bluuebunny/crossref_metadata_2025_split huggingface dataset:
Allometry and Metabolic Scaling in Ecology
Authors: Anderson‐Teixeira Kristina J , Savage Van M , Allen Andrew P , Gillooly James F 
Published: December 2009

Abstract

Body size affects the structure and function of all levels of biological organization. In ecological systems, body size strongly influences individuals (e.g. rates of individual growth, reproduction and mortality), populations (e.g. population growth rate, abundance and space use), communities (e.g. community abundance, food‐web structure and interspecific interactions) and ecosystems (e.g. flux, storage and turnover of materials and energy). This is because individual metabolic rate – the rate at which an organism takes up and utilizes energy and materials – is largely controlled by body size. Here we review how body‐size allometries at the individual level affect the structure and function of populations, communities and ecosystems. We use these results to identify and highlight exciting new applications of allometric theory in ecology.

Key concepts:

Body size sets an organism's metabolic rate and thereby controls its rates of growth, reproduction and mortality.

Body size is a key predictor of population growth rate, density and carrying capacity through its effects on individual‐level rates of birth, death and resource use.

Body size influences community structure through its effects on individual‐level resource demands, individual life histories and interspecific interactions.

Body size affects predator–prey dynamics and food‐web interactions partially through its effects on metabolic rate.

The contribution of biota to the cycling of energy and materials in ecosystems is affected by species’ size distributions, and by the flux, storage and turnover of energy and elements in individuals which, in turn, is controlled by metabolic rate.

Allometric models provide a baseline for understanding the structure and function of complex ecological systems, and a means to quantitatively link different levels of biological organization.
Cell Death inC. elegans
Authors: Sendoel Ataman , Hengartner Michael O 
Published: December 2009

AbstractProgrammed cell death plays a central role in the development of most multicellular animals. During the development ofCaenorhabditis elegans, a total of 1090 cells are generated, 131 of which are destined to die. Genetic studies focusing on the control of the fate of these 131 cells revealed an evolutionary conserved set of genes essential for all programmed cell deaths inC. elegans. In a cell undergoing apoptosis, the BH3‐only domain proteinEGL‐1binds to theCED‐9–CED‐4complex on the outer mitochondrial membrane resulting in the release ofCED‐4, which in turn activates the effector caspaseCED‐3. These at the time pioneering findings establishedC. elegansas a prime model system to study apoptosis, a system that still today provides a stage for new inspiring science, such as studies onC. elegansapoptotic cell clearance and on deoxyribonucleic acid (DNA) damage‐induced apoptosis.Key concepts:Caenorhabditis elegansas a model organism has been introduced by Sidney Brenner in the 1960s.The completeC. eleganscell lineage was described in 1983 by John Sulston.The cell lineage inC. elegansis invariant: during the development of an animal, a total of 1090 cells are generated, 131 of which are destined to die.The basis for analysing programmed cell death inC. eleganswas delineation of the complete cell lineage.There are three waves of programmed cell death inC. elegans: a first wave can be observed in embryos, the second smaller wave during the second larval stage, whereas the third wave occurs in the adult germline.Germline apoptosis is a stochastic process in which half of the germ cells undergo apoptotic cell death.CED‐4 and CED‐3 are killer proteins essential for all programmed cell deaths inC. elegans.CED‐9 is homologous to Bcl‐2 and protects from cell death.In a cell undergoing apoptosis, the BH3‐only domain protein EGL‐1 inhibits CED‐9 from inhibiting CED‐4.The central cell death pathway is conserved through evolution; homologues of EGL‐1, CED‐9, CED‐4 and CED‐3 are present in mammals, where they control the mitochondrial pathway for apoptosis.Apoptotic cell clearance is controlled via two partially redundant intracellular signalling cascades that converge at the Rac1 homologue CED‐10.DNA damage‐induced germline apoptosis is triggered by a genomic integrity checkpoint and activates a pathway including the p53 homologue CEP‐1.
Structures, Domains and Functions in Cell Death (
DD
,
DED
,
CARD
,
PYD
)
Authors: Wu Hao , Lo Yu‐Chih 
Published: December 2009

