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0 | 1 | 1_8_6 | How does the second law of thermodynamics apply to spontaneity? | how | [] | [
"The second law of thermodynamics states that spontaneous processes, those requiring no outside input of energy, increase the entropy (disorder) of the universe."
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2 | 3 | 1_10_1_3 | How does carbon dioxide get into a plant? | how | [] | [
"The Calvin cycle is named for Melvin Calvin, who, along with his colleagues, began to elucidate its steps in the late 1940s. The cycle begins by incorporating CO2 from the air into organic molecules already present in the chloroplast. This initial incorporation of carbon into organic compounds is known as carbon fixation."
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4 | 5 | 1_10_3 | How does carbon dioxide get into a plant? | how | [] | [
"Phase 1: Carbon fixation. The Calvin cycle incorporates each CO2 molecule, one at a time, by attaching it to a five-carbon sugar named ribulose bisphosphate (abbreviated RuBP). The enzyme that catalyzes this first step is RuBP carboxylase, or rubisco. (This is the most abundant protein in chloroplasts and is also thought to be the most abundant protein on Earth. ) The product of the reaction is a six-carbon intermediate so unstable that it immediately splits in half, forming two molecules of 3-phosphoglycerate (for each CO2 fixed)."
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6 | 7 | 1_10_1_1 | How does carbon dioxide get into a plant? | how | [] | [
"Carbon dioxide enters the leaf, and oxygen exits, by way of microscopic pores called stomata (singular, stoma; from the Greek, meaning \"mouth\")."
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8 | 9 | 1_10_4 | How does carbon dioxide get into a plant? | how | [] | [
"The CO2 required for photosynthesis enters a leaf via stomata, the pores on the leaf surface (see Figure 10.4)."
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10 | 11 | 1_35_3_2_2 | How does carbon dioxide get into a plant? | how | [] | [
"Mesophyll consists mainly of parenchyma cells specialized for photosynthesis. The mesophylls of many eudicots have two distinct layers: palisade mesophyll and spongy mesophyll. Palisade mesophyll consists of one or more layers of elongated parenchyma cells on the upper part of the leaf. Spongy mesophyll is below the palisade mesophyll. These parenchyma cells are more loosely arranged, with a labyrinth of air spaces through which CO2 and oxygen circulate around the cells and up to the palisade region. The air spaces are particularly large in the vicinity of stomata, where CO2 is taken up from the outside air and O2 is discharged."
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12 | 13 | 1_36_4 | How does carbon dioxide get into a plant? | how | [] | [
"The large surface area enhances light absorption for photosynthesis. The high surface-to-volume ratio aids in CO2 absorption during photosynthesis as well as in the release of O2, a by-product of photosynthesis. Upon diffusing through the stomata, CO2 enters a honeycomb of air spaces formed by the spongy mesophyll cells (see Figure 35.18). Because of the irregular shapes of these cells, the leaf's internal surface area may be 10 to 30 times greater than the external surface area."
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14 | 15 | 1_11_3_2 | How does a phosphorylation cascade affect a signal? | how | [] | [
"Figure 11.10 A phosphorylation cascade. In a phosphorylation cascade, a series of different molecules in a pathway are phosphorylated in turn, each molecule adding a phosphate group to the next one in line. In this example, phosphorylation activates each molecule, and dephosphorylation returns it to its inactive form. The active and inactive forms of each protein are represented by different shapes to remind you that activation is usually associated with a change in molecular shape. Many of the relay molecules in signal transduction pathways are protein kinases, and they often act on other protein kinases in the pathway. Figure 11.10 depicts a hypothetical pathway containing three different protein kinases that create a \"phosphorylation cascade. \" The sequence shown is similar to many known pathways, including those triggered in yeast by mating factors and in animal cells by many growth factors. The signal is transmitted by a cascade of protein phosphorylations, each bringing with it a \nshape change."
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16 | 17 | 1_11_3_2 | How does a phosphorylation cascade affect a signal? | how | [] | [
"Equally important in the phosphorylation cascade are the protein phosphatases, enzymes that can rapidly remove phosphate groups from proteins, a process called dephosphorylation. By dephosphorylating and thus inactivating protein kinases, phosphatases provide the mechanism for turning off the signal transduction pathway when the initial signal is no longer present. Phosphatases also make the protein kinases available for reuse, enabling the cell to respond again to an extracellular signal. The phosphorylation-dephosphorylation system acts as a molecular switch in the cell, turning activities on or off, or up or down, as required."
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18 | 19 | 1_11_6 | How does a phosphorylation cascade affect a signal? | how | [] | [
"11.3 Transduction: Cascades of molecular interactions relay signals from receptors to target molecules in the cell (pp. 214-219) At each step in a signal transduction pathway, the signal is transduced into a different form, which commonly involves a shape change in a protein. Many signal transduction pathways include phosphorylation cascades, in which a series of protein kinases each add a phosphate group to the next one in line, activating it. Enzymes called protein phosphatases remove the phosphate groups. The balance between phosphorylation and dephosphorylation regulates the activity of proteins involved in the sequential steps of a signal transduction pathway."
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20 | 21 | 1_17_4_2_3 | How does a release factor differ from tRNA? | how | [] | [
"A release factor, a protein shaped like an aminoacyl tRNA, binds directly to the stop codon in the A site. The release factor causes the addition of a water molecule instead of an amino acid to the polypeptide chain. (There are plenty of water molecules available in the aqueous cellular environment. ) This reaction breaks (hydrolyzes) the bond between the completed polypeptide and the tRNA in the P site, releasing the polypeptide through the exit tunnel of the ribosome's large subunit."
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22 | 23 | 1_5_5_4 | How does a release factor differ from tRNA? | how | [] | [
"Consider, for example, the type of RNA called transfer RNA (tRNA), which brings amino acids to the ribosome during the synthesis of a polypeptide. A tRNA molecule is about 80 nucleotides in length. Its functional shape results from base pairing between nucleotides where complementary stretches of the molecule run antiparallel to each other (Figure 5.27b)."
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24 | 25 | 1_17_4_1 | How does a release factor differ from tRNA? | how | [] | [
"As a molecule of mRNA is moved through a ribosome, codons are translated into amino acids, one by one. The interpreters are tRNA molecules, each type with a specific anticodon at one end and a corresponding amino acid at the other end. A tRNA adds its amino acid cargo to a growing polypeptide chain when the anticodon hydrogen-bonds to a complementary codon on the mRNA. The figures that follow show some of the details of translation in a bacterial cell. In the process of translation, a cell \"reads\" a genetic message and builds a polypeptide accordingly. The message is a series of codons along an mRNA molecule, and the translator is called transfer RNA (tRNA). The function of tRNA is to transfer amino acids from the cytoplasmic pool of amino acids to a growing polypeptide in a ribosome. A cell keeps its cytoplasm stocked with all 20 amino acids, either by synthesizing them from other compounds or by taking them up from the surrounding solution. The ribosome, a structure made of proteins \nand RNAs, adds each amino acid brought to it by tRNA to the growing end of a polypeptide chain (Figure 17.14)."
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26 | 27 | 1_17_4_1_1 | How does a release factor differ from tRNA? | how | [] | [
"A tRNA molecule consists of a single RNA strand that is only about 80 nucleotides long (compared to hundreds of nucleotides for most mRNA molecules). Because of the presence of complementary stretches of nucleotide bases that can hydrogen-bond to each other, this single strand can fold back upon itself and form a molecule with a three-dimensional structure. Flattened into one plane to clarify this base pairing, a tRNA molecule looks like a cloverleaf (Figure 17.15a). The tRNA actually twists and folds into a compact three-dimensional structure that is roughly L-shaped (Figure 17.15b). The loop extending from one end of the L includes the anticodon, the particular nucleotide triplet that base-pairs to a specific mRNA codon. From the other end of the L-shaped tRNA molecule protrudes its 3' end, which is the attachment site for an amino acid. Thus, the structure of a tRNA molecule fits its function. Figure 17.16 An aminoacyl-tRNA synthetase joining a specific amino acid to a tRNA."
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28 | 29 | 1_17_4_2_3 | How does release factor release a polypeptide from the ribosome? | how | [] | [
"A release factor, a protein shaped like an aminoacyl tRNA, binds directly to the stop codon in the A site. The release factor causes the addition of a water molecule instead of an amino acid to the polypeptide chain. (There are plenty of water molecules available in the aqueous cellular environment. ) This reaction breaks (hydrolyzes) the bond between the completed polypeptide and the tRNA in the P site, releasing the polypeptide through the exit tunnel of the ribosome's large subunit."
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30 | 31 | 1_27_2_2 | How does recombination occur in bacteria? | how | [] | [
"Although new mutations are a major source of variation in prokaryotic populations, additional diversity arises from genetic recombination, the combining of DNA from two sources. In eukaryotes, the sexual processes of meiosis and fertilization combine DNA from two individuals in a single zygote. But meiosis and fertilization do not occur in prokaryotes. Instead, three other mechanisms: transformation, transduction, and conjugation: can bring together prokaryotic DNA from different individuals (that is, cells). When the individuals are members of different species, this movement of genes from one organism to another is called horizontal gene transfer. Although scientists have found evidence that each of these mechanisms can transfer DNA within and between species in both domain Bacteria and domain Archaea, to date most of our knowledge comes from research on bacteria."
