Does the edge effect promote biodiversity? I define the edge effect as:

A term used to describe what occurs at habitat boundaries where two bordering communities influence one another.

My question is whether it generally leads to an increase or decrease in biodiversity (both evenness and richness) and why.

Also, what are the biogeographic factors that impact biodiversity relating to this edge effect?

I believe that species diversity would increase, as at such habitat boundaries species that inhabit the bordering habitats and those that can also be found in habitat boundaries would be present.

I do remember reading that light intensity increases due to the edge effect and thus also allows for shade-intolerant species to thrive, but I do not understand why.

EDGE EFFECT PROMOTES BIODIVERSITY.
EDGE EFFECT OCCURS IN ECOTYPE.
ECOTYPE IS THE TRANSISSION ZONE WHERE TWO COMMUNITIES MERGE.
HENCE SPECIES RICHNESS IS FAIRLY HIGHER THAN THAT OF THE SURROUNDING ECOSYSTEMS.
IF ANY OF THE SPECIES TENDS TO EXPLOIT THE RESOURCES OF THE ECOTYPE IT WHOULD HAVE TO MODIFY ITS CHARACTERISTICS BY THE PROCESS OF  ADAPTIVE RADIATION AND EVOLUTION .
HENCE NEW SPECIES EMERGES PROMOTING BIODIVERSITY.


Why do cells not store glucose? I understand that glucose is soluble and hence it is not stored by cells. However, my teacher said that I also have to say that "it would have an osmotic effect on the cell." I don't understand what that means.

The issue here can be explained by colligative properties:

In short, colligative properties are properties that depend upon the concentration of the molecules, but not upon the type of those molecules. And osmotic pressure is a colligative property.

That being said, have in mind that 10 molecules of a huge polysaccharide in a given volume or 10 molecules of a small monosaccharide in the same given volume will have the same osmotic pressure.

So, let's imagine that the cell needs a given amount of glucose. Let's say 1000 molecules, just for an oversimplified example. The osmotic pressure can be calculated by (assuming Van't Hoff factor is 1):

  π = MRT

Where M is the molar concentration, R is the ideal gas constant and T is the absolute temperature.

Thus, the osmotic pressure created by those 1000 molecules can be calculated taking into account their molar concentration.

However, If we simply polymerize those 1000 glucose molecules into a huge polysaccharide (be it starch, glycogen or cellulose, it doesn't matter)...

  1000 molecules of glucose → 1 molecule of starch

... the molar concentration will be 1000 times smaller, and the osmotic pressure will drop 1000 times.

As the actual numbers are way higher than this simplified example, we can clearly understand that cells avoid storing glucose to prevent a deadly osmotic pressure, in which the cell bursts due to the amount of water that moves in (specially animal cells, which have no walls that could prevent the membrane from rupturing).

You maybe asked the question Why cells do not store glucose?
Answer: Cells actually store glucose in the form of glycogen.
Glucose is soluble or dissolved and it has a higher osmotic effect so cells can swell up which means it can become larger due to storing glucose directly.
i hope it is super clear to you and you might find helpful


Extinction of species I barely know anything about biology and realize that this might be a stupid question, but I'll ask anyway! I know that species "transform" into other species through the process of evolution. Many species around today still co-exist with the species in which they evolved from, right? Actually, is it correct to say that all species coexist with some common ancestor?

Anyway, my question is; if the monkeys that we evolved from are still around today, then where are all the in-between species. Are there still early humans, like Neanderthal's or Hominids or what have you still roaming around some where?

If all early forms of humans are gone, is it because the more modern humans had a greater evolutionary advantage? But wouldn't these less modernized humans have those same advantages over the less evolved monkeys?

This is a common misconception about evolution, many skeptics ask something along the lines of "If humans evolved from monkeys, why are there still monkeys?" The answer is that evolution is not a linear process of one species becoming the next species becoming the next. Species branch off much more like a tree. At some point in the past the last common ancestor of humans and monkeys split into two directions, one that became the apes including humans, and one that became modern monkeys. Evolution did not stop for either branch, but only our branch became humans, after several more branchings. Sometimes species adapt and evolve without major changes in morphology, for example modern turtles look a lot like turtles from 100 million years ago, but this doesn't mean they haven't evolved.

The intermediate species are often lost with time as environmental conditions and competition changes. For example, if one early human group found itself competing with a slightly more advanced human group with better tools, the more primitive group would have trouble getting enough food and eventually die off, leaving the more advanced group to pass its genes on.

Now, if those more primitive humans were more suited to a particular niche, they could survive there. Lets say they could climb trees better ( assume REALLY primitive ancestors, barely out of the forest ), they might survive in the forested areas while the more advanced groups become dominant in the grasslands. Something like this is why our ancestors didn't totally displace monkeys, the monkeys were better suited for their forested ecosystem. If those same monkeys had to live on dry savannas we would have eaten them all long ago.

I know that species "transform" into other species through the process
  of evolution.

I don't think you are thinking about that right.

We have a population of organisms that are breeding together.  We humans label that a 'species'.  That population has descendants, and over time, the population changes, and when we humans think that the new population look sufficiently different from the old, we label them a new species.

  Many species around today still co-exist with the species in which
  they evolved from, right?

You might have founder situations, where a small sub population breaks off and inhabits a new environment, and changes a great deal more over time than the original population does, such that we continue to label the original population the same species, while we label the offshoot a different species.  But I think what happens more often is that the alleles that cause humans to label a population a distinct 'species' dwindle to nothing in the descendants, and then we say that the original species is extinct, replaced by the new one.  but that's a matter of labels: there is continuity in that the new 'species' is just the descendants of the older one.

  Actually, is it correct to say that all species coexist with some
  common ancestor?

No.  Can you even name any examples where you think this is true?

  if the monkeys that we evolved from are still around today,

What on earth makes you think that's remotely true?  For one thing we aren't descended from monkeys.  We are descended from primates that were more like apes, not monkeys.  There is no living population of primates that we would categorize as being the same species as that non-homo sapiens ancestor population.

  Are there still early humans, like Neanderthal's or Hominids or what
  have you still roaming around some where?

I'm confused how you think an organism or a population existing in the 21st century could be "early". All the hominids walking around today are members of homo sapiens sapiens.


Which animal that lives in the forest makes this noise? Which animal makes this noise? Link to audio file

The file was recorded next to a forest in Germany.

It is a bird sound and most probaby a young bird of prey. It might be a young buzzard. Or, if it's in the eveving or night it might be the sound of a young owl.


Can we identify an individual from their palm lines Can we identify an individual from their palm lines. Is there any uniqueness for palm lines among family members ?

It was tricky searching for this through the morass of palmistry sites.  But, in the field of biometrics, I found the article "Palm Print Recognition", which states that (bolding mine):

  Because fingerprints and palms have both uniqueness and permanence..

it has been used for identification the same as fingerprints. The only reason it is not as widespread as fingerprints is largely due to logistics such as computer processing.

Studies show correlations between palm primary lines and lip lines and palatal rugae patterns.Familial uniqueness should be there.


How valid is the theory of human's chimp-pig origin? Edit: I have also asked the question on skeptics.stackexchange.com and it has been answered there. Here is the link.

There is a person called Dr. Eugene McCarthy who has a theory that the origin of humans come from pig-chimp hybridization (online article about his theory). How acceptable is his theory in comparison to the other common theories?

Briefly, the "theory" makes no genetic sense. Pig and human genomes have both been sequenced, and their sequences are completely incompatible with this model.

The "theory" is completely idiotic in many other ways -- debunking it almost becomes difficult because there are so many ways it fails to make sense -- but the genetics alone make it impossible.

both Suidae and Primates  like every creature on earth have a common ancestor in history , but they are simply too different to breed together .

Therefore the theory makes no sense , unless it uses pig and chimp in a metaphoric sense .


Are there macrophages in the blood vessels and within the blood stream? Monocytes are phagocytes that "evolve" or "differentiate" into macrophages. I read that there are monocytes in the blood stream and vessels and that macrophages are found mainly in other tissues and in the lymphatic system.