Abstract

The death domain (DD), death effector domain (DED), caspase‐recruitment domain (CARD) and pyrin domain (PYD) are subfamilies of the DD superfamily. By mediating homotypic interactions, these proteins play important roles in the assembly and activation of apoptotic signalling complexes. They are responsible for caspase recruitment and for formation of oligomeric platforms for signalling. DD superfamily proteins have a common six‐helical bundle fold and show different surface features for each of the subfamilies. Most interestingly, the homotypic interactions within each subfamily are mostly mediated by asymmetric contacts, in which different surfaces of the interaction partners are adjacent to each other. The DD superfamily proteins appear to use three common types of asymmetric interactions to assemble into large oligomeric complexes.

Key concepts

Death domains (DDs), death effector domains (DEDs), caspase‐recruitment domains (CARDs) and pyrin domains (PYDs) are protein:protein interaction modules for formation of caspase‐activating complexes.

DDs, DEDs, CARDs and PYDs share a common six‐helical bundle fold.

Interactions within these domains are mostly asymmetric and conserved.
Evolution of Caspase‐1 Inhibitors
Authors: da Cunha Julia Pinheiro Chagas , Galante Pedro Alexandre F , de Souza Sandro José 
Published: December 2009

Abstract

CARD only protein 1 (
COP1
), inhibitory caspase recruitment domain (INCA) and ICEBERG are caspase recruitment domain (CARD)‐only proteins that inhibit the activation of cysteine‐dependent
ASPartyl‐specific proteASE
(caspase)‐1 or CASP‐1. Although CASP‐1 is widespread in vertebrates, CASP‐1 inhibitors are exclusively found in primates. The most ancient CASP‐1 inhibitor was found in the genome of a tree shrew, an ancestor of primates. The inhibitors are mapped in tandem at human chromosome 11 and their origin is directly and indirectly related to CASP‐1 gene duplications. Different stop codons arose in the duplicated copies just upstream of the catalytic domain of CASP‐1 generating CARD‐only proteins. In this review we discuss the most recent findings regarding the evolution of both caspases and their inhibitors.

Key concepts

COP, INCA and ICEBERG are CASP‐1 inhibitors.

COP, INCA and ICEBERG arose directly or indirectly from CASP‐1 duplications.

Procaspase‐1 contains a CARD and peptidase C14 domain, but the inhibitors contain only the CARD domain.

Stop codons upstream of the peptidase C14 domain where important for the generation of CASP‐1 inhibitors.
Evolution of Traits Deduced from Genome Comparisons
Authors: Tung Jenny , Wray Gregory A 
Published: December 2009

Abstract

One of the major aims in evolutionary enomics is to leverage comparative genomic data sets to understand the evolution of adaptively important traits. These comparisons may occur at multiple scales, but can be roughly classed into those that focus on differences between closely related species and those that aim to explain broad patterns across diverse groups of organisms. Perhaps the most significant contributions of genome comparisons thus far have been in highlighting broad evolutionary trends, such as identifying gene sets or pathways that have been adaptively important in the evolution of specific lineages, including our own. In contrast, the establishment of concrete links between genetic variation and specific traits remains rare, despite a handful of exciting early successes. We anticipate that the addition of more genome sequences will rapidly advance the field. In particular, we look forward to increasing integration between comparative genomic analyses and ecological and phenotypic data sets.

Key concepts:

Comparisons between closely related species allow investigators to search for the genetic basis of recently evolved differences that distinguish those species.

Comparisons across organisms that share a distant common ancestor allow investigators to search for the genetic basis of major shared differences that define these groups of related organisms.

Genome comparisons often identify broad trends in trait evolution instead of specific genetic differences that influence a specific trait.

Identification of specific genes that influence a specific trait requires not only genome‐scale comparisons but also statistical filtering and experimental validation.