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32 | 33 | 1_27_2_2_1 | How does recombination occur in bacteria? | how | [] | [
"In transformation, the genotype and possibly phenotype of a prokaryotic cell are altered by the uptake of foreign DNA from its surroundings. For example, a harmless strain of Streptococcus pneumoniae can be transformed into pneumonia-causing cells if the cells are placed in a medium containing DNA from a pathogenic strain (see p. 306). This transformation occurs when a nonpathogenic cell takes up a piece of DNA carrying the allele for pathogenicity and replaces its own allele with the foreign allele, an exchange of homologous DNA segments. The cell is now a recombinant: Its chromosome contains DNA derived from two different cells. For many years after transformation was discovered in laboratory cultures, most biologists thought the process to be too rare and haphazard to play an important role in natural bacterial populations. But researchers have since learned that many bacteria have cell-surface proteins that recognize DNA from closely related species and transport it into the cell. \nOnce inside the cell, the foreign DNA can be incorporated into the genome by homologous DNA exchange. Figure 27.11 Transduction. Phages may carry pieces of a bacterial chromosome from one cell (the donor) to another (the recipient). If recombination occurs after the transfer, genes from the donor may be incorporated into the recipient's genome. In transduction, phages (from \"bacteriophages,\" the viruses that infect bacteria) carry prokaryotic genes from one host cell to another. In most cases, transduction results from accidents that occur during the phage replicative cycle (Figure 27.11). A virus that carries prokaryotic DNA may not be able to replicate because it lacks some or all of its own genetic material. However, the virus can attach to another prokaryotic cell (a recipient) and inject prokaryotic DNA acquired from the first cell (the donor). If some of this DNA is then incorporated into the recipient cell's chromosome by DNA recombination, a recombinant cell is formed."
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34 | 35 | 1_27_2_2_2 | How does recombination occur in bacteria? | how | [] | [
"Figure 27.12 Bacterial. The E. coli donor cell (left) extends a pilus that attaches to a recipient cell, a key first step in the transfer of DNA. The pilus is a flexible tube of protein subunits (TEM). In a process called conjugation, DNA is transferred between two prokaryotic cells (usually of the same species) that are temporarily joined. In bacteria, the DNA transfer is always one-way: One cell donates the DNA, and the other receives it. The best-understood mechanism is that used by E. coli, and we will focus on this organism for the rest of this section. In E. coli, a pilus of the donor cell attaches to the recipient (Figure 27.12). The pilus then retracts, pulling the two cells together, much like a grappling hook. The next step is thought to be the formation of a temporary \"mating bridge\" between the two cells, through which the donor may transfer DNA to the recipient. This is an unsettled issue, however, and recent evidence indicates that DNA may pass directly through the pilus, \nwhich is hollow. In either case, the ability to form pili and donate DNA during conjugation results from the presence of a particular piece of DNA called the F factor (F for fertility). The F factor of E. coli consists of about 25 genes, most required for the production of pili. The F factor can exist either as a plasmid or as a segment of DNA within the bacterial chromosome. The F Factor as a Plasmid Figure 27.13 Conjugation and recombination in E. coli. The DNA replication that accompanies transfer of an F plasmid or part of an Hfr bacterial chromosome is called rolling circle replication. In effect, the intact circular parental DNA strand \"rolls\" as its other strand peels off and a new complementary strand is synthesized. The F factor in its plasmid form is called the F plasmid. Cells containing the F plasmid, designated F+ cells, function as DNA donors during conjugation. Cells lacking the F factor, designated F-', function as DNA recipients during conjugation. The F+ condition is transferable in the \nsense that an F+ cell converts an F-' cell to F+ if a copy of the entire F+ plasmid is transferred (Figure 27.13a). The F Factor in the Chromosome Chromosomal genes can be transferred during conjugation when the donor cell's F factor is integrated into the chromosome. A cell with the F factor built into its chromosome is called an Hfr cell (for high frequency of recombination). Like an F+ cell, an Hfr cell functions as a donor during conjugation with an F-' cell (Figure 27.13b). When chromosomal DNA from an Hfr cell enters an F-' cell, homologous regions of the Hfr and F-' chromosomes may align, allowing segments of their DNA to be exchanged. This results in the production of a recombinant bacterium that has genes derived from two different cells: a new genetic variant on which evolution can act."
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36 | 37 | 1_43_2 | How is a lymphocyte activated? | how | [] | [
"Vertebrates are unique in having adaptive immunity in addition to innate immunity. The adaptive response relies on T cells and B cells, which are types of white blood cells called lymphocytes. Like all blood cells, lymphocytes originate from stem cells in the bone marrow. Some lymphocytes migrate from the bone marrow to the thymus, an organ in the thoracic cavity above the heart (see Figure 43.7). These lymphocytes mature into T cells. Lymphocytes that remain and mature in the bone marrow develop as B cells. (Lymphocytes of a third type remain in the blood and become the natural killer cells active in innate immunity. ) Any substance that elicits a response from a B cell or T cell is called an antigen. In adaptive immunity, recognition occurs when a B cell or T cell binds to an antigen, such as a bacterial or viral protein, via a protein called an antigen receptor. An antigen receptor is specific enough to bind to just one part of one molecule from a particular pathogen, such as a \nspecies of bacteria or strain of virus. Although the cells of the immune system produce millions of different antigen receptors, all of the antigen receptors made by a single B or T cell are identical. Infection by a virus, bacterium, or other pathogen triggers activation of B and T cells with antigen receptors specific for parts of that pathogen. B and T cells are shown here with only a few antigen receptors, but there are actually about 100,000 antigen receptors on the surface of a single B or T cell. Antigens are usually foreign and are typically large molecules, either proteins or polysaccharides. Many antigens protrude from the surface of foreign cells or viruses. Other antigens, such as toxins secreted by bacteria, are released into the extracellular fluid. The small, accessible portion of an antigen that binds to an antigen receptor is called an epitope, or antigenic determinant. An example is a group of amino acids in a particular protein. A single antigen usually has several different epitopes, each \nbinding a receptor with a different specificity. Because all antigen receptors produced by a single B cell or T cell are identical, they bind to the same epitope. Each B cell or T cell thus displays specificity for a particular epitope, enabling it to respond to any pathogen that produces molecules containing that same epitope. The antigen receptors of B cells and T cells have similar components, but they encounter antigens in different ways."
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38 | 39 | 1_43_2_3 | How is a lymphocyte activated? | how | [] | [
"Receptor diversity and self-tolerance arise as a lymphocyte matures. Proliferation of cells and the formation of immunological memory occur later, after a mature lymphocyte encounters and binds to a specific antigen."
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40 | 41 | 1_43_2_3_3 | How is a lymphocyte activated? | how | [] | [
"To begin with, an antigen is presented to a steady stream of lymphocytes in the lymph nodes (see Figure 43.7) until a match is made. A successful match then triggers changes in cell number and activity for the lymphocyte to which an antigen has bound. The binding of an antigen receptor to an epitope initiates events that activate the lymphocyte. Once activated, a B cell or T cell undergoes multiple cell divisions. For each activated cell, the result of this proliferation is a clone, a population of cells that are identical to the original cell. Some cells from this clone become effector cells, short-lived cells that take effect immediately against the antigen and any pathogens producing that antigen. The effector forms of B cells are plasma cells, which secrete antibodies. The effector forms of T cells are helper T cells and cytotoxic T cells, whose roles we'll explore in Concept 43.3. The remaining cells in the clone become memory cells, long-lived cells that can give rise to effector \ncells if the same antigen is encountered later in the animal's life. Figure 43.14 Clonal selection. This figure illustrates clonal selection, using B cells as an example. In response to a specific antigen and to immune cell signals (not shown), one B cell divides and forms a clone of cells. The remaining B cells, which have antigen receptors specific for other antigens, do not respond. The clone of cells formed by the selected B cell gives rise to memory B cells and antibody-secreting plasma cells. T cells also undergo clonal selection, generating memory T cells and effector T cells (cytotoxic T cells and helper T cells). Figure 43.14 summarizes the proliferation of a lymphocyte into a clone of cells in response to binding to an antigen, using B cells as an example. This process is called clonal selection because an encounter with an antigen selects which lymphocyte will divide to produce a clonal population of thousands of cells specific for a particular epitope."
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42 | 43 | 1_43_5 | How is a lymphocyte activated? | how | [] | [
"43.2 In adaptive immunity, receptors provide pathogen-specific recognition (pp. 935-940) Adaptive immunity relies on lymphocytes that arise from stem cells in the bone marrow and complete their maturation in the bone marrow (B cells) or in the thymus (T cells). Lymphocytes have cell-surface antigen receptors for foreign molecules. All receptor proteins on a single B or T cell are the same, but there are millions of B and T cells in the body that differ in the foreign molecules that their receptors recognize. Upon infection, B and T cells specific for the pathogen are activated. Some T cells help other lymphocytes; others kill infected host cells. B cells called plasma cells produce soluble receptor proteins called antibodies, which bind to foreign molecules and cells. The activated lymphocytes called memory cells defend against future infections by the same pathogen. Recognition of foreign molecules involves the binding of variable regions of receptors to an epitope, a small region of \nan antigen. B cells and antibodies recognize epitopes on the surface of antigens circulating in the blood or lymph. T cells recognize protein epitopes in small antigen fragments (peptides) that are presented on the surface of host cells, complexed with cell-surface proteins called MHC (major histocompatibility complex) molecules. The four major characteristics of B and T cell development are the generation of cell diversity, self-tolerance, proliferation, and immunological memory."
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44 | 45 | 1_43_5 | How is a lymphocyte activated? | how | [] | [
"43.3 Adaptive immunity defends against infection of body fluids and body cells (pp. 940-946) Helper T cells interact with antigen fragments displayed by class II MHC molecules on the surface of dendritic cells, macrophages, and B cells (antigen-presenting cells). Activated helper T cells secrete cytokines that stimulate other lymphocytes as part of the response to nearly all antigens. Cytotoxic T cells bind to a complex of an antigen fragment and a class I MHC molecule on infected host cells. In the cell-mediated immune response, activated cytotoxic T cells secrete proteins that initiate destruction of infected cells. All T cells have an accessory protein that enhances binding to MHC-antigen fragment complexes. In the humoral immune response, B cell antigen receptors and antibodies bind to extracellular foreign substances in blood and lymph. The binding of antibodies helps eliminate antigens by phagocytosis and complement-mediated lysis. The five major antibody classes differ in \ndistribution and function. Active immunity develops in response to infection or to immunization with a nonpathogenic form or part of a pathogen. Active immunity includes a response to and immunological memory for that pathogen."