My question: are there macrophages (and not merely monocytes) in the blood vessels and within the blood stream? And if there are, are they numerous there or sparse?

Usually, monocytes and neutrophils are present(there are other cells like Lymphocytes and other leukocytes), the only time a macrophage will be present is when inflammation occurs, I suspect this is due to the large size of the macrophage, it would be difficult for it to travel in the bloodstream, as it is quite big, compared to the small size of a monocyte. During inflammation, vascular dilation and permeability increase, which makes it easier for cells and proteins to diffuse across the endothelium.

A source that macrophages are present in all tissues: https://www.researchgate.net/publication/227897252_Macrophages_in_the_embryo_and_beyond_Much_more_than_just_giant_phagocytes

A source that talks about all the leukocytes and lymphocytes present in the blood normally: http://www.histology.leeds.ac.uk/blood/blood_wbc.php

Macrophages are white blood cells and I’m pretty sure that leukocytes are present in blood that flows throughout the body and hence they are found in tissues. Typically, more number of macrophages are present in the blood when there is some form of invasion by bacteria or virus.


Is there any organism that is born with all the nutrients and resources needed for their entire lifetime? I understand that adult mayflies have no mouth, but they do take in oxygen through openings in their exoskeleton.

Is there any organism that does not need to ingest any type of nutrition and does not need to take in something for cellular respiration?

You may need to clarify your question: As written, this would be the biological equivalent of a perpetual motion machine. No such organism could reproduce without either violating the first and second laws of thermodynamics, or ultimately evaporating into nothingness as it divides.

Luna moth , so I expect there are other moths.


How to convert PDB file of Amino Acids to rotamer tuples list of all AAs instances Either by Python command, or via specific application (like Chimera) publicly available. Please provide example or link to one of.

I have to detect AA location within MAP (density) 3D matrix. And to verify with PDB format (which models same 3D structure). Each AA may have different rotamer (aka 3 angles usually used to describe AA exact position related to carbon C_alpha atom (the atom which AA side chain exits from). To justify inaccuracies - I need to show that (among other reasons) - inaccuracy is caused since not all possible rotamers existed in my training set (I use machine learning classification to decide what AA is it, and where it stands within cryo- EM scan).

I’m not sure if it is what you are after, but I have used Roland Dunbrack's dihedral perl script to get dihedral angles, the header of which is:

 RL_Dunbrack@fccc.edu

 usage
 dihedral.pl filename [chain]

 dihedral.pl pdb2hla.ent
     will print out all dihedrals from file pdb2hla.ent
 dihedral.pl pdb2hla.ent A
     will print out dihedrals only from chain A

I don’t know if it’s on his website as I got it from him personally. If not, or even if it’s not what you need, email him — he is likely to be able to help you.


What determines the spiral direction of plants? Some plants and vines spiral clockwise as they go along (right direction) and some spiral anticlockwise (left direction). What determines which direction they spiral along? At first, I believed it to be determined by which hemisphere you are in (influenced by the Coriolis Effect), and this result could be tested by finding spirals in both northern and southern hemispheres and comparing their directions. However, the very first spiral I found seemed to cripple that idea.

The spiral I found spirals first in the right direction, then suddenly decides to spiral in the left direction, and then further along in the right direction again. Since the Earth does not arbitrarily change its rotational direction, this phenomenon must be explained by some other explanation. The change in rotational direction seems to be abrupt, almost like a catastrophic event. A few that I thought of:

1: Arbitrary. The spiral seeks merely to latch onto something, and will try both directions to see if either work out.

2: The spiral is somehow influenced by the night day cycles. Since the spiral switches from right to left back to right having been subjected to two sudden changes, the only large changes I can think of is the day night cycle.

-I live in Australia by the way

First of all, you assumption seems to be incorrect. Plants in same part of the world can twine in opposite directions.

Little seems to be known exactly. Gravity has nothing to do with plant's chirality (or "handedness") or spiraling:

  How plants do this is still unknown. Darwin proposed that it was "autonomously induced." This came to be known as the internal oscillator theory. In the 1960's the gravitropic overshoot theory explained mathematically how circumnutation could spontaneously occur as a result of forces related to gravity and growth. Recent experiments on the Space Shuttle have demonstrated that gravity is not necessary for circumnutation.

Here is another link to a blog, but it does contain reference to original paper on observation of chirality. Main conclusion, taken from the abstract, is:

  The predominance of right-handed helical growth in climbing plants cannot be explained by hypotheses attempting to link plant growth behaviour and global location. One alternative hypothesis for our findings is that the widespread phenomenon of anticlockwise twining arises as a function of microtubule orientation operating at a subcellular level.

To elaborate a little on that, remember that actin filaments as well as microtubules are all chiral polymers. That is, they form spiral structures with defined orientation. Even more, microtubules all start roughly from the nucleus away to membrane, so this might suggest cellular mechanism for preference toward twining chirality. However, this does not address your observation that given plant changes direction of growth twice.

I have been told that the direction of twist should be clockwise as long as the growth is vertical. This would mean the tendrils going out horizontal could go either way but the twisting vines should be prodominately clockwise as they grow upward. Googling pictures of American Bittersweet vines provides a good example of this.

Tendrils that have twists in both directions are better suited to holding up under tension as they tend to be able to just untwist without kinking when pulled on. You might see this occur during high winds for example. What I am suggesting is that tendrils may be a special case as they have a unique fuction and often a non-vertical orientation.


Why do food items expire? Why do food items and medicines expire after sometime?

Expiring food items is obvious: for fresh food, it's almost always due to bacterial or fungal decay (spoilage).

Oxidization and sunlight doesn't really ruin food; it might alter the taste or decrease its appeal, although it remains edible even by first-world standards. However, it might destroy vitamins and other nutrients.

Medicines are a different matter. Some chemical compounds are slightly unstable, with half-lives measured in years. Instability can cause the compounds to randomly break into subcompounds that are ineffective for treating the intended condition at best and poisonous at worst. Unlike food, it's imperative to keep medicines away from sunlight (and oxidation in some cases) as both of these can further promote instability and breakage into subcompounds.

On the comment that Charles posted about medicine shelf life being much longer than advertised: The reason why they underestimate the shelf life is that it's better to have people throwing out potentially OK medicine than to have it sitting on a shelf for 20 years, going bad and sickening people, and prompting numerous lawsuits against the manufacturer. This type of deliberate underestimation in the name of safety is common in engineering - usually with weight limits advertised below the real weight limit. For example, an elevator able to haul 6000 pounds might be advertised as only 2000 because the manufacturer knows there's always going to be a few idiots who disregard the posted limit.

Food expires because its growing. Constantly. Every ingredient you put into making specific foods has a Date when its time has ended. Just like our bodies as we age. We are one year closer to expireing. We Grow old and Our skin starts to Wrinkle. Its just a way of life. If nothing ever expired we would over populate everything. Not to mention, if our foods didnt expire they wouldnt break down in our Bodies making it hard to gain nutrients from. Ending in a result of Death. We need the foods to break down in order to survive.


Have humans finished evolving? I thought that massive changes among organisms are over long periods of time. This is caused by, to my knowledge:

Evolutionary pressure
Natural/artificial selection
Mutations
Genetic drift

Will mutations be the only factor in human change? Will humans change at all over a long time?

Issue in your introduction

I thought that massive changes among organisms are over long periods of time.

Actually, some evolutionary events can happen on a very short time scale. A single mutation can have a massive impact on the phenotype of an individual (see for example Doebley 2004). If this new phenotype has much higher fitness, then the mutation might spread over the whole population in a matter of weeks (typically if the population is not too large, without barriers to gene flow and more importantly if the generation time is short).

This is caused by, to my knowledge:

Evolutionary pressure

Natural/artificial selection

Non-detrimental mutations

The term evolutionary pressure typically encompass natural and artificial selection, mutations (regardless of their mutational effect, that is regardless of whether they are beneficial or detrimental) and other processes that you don't mention (such as genetic drift for example; you have now edited your post to include drift).
Answer to your questions

Will mutations be the only factor in human change?