Identification of regions of the genome that evolved under positive selection or that are functionally important is a useful method for narrowing down genome‐wide differences to those that are most likely to have phenotypic effects.
Evolution and Organization of Monotreme Sex Chromosomes
Authors: Grützner Frank 
Published: December 2009

Abstract

Monotremes have an unusually complex sex chromosome system which shares extensive homology to bird sex chromosomes and no homology to sex chromosomes in other mammals. This has entirely changed the way we think about the evolution of sex chromosomes in mammals as it suggests that birds and early mammals shared the sex chromosomes which evolved in the reptilian common ancestor. The sex chromosomes of marsupial and eutherian mammals have evolved much later, after the divergence of monotremes. With 10 sex chromosomes in platypus and 9 sex chromosomes in echidna, monotremes feature the most complex sex chromosomes system described in any mammal. This remarkably complex sex chromosome system raises fundamental questions about its evolution, meiotic organization and dosage compensation and about sex determination in monotremes.

Key concepts

Monotremes
are the only egg‐laying mammals. Because they diverged earlier than any other living mammal they provide unique insights into mammalian evolution.

Sex chromosomes
can be found in various plant and animal species and play an important role in determining sex. In contrast to autosomes most sex chromosomes show cytologically detectable differences in the heterogametic sex (e.g. X‐ and Y‐chromosome in male mammals and Z‐ and W‐chromosome in female birds).

Most sex chromosome systems comprise one or two chromosomes (XX/XY, X0/XX, ZZ/ZW) but translocations between autosomes and sex chromosomes can occasionally lead to
multiple sex chromosomes
.

Sex chromosomes evolved
from autosomes by suppression of recombination and accumulation of sexual antagonistic genes (genes that are beneficial for one of the two sexes), which leads to differentiation of the two sex chromosomes.

At
meiosis
homologous chromosomes pair, recombine and segregate into haploid gametes (sperms and eggs).

Sex chromosome pairing at meiosis is incomplete and leads to
meiotic sex chromosome inactivation
of both X‐ and Y‐chromosome which become visible as so‐called sex body during male meiosis.

The massive gene loss on Y‐ and W‐chromosome leads to a dosage imbalance between homogametic (ZZ or XX) and heterogametic (XY or ZW) sex.
Dosage compensation mechanisms
lead to silencing or upregulation of genes on X‐ or Z‐chromosome to balance gene dosage between sexes.

In most mammals, dosage compensation is achieved by
X‐chromosome inactivation
of one of the X‐chromosomes in XX females.

Sex determination
is a developmental process where two very different organs (i.e. testis and ovary) develop from undifferentiated germ cells during a critical window at early embryo development.
OPA
1 and Its Clinical Implications
Authors: Trevisson Eva , Salviati Leonardo , Scorrano Luca 
Published: December 2009

Abstract

Autosomal dominant optic atrophy (ADOA) or Kjer disease (MIM #
165500
) is a primary inherited nonsyndromic optic neuropathy that results in loss of retinal ganglion cells, leading to the clinical appearance of optic atrophy. It is caused by mutations in
optic atrophy 1
(
OPA1
), a dynamin‐related protein of the inner mitochondrial membrane. Recent evidence supports a role for
OPA1
in the regulation of the process of cristae remodelling during apoptosis, by which the complete release of mitochondrial stores of cytochrome
c
is achieved, supporting a role for apoptosis in the pathogenesis of ADOA. Here we review the basic clinical features of ADOA, the biology of
OPA1
and its role in the regulation of mitochondrial shape changes during apoptosis.

Key concepts

Mitochondrial shape changes during apoptosis.

Cristae are the main store of cytochrome
c
.

The complete release of cytochrome
c
is accompanied by the remodelling of the cristae.

The dynamin‐related protein OPA1 regulates the shape of the cristae.

Dis‐oligomerization of OPA1 is a key event in the release of cytochrome
c
during apoptosis.
Stem Cell Niches in
Drosophila
Authors: Yamashita Yukiko M 
Published: December 2009

Abstract

Adult stem cells supply a continual source of highly differentiated cells throughout the life of an organism. They are able to maintain an undifferentiated state and possess unlimited proliferation capacity. Many stem cells reside in a special microenvironment known as a niche that specifies stem cell identity and protects them from differentiation by providing essential molecular signals. Because of its essential requirement to maintain stem cells, the stem cell niche also limits the number of stem cells, safeguarding against cancer.