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46 | 47 | 1_8_2_3_2 | How do cells avoid coming to equilibrium? | how | [] | [
"Like most systems, a living cell is not in equilibrium. The constant flow of materials in and out of the cell keeps the metabolic pathways from ever reaching equilibrium, and the cell continues to do work throughout its life. This principle is illustrated by the open (and more realistic) hydroelectric system in Figure 8.7b. However, unlike this simple single-step system, a catabolic pathway in a cell releases free energy in a series of reactions. An example is cellular respiration, illustrated by analogy in Figure 8.7c. Some of the reversible reactions of respiration are constantly \"pulled\" in one direction: that is, they are kept out of equilibrium. The key to maintaining this lack of equilibrium is that the product of a reaction does not accumulate but instead becomes a reactant in the next step; finally, waste products are expelled from the cell. The overall sequence of reactions is kept going by the huge free-energy difference between glucose and oxygen at the top of the energy \"\nhill\" and carbon dioxide and water at the \"downhill\" end. As long as our cells have a steady supply of glucose or other fuels and oxygen and are able to expel waste products to the surroundings, their metabolic pathways never reach equilibrium and can continue to do the work of life."
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48 | 49 | 1_17_1_2 | How does an mRNA strand compare to its coding strand? | how | [] | [
"Transcription is the synthesis of RNA using information in the DNA. The two nucleic acids are written in different forms of the same language, and the information is simply transcribed, or \"rewritten,\" from DNA to RNA. Just as a DNA strand provides a template for making a new complementary strand during DNA replication, it also can serve as a template for assembling a complementary sequence of RNA nucleotides. For a protein-coding gene, the resulting RNA molecule is a faithful transcript of the gene's protein-building instructions. This type of RNA molecule is called messenger RNA (mRNA) because it carries a genetic message from the DNA to the protein-synthesizing machinery of the cell."
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50 | 51 | 1_17_1_3_1 | How does an mRNA strand compare to its coding strand? | how | [] | [
"The series of words in a gene is transcribed into a complementary series of nonoverlapping, three-nucleotide words in mRNA, which is then translated into a chain of amino acids (Figure 17.4). During transcription, the gene determines the sequence of nucleotide bases along the length of the RNA molecule that is being synthesized. For each gene, only one of the two DNA strands is transcribed. This strand is called the template strand because it provides the pattern, or template, for the sequence of nucleotides in an RNA transcript. For any given gene, the same strand is used as the template every time the gene is transcribed. For other genes on the same DNA molecule, however, the opposite strand may be the one that always functions as the template. An mRNA molecule is complementary rather than identical to its DNA template because RNA nucleotides are assembled on the template according to base-pairing rules (see Figure 17.4). The pairs are similar to those that form during DNA \nreplication, except that U, the RNA substitute for T, pairs with A and the mRNA nucleotides contain ribose instead of deoxyribose."
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52 | 53 | 1_17_1_3_1 | How does an mRNA strand compare to its coding strand? | how | [] | [
"In the example in Figure 17.4, the nucleotide triplet ACC along the DNA (written as 3'-ACC-5') provides a template for 5'-UGG-3' in the mRNA molecule. The mRNA nucleotide triplets are called codons, and they are customarily written in the 5' → 3' direction. In our example, UGG is the codon for the amino acid tryptophan (abbreviated Trp). The term codon is also used for the DNA nucleotide triplets along the nontemplate strand. These codons are complementary to the template strand and thus identical in sequence to the mRNA, except that they have T instead of U. (For this reason, the nontemplate DNA strand is sometimes called the \"coding strand. \")"
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54 | 55 | 1_25_1_4 | How does the structure of a ribosome's active site support the RNA world hypothesis? | how | [] | [
"In a particular environment, RNA molecules with certain base sequences are more stable and replicate faster and with fewer errors than other sequences. The RNA molecule whose sequence is best suited to the surrounding environment and has the greatest ability to replicate itself will leave the most descendant molecules. Occasionally, a copying error will result in a molecule that folds into a shape that is even more stable or more adept at self-replication than the ancestral sequence. Similar selection events may have occurred on early Earth. Thus, the molecular biology of today may have been preceded by an \"RNA world,\" in which small RNA molecules that carried genetic information were able to replicate and to store information about the vesicles that carried them."
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56 | 57 | 1_8_2_2 | How are free energy and a system's likelihood to change related? | how | [] | [
"Unstable systems (top) are rich in free energy, G. They have a tendency to change spontaneously to a more stable state (bottom), and it is possible to harness this \"downhill\" change to perform work. We can think of free energy as a measure of a system's instability: its tendency to change to a more stable state. Unstable systems (higher G) tend to change in such a way that they become more stable (lower G)."
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58 | 59 | 1_12_3_3 | How do malignant tumor cells spread? | how | [] | [
"Figure 12.20 The growth and metastasis of a malignant breast tumor. The cells of malignant (cancerous) tumors grow in an uncontrolled way and can spread to neighboring tissues and, via lymph and blood vessels, to other parts of the body. The spread of cancer cells beyond their original site is called metastasis. The abnormal behavior of cancer cells can be catastrophic when it occurs in the body. The problem begins when a single cell in a tissue undergoes transformation, the process that converts a normal cell to a cancer cell. The body's immune system normally recognizes a transformed cell as an insurgent and destroys it. However, if the cell evades destruction, it may proliferate and form a tumor, a mass of abnormal cells within otherwise normal tissue. The abnormal cells may remain at the original site if they have too few genetic and cellular changes to survive at another site. In that case, the tumor is called a benign tumor. Most benign tumors do not cause serious problems and \ncan be completely removed by surgery. In contrast, a malignant tumor includes cells whose genetic and cellular changes enable them to spread to new tissues and impair the functions of one or more organs. An individual with a malignant tumor is said to have cancer; Figure 12.20 shows the development of breast cancer. The changes that have occurred in cells of malignant tumors show up in many ways besides excessive proliferation. These cells may have unusual numbers of chromosomes, though whether this is a cause or an effect of transformation is a current topic of debate. Their metabolism may be disabled, and they may cease to function in any constructive way. Abnormal changes on the cell surface cause cancer cells to lose attachments to neighboring cells and the extracellular matrix, allowing them to spread into nearby tissues. Cancer cells may also secrete signaling molecules that cause blood vessels to grow toward the tumor. A few tumor cells may separate from the original tumor, enter blood vessels and \nlymph vessels, and travel to other parts of the body. There, they may proliferate and form a new tumor. This spread of cancer cells to locations distant from their original site is called metastasis (see Figure 12.20)."
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60 | 61 | 1_12_4 | How do malignant tumor cells spread? | how | [] | [
"Cancer cells elude normal cell cycle regulation and divide out of control, forming tumors. Malignant tumors invade surrounding tissues and can undergo metastasis, exporting cancer cells to other parts of the body, where they may form secondary tumors."
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62 | 63 | 1_18_5_3 | How do malignant tumor cells spread? | how | [] | [
"The model of a multistep path to cancer is well supported by studies of one of the best-understood types of human cancer, colorectal cancer. About 135,000 new cases of colorectal cancer are diagnosed each year in the United States, and the disease causes 60,000 deaths each year. Like most cancers, colorectal cancer develops gradually (Figure 18.25). The first sign is often a polyp, a small, benign growth in the colon lining. The cells of the polyp look normal, although they divide unusually frequently. The tumor grows and may eventually become malignant, invading other tissues. The development of a malignant tumor is paralleled by a gradual accumulation of mutations that convert proto-oncogenes to oncogenes and knock out tumor-suppressor genes. A ras oncogene and a mutated p53 tumor-suppressor gene are often involved. About half a dozen changes must occur at the DNA level for a cell to become fully cancerous. These changes usually include the appearance of at least one active oncogene \nand the mutation or loss of several tumor-suppressor genes. Furthermore, since mutant tumor-suppressor alleles are usually recessive, in most cases mutations must knock out both alleles in a cell's genome to block tumor suppression. (Most oncogenes, on the other hand, behave as dominant alleles. ) The order in which these changes must occur is still under investigation, as is the relative importance of different mutations."
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64 | 65 | 1_14_1_1 | Since DNA had not yet been discovered, how was Mendel able to determine how traits are passed from parents to offspring? | how | [] | [
"Around 1857, Mendel began breeding garden peas in the abbey garden to study inheritance. Although the question of heredity had long been a focus of curiosity at the monastery, Mendel's fresh approach allowed him to deduce principles that had remained elusive to others. One reason Mendel probably chose to work with peas is that they are available in many varieties. For example, one variety has purple flowers, while another variety has white flowers. A heritable feature that varies among individuals, such as flower color, is called a character. Each variant for a character, such as purple or white color for flowers, is called a trait. Other advantages of using peas are their short generation time and the large number of offspring from each mating. Furthermore, Mendel could strictly control mating between plants."
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66 | 67 | 1_14_1_1 | Since DNA had not yet been discovered, how was Mendel able to determine how traits are passed from parents to offspring? | how | [] | [
"In nature, pea plants usually self-fertilize: Pollen grains from the stamens land on the carpel of the same flower, and sperm released from the pollen grains fertilize eggs present in the carpel. To achieve cross-pollination (fertilization between different plants), Mendel removed the immature stamens of a plant before they produced pollen and then dusted pollen from another plant onto the altered flowers (Figure 14.2). Each resulting zygote then developed into a plant embryo encased in a seed (pea). Mendel could thus always be sure of the parentage of new seeds."