By "human change", I will assume you mean "human evolution". The answer is: no, mutations are not the only process that leads to human evolution. All standard evolutionary processes are at play in humans as they are in other species. You might want to have a look at the posts Human Evolution in Modern Times and How is evolution possible in contemporary humans?.

Will humans change at all over a long time?

Yes, humans are currently (and will continue to do so in the future) evolving. Again, you might want to have a look at the linked posts.
Want to know more?
Your questions are quite introductory and show a number of misunderstanding you have about evolution. I would recommend having a quick look at Understanding Evolution by UC Berkeley which is a very introductory course to evolutionary biology that is fast and easy to follow.

The genes associated with people who have more surviving and reproducing children will be more prevalent in the future. If you live in a multicultural society where different ethnic groups have different amounts of children you can get a perception of how the humans in your country will evolve over time. Also if you live in a country where there is a huge influx of people who are genetically different from the people who already live there, that will have a serious impact on the short-term change. But basically, if you want to get a hunch of where humans are evolving where you live, you can have a look at the people producing offspring and try to find out if they are different somehow in their genetic composition compared to the population at large. If stupid people are having more children, people will be dumber, if taller people are having more children, people will be taller etc.


What is this spider found in day time? .

South India
Arm to arm about 3 inch in length. Day time. was hiding inside a cardboard storage box.

It's definitely a species of Huntsman spider maybe of the genus "heteropoda" or "olios". Sorry I couldn't be more help.


Do plants need sleep? Turns out that you can do indoor farming these days via hydroponics and specialised LED lights. My mother, who has a large garden, warns me from exploring this as a hobby. She mentions that 'plants need to sleep too' and that having a LED light on them 100% of the time might be bad for them.

Is there any sense in this? Is it true that plants would grow suboptimally if the sun was on them 100% of the time or would they in fact grow quicker? Is there any research on this?

The quote as phrased is a bit non-sensical really because it mostly hinges on what you define as 'sleep' or 'rest'. Plants, like most living things, including us, are far from dormant at night.

It's true that diurnal patterns govern the behaviour of most, if not all, living things that are exposed to them (1). Plants are no exception to this.

For example, photosynthesis is a 2-component process. With the so called 'dark' and 'light' reactions of photosynthesis (more correctly "light-dependent" and "light-independent"). Though both happen during the day and night, it is at it's peak during peak sunlight.

In CAM plants, to avoid dessication, there is differential carbon fixation because the stomata are kept shut during the hot daylight hours.

Respiration however, where the produced food is converted to energy, primarily happens at night.

The Khan Academy has a great 'walkthrough' of the steps of photosynthesis:
https://www.khanacademy.org/science/biology/photosynthesis-in-plants/the-light-dependent-reactions-of-photosynthesis/a/light-dependent-reactions

(1). The diurnal course of plant water potential, stomatal conductance and transpiration in a papyrus (Cyperus papyrus L.) canopy
https://link.springer.com/article/10.1007/BF00379885

Plants need no rest as long as there is a constant source of nutrients and they are kept in the right environment they will not be damaged or die or get "tired". However Plants can be subjected to the seasons where they rest in the winter ect. due to the lack of resources and essential elements.

You can however make them grow better by subjecting them to blue and red light as this is the light they respond to the best out of the whole spectrum of light.

https://www.popsci.com/blog-network/our-modern-plagues/do-plants-sleep
https://homeguides.sfgate.com/24hour-light-schedule-bad-plants-95954.html


What is an 'ex vivo' experiment? Simple terminology question:

Is there a hard boundary between in vitro and ex vivo?
Is there a hard boundary between in vivo and ex vivo?

Suppose a sensory neuron is electrically recorded in the following settings:

Surgically accessing through the animal's skin, and patch-clamped,
Tissue surrounding the neuron is almost separated, but still dangling from the larger part of the animal, and patch-clamped,
Same as above, but the slight dangling connection is cut,
The sensory neuron is isolated and put in an artificially oxygenated medium

The sensory neuron is assumed to have purely feedforward signal, and is perfectly healthy in all conditions. Which conditions, if any, are in vivo, in vitro, or ex vivo? (Feel free to propose better hypothetical experiments. I know this example is not the best.)

Am I the only one confused about these terminologies?

Ex vivo simply means "outside the normal, living organism", whereas in vitro means "within glass", usually in a cultured system.  They are not exactly same as there is no need for the work to be done in a culture system, although both are not in vivo.  Harvested tissue could be examined ex vivo without being in a test tube, or surgical systems could be tested ex vivo on artificial organ models.  In vivo requires the natural, living organism, although it depends on just how much you are perturbing the natural.

To answer your scenarios,

in vivo
ex vivo, as it is not within the normal organism, although I could understand someone taking issue with that; definitely not in vivo, which is usually for normal conditions only, even including temperature.
ex vivo
If you mean the artificially oxygenated environment of a tissue culture system, then in vitro; if you mean the artificially oxygenated environment of a lab bench with an open $O_2$ valve, then ex vivo would suffice.

The term in vivo refers to a medical test, experiment or procedure that is done on (or in) a living organism, such as a laboratory animal or human.

The term in vitro, in contrast to in vivo, refers to a medical study or experiment which is done in the laboratory within the confines of a test tube or laboratory dish.

In contrast to in vitro studies, in vivo studies are needed to see how the body as a whole will respond to a particular substance. In some cases in vitro studies of a drug will be promising, but subsequent in vivo studies fail to show any efficacy (or, on the other hand, find a drug to be unsafe) when used within the multiple metabolic processes that are continually taking place in the body.


What evolutionary explanations are there for death? I know death and cancer doesn't hurt humans' reproductive success. It's not helping either.

Why do we die? Why dying humans (all of us) are common? What's the point of dying?

Death is not only for humans. All 'complicated enough' organisms die (with a notable exception of Hydra, though you may argue when it comes to the complexity). It is is easier to create a new organism from scratch than to repair both internal factors (free radicals, metabolic by-products, ...) and external (physical damage, exposure to toxins, ...).
Underlying causes of death actually can be evolutionary beneficial. For example, shortening of telomeres offers protection against cancer (on a cellular level), but also bounds lifespan.
So actually they may be evolutionary competition (within the same species) of young and old. Mutations helping young but harming older may be preferred to the opposite ones.

The evolutionary explanation is quite simple. Without death, evolution couldn't take place in the first place at all.

Who knows that jellyfish are immortal? Did they continuously evolve from one cell (without reproduction)? I don't think so. Who knows if today present jellyfish were already alive 1000 000 years ago (i.e. without parents)? I think this is the case for any living creature.

That's why telomeres get shorter and shorter when growing older. In the case of cancer, these telomeres stay the same with each division of the parent cell, so it grows wildly. Which all species would probably do so too.


How did sneezing evolve? Did we develop the sneezing mechanism to get rid of pathogens like bacteria and viruses in our nose?

Or did pathogens develop a way to make us sneeze to propagate themselves?

Or did we develop the sneezing mechanism, and then pathogens hijacked this pathway to benefit themselves?

I'm trying to understand why we sneeze so much when we get sick - is it our bodies trying to help us, or is it something the pathogen is causing to help itself spread? And if it's both, how did that happen?

Sneezing itself is a part of long story of human evolution.

Sneezing for early humans was as common as eating is for us. Early humans lived in caves which were full of dust and insects so whenever they wake up from sleep they sneezed intentionally to remove the dust and small insects from their nose, slowly this behaviour of early humans was proved to be beneficial and muscle memories remembered the Activity as a daily routine work and performed it to remove dust and any irritant in their nose or nasal cavity.
As they evolved they passed on their daily routine works to their descendants and this was also passed on , this way sneezing was slowly incorporated into the muscle memories and it exists till now as a way to relax is from external allergens.