Drosophila melanogaster

has served as an ideal model system to study stem cells and their niches, thanks to the well‐understood signalling pathways, elegant genetics and relatively simple anatomy. Studies in

Drosophila

have provided a fundamental framework for understanding mammalian stem cells and their niches. Here, I give an overview of how stem cells are regulated by their niches in

Drosophila

.

Key concepts

Adult stem cells: Cells found in adult tissues that are capable of proliferation over a prolonged time period (throughout the life of the organism) and of further differentiation to produce various types of differentiated cells in the tissue.

Self‐renewal: The phenomenon by which stem cells produce stem cells on cell division. Stem cell characteristics, including undifferentiated state, proliferative potential and developmental potential to differentiate, are maintained.

Niche: A microenvironment in which stem cell characteristics (such as stem cell identity and proliferation potential) are maintained.

Asymmetric stem cell division: A form of stem cell division in which one stem cell and one differentiated cell are created, thereby maintaining stem cell number.
Cytoskeleton in Axon Growth
Authors: Stiess Michael , Bradke Frank 
Published: December 2009

Abstract

During development, neurons extend two different types of processes, typically several short dendrites and one long axon. The axon forms synapses with dendrites of other neurons to integrate into a neuronal network. Axons can extend to enormous lengths. Their growth is guided and exactly controlled to guarantee the correct neuronal connections. Microtubules and actin filaments, the two major cytoskeletal elements, are the key players in these processes. They form the backbone for axon extension, provide the construction material for axon elongation, and are the site of convergence of extracellular and intrinsic signals. Correct path finding of the axon is ensured by a specialized and highly dynamic structure at the tip of the growing axon, the growth cone. Its dynamic cytoskeleton is the machinery that establishes, controls and directs axon growth. Overall, the cytoskeleton determines the distinction of axons and dendrites and aberrant changes in the cytoskeleton are a major cause of regenerative failure after spinal cord injury.

Key concepts:

The growth cone is the highly motile tip of a growing axon, where the axon becomes elongated.

Growth cone motility is regulated by cytoskeletal dynamics.

Actin filaments determine growth cone shape and are involved in path finding.

Microtubules give structure to the axon shaft and are essential for axon elongation.

Guidance cues act on the cytoskeleton in the growth cone.

A dynamic interaction between actin filaments and microtubules is necessary to steer axon growth.

The cytoskeleton regulates neuronal polarity.

Injury induced pathological changes of the cytoskeleton are a major cause for lack of regeneration after spinal cord injury.
Theory of Cooperation
Authors: Gardner Andy , Griffin Ashleigh S , West Stuart A 
Published: December 2009

Abstract

Cooperation is defined as any adaptation that has evolved, at least in part, to increase the reproductive success of the actor's social partners. Inclusive fitness theory reveals that cooperation can be favoured by natural selection owing to either direct fitness benefits (mutually beneficial cooperation) or indirect fitness benefits (altruistic cooperation). Direct fitness benefits can arise as a simple byproduct of cooperation, or else owing to the existence of enforcement mechanisms, which may be fixed or conditioned according to the individual's cooperative behaviour. Indirect fitness benefits can arise when cooperation occurs between genetically similar individuals, as a consequence of limited dispersal, kin discrimination or greenbeard mechanisms. These theoretical mechanisms are illustrated with empirical examples, from laboratory experiments to field studies.

Key concepts:

The function of Darwinian adaptation is to maximize the organism's inclusive fitness.

Inclusive fitness describes how well an organism transmits copies of its genes to future generations.

Direct fitness is the part of inclusive fitness that comes from the organism's own reproductive success.

Indirect fitness is the part of inclusive fitness that comes from the reproductive success of the organism's genetic relatives.

Cooperation is any adaptation whose function is, at least in part, to increase the reproductive success of a social partner.

Cooperation is mutually beneficial if the actor also benefits and altruistic if the actor suffers a net loss of reproductive success.

Mutually beneficial cooperation is favoured by direct fitness benefits.

Direct fitness benefits can arise as a byproduct or owing to enforcement mechanisms.

Altruistic cooperation is favoured by indirect fitness benefits.