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68 | 69 | 1_14_1_1 | Since DNA had not yet been discovered, how was Mendel able to determine how traits are passed from parents to offspring? | how | [] | [
"Mendel chose to track only those characters that occurred in two distinct, alternative forms. For example, his plants had either purple flowers or white flowers; there were no colors intermediate between these two varieties. Had Mendel focused instead on characters that varied in a continuum among individuals: seed weight, for example: he would not have discovered the particulate nature of inheritance. (You'll learn why later. ) Mendel also made sure that he started his experiments with varieties that, over many generations of self-pollination, had produced only the same variety as the parent plant."
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70 | 71 | 1_14_1_1 | Since DNA had not yet been discovered, how was Mendel able to determine how traits are passed from parents to offspring? | how | [] | [
"In a typical breeding experiment, Mendel cross-pollinated two contrasting, true-breeding pea varieties: for example, purple-flowered plants and white-flowered plants (see Figure 14.2). This mating, or crossing, of two true-breeding varieties is called hybridization. The true-breeding parents are referred to as the P generation (parental generation), and their hybrid offspring are the F1 generation (first filial generation, the word filial from the Latin word for \"son\"). Allowing these F1 hybrids to self-pollinate (or to cross-pollinate with other F1 hybrids) produces an F2 generation (second filial generation). Mendel usually followed traits for at least the P, F1, and F2 generations. Had Mendel stopped his experiments with the F1 generation, the basic patterns of inheritance would have escaped him. Mendel's quantitative analysis of the F2 plants from thousands of genetic crosses like these allowed him to deduce two fundamental principles of heredity, which have come to be called the \nlaw of segregation and the law of independent assortment."
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72 | 73 | 1_14_1_2 | Since DNA had not yet been discovered, how was Mendel able to determine how traits are passed from parents to offspring? | how | [] | [
"If the blending model of inheritance were correct, the F1 hybrids from a cross between purple-flowered and white-flowered pea plants would have pale purple flowers, a trait intermediate between those of the P generation. Notice in Figure 14.2 that the experiment produced a very different result: All the F1 offspring had flowers just as purple as the purple-flowered parents. What happened to the white-flowered plants' genetic contribution to the hybrids? If it were lost, then the F1 plants could produce only purple-flowered offspring in the F2 generation. But when Mendel allowed the F1 plants to self-pollinate and planted their seeds, the white-flower trait reappeared in the F2 generation. Mendel used very large sample sizes and kept accurate records of his results: 705 of the F2 plants had purple flowers, and 224 had white flowers. These data fit a ratio of approximately three purple to one white (Figure 14.3). Mendel reasoned that the heritable factor for white flowers did not \ndisappear in the F1 plants, but was somehow hidden, or masked, when the purple-flower factor was present. In Mendel's terminology, purple flower color is a dominant trait, and white flower color is a recessive trait. The reappearance of white-flowered plants in the F2 generation was evidence that the heritable factor causing white flowers had not been diluted or destroyed by coexisting with the purple-flower factor in the F1 hybrids."
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74 | 75 | 1_14_1_3 | Since DNA had not yet been discovered, how was Mendel able to determine how traits are passed from parents to offspring? | how | [] | [
"Mendel derived the law of segregation from experiments in which he followed only a single character, such as flower color. All the F1 progeny produced in his crosses of true-breeding parents were monohybrids, meaning that they were heterozygous for the one particular character being followed in the cross. We refer to a cross between such heterozygotes as a monohybrid cross. Mendel identified his second law of inheritance by following two characters at the same time, such as seed color and seed shape. Seeds (peas) may be either yellow or green. They also may be either round (smooth) or wrinkled. From single-character crosses, Mendel knew that the allele for yellow seeds is dominant (Y), and the allele for green seeds is recessive (y)."
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76 | 77 | 1_14_3 | Since DNA had not yet been discovered, how was Mendel able to determine how traits are passed from parents to offspring? | how | [] | [
"For the work that led to his two laws of inheritance, Mendel chose pea plant characters that turn out to have a relatively simple genetic basis: Each character is determined by one gene, for which there are only two alleles, one completely dominant and the other completely recessive."
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78 | 79 | 1_8_2_2 | How does equilibrium describe a state of maximum stability? | how | [] | [
"Another term that describes a state of maximum stability is equilibrium, which you learned about in Chapter 2 in connection with chemical reactions. There is an important relationship between free energy and equilibrium, including chemical equilibrium. Recall that most chemical reactions are reversible and proceed to a point at which the forward and backward reactions occur at the same rate. The reaction is then said to be at chemical equilibrium, and there is no further net change in the relative concentration of products and reactants. As a reaction proceeds toward equilibrium, the free energy of the mixture of reactants and products decreases. Free energy increases when a reaction is somehow pushed away from equilibrium, perhaps by removing some of the products (and thus changing their concentration relative to that of the reactants). For a system at equilibrium, G is at its lowest possible value in that system."
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80 | 81 | 1_22_2_1_2 | How does natural selection act on a sexually-reproducing population? | how | [] | [
"Darwin realized that explaining such adaptations was essential to understanding evolution. As we'll explore further, his explanation of how adaptations arise centered on natural selection, a process in which individuals that have certain inherited traits tend to survive and reproduce at higher rates than other individuals because of those traits. By the early 1840s, Darwin had worked out the major features of his hypothesis. He set these ideas on paper in 1844, when he wrote a long essay on descent with modification and its underlying mechanism, natural selection."
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82 | 83 | 1_22_2_2_2 | How does natural selection act on a sexually-reproducing population? | how | [] | [
"An organism's heritable traits can influence not only its own performance, but also how well its offspring cope with environmental challenges. For example, an organism might have a trait that gives its offspring an advantage in escaping predators, obtaining food, or tolerating physical conditions. When such advantages increase the number of offspring that survive and reproduce, the traits that are favored will likely appear at a greater frequency in the next generation. Thus, over time, natural selection resulting from factors such as predators, lack of food, or adverse physical conditions can lead to an increase in the proportion of favorable traits in a population. How rapidly do such changes occur? Darwin reasoned that if artificial selection can bring about dramatic change in a relatively short period of time, then natural selection should be capable of substantial modification of species over many hundreds of generations. Even if the advantages of some heritable traits over others \nare slight, the advantageous variations will gradually accumulate in the population, and less favorable variations will diminish. Over time, this process will increase the frequency of individuals with favorable adaptations and hence refine the match between organisms and their environment (see Figure 1.20)."
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84 | 85 | 1_22_2_2_3 | How does natural selection act on a sexually-reproducing population? | how | [] | [
"Let's now recap the main ideas of natural selection: Natural selection is a process in which individuals that have certain heritable traits survive and reproduce at a higher rate than other individuals because of those traits."
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86 | 87 | 1_22_2_2_3 | How does natural selection act on a sexually-reproducing population? | how | [] | [
"Over time, natural selection can increase the match between organisms and their environment (Figure 22.12). If an environment changes, or if individuals move to a new environment, natural selection may result in adaptation to these new conditions, sometimes giving rise to new species. One subtle but important point is that although natural selection occurs through interactions between individual organisms and their environment, individuals do not evolve. Rather, it is the population that evolves over time. A second key point is that natural selection can amplify or diminish only those heritable traits that differ among the individuals in a population. Thus, even if a trait is heritable, if all the individuals in a population are genetically identical for that trait, evolution by natural selection cannot occur. Third, remember that environmental factors vary from place to place and over time. A trait that is favorable in one place or time may be useless: or even detrimental: in other \nplaces or times. Natural selection is always operating, but which traits are favored depends on the context in which a species lives and mates."
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88 | 89 | 1_22_4 | How does natural selection act on a sexually-reproducing population? | how | [] | [
"22.1 The Darwinian revolution challenged traditional views of a young Earth inhabited by unchanging species (pp. 453-455) Darwin proposed that life's diversity arose from ancestral species through natural selection, a departure from prevailing views. In contrast to catastrophism (the principle that events in the past occurred suddenly by mechanisms not operating today), Hutton and Lyell thought that geologic change results from mechanisms that operated in the past in the same manner as at the present time (uniformitarianism). Lamarck hypothesized that species evolve, but the underlying mechanisms he proposed are not supported by evidence. ?Why was the age of Earth important for Darwin's ideas about evolution? 22.2 Descent with modification by natural selection explains the adaptations of organisms and the unity and diversity of life (pp. 455-460) Darwin's experiences during the voyage of the Beagle gave rise to his idea that new species originate from ancestral forms through the \naccumulation of adaptations. He refined his theory for many years and finally published it in 1859 after learning that Wallace had come to the same idea. In The Origin of Species, Darwin proposed that evolution occurs by natural selection. ?Describe how overreproduction and heritable variation relate to evolution by natural selection. 22.3 Evolution is supported by an overwhelming amount of scientific evidence (pp. 460-467) Researchers have directly observed natural selection leading to adaptive evolution in many studies, including research on soapberry bug populations and on MRSA. Organisms share characteristics because of common descent (homology) or because natural selection affects independently evolving species in similar environments in similar ways (convergent evolution)."
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90 | 91 | 1_23 | How does natural selection act on a sexually-reproducing population? | how | [] | [
"23.4 Natural selection is the only mechanism that consistently causes adaptive evolution"
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92 | 93 | 1_23_0_0 | How does natural selection act on a sexually-reproducing population? | how | [] | [
"One common misconception about evolution is that individual organisms evolve. It is true that natural selection acts on individuals: Each organism's traits affect its survival and reproductive success compared with other individuals. But the evolutionary impact of natural selection is only apparent in the changes in a population of organisms over time."
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94 | 95 | 1_23_3 | How does natural selection act on a sexually-reproducing population? | how | [] | [
"The three mechanisms that alter allele frequencies directly and cause most evolutionary change are natural selection, genetic drift, and gene flow (violations of conditions 3-5)."