There are several other theories too about evolution of sneezing and it itself demands great research .
 There is also a video on Veritasium on YouTube regarding the Sneezing whenever one sees light , this video too discusses this theory.
You should check that out too.


Can there be an equilibrium between humanity's increase of carbon dioxide output with plants since plants harness CO2? Is it possible that, prior to hitting a thermal equilibrium in the atmosphere, the increase in CO2 that humanity puts out every year will come to an equilibrium due to the consumption by the world's plants, which may respond by growing, reproducing and feeding more off of the additional CO2 in the atmosphere at a faster rate?

Yes, with 2 caveats.

More CO2 encourages plant growth up to the local plants' limit. After that limit, the plants are saturated and extra CO2 backlogs into the air. If you intend to prevent atmospheric CO2 buildup, you're better off gradually supplying CO2 rather than deploying it in large surges.

The other caveat is dead trees and other plants that should be harvested or logged to make way for new growth (while providing lumber, fuel, and employment).


How did giant sauropods satisfy their daily energy needs, considering their relatively small mouths? Gigantic sauropod dinosaurs had relatively small heads (and consequently small mouths) in comparison to their overall body mass.

In the book "Dinosaur Odyssey: Fossil Threads in the Web of Life" (by Scott D. Sampson) the author says (on pp. 218-219) that

  The sheer size of the biggest sauropods has long shrouded them in
  mystery. How could such gigantic animals with such small heads (at
  least compared to their body sizes) manage to consume enough food to
  sustain themselves? The mystery deepens when we look inside the
  mouths of sauropods. Cows are typical of big mammalian herbivores
  (e.g. elephants, deer, antelope, and the like) in possessing oversized
  teeth well suited for processing large amounts of fodder. Chewing
  serves not only to break food-items into bite-size chunks' it also
  grinds up the plant matter and begins the process of digestion by
  making the bits of vegetation more susceptible to chemical attack. By
  comparison, sauropods have puny teeth well suited to tearing or, at
  best, slicing, but not for grinding.

(emphasis added)

I don't remember Dr. Scott providing an explicit answer to the question "How could such gigantic animals with such small heads (at least compared to their body sizes) manage to consume enough food to sustain themselves?" but somewhere in the book he did mention that the earth's ecosystem may have been rather different back then.

However, since the book came out nearly a decade ago, I was curious on whether any other findings have been made since then.

How did sauropods manage to consume enough food to sustain themselves? Was it because of some differences in the ecosystem that are now lost?

Unlike mammals, saurischian dinosaurs don't have to chew their food. Like birds they have a gizzard to do that instead.

Look at a modern ostriches: they have a very small head because the head is only used to gather food not process it. Mammals process food in the head (chewing) so the head has to be large to support the muscles, teeth, and other apparatus for this. On the other hand, birds and sauropods use stones in the gizzard to grind up their food, so all that space is taken up in the torso instead of the head.  Ornithischian dinosaurs, which do chew, have large heads just like mammals.

Additionally since the mouth is not occupied chewing the time that would be lost chewing can be spent feeding instead. This can be a lot of time a cow spends 8 hours a day just chewing.

Source

Note several things:

Their long neck allow them access to a lot of food enabling to broswe with minimal movement and energy consumption.
The sauropods had very big and long digestive system, and they probably also used gastroliths. These allowed them to process the food without chewing it in their mouths.
I didn't relate to the question rather they were "cold blooded" or "warm blooded". If they were partially cold blooded (mesothermic) then they would need less food than a warm blooded critter of their size.
I guess the vast majority of their diurnal activity was eating... a lot.

Hope it helps.


Why aren't all infections immune-system resistant? It's been less than a century since the widespread use of antibotics started, and already we're seeing bacteria that have evolved immunities to the antibotics we use.

On the other hand, we've been using immune systems to to fight bacteria for millions of years, and bacteria evolve much faster than humans do.  Why have bacteria not evolved immunities that let them completely overwhelm our immune systems and kill us all?

First of, not all infections are mediated by bacteria and not all bacteria are infectious. Also, not all parasitic bacteria lead to a strong infection or important health problem that cause any non-negligible selection pressure. Following the implicit logic of your post I will talk about infectious bacteria which cause "noticeable harm".

The mistake in your thinking is in the sentence

  bacteria evolve much faster than humans do

While it is true that the mutation rate of base pair is higher and that the generation time is lower, the statement bacteria evolve much faster than humans do is made way too general and lead to your mistake here.

Infectious bacteria are selected to deal with the host immune system and the host is also selected to deal with the the parasite. Both virulence and penetrance evolve in this evolutionary arms race.

The evolution of host-parasite interaction is a very large field of study and it would take several books (and several books have been written on the subject; see this Amazon search) to summarize it. For some theoretical insights into the evolution of host and parasites, you might be interested in the book by Martin Nowak Evolutionary Dynamics: Exploring the equations of life

You will also note that a parasite does not have any "direct interest" in killing (or even harming) its host (thanks @jamesqf for his comment). You might want to have a look at the post Why do parasites sometimes kill their hosts?

Immune-system resistance is especially difficult due to how immunity works.

First, I make 2 assumptions in my explanation:

the pathogen isn't specially designed to dodge the immune system and it isn't able to hide dormant in cells
the immune system is healthy and normal

When a pathogen is present, the immune system samples pieces of it (epitopes) and works on "randomly" putting together antibodies that bind to that epitope. Once a match is found, the qualifying antibody proliferates and is deployed in full force. Each copy of the matching antibody binds to the offending pathogen on contact with good probability - think of it as a microscopic football tackle. Cell-like pathogens (bacteria, fungi, and protozoa) thoroughly covered in antibodies can't consume nutrients, attack cells, and in extreme cases they can't excrete toxins because exocytosis proteins are blocked in antibodies. Viruses covered in antibodies have their surface structures blocked, thoroughly preventing binding to host cells.

The only reason why antibiotics are "easy" to gain resistance to by comparison is that they don't change on their own. The ones most vulnerable to resistance rely on tricking bacteria into eating them (endocytosis), which quickly selects for bacteria that work around the vulnerable protein channel. In other cases, bacteria develop something that inactivates antibiotics.

There has recently been work on antibiotics that force their way into bacterial cells, effectively punching large holes in the membrane. These would be difficult to develop resistance to, especially if they operate via electrical potential or grab onto a wide variety of bacterial epitopes.

Additionally, bacteria would be in a lot of trouble if humans developed antibiotic-generator implants that work as a secondary immune system. Consider a technology that scans for pathogenic bacteria, builds computerized 3D models of them, and then uses a biochemical 3D printer chip to construct custom antibiotics after preliminary safety checks to verify that the custom antibiotic in question wouldn't have dangerous side effects.


Does vitamin D affect melanin concentration? I am aware of the affect on vitamin D production by melanin (in sunlight) but I can not find any information regarding a reverse connection.

Darker skin, as opposed to common belief, probably did not develop as cancer protection. Cancer is usually something that attacks the body in a subsequent life. Even pale individuals under the sun are likely to survive far beyond their reproductive era before they are wiped off by skin cancer.

Instead, it is believed that folic acid manufacturing is the highest selection pressure causing darker skin. Folic acid (vitamin B9) which is used all over the flesh, especially during pregnancy and childhood, will decompose in sunlight.

So the skin tone tries to discover the ideal equilibrium between vitamin D and minimal folic acid breakdown.

As a consequence, if you genuinely have enough vitamin D in your diet, there is no need for lighter skin (and further proof for the vitamin-d hypothesis). That is why the Inuit have lighter skin than expected for their extreme location: the intake of vitamin D is large, so the folic acid part of the equation "wins" and pale skin is not preferable. This is why Inuit individuals do not need so much sun.

Source:

scienceline.org/2007/06/ask-dricoll-inuiteskimos/

pnas.org/content/107/Supplement_2/8962


What's a non-allelic gene? Non-allelic or non-alletic

I stumbled across the term in my Human Genetics textbook. It didn't explain it there, and a quick google search only showed scientific papers that refer to 'recombinations with non-allelic genes' without explaining what they are.