Indirect fitness benefits can arise as a consequence of limited dispersal, kin discrimination or greenbeard mechanisms.
From Reactive Oxygen and Nitrogen Species to Therapy
Authors: McKercher Scott R , Nakamura Tomohiro , Lipton Stuart A 
Published: December 2009

Abstract

Excessive free radicals, including reactive oxygen species (ROS) and nitric oxide (NO), contribute to pathological production of misfolded proteins, synaptic damage and apoptosis. Misfolded protein aggregates occur in several chronic neurodegenerative disorders, including Parkinson and Alzheimer diseases. In rare cases, the cause is a genetic mutation; the majority is sporadic and may be a response to environmental factors that generate free radicals. Overactivity of the
N
‐methyl‐
d
‐aspartate (NMDA)‐subtype of glutamate receptor can generate ROS and NO species that mediate protein misfolding, synaptic damage and apoptosis, and thus, neurodegenerative disease. We review current evidence that excessive ROS and NO contribute to protein misfolding by
S
‐nitrosylation of the
E3 ubiquitin ligase
parkin and
protein‐disulfide isomerase
. We also discuss NMDA receptor antagonists memantine and NitroMemantine, drugs that block excessive glutamate excitation, thereby limiting production of ROS and NO, and therapeutic electrophiles, drugs that protect cells from oxidative stress by activating the Nrf2 transcriptional pathway.

Key Concepts:

S
‐nitrosylation or transfer of the NO group to critical cysteine thiol can regulate protein function.

Under pathological circumstances, aberrant
S
‐nitrosylation reactions can contribute to protein misfolding, neuronal injury and neurodegeneration.
The Molecular Genetics of Type 2 Diabetes: Past, Present and Future
Authors: Tan Jonathan T , Chia Kee Seng , Ku Chee Seng 
Published: December 2009

Abstract

Type 2 diabetes is a metabolic disorder which is characterized by elevated blood glucose levels. This common disease affects more than 170 million individuals worldwide. It is a complex disease caused by a combination of multiple genetic factors and environmental exposures. Early attempts to decipher the genetics of type 2 diabetes achieved limited success with only a handful of loci identified showing convincing association. However, with the advent of genome‐wide association studies, much progress has been made in recent years in understanding the genetics of type 2 diabetes. Over a dozen novel susceptibility loci showing consistent and robust associations across different populations have been identified, with the risk associated with the majority of these loci exerting their effect through pancreatic β‐cell dysfunction, leading to impairment in insulin secretion, in the patho‐physiology of diabetes.

Key concepts

Type 2 diabetes is characterized by hyperglycaemia (elevated blood glucose level) as a consequence of the body's inability to maintain blood glucose homeostasis.

This common disease affects more than 170 million individuals worldwide, and this has been projected to increase to over 360 million by 2030.

It is a polygenic disease with many genetic variants, each contributing a modest effect with additional gene–gene and gene–environment interactions adding further complexity.

As with many other complex diseases, the molecular pathways or mechanisms underlying the development of type 2 diabetes have remained poorly understood.

Genetic studies of diseases have traditionally relied on two methods to discover the responsible genes: whole genome linkage mapping and candidate gene association studies.

Genetic studies of the past were largely unsuccessful with only a handful of loci showing convincing association with type 2 diabetes.

Genome‐wide association study is a comprehensive and unbiased approach of interrogating a large number of genetic markers across the genome to identify statistical association between genetic variants and phenotypes.

In contrast to linkage studies, it is usually carried out in unrelated individuals, and unlike candidate gene studies, it does not require any prior supposition of the biological function of genes or pathogenesis of the disease.

The findings from genome‐wide association studies have made some advances in our understanding and knowledge of the genetic basis of this common disease, and it has also implicated the importance of β‐cell dysfunction and impairment in insulin secretion in the patho‐physiology of type 2 diabetes.

Cumulatively, all the type 2 diabetes susceptibility SNPs that have been identified account for only a small proportion of the heritability (approximately 10%); with the majority of the genetic predisposition remaining unexplained, indicating that much still remains to be discovered and understood of the genetic basis of this complex disease.