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96 | 97 | 1_23_3_1 | How does natural selection act on a sexually-reproducing population? | how | [] | [
"As you read in Chapter 22, Darwin's concept of natural selection is based on differential success in survival and reproduction: Individuals in a population exhibit variations in their heritable traits, and those with traits that are better suited to their environment tend to produce more offspring than those with traits that are not as well suited. In genetic terms, we now know that selection results in alleles being passed to the next generation in proportions that differ from those in the present generation."
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98 | 99 | 1_23_4 | How does natural selection act on a sexually-reproducing population? | how | [] | [
"Evolution by natural selection is a blend of chance and \"sorting\": chance in the creation of new genetic variations (as in mutation) and sorting as natural selection favors some alleles over others. Because of this favoring process, the outcome of natural selection is not random. Instead, natural selection consistently increases the frequencies of alleles that provide reproductive advantage and thus leads to adaptive evolution."
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100 | 101 | 1_23_4_1_2 | How does natural selection act on a sexually-reproducing population? | how | [] | [
"Natural selection can alter the frequency distribution of heritable traits in three ways, depending on which phenotypes in a population are favored. These three modes of selection are called directional selection, disruptive selection, and stabilizing selection. Figure 23.13 Modes of selection. These cases describe three ways in which a hypothetical deer mouse population with heritable variation in fur coloration from light to dark might evolve. The graphs show how the frequencies of individuals with different fur colors change over time. The large white arrows symbolize selective pressures against certain phenotypes. Directional selection occurs when conditions favor individuals exhibiting one extreme of a phenotypic range, thereby shifting a population's frequency curve for the phenotypic character in one direction or the other (Figure 23.13a). Directional selection is common when a population's environment changes or when members of a population migrate to a new (and different) \nhabitat. For instance, an increase in the size of seeds available as food led to an increase in beak depth in a population of Galapagos finches (see Figure 23.1). Disruptive selection (Figure 23.13b) occurs when conditions favor individuals at both extremes of a phenotypic range over individuals with intermediate phenotypes. One example is a population of black-bellied seedcracker finches in Cameroon whose members display two distinctly different beak sizes. Small-billed birds feed mainly on soft seeds, whereas large-billed birds specialize in cracking hard seeds. It appears that birds with intermediate-sized bills are relatively inefficient at cracking both types of seeds and thus have lower relative fitness. Stabilizing selection (Figure 23.13c) acts against both extreme phenotypes and favors intermediate variants. This mode of selection reduces variation and tends to maintain the status quo for a particular phenotypic character. For example, the birth weights of most human babies lie in the range of 3-4 \nkg (6.6-8.8 pounds); babies who are either much smaller or much larger suffer higher rates of mortality. Regardless of the mode of selection, however, the basic mechanism remains the same. Selection favors individuals whose heritable phenotypic traits provide higher reproductive success than do the traits of other individuals."
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102 | 103 | 1_23_4_5 | How does natural selection act on a sexually-reproducing population? | how | [] | [
"Though natural selection leads to adaptation, nature abounds with examples of organisms that are less than ideally \"engineered\" for their lifestyles. There are several reasons why. Selection can act only on existing variations. Natural selection favors only the fittest phenotypes among those currently in the population, which may not be the ideal traits."
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104 | 105 | 1_23_5 | How does natural selection act on a sexually-reproducing population? | how | [] | [
"23.4 Natural selection is the only mechanism that consistently causes adaptive evolution (pp. 480-485) One organism has greater relative fitness than a second organism if it leaves more fertile descendants than the second organism. The modes of natural selection differ in how selection acts on phenotype (the white arrows in the summary diagram below represent selective pressure on a population). Unlike genetic drift and gene flow, natural selection consistently increases the frequencies of alleles that enhance survival and reproduction, thus improving the match between organisms and their environment."
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106 | 107 | 1_9_6_3 | How does phosphofructokinase play a role in regulating glycolysis? | how | [] | [
"Allosteric enzymes at certain points in the respiratory pathway respond to inhibitors and activators that help set the pace of glycolysis and the citric acid cycle. Phosphofructokinase, which catalyzes an early step in glycolysis (see Figure 9.9), is one such enzyme. It is stimulated by AMP (derived from ADP) but is inhibited by ATP and by citrate. This feedback regulation adjusts the rate of respiration as the cell's catabolic and anabolic demands change."
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108 | 109 | 1_9_6_3 | How does phosphofructokinase play a role in regulating glycolysis? | how | [] | [
"As shown in Figure 9.20, one important switch is phosphofructokinase, the enzyme that catalyzes step 3 of glycolysis (see Figure 9.9). That is the first step that commits the substrate irreversibly to the glycolytic pathway. By controlling the rate of this step, the cell can speed up or slow down the entire catabolic process. Phosphofructokinase can thus be considered the pacemaker of respiration. Phosphofructokinase is an allosteric enzyme with receptor sites for specific inhibitors and activators. It is inhibited by ATP and stimulated by AMP (adenosine monophosphate), which the cell derives from ADP. As ATP accumulates, inhibition of the enzyme slows down glycolysis. The enzyme becomes active again as cellular work converts ATP to ADP (and AMP) faster than ATP is being regenerated. Phosphofructokinase is also sensitive to citrate, the first product of the citric acid cycle. If citrate accumulates in mitochondria, some of it passes into the cytosol and inhibits phosphofructokinase. \nThis mechanism helps synchronize the rates of glycolysis and the citric acid cycle. As citrate accumulates, glycolysis slows down, and the supply of acetyl groups to the citric acid cycle decreases. If citrate consumption increases, either because of a demand for more ATP or because anabolic pathways are draining off intermediates of the citric acid cycle, glycolysis accelerates and meets the demand. Metabolic balance is augmented by the control of enzymes that catalyze other key steps of glycolysis and the citric acid cycle."
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110 | 111 | 1_14_4_2_3 | How does the gene for sickle cell anemia show heterozygote advantage? | how | [] | [
"About one out of ten African-Americans have sickle-cell trait, an unusually high frequency of heterozygotes for an allele with severe detrimental effects in homozygotes. Why haven't evolutionary processes resulted in the disappearance of this allele among this population? One explanation is that having a single copy of the sickle-cell allele reduces the frequency and severity of malaria attacks, especially among young children. The malaria parasite spends part of its life cycle in red blood cells (see Figure 28.10), and the presence of even heterozygous amounts of sickle-cell hemoglobin results in lower parasite densities and hence reduced malaria symptoms. Thus, in tropical Africa, where infection with the malaria parasite is common, the sickle-cell allele confers an advantage to heterozygotes even though it is harmful in the homozygous state."
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112 | 113 | 1_18_1 | How can a bacterial cell regulate which genes get expressed? | how | [] | [
"Second, cells can adjust the production level of certain enzymes; that is, they can regulate the expression of the genes encoding the enzymes. If, in our example, the environment provides all the tryptophan the cell needs, the cell stops making the enzymes that catalyze the synthesis of tryptophan (Figure 18.2b). In this case, the control of enzyme production occurs at the level of transcription, the synthesis of messenger RNA coding for these enzymes. More generally, many genes of the bacterial genome are switched on or off by changes in the metabolic status of the cell. One basic mechanism for this control of gene expression in bacteria, described as the operon model, was discovered in 1961 by Francois Jacob and Jacques Monod at the Pasteur Institute in Paris. Let's see what an operon is and how it works, using the control of tryptophan synthesis as our first example."
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114 | 115 | 1_18_1_1 | How can a bacterial cell regulate which genes get expressed? | how | [] | [
"E. coli synthesizes the amino acid tryptophan from a precursor molecule in the multistep pathway shown in Figure 18.2. Each reaction in the pathway is catalyzed by a specific enzyme, and the five genes that code for the subunits of these enzymes are clustered together on the bacterial chromosome. A single promoter serves all five genes, which together constitute a transcription unit. (Recall from Chapter 17 that a promoter is a site where RNA polymerase can bind to DNA and begin transcription. ) Thus, transcription gives rise to one long mRNA molecule that codes for the five polypeptides making up the enzymes in the tryptophan pathway. The cell can translate this one mRNA into five separate polypeptides because the mRNA is punctuated with start and stop codons that signal where the coding sequence for each polypeptide begins and ends. Figure 18.3 The trp operon in E. coli: regulated synthesis of repressible enzymes. Tryptophan is an amino acid produced by an anabolic pathway catalyzed \nby repressible enzymes. (a) The five genes encoding the polypeptide subunits of the enzymes in this pathway (see Figure 18.2) are grouped, along with a promoter, into the trp operon. The trp operator (the repressor binding site) is located within the trp promoter (the RNA polymerase binding site). (b) Accumulation of tryptophan, the end product of the pathway, represses transcription of the trp operon, thus blocking synthesis of all the enzymes in the pathway and shutting down tryptophan production."
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116 | 117 | 1_18_1_1 | How can a bacterial cell regulate which genes get expressed? | how | [] | [
"A key advantage of grouping genes of related function into one transcription unit is that a single \"on-off switch\" can control the whole cluster of functionally related genes; in other words, these genes are coordinately controlled. When an E. coli cell must make tryptophan for itself because the nutrient medium lacks this amino acid, all the enzymes for the metabolic pathway are synthesized at one time. The switch is a segment of DNA called an operator. Both its location and name suit its function: Positioned within the promoter or, in some cases, between the promoter and the enzyme-coding genes, the operator controls the access of RNA polymerase to the genes. All together, the operator, the promoter, and the genes they control: the entire stretch of DNA required for enzyme production for the tryptophan pathway: constitute an operon. The trp operon (trp for tryptophan) is one of many operons in the E. coli genome (Figure 18.3). If the operator is the operon's switch for controlling \ntranscription, how does this switch work? By itself, the trp operon is turned on; that is, RNA polymerase can bind to the promoter and transcribe the genes of the operon. The operon can be switched off by a protein called the trp repressor. The repressor binds to the operator and blocks attachment of RNA polymerase to the promoter, preventing transcription of the genes. A repressor protein is specific for the operator of a particular operon."