It is my understanding that a non-allelic gene is one that affects another's traits, but is not as a typical dominant / recessive manner. If I am correct, this is the same thing as  epistasis - meaning that one gene modifies how another is expressed.
There exists epistatic genes for horse coat color. One gene is the coat color itself (horses may have either brown or red color alleles at this loci), the second gene is for a protein that allows the coat color gene to be expressed.
For example, a horse has two brown alleles at the coat color locus. It also has a wild type gene in the second (modifier) position. This modifier allows the color brown to be expressed and the horse is brown.
B/B, wt/wt --> Brown
If the horse has the two brown alleles, but has a mutant allele at the modifier position, then coat color is not expressed and the horse is white.
B/B, mt/mt --> white

Because the modifier alleles are separate genes from the coat color alleles, the two are non-allelic - yet they both affect the same trait in some way.

I hope this helps.

Alleles of two or more independent genes interact to produce a phenotypic expression different from normal expression


Mathematical representation of "gene signatures" According to Wikipedia's definition, "a gene signature is a group of genes in a cell whose combined expression pattern is uniquely characteristic of a biological phenotype or medical condition."

While the above definition is very useful to understand the concept, I am looking for a "more practical" definition or, rather, a mathematical representation (e.g., a vector) of gene signatures. Hence my question.

There are mathematical definitions of "gene signature". Please have a look at the supplemental material of Subramanian et al. PNAS 2005, one of the first papers on "gene signatures", and a method and tool which is still commonly used in basic research.

Note that Subramanian et al. have multiple definitions and that copying them here would exceed the scope of this page.

There is no mathematical definition of genetic signature. Please first have a look at Is there a formal definition of signature of natural selection?. As explain the term genetic signature is used in a very broad sense.

There are a number of processes for which one might be looking for a signature of this process. Such signature can take the form of various statistics. For example, a historically important statistics is Tajima's D defined as

$$D = \frac{\Pi - S/a}{SE}$$

, where $\Pi$ is the average number of pairwise differences between two randomly sampled haplotypes, $S$ is the number of segregating sites, $a=\sum_i^{k-1}1/i$, where $k$ is the number of sampled haplotypes. $SE$ is the standard error for the numerator which takes a complicated formulation (have a look at Tajima 1989 for more information).


What E-value BLAST cut-off is best? What is the best cut-off for e-value in BLAST?
Some say 0.01 ,others 0.0001?
Even BLAST tutorials don't give a very clear idea about which cutoff suits which purpose?
Could some experts give me a clear idea on this.
Why are we using 0.0001 and not 0.00011?

There is no perfect cut-off. It always depends on what you're doing. The e-value is basically a measure of how many such alignments you would expect to find in a database this size by chance. Therefore, e-values greater than 1 mean that you'd expect at least one alignment similar to what you've found by chance alone.

As others have stated, the e-value is not a rigorous measure of significance. It depends on

The length of your alignment.
The alignment's bit-score score (this takes into account amino acid substitution scores based on the matrix being used, BLOSUM65 by default).
The size of the database you are searching in.

I have at different times and for different projects used e-values ranging from 10 to 1e-100 or less. You always need to take into account what you are looking for. For example, to run a tBLASTn looking for distant homologs, you'd use a relatively high e-value, say 1e-10 or even 1 or greater depending on the details. For example, the default e-value for ncbi-tBLASTn is 10.

To find extremely similar sequences in closely related species, you'd use a much smaller one. Say 1e-20 or 1e-50. Normally, you tweak these settings after seeing your results.

After running a few hundred blasts, you get the hang of it and you can have a pretty good estimate of the e-value cutoff you want to use. Until you get that experience, you will have to use trial and error. Just remember that the conclusions you can draw from your data will be heavily influenced by that e-value. Don't try to publish something claiming you've found a homolog if the supporting BLAST hit has an e-value of 45 for example.

Personally, when looking at BLAST out files, I check the e-value, the alignment's length (as a percentage of the query), the alignment's %id score and the bit score itself. Of these, the most reliable is the bit-score but, again, that too changes depending on what question you are attempting to answer.

The e-value is required to have confidence in the hit, along with hit. Generally, an e-value of e-4 is preferred because, this cutoff is found to be sufficient enough by blast to confirm a hit as homolog. But, for a hit, an e-value greater than e-4 does not mean it is a homolog neither we can say it is not a homolog. We cannot surely infer anything from these hits. Therefore, researchers choose a value


Why only 6 water molecules are formed in the aerobic degradation of glucose? I am studying the aerobic degradation of glucose and it seems that for every glucose molecule we should obtain $\ce{10H2O}$ molecules. However, it is known that we only obtain 6.

$\ce{C6H12O6 + 6O2 -> 6CO2 + 6H2O}$

(I am not going to focus in all products and reactants, but just in the important ones for the formation of water molecules)

First, in the glycolysis, for each molecule of glucose we obtain two water molecules, $\ce{2NADH+}$ and 2 pyruvate molecules. By the oxidation of two pyruvate molecules we obtain $\ce{2NADH+}$ and 2 acetyl Co-A molecules. So we are going to pass twice through the Krebs cycle, obtaining $\ce{6NADH+}$ and $\ce{2FADH2}$, and requiring 4 water molecules.

So, when we arrive to the electron transport chain, we have a negative balance of 2 water molecules, and we have $\ce{10NADH+}$ and $\ce{2FADH2}$. We have been told that for every of these molecules 2 electrons go to the electron transport chain, that means that a total of 24 electrons go to the system. The problem comes here:

$\ce{4e- + 4H+ + O2 = 2H2O}$

So, bearing in mind that we have $24e^-$, 12 water molecules should be formed, so at the end, we have gained 10 water molecules, but we know that the number of water molecules formed should be 6. So, clearly there is something wrong in my explanation. I would be very pleased if you could tell me what is wrong.

Thanks in advance.

Your confusion comes entirely from this equation:

$\ce{C6H12O6 + 6O2 -> 6CO2 + 6H2O}$

This reaction is the combustion of glucose. This is not how glucose is oxidized in cells! Why so many biology texts and courses present this equation when introducing metabolism is beyond me.

Indeed, your tracking of water molecules is correct: starting with one glucose molecule, 2 waters are produced in glycolysis, 4 are consumed in the tricarboxylic acid cycle and 12 are produced during oxidation of NADH/QH2 (ie FADH2). This gives a net total of 10 produced.

Why is this different from the combustion of glucose? The answer lies in the oxygens introduced by inorganic phosphate during substrate level phosphorylation. Consider the balanced net reaction for the biological oxidation of glucose (simplified by ignoring ATP produced by oxidative phosphorylation and substituting ADP/ATP for GDP/GTP):

$\ce{C6H12O6 + 6O2 + 4ADP + 4P_i + 4H+ -> 6CO2 + 4ATP + 10H2O}$

In particular, consider the formation of ATP from ADP and Pi (HPO42-). In both substrate level phosphorylation reactions (catalyzed by GADPH/PGK in glycolysis and succinate-CoA ligase in the tricarboxylic acid cycle), inorganic phosphate nucleophilically attacks the activated carbonyl (thioester) of the substrate and is then transferred to ADP (to form ATP):

The oxygens of the original inorganic phosphate are coloured red. The key point is that an oxygen atom from HPO42- is transferred to the substrate. This oxygen is later removed in the form of carbon dioxide, via oxidative decarboxylation, during the conversion of pyruvate to acetyl-CoA and in the tricarboxylic acid cycle. This occurs four times for each glucose molecule entering glycolysis and is accompanied by the reduction of NAD+ to NADH. Given that NADH is used to reduce molecular oxygen during the electron transport chain:

$\ce{NADH + H+ + 1/2O2 -> NAD+ + H2O}$

...this explains where the four, apparently extra, water molecules come from when comparing the combustion of glucose with its biological oxidation.

Two waters come in at each turn of the TCA cycle, one at citrate synthase and one at fumarase. Additionally, I don't think it's right to say that you get a net water from glycolysis (in fact if you look at what you wrote, the oxygens don't balance). I think what you're missing is you also get an ATP, and the water you do get at the 2PG->PEP step is really part of the net reaction ADP + phosphate -> ATP + water.

To really balance the waters you have to consider all the substrates and byproducts of glucose oxidation, including the ATP/GTP.


How can parentage test be accurately done even though crossing over occurs? As crossing over occurs when gametes are secreted, so when a zygote is formed after fertilization, the base pairs of DNA in the child should be different from that of the parents. So when gel electrophoresis occurs, the position of DNA fragments of the child shouldn't be the same as half of their father and mother. But why is this statement wrong? sorry for bad English.

Crossing over is an event that occurs during meiosis, which produces the gametes. This crossing over occurs between 2 homologous chromosomes, which are both from the parent. Hence, even though crossing over occurs, the recombinant chromosome that is passed down to the child will contain an allele that matches with the allele on one of the parent's chromosomes. Within the allele, the base pair sequence would not change.


Blebbistatin effect on vesicles Blebbistatin is a drug that specifically inhibits the assembly of myosin in the cytoskeleton. What effect would you expect blebbistatin to have on intracellular vesicles?

The formation of vesicles would cease.
The movement of vesicles within the cell would cease.
The vesicle membranes would fail and release their contents into the cytoplasm.
The vesicles would be unable to fuse with the plasma membrane.

I don't readily see how Blebbistatin would effect intracellular vesicles; I believe this ignorance comes from not knowing what myosin is and how it interacts in the cytoskeleton.

Blebbistatin inhibits myosin II by blocking it's attachment with actin. Myosin II and other actin based motors have shown to be involved in vesicle budding from trans golgi network. Given this information, I think correct answer will be

  The formation of vesicles would cease.

Following cartoon from (Stow et al 1998) shows proposed mechanism,

However looking at this paper, option (2) The movement of vesicles within the cell would cease, also sounds reasonable.

Blebbistatin blocks effectively the Myosin II light chain kinase (MLCK)activity, and myosin being a motor protein, plays an important role in vesicle traffciking thereby affecting the process of endo and exocytosis.
With this information, I think it would be logical to say that blebbistatin will cease the formation of vesicles, the vesicle movement and inturn will inhibit the ability to fuse with the plasma membrane.
It looks to me more like a cumulative effect of blebbistatin on the intracellular vesicles.


Why are cells affected by time? We as individuals die when we get old. But why are cells affected by time? We are constantly providing energy to the cells through food, but the cells die after a certain time. Why does this happen?

Individual cells don't live forever because they are damaged by their environment, for example by chemicals, radiation and mechanical wear and tear, or by other organisms (see this review). In multicellular organisms, such "worn out" cells are typically dismantled by programmed cell death and new cells are generated to take their place.

The life span of animal cells varies widely depending on their location and function. For example, epithelial cells lining the skin and intestines are exposed to a harsh environment, and consequently live only a couple of days. At the other extreme, neurons, which are safely lodged in the protected brain tissue, can live as long as the individual (or even longer).

Note that the life span of a given cell is very different from replicative age, which refers to the number of divisions a cell lineage has undergone, measured from some progenitor cell. Most animal cells are allowed only a limited number of cell divisions (known as the Hayflick limit) and thus their lineage is "mortal", while that of microorganisms are not.

I love questions like this! my reasoning is that while cells certainly have processes and mechanisms that exploit entropy, the bitter reality is that eventually something like our own cells will be subjected to entropy and will ultimately die and be disassociated. Every second a cell produces ATP to survive it is put under more and more oxidative stress and this is why cells age and ultimately die. It is also why less metabolically taxing lifeforms like a plant, can live for hundreds of years, as opposed to a mouse, which lives for like 3 years (an animal with a high metabolism)

my english is terrible so in short: energy is oxidation, oxidation reactions are entropy favored, this causes things to age. higher metabolism = more oxidation = shorter lifespan. Plants dont get up and run so they can live longer than animals which do


Is there an advantage to antibacterial soap? There are plenty of different hand soaps out there, as well as hand sanitizers. Is there an advantage to soaps that claim that they're antibacterial vs soaps that just say soap?

In particular I'm looking at Softsoap who offers normal soap and antibacterial soap.

Examples:

Normal:

Antibacterial:

Short answer: There is no benefit for their use in households.

Long answer: These soaps (see here for the complete list) contain the so called quaternary ammonium compounds Benzalkonium chloride and Cetrimonium chloride which indeed have antimicrobial properties.

While they do not promote resistance to these compounds (see reference 1), their use is still not recommended, as their permanent use might dry out the skin, can cause contact allergies and the products released into the environment are also problematic.

There are two studies, which compared the use of normal soap (which has some antibacterial properties on its own) to antibacterial soaps in household environments and found no differences. See article linked in reference 2 for a summary and references 3 and 4 for details on the studies.

This doesn't mean that antibacterial soaps are useless at all, they simply make no sense in households. For hospitals or doctors they are an important tool to protect their patients before operations. But here detailed instructions for how long and how the hands have to be washed are provided. Hand washing is also followed by another disinfection step, which helps with efficiency. But this is very much different from the way people wash their hands at home. See reference 5 for some opinions here.

References:

Use of germicides in the home and the healthcare setting: is there a
relationship between germicide use and antibiotic resistance?
Plain soap as effective as antibacterial but without the risk
Consumer antibacterial soaps: effective or just risky?
Effect of antibacterial home cleaning and handwashing products on
infectious disease symptoms: a randomized, double-blind trial.
The Burning Question: Is It Safe to Use Antibacterial Soap?

Human immune defense response is primed by cell damage products as it does not have prior knowledge about bacterial or viral "malware".

The whole purpose of disinfectant substances is damaging cells and potential organic disease carriers.  As those substances are not discriminating, frequent use of them will prime your immune defense against benign organic matter as well.  In combination with solvents that remove protective layers of fat and thus increase the permeation of this kind of cell waste into top skin layers, this sounds like a recipe for allergies and neurodermitic reactions in the long run.

There is a high correlation of countries (and eras) with high standards of living including household hygiene and autoimmune response problems.  Finding actual causations is work in progress.

While that is still the case, it is my gut feeling that contact with disinfectants should be reserved to cases of tangible risk.


What's the evidence against SARS-CoV-2 being engineered by humans? A couple of colleagues suggested in a discussion that the virus that causes COVID-19 appears to be made by humans, since nature could not have produced such an efficient virus — that spreads so fast and whose patients are contagious quite some time before showing signs of infection.

Since my knowledge of biology is very limited, my only counterargument for such a conspiracy theory was along the following lines:

there is a consensus that the most probable source of the first infection was in an animal market in China.
since that animal market was actually composed of a plethora of animals belonging to various species (mixed with humans), a virus had a bigger chance of evolving a mutation that might infect an individual from another species (a thing that is way less unlikely in the wild since many of those animals do not sit close to each others or next to humans).

Clearly, I have made a little story that might be quite far away from how SARS-CoV-2 infected humans, so I am interested in a scientific arguments to support my cause.

Question: What are the main scientific arguments that can be used to debunk COVID-19 being engineered by humans?

Answers that also include explanations more accessible to laymen are greatly welcomed.