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118 | 119 | 1_10_4_3 | How can CAM plants take carbon dioxide in at night when photosynthesis requires light? | how | [] | [
"A second photosynthetic adaptation to arid conditions has evolved in many succulent (water-storing) plants, numerous cacti, pineapples, and representatives of several other plant families. These plants open their stomata during the night and close them during the day, just the reverse of how other plants behave. Closing stomata during the day helps desert plants conserve water, but it also prevents CO2 from entering the leaves. During the night, when their stomata are open, these plants take up CO2 and incorporate it into a variety of organic acids. This mode of carbon fixation is called crassulacean acid metabolism, or CAM, after the plant family Crassulaceae, the succulents in which the process was first discovered. The mesophyll cells of CAM plants store the organic acids they make during the night in their vacuoles until morning, when the stomata close. During the day, when the light reactions can supply ATP and NADPH for the Calvin cycle, CO2 is released from the organic acids \nmade the night before to become incorporated into sugar in the chloroplasts."
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120 | 121 | 1_10_5 | How can CAM plants take carbon dioxide in at night when photosynthesis requires light? | how | [] | [
"CAM plants open their stomata at night, incorporating CO2 into organic acids, which are stored in mesophyll cells. During the day, the stomata close, and the CO2 is released from the organic acids for use in the Calvin cycle."
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122 | 123 | 1_13_4_1_2 | How does crossover provide more variation for natural selection to act on? | how | [] | [
"Figure 13.11 The results of crossing over during meiosis. As a consequence of the independent assortment of chromosomes during meiosis, each of us produces a collection of gametes differing greatly in their combinations of the chromosomes we inherited from our two parents. Figure 13.10 suggests that each chromosome in a gamete is exclusively maternal or paternal in origin. In fact, this is not the case, because crossing over produces recombinant chromosomes, individual chromosomes that carry genes (DNA) derived from two different parents (Figure 13.11). In meiosis in humans, an average of one to three crossover events occur per chromosome pair, depending on the size of the chromosomes and the position of their centromeres. Crossing over begins very early in prophase I as homologous chromosomes pair loosely along their lengths. Each gene on one homolog is aligned precisely with the corresponding gene on the other homolog. In a single crossover event, the DNA of two nonsister chromatids: \none maternal and one paternal chromatid of a homologous pair: is broken by specific proteins at precisely corresponding points, and the two segments beyond the crossover point are each joined to the other chromatid. Thus, a paternal chromatid is joined to a piece of maternal chromatid beyond the crossover point, and vice versa. In this way, crossing over produces chromosomes with new combinations of maternal and paternal alleles (see Figure 13.11)."
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124 | 125 | 1_23_1_2_4 | How does crossover provide more variation for natural selection to act on? | how | [] | [
"During meiosis, homologous chromosomes, one inherited from each parent, trade some of their alleles by crossing over. These homologous chromosomes and the alleles they carry are then distributed at random into gametes."
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126 | 127 | 1_13_4_1_2 | How does crossover provide more variation for natural selection to act on? | how | [] | [
"The important point for now is that crossing over, by combining DNA inherited from two parents into a single chromosome, is an important source of genetic variation in sexual life cycles."
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128 | 129 | 1_13_5 | How does crossover provide more variation for natural selection to act on? | how | [] | [
"Crossing over involves breakage and rejoining of the DNA of nonsister chromatids in a homologous pair, resulting in recombinant chromatids that will become recombinant chromosomes."
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130 | 131 | 1_15_3_2_2 | How does crossover provide more variation for natural selection to act on? | how | [] | [
"Subsequent experiments demonstrated that this process, now called crossing over, accounts for the recombination of linked genes. In crossing over, which occurs while replicated homologous chromosomes are paired during prophase of meiosis I, a set of proteins orchestrates an exchange of corresponding segments of one maternal and one paternal chromatid (see Figure 13.11). In effect, end portions of two nonsister chromatids trade places each time a crossover occurs."
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132 | 133 | 1_43_3_1 | How do cytotoxic T lymphocytes kill viral cells? | how | [] | [
"Activated helper T cells also help stimulate cytotoxic T cells, as we'll discuss next."
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134 | 135 | 1_43_3_2 | How do cytotoxic T lymphocytes kill viral cells? | how | [] | [
"In the cell-mediated immune response, cytotoxic T cells are the effector cells. The term cytotoxic refers to their use of toxic gene products to kill infected cells. To become active, they require signaling molecules from helper T cells as well as interaction with a cell that presents an antigen. Once activated, cytotoxic T cells can eliminate cells that are infected by viruses or other intracellular pathogens. Figure 43.17 The killing action of cytotoxic T cells on an infected host cell. An activated cytotoxic T cell releases molecules that make pores in an infected cell's membrane and enzymes that break down proteins, promoting the cell's death. Fragments of foreign proteins produced in infected host cells associate with class I MHC molecules and are displayed on the cell surface, where they can be recognized by cytotoxic T cells (Figure 43.17). As with helper T cells, cytotoxic T cells have an accessory protein that binds to the MHC molecule, helping keep the two cells in contact \nwhile the T cell is activated. The targeted destruction of an infected host cell by a cytotoxic T cell involves the secretion of proteins that disrupt membrane integrity and trigger apoptosis (see Figure 43.17). The death of the infected cell not only deprives the pathogen of a place to reproduce, but also exposes cell contents to circulating antibodies, which mark them for disposal. After destroying an infected cell, the cytotoxic T cell can move on and kill other cells infected with the same pathogen."
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136 | 137 | 1_43_5 | How do cytotoxic T lymphocytes kill viral cells? | how | [] | [
"43.3 Adaptive immunity defends against infection of body fluids and body cells (pp. 940-946) Helper T cells interact with antigen fragments displayed by class II MHC molecules on the surface of dendritic cells, macrophages, and B cells (antigen-presenting cells). Activated helper T cells secrete cytokines that stimulate other lymphocytes as part of the response to nearly all antigens. Cytotoxic T cells bind to a complex of an antigen fragment and a class I MHC molecule on infected host cells. In the cell-mediated immune response, activated cytotoxic T cells secrete proteins that initiate destruction of infected cells. All T cells have an accessory protein that enhances binding to MHC-antigen fragment complexes."
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138 | 139 | 1_45_3_1 | How does the hypothalamus affect the anterior pituitary? | how | [] | [
"In vertebrates, the hypothalamus plays a central role in integrating the endocrine and nervous systems. One of several endocrine glands located in the brain (Figure 45.14), the hypothalamus receives information from nerves throughout the body, including the brain. In response, the hypothalamus initiates endocrine signaling appropriate to environmental conditions. In many vertebrates, for example, nerve signals from the brain pass sensory information to the hypothalamus about seasonal changes. The hypothalamus, in turn, regulates the release of reproductive hormones required during the breeding season. Signals from the hypothalamus travel to the pituitary gland, a gland located at its base (see Figure 45.14). Roughly the size and shape of a lima bean, the pituitary has discrete posterior and anterior parts, or lobes, that secrete different sets of hormones."
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140 | 141 | 1_45_3_1 | How does the hypothalamus affect the anterior pituitary? | how | [] | [
"In contrast, the anterior pituitary is an endocrine gland that synthesizes and secretes hormones in response to signals from the hypothalamus. Many anterior pituitary hormones act as tropic hormones, meaning that they regulate the function of other endocrine cells or glands."
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142 | 143 | 1_45_3_1_2 | How does the hypothalamus affect the anterior pituitary? | how | [] | [
"Endocrine signals generated by the hypothalamus regulate hormone secretion by the anterior pituitary (Figure 45.16). Each hypothalamic hormone is either a releasing hormone or an inhibiting hormone, reflecting its role in promoting or inhibiting release of one or more specific hormones by the anterior pituitary. Prolactin-releasing hormone, for example, is a hypothalamic hormone that stimulates the anterior pituitary to secrete prolactin, which has activities that include stimulating milk production. Every anterior pituitary hormone is controlled by at least one releasing hormone. Some, such as prolactin, have both a releasing hormone and an inhibiting hormone. The hypothalamic releasing and inhibiting hormones are secreted near capillaries at the base of the hypothalamus. The capillaries drain into short blood vessels, called portal vessels, which subdivide into a second capillary bed within the anterior pituitary. In this way, the releasing and inhibiting hormones have direct access \nto the gland they control. Hormones secreted by the anterior pituitary regulate a diverse set of processes in the human body, including metabolism, osmoregulation, and reproductive activity."
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144 | 145 | 1_8_3_2 | How can an endergonic cellular process be made exergonic? | how | [] | [
"In this example, the exergonic process of ATP hydrolysis is used to drive an endergonic process: the cellular synthesis of the amino acid glutamine from glutamic acid and ammonia. For example, with the help of specific enzymes, the cell is able to use the energy released by ATP hydrolysis directly to drive chemical reactions that, by themselves, are endergonic. If the deltaG of an endergonic reaction is less than the amount of energy released by ATP hydrolysis, then the two reactions can be coupled so that, overall, the coupled reactions are exergonic (Figure 8.9). This usually involves the transfer of a phosphate group from ATP to some other molecule, such as the reactant. The recipient with the phosphate group covalently bonded to it is then called a phosphorylated intermediate. The key to coupling exergonic and endergonic reactions is the formation of this phosphorylated intermediate, which is more reactive (less stable) than the original unphosphorylated molecule."
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146 | 147 | 1_8_6 | How can an endergonic cellular process be made exergonic? | how | [] | [
"ATP is the cell's energy shuttle. Hydrolysis of its terminal phosphate yields ADP and phosphate and releases free energy. Through energy coupling, the exergonic process of ATP hydrolysis drives endergonic reactions by transfer of a phosphate group to specific reactants, forming a phosphorylated intermediate that is more reactive."