At the moment, there is very little scientific literature about this, but I found two papers that address the problem and are fairly easy to understand. You can find them in the references. Reference 1 is probably the most interesting and is the basis for this answer.
Edit: It is also interesting to read reference 2 on the origin of SARS-CoV-2; the article also addresses some of the conspiracy theories.
As far as I can see, there are a few major points taken up by conspiracy theories.
1. SARS-CoV-2 leaked from a lab in which research on the Bat CoV (RaTG13) was done:
Unlikely, since the viruses share only around 96% sequence homology, which translates into more than 1100 sites where the sequence of SARS-CoV-2 viruses is different from RaTG13. The mutations are distributed throughout the viral genome in a natural evolutionary pattern, making it highly unlikely that SARS-CoV-2 is a direct descendant from RaTG13. For comparison, the original SARS-CoV and the intermediate host palm civet SARS-like CoV from which it originated shared 99.8% sequence homology, showing a much closer relation.
2. The S (spike) protein from bat SARS-CoV cannot be used to enter human cells via the human ACE2 receptor and therefore has been adapted in the lab:
This is untrue, since a 2013 study of a novel bat coronavirus was published showing the ability of the virus to enter cells via the ACE2 receptor. See reference 3 for details.
3. The spike protein of SARS-CoV contains a unique inserted sequence (1378 bp) located in the middle of its spike glycoprotein gene that had no match in other coronaviruses:
As shown in reference 4, the sequence comparison of the SARS-CoV-2 with closely related other coronaviruses shows that this sequence is not unique to the new virus but is already present in older strains. It shows some difference due to inserted mutations.
4. The claim that SARS-CoV-2 contains four insertions from HIV-1:
The paper claiming this has now been retracted due to severe criticism, and additionally a renowned HIV expert published an analysis (reference 5) demonstrating that the HIV-1 claimed insertions are random rather than targeted.
5. The claim that the SARS-CoV-2 virus is completely man-made:
To design such a "weapon grade" virus in the lab, the design would usually start from a known virus backbone and then introduce logical changes (for example, complete genes from other viruses). This cannot be seen in the genome of the virus; rather, you see randomly distributed changes throughout the genome coming from virus evolution and not directed cloning. It is more likely that this virus originates from the recombination of a bat CoV (to which it is closely, but not directly related) and another, not yet known CoV in an intermediate host, like the palm civet for the 2003 CoV.
References:

No credible evidence supporting claims of the laboratory engineering
of SARS-CoV-2
The proximal origin of SARS-CoV-2
Isolation and characterization of a bat SARS-like coronavirus that
uses the ACE2 receptor
Is SARS-CoV-2 originated from laboratory? A rebuttal to the claim of
formation via laboratory recombination
HIV-1 did not contribute to the 2019-nCoV genome

A conclusive proof of CoV2's artificial origin would be finding lab records or samples dated before the epidemic, or finding an obvious unique marker sequence in the cDNA. To date there is no such conclusive proof.

All other "proofs" I have seen are just hypotheses, and they all can be explained by natural processes too. In fact, if your opponents refuses to consider natural causes, such hypotheses become infalsifiable, like the Russel's teapot: any naturally occurring coronavirus can also be recreated in the lab. Here's an article from 2003 in which researchers describe how they have recreated SARS-CoV using a panel of cDNA fragments, which produced a virus identical to the natural strain (except for marker mutations).

For instance, here's a closer look on the infamous "unique sequence in S protein" (called Receptor Binding Domain) of CoV2, compared to RaTG13 (bat coronavirus) and MP789 (pangolin coronavirus):

source

As you can see, the "uniqueness" of this sequence is questionable if we consider that RaTG13 could have combined with a part of MP789 (in the red frame) and accumulated some additional mutations to produce CoV2. The conclusion that such recombination happened artificially can only be drawn if you see no possibility those two viruses could have met in the wild.

There's also a philosophical side to what should be considered "artificial". Two viruses recombining in the wild is natural. How about two viruses recombining in a market? What about a lab cage or waste?


At what point do scientists consider something sentient vs random and/or genetic? When I was thinking about sentience from a scientific point of view, I was confused about the bio-electric mental difference between a paramecium, dog, human, and supercomputer.

At what point does electricity go from being random and genetic to creating logic gates for perceived "sentience" / intelligence?

if you have 300 neurons and 10 of them can put you in a depressed state, you are a sad eukariote.

To compare the logic gates of a worm and a mouse? which one is sentient? a slug literally has 10k neurons and a fly has 250k. that would make a slug 25 time sless sentient than a human, and a dog less sentient than a human, but a human is equally as sentient as a dog so numerically there may be now lower bounds.

Logic Gates are electronic switches which provide routing for AND/OR/NOT/EQUALS of data types, or objects. They come into existence when you have the first cilia and sensory cells. 20 nerves are a signal routing engine, logic system.

A neuron can roughly represented by 4-8 transistors, and a logic gate is a simple transistor routing/instruction, so a worm has about 2000 logic gate equivalents. https://en.wikipedia.org/wiki/List_of_animals_by_number_of_neurons

A logic gate is digital, a brain is analogue, no software, , so you inadvertantly weave smoke and mirrors to clarify your question.

The question evokes electrical sentience, synapses are electrochemical, slower than electricity and can varied in many ways chemically, and they are self organizing.

feeling, aware and knowing (reductionism of sentience) are much more debated topics in science. Relative to random and genetic logic gates for intelligence, that's unclear and you are discussing free will and decision (philosophy), intelligence has unclear relation to sentience/emotion.

Your question is confusing a vast range of scientific measures by using the term sentience, which is rarely used in science. Scientists write informally about sentience as an ethical issue based on their experience, but there's only fringe research on animal sentience. https://scholar.google.fr/scholar?hl=en&as_sdt=0%2C5&q=sentience+fish&btnG=

Animal psychology is a scientific topic, and sentience is metaphysical, it means feeling, aware and knowing, it's incommensurate and imprecise.

So scientists don't consider there to be such a point of sentience. They measure certain markers of sentience, such as

self awareness,

stress response,

emotional queues,

counting,

comparing,

memory,

puzzle solving,

social behaviour,

hormones, that kind of thing.

There are perhaps a 2 publications about sentience in fish, none about lizards or insects, and there are thousands of books and opinions about sentience in insects and other animals.

The brain increases in size from a dozens to billions of neurons. So the progression is in stages, so awareness is likely to be a complex series of steps.

A good animal psychologist can give you an entire book about the onsent of emotions and knowing in animals.


Can a woman possessing 1 mutated allele show attenuated color-vision deficiency? Women possess two X chromosomes. However, during development, when the embryo has about 32 - 64 cells, one of these chromosomes is randomly inactivated (in each cell) by an lncRNA named Xist. As a consequence, females are mosaics.

I was interested if this might affect phenotypes of X-linked genetic diseases, for example...

1) Is it possible for a woman who is heterozygote to color vision deficiency be "partially" color blind, considering that some of her cones will only possess the mutated allele?

2) Is it possible that a heterozygote female who carries a dominant allele for a X-linked disease be asymptomatic?

Any references on these issues are welcome.

Short answer
Skewed X-inactivation may lead to phenotypic manifestation of X-linked color blindness.

Background
What an interesting question!

In a study by Jorgensen et al. (1992) two female identical twins that were heterozygotes for X-linked deuteranomaly were investigated. Phenotypically, deuteranomaly refers to anomalous trichromacy, i.e., reduced perception of a color. Note that deuteranopes are totally color blind. Deuteronomaly in the twins was associated with a defective gene derived from their father. Interestingly, while monozygotic twins are genetically identical, one of the twins was phenotypically deuteranomalous, while the other had normal color vision.

Analysis of skin cells of the color vision-defective twin revealed that almost all skin cells had the paternal abnormal X chromosome active, explaining her color-vision defect. In contrast, skin cells from her sister with normal color vision had predominantly the maternal X chromosome active. Hence, deuteranomaly in one of the twins could be explained by an extremely skewed X inactivation.

As pointed out by @mdperry, extreme skewed X-inactivation is rare, and most heterzygous females for color blindness (carriers) are indeed asymptomatic (Jordan & Mollon, 1993). Regarding your second question, all gene mutations leading to color blindness are recessive (NIH).