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148 | 149 | 1_8_3_3 | How is ATP regeneration an anabolic process? | how | [] | [
"An organism at work uses ATP continuously, but ATP is a renewable resource that can be regenerated by the addition of phosphate to ADP (Figure 8.11). The free energy required to phosphorylate ADP comes from exergonic breakdown reactions (catabolism) in the cell. This shuttling of inorganic phosphate and energy is called the ATP cycle, and it couples the cell's energy-yielding (exergonic) processes to the energy-consuming (endergonic) ones."
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150 | 151 | 1_8_3_3 | How is ATP regeneration an anabolic process? | how | [] | [
"Because both directions of a reversible process cannot be downhill, the regeneration of ATP from ADP and Ⓟi is necessarily endergonic: ADP + Ⓟi → ATP + H2O ΔG = +7.3 kcal/mol (+30.5 kJ/mol) (standard conditions) Since ATP formation from ADP and Ⓟi is not spontaneous, free energy must be spent to make it occur. Catabolic (exergonic) pathways, especially cellular respiration, provide the energy for the endergonic process of making ATP. Plants also use light energy to produce ATP. Thus, the ATP cycle is a revolving door through which energy passes during its transfer from catabolic to anabolic pathways."
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152 | 153 | 1_9_1_1 | How is the change in free energy that occurs during glucose oxidation used in the cell? | how | [] | [
"Although carbohydrates, fats, and proteins can all be processed and consumed as fuel, it is helpful to learn the steps of cellular respiration by tracking the degradation of the sugar glucose (C6H12O6): C6H12O6 + 6 O2 → 6 CO2 + 6 H2O + Energy (ATP + heat) Glucose is the fuel that cells most often use; we will discuss other organic molecules contained in foods later in the chapter. This breakdown of glucose is exergonic, having a free-energy change of -'686 kcal (2,870 kJ) per mole of glucose decomposed (deltaG = -'686 kcal/mol). Recall that a negative deltaG indicates that the products of the chemical process store less energy than the reactants and that the reaction can happen spontaneously: in other words, without an input of energy. Catabolic pathways do not directly move flagella, pump solutes across membranes, polymerize monomers, or perform other cellular work. Catabolism is linked to work by a chemical drive shaft: ATP, which you learned about in Chapter 8. To keep \nworking, the cell must regenerate its supply of ATP from ADP andi (see Figure 8.11). To understand how cellular respiration accomplishes this, let's examine the fundamental chemical processes known as oxidation and reduction."
] |
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154 | 155 | 1_9_1_2 | How is the change in free energy that occurs during glucose oxidation used in the cell? | how | [] | [
"How do the catabolic pathways that decompose glucose and other organic fuels yield energy? The answer is based on the transfer of electrons during the chemical reactions. The relocation of electrons releases energy stored in organic molecules, and this energy ultimately is used to synthesize ATP."
] |
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156 | 157 | 1_9_1_2_2 | How is the change in free energy that occurs during glucose oxidation used in the cell? | how | [] | [
"But the energy-yielding redox process of greatest interest to biologists is respiration: the oxidation of glucose and other molecules in food. Examine again the summary equation for cellular respiration, but this time think of it as a redox process: As in the combustion of methane or gasoline, the fuel (glucose) is oxidized and oxygen is reduced. The electrons lose potential energy along the way, and energy is released. In general, organic molecules that have an abundance of hydrogen are excellent fuels because their bonds are a source of \"hilltop\" electrons, whose energy may be released as these electrons \"fall\" down an energy gradient when they are transferred to oxygen. The summary equation for respiration indicates that hydrogen is transferred from glucose to oxygen. But the important point, not visible in the summary equation, is that the energy state of the electron changes as hydrogen (with its electron) is transferred to oxygen. In respiration, the oxidation of glucose \ntransfers electrons to a lower energy state, liberating energy that becomes available for ATP synthesis."
] |
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158 | 159 | 1_9_1_2_3 | How is the change in free energy that occurs during glucose oxidation used in the cell? | how | [] | [
"Electrons lose very little of their potential energy when they are transferred from glucose to NAD+. Each NADH molecule formed during respiration represents stored energy that can be tapped to make ATP when the electrons complete their \"fall\" down an energy gradient from NADH to oxygen. Figure 9.5 An introduction to electron transport chains. (a) The one-step exergonic reaction of hydrogen with oxygen to form water releases a large amount of energy in the form of heat and light: an explosion. (b) In cellular respiration, the same reaction occurs in stages: An electron transport chain breaks the \"fall\" of electrons in this reaction into a series of smaller steps and stores some of the released energy in a form that can be used to make ATP."
] |
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160 | 161 | 1_9_1_3 | How is the change in free energy that occurs during glucose oxidation used in the cell? | how | [] | [
"The harvesting of energy from glucose by cellular respiration is a cumulative function of three metabolic stages: Biochemists usually reserve the term cellular respiration for stages 2 and 3. We include glycolysis, however, because most respiring cells deriving energy from glucose use glycolysis to produce the starting material for the citric acid cycle. Figure 9.6 An overview of cellular respiration. During glycolysis, each glucose molecule is broken down into two molecules of the compound pyruvate. In eukaryotic cells, as shown here, the pyruvate enters the mitochondrion. There it is oxidized to acetyl CoA, which is further oxidized to CO2 in the citric acid cycle. NADH and a similar electron carrier, a coenzyme called FADH2, transfer electrons derived from glucose to electron transport chains, which are built into the inner mitochondrial membrane. (In prokaryotes, the electron transport chains are located in the plasma membrane. ) During oxidative phosphorylation, electron transport \nchains convert the chemical energy to a form used for ATP synthesis in the process called chemiosmosis."
] |
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162 | 163 | 1_9_1_3 | How is the change in free energy that occurs during glucose oxidation used in the cell? | how | [] | [
"Some of the steps of glycolysis and the citric acid cycle are redox reactions in which dehydrogenases transfer electrons from substrates to NAD+, forming NADH. In the third stage of respiration, the electron transport chain accepts electrons from the breakdown products of the first two stages (most often via NADH) and passes these electrons from one molecule to another. At the end of the chain, the electrons are combined with molecular oxygen and hydrogen ions (H+), forming water (see Figure 9.5b). The energy released at each step of the chain is stored in a form the mitochondrion (or prokaryotic cell) can use to make ATP from ADP. This mode of ATP synthesis is called oxidative phosphorylation because it is powered by the redox reactions of the electron transport chain. Figure 9.7 Substrate-level phosphorylation. Some ATP is made by direct transfer of a phosphate group from an organic substrate to ADP by an enzyme. (For examples in glycolysis, see Figure 9.9, steps 7 and 10. )"
] |
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164 | 165 | 1_8_1_3_2 | How does the highly-ordered structure of an organism not contradict the second law of thermodynamics? | how | [] | [
"We can now state the second law of thermodynamics: Every energy transfer or transformation increases the entropy of the universe. Although order can increase locally, there is an unstoppable trend toward randomization of the universe as a whole."
] |
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166 | 167 | 1_8_1_3_3 | How does the highly-ordered structure of an organism not contradict the second law of thermodynamics? | how | [] | [
"During the early history of life, complex organisms evolved from simpler ancestors. For example, we can trace the ancestry of the plant kingdom from much simpler organisms called green algae to more complex flowering plants. However, this increase in organization over time in no way violates the second law. The entropy of a particular system, such as an organism, may actually decrease as long as the total entropy of the universe: the system plus its surroundings: increases. Thus, organisms are islands of low entropy in an increasingly random universe."
] |
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168 | 169 | 1_4_2_2 | How do the carbon atoms of an organic molecule contribute to its shape? | how | [] | [
"Carbon chains form the skeletons of most organic molecules. The skeletons vary in length and may be straight, branched, or arranged in closed rings (Figure 4.5). Some carbon skeletons have double bonds, which vary in number and location. Such variation in carbon skeletons is one important source of the molecular complexity and diversity that characterize living matter. In addition, atoms of other elements can be bonded to the skeletons at available sites."
] |
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170 | 171 | 1_8_2_3_2 | How can one disrupt a system in equilibrium? | how | [] | [
"Like most systems, a living cell is not in equilibrium. The constant flow of materials in and out of the cell keeps the metabolic pathways from ever reaching equilibrium, and the cell continues to do work throughout its life."
] |
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172 | 173 | 1_8_2_3_2 | How can one disrupt a system in equilibrium? | how | [] | [
"Some of the reversible reactions of respiration are constantly \"pulled\" in one direction: that is, they are kept out of equilibrium. The key to maintaining this lack of equilibrium is that the product of a reaction does not accumulate but instead becomes a reactant in the next step; finally, waste products are expelled from the cell. The overall sequence of reactions is kept going by the huge free-energy difference between glucose and oxygen at the top of the energy \"hill\" and carbon dioxide and water at the \"downhill\" end."
] |
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174 | 175 | 1_18_0_0 | How are genes expressed? | how | [] | [
"Figure 18.1 What regulates the precise pattern of gene expression in the developing wing of a fly embryo? An adult fruit fly, for example, develops from a single fertilized egg, passing through a wormlike stage called a larva. At every stage, gene expression is carefully regulated, ensuring that the right genes are expressed only at the correct time and place. In the larva, the adult wing forms in a disk-shaped pocket of several thousand cells, shown in Figure 18.1. The tissue in this image has been treated to reveal the mRNA for three genes: labeled red, blue, and green: using techniques covered in Chapter 20. (Red and green together appear yellow. ) The intricate pattern of expression for each gene is the same from larva to larva at this stage, and it provides a graphic display of the precision of gene regulation. But what is the molecular basis for this pattern? Why is one particular gene expressed only in the few hundred cells that appear blue in this image and not in the other \ncells? In this chapter, we first explore how bacteria regulate expression of their genes in response to different environmental conditions. We then examine how eukaryotes regulate gene expression to maintain different cell types. Gene expression in eukaryotes, as in bacteria, is often regulated at the stage of transcription, but control at other stages is also important."
] |
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176 | 177 | 1_18_2 | How are genes expressed? | how | [] | [
"All organisms, whether prokaryotes or eukaryotes, must regulate which genes are expressed at any given time. Both unicellular organisms and the cells of multicellular organisms must continually turn genes on and off in response to signals from their external and internal environments. Regulation of gene expression is also essential for cell specialization in multicellular organisms, which are made up of different types of cells, each with a distinct role. To perform its role, each cell type must maintain a specific program of gene expression in which certain genes are expressed and others are not."
] |
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178 | 179 | 1_18_2_3_2 | How are genes expressed? | how | [] | [
"The specific transcription factors made in a cell determine which genes are expressed. In this example, the genes for albumin and crystallin are shown at the top, each with an enhancer made up of three different control elements. Although the enhancers for the two genes share one control element (gray), each enhancer has a unique combination of elements. All the activators required for high-level expression of the albumin gene are present only in liver cells (a), whereas the activators needed for expression of the crystallin gene are present only in lens cells (b). For simplicity, we consider only the role of activators here, although the presence or absence of repressors may also influence transcription in certain cell types. Even with only a dozen control element sequences available, a very large number of combinations are possible. A particular combination of control elements will be able to activate transcription only when the appropriate activator proteins are present, which may \noccur at a precise time during development or in a particular cell type. Figure 18.11 illustrates how the use of different combinations of just a few control elements can allow differential regulation of transcription in two cell types. This can occur because each cell type contains a different group of activator proteins. How these groups came to differ will be explored in Concept 18.4."
] |
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180 | 181 | 1_18_2_3_3 | How are genes expressed? | how | [] | [
"How does the eukaryotic cell deal with genes of related function that need to be turned on or off at the same time? Earlier in this chapter, you learned that in bacteria, such coordinately controlled genes are often clustered into an operon, which is regulated by a single promoter and transcribed into a single mRNA molecule. Thus, the genes are expressed together, and the encoded proteins are produced concurrently. With a few minor exceptions, operons that work in this way have not been found in eukaryotic cells. Co-expressed eukaryotic genes, such as genes coding for the enzymes of a metabolic pathway, are typically scattered over different chromosomes. In these cases, coordinate gene expression depends on the association of a specific combination of control elements with every gene of a dispersed group. The presence of these elements can be compared to the raised flags on a few mailboxes out of many, signaling to the mail carrier to check those boxes. Copies of the activators that \nrecognize the control elements bind to them, promoting simultaneous transcription of the genes, no matter where they are in the genome. Coordinate control of dispersed genes in a eukaryotic cell often occurs in response to chemical signals from outside the cell. A steroid hormone, for example, enters a cell and binds to a specific intracellular receptor protein, forming a hormone-receptor complex that serves as a transcription activator (see Figure 11.9). Every gene whose transcription is stimulated by a particular steroid hormone, regardless of its chromosomal location, has a control element recognized by that hormone-receptor complex. This is how estrogen activates a group of genes that stimulate cell division in uterine cells, preparing the uterus for pregnancy. Many signaling molecules, such as nonsteroid hormones and growth factors, bind to receptors on a cell's surface and never actually enter the cell. Such molecules can control gene expression indirectly by triggering signal transduction pathways \nthat lead to activation of particular transcription activators or repressors (see Figure 11.15). Coordinate regulation in such pathways is the same as for steroid hormones: Genes with the same control elements are activated by the same chemical signals."
] |
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182 | 183 | 1_21_3_2 | How are genes expressed? | how | [] | [
"What genetic attributes allow humans (and other vertebrates) to get by with no more genes than nematodes? An important factor is that vertebrate genomes \"get more bang for the buck\" from their coding sequences because of extensive alternative splicing of RNA transcripts. Recall that this process generates more than one functional protein from a single gene (see Figure 18.13). A typical human gene contains about ten exons, and an estimated 93% or so of these multi-exon genes are spliced in at least two different ways. Some genes are expressed in hundreds of alternatively spliced forms, others in just two. It is not yet possible to catalog all of the different forms, but it is clear that the number of different proteins encoded in the human genome far exceeds the proposed number of genes."
] |
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184 | 185 | 1_17_6_2 | How are genes expressed? | how | [] | [
"Thus, we arrive at the following definition: A gene is a region of DNA that can be expressed to produce a final functional product that is either a polypeptide or an RNA molecule. When considering phenotypes, however, it is often useful to start by focusing on genes that code for polypeptides. In this chapter, you have learned in molecular terms how a typical gene is expressed: by transcription into RNA and then translation into a polypeptide that forms a protein of specific structure and function. Proteins, in turn, bring about an organism's observable phenotype. A given type of cell expresses only a subset of its genes."
] |
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186 | 187 | 1_17_0_0 | How are genes expressed? | how | [] | [
"Gene expression is the process by which DNA directs the synthesis of proteins (or, in some cases, just RNAs). The expression of genes that code for proteins includes two stages: transcription and translation."
] |
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188 | 189 | 1_17_1_2 | How are genes expressed? | how | [] | [
"Genes are typically hundreds or thousands of nucleotides long, each gene having a specific sequence of nucleotides. Each polypeptide of a protein also has monomers arranged in a particular linear order (the protein's primary structure), but its monomers are amino acids. Thus, nucleic acids and proteins contain information written in two different chemical languages. Getting from DNA to protein requires two major stages: transcription and translation. Transcription is the synthesis of RNA using information in the DNA. The two nucleic acids are written in different forms of the same language, and the information is simply transcribed, or \"rewritten,\" from DNA to RNA. Just as a DNA strand provides a template for making a new complementary strand during DNA replication, it also can serve as a template for assembling a complementary sequence of RNA nucleotides. For a protein-coding gene, the resulting RNA molecule is a faithful transcript of the gene's protein-building instructions. This \ntype of RNA molecule is called messenger RNA (mRNA) because it carries a genetic message from the DNA to the protein-synthesizing machinery of the cell. (Transcription is the general term for the synthesis of any kind of RNA on a DNA template. Later, you will learn about some other types of RNA produced by transcription. ) Translation is the synthesis of a polypeptide using the information in the mRNA. During this stage, there is a change in language: The cell must translate the nucleotide sequence of an mRNA molecule into the amino acid sequence of a polypeptide. The sites of translation are ribosomes, complex particles that facilitate the orderly linking of amino acids into polypeptide chains. Transcription and translation occur in all organisms, both those that lack a membrane-bounded nucleus (bacteria and archaea) and those that have one (eukaryotes)."
] |
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190 | 191 | 1_17_1_3_1 | How are genes expressed? | how | [] | [
"Experiments have verified that the flow of information from gene to protein is based on a triplet code: The genetic instructions for a polypeptide chain are written in the DNA as a series of nonoverlapping, three-nucleotide words. The series of words in a gene is transcribed into a complementary series of nonoverlapping, three-nucleotide words in mRNA, which is then translated into a chain of amino acids (Figure 17.4)."
] |
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192 | 193 | 1_12_1_2 | How are sister chromatids connected to each other? | how | [] | [
"Each duplicated chromosome has two sister chromatids, which are joined copies of the original chromosome (Figure 12.4). The two chromatids, each containing an identical DNA molecule, are initially attached all along their lengths by protein complexes called cohesins; this attachment is known as sister chromatid cohesion. Each sister chromatid has a centromere, a region containing specific DNA sequences where the chromatid is attached most closely to its sister chromatid. This attachment is mediated by proteins bound to the centromeric DNA sequences and gives the condensed, duplicated chromosome a narrow \"waist."
] |
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194 | 195 | 1_12_4 | How are sister chromatids connected to each other? | how | [] | [
"In preparation for cell division, chromosomes are duplicated, each one then consisting of two identical sister chromatids joined along their lengths by sister chromatid cohesion and held most tightly together at a constricted region at the centromeres of the chromatids."
] |
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196 | 197 | 1_13_3_2 | How are sister chromatids connected to each other? | how | [] | [
"How do sister chromatids stay together through meiosis I but separate from each other in meiosis II and mitosis? Sister chromatids are attached along their lengths by protein complexes called cohesins."
] |
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198 | 199 | 1_17_2_1 | How does RNA polymerase know when to stop transcription? | how | [] | [
"Unlike DNA polymerases, however, RNA polymerases are able to start a chain from scratch; they don't need a primer. Specific sequences of nucleotides along the DNA mark where transcription of a gene begins and ends. The DNA sequence where RNA polymerase attaches and initiates transcription is known as the promoter; in bacteria, the sequence that signals the end of transcription is called the terminator."
] |
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in Dataset Viewer.
Dataset Card for BiologyHowWhyCorpus
This dataset consists of 185 "how" and 193 "why" biology questions authored by a domain expert, with one or more gold answer passages identified in an undergraduate textbook. The expert was not constrained in any way during the annotation process, so gold answers might be smaller than a paragraph or span multiple paragraphs. This dataset was used for the question-answering system described in the paper “Discourse Complements Lexical Semantics for Non-factoid Answer Reranking” (ACL 2014).
Citation Information
@inproceedings{jansen-etal-2014-discourse,
title = "Discourse Complements Lexical Semantics for Non-factoid Answer Reranking",
author = "Jansen, Peter and
Surdeanu, Mihai and
Clark, Peter",
booktitle = "Proceedings of the 52nd Annual Meeting of the Association for Computational Linguistics (Volume 1: Long Papers)",
month = jun,
year = "2014",
address = "Baltimore, Maryland",
publisher = "Association for Computational Linguistics",
url = "https://aclanthology.org/P14-1092",
doi = "10.3115/v1/P14-1092",
pages = "977--986",
}
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