References
- Jordan & Mollon, Vis Res (1993); 33(1): 1495-1508
- Jorgensen et al. Am J Hum Genet (1992); 51: 291-8

Your theoretical understanding of the ramifications of X-chromosome inactivation is excellent (e.g., the two situations you described).  However, it is important to consider the size of the resulting clones. At that early stage of embryogenesis only ~ half (or less) of those cells will go on to contribute to the fetus, the rest will form the placenta. Also at this stage each cell is likely totipotent, and capable of contributing to all of the different tissues, but eventually the daughters of these cells will become committed, or determined in their developmental lineage. Depending on how much mixing of cells occurs prior to determination, I think it unlikely that within one retina the cone cells would originate from more than a single clone--so I would think that either they all are + or the all are mutant. Since there is L-R symmetry between the two optic cups that will give rise to the developing eyes, I think it is more likely that one female could have one eye that is mutant and one eye that is +.  Given that the prevalence of red-green color-blindness in males approaches 7 % of the population, we can infer that heterozygous females are very common, yet to the best of my knowledge there are not millions of females with partial color-blindness--they either have it (m/m), or they don't (+/+ & m/+). So I think a mosaic female with one eye color-blind and one eye normal must be exceedingly rare.
Re: autosomal dominant diseases, it all depends on the tissue(s) and the affected developmental stage. The OMIM, Mendelian inheritance in Man database may have some discussion of this interesting point(?).


what's the difference between traditional genetic engineering and and CRISPR? While at school, I learnt about restriction enzymes and how you could insert foreign DNA into an organism.

When I first heard about CRISPR I thought it was very similar except much more precise/targeted.

It seems however that CRISPR only allows editing (substituting nucleotides)

What are the differences, advantages, etc?

Bacteria and archaea evolved CRISPR as part of their adaptive immune system to protect themselves from invading viruses and foreign plasmids. The defence system relies on small, non-coding RNA molecules (CRISPR RNAs/guide RNA) that in association with a CRISPR associated (Cas) protein silence foreign sequences by means of cleavage. Twenty nucleotides at the 5’ end of the CRISPR RNA, corresponding to the protospacer region, direct the Cas9 protein to a specific sequence within the DNA using predictable Watson and Crick base pairing between the target DNA and the guide RNA, triggering enzymatic cleavage of the foreign DNA. Essential for cleavage is the presence of a sequence motif immediately downstream of the target region, known as the protospacer-adjacent motif (PAM),the PAM sequence in S. pyogenes (the most widely used system) is NGG. Because a sequence match also exists between the guide RNA and the host’s DNA that encodes it, it is vital that the guide RNA identifies bona fide targets without attacking the host chromosome. Discrimination between the target and host protospacer is achieved by the Cas effector recognition of a PAM sequence that initiates binding and cleavage of the foreign DNA. Changing the DNA target site that is specified by the 20 nucleotides at the 5’ end of the guide RNA redirects the system to target a different DNA sequence, making it a highly versatile and programmable tool. In 2012, the CRISPR system was  programmed to cleave specific DNA sites in vitro and since then, the system has been widely used in many gene modification applications.

CRISPR allow so much more than just substituting nucletodies. Like you say, CRISPR is a much more precise system than restriction enzymes, the guide RNA for CRISPR systems is typically around 20 nucleotides long so it can theoretically be used to target a unique site in the genome (4^20 = 10^12, so only the recognition site is expected to feature once 1 in 10^12 bases, N.B. the human genome is only 3x10^9 base pairs in size).

There are several options using the CRISPR with an active Cas9 protein, the first is to create a gene knockout, which removes the function of a gene. Gene knockouts can be performed by targeting the CRISPR-Cas9 system to the start of the gene and cleaving both strands of the DNA to generate a double stranded break which will be repaired most likely by the cellular repair pathway non homologous end joining (NHEJ). NHEJ results in insertions or deletions and so will most likely result in a frameshift mutation which alters a large amount of the amino acid sequence in the gene or introduces an early stop codon, so the protein produced is non functional. Alternatively a conserved residue (e.g. a catalytically important residue) in the protein can be targeted and mutation of this can remove the catalytic function or recognition domain in an enzyme or protein. NHEJ can also be used to mutate DNA that codes for RNA products. Additionally, the CRISPR system can be targeted to regions outside of the coding sequence such as the promoter or enhancers and silencers/operators (depending on whether prokaryotic or eukaryotic), which can also remove the functionality of the gene.

The CRISPR system can also be introduced to the cell  together with a single-stranded or double-stranded DNA template to make very small and precise changes to the DNA (e.g. single base mutations), or insert DNA sequences up to thousands of bases in length so that entire genes can be incorporated into the target region. This more precise editing method also involves the double stranded break formation by the cas9 protein, but relies on different cellular repair pathways: homology directed repair, the most common form of which is homologous recombination. Importantly, the template DNA must have homologous sequences to the DNA flanking either side of the double stranded break. In the presence of the correct exogenous DNA template, homology directed repair can occur in which the exogenous template DNA is incorporated into the target DNA in exchange for the damaged DNA.

Other use of CRIPSR include using a catalytically inactive cas9 protein (dead Cas9). This system is unable to cleave DNA, but is still able to target specific sites in the DNA. dead Cas9 can be fused to or recruit effector proteins for regulating gene expression at the transcriptional level, as well as guiding enzymes capable of precise base editing without introducing double stranded breaks. The dead cas9 system can be fused to transcription repressor domains such as the Krüppel-associated box (KRAB) or transcriptional acitvators such as VP64 for effective and specific repression or activation of gene expression at sites that don't contain recongion sequences for these effectors. dead Cas9 can also be used to recruit epigenetic modifitying enzymes such as methylases and acetylases to regulate gene expression this way. Additionally, this system can be fused to DNA base editors, which are enzymes created by directed evolution that are capable of causing efficient and specific point mutations in DNA and RNA (this is much more specific and effective than point mutations using homology directed repair), although RNA editing required using cas13.

Gene editing can be used to repair disease causing mutations, introduce new genes with novel functions into organisms' genomes, transiently alter gene expression to treat diseases; create knockout, knockdown and knock in strains for studying the effects of genetic factors on phenotype and even more.

In contrast, restriction enzymes typically have recognition site of 6 nucleotides and so they will cut at many orders of magnitude more sites than CRISPR will (4^6 = 4096, so 1 in 4096 nucleotides are expected to be a cut site for restriction enzymes) so they are not suitable for specific editing of genomes as they will cause non specific fragmentation of genomic DNA, which will kill the organism, so CRISPR is a much better enzyme for editing genomes. Instead, restriction enzymes are used in molecular cloning to generate sticky overhangs (or blunt ends) for the assembly of DNA molecules to generate recombinant DNA.

Although the PAM appears to limit the number of target sites that the CRISPR system can be targeted to (around 1 in every 16), through directed evolution, a Cas9 variant with increased PAM compatibility has been developed. This new Cas9 is capable of recognizing PAM sequences including NG, GAA, and GAT, this makes it  more versatile and greatly expands the number of targets available for site-sensitive genome editing applications.

Whilst CRISPR based gene editing is very exciting, a lot of work is still needed to: increase the specificity of the system as it causes numerous off site mutations, which can be lethal to cells; to increase the effectiveness of delivery of the system in vivo to large organisms such as humans; to reduce the immunogenicity of the system (it can trigger an immune response in humans) so that it is safe to use; as well as increase our understanding of the affect of making specific mutations in humans (e.g. which mutations can treat diseases safely).

References/further reading:

Jinek, M. et al. A programmable dual-RNA-guided DNA endonuclease in adaptive bacterial immunity. Science (80-. ). 337, 816–821 (2012).

Repurposing CRISPR as an RNA-Guided Platform for Sequence-Specific Control of Gene Expression. Cell 152, 1173–1183 (2013).

Liu, X. S. et al. Editing DNA Methylation in the Mammalian Genome. Cell 167, 233–247.e17 (2016).

Zalatan, J. G. et al. Engineering complex synthetic transcriptional programs with CRISPR RNA scaffolds. Cell 160, 339–50 (2015).

Hu, J. H. et al. Evolved Cas9 variants with broad PAM compatibility and high DNA specificity. Nature (2018). doi:10.1038/nature26155

Cox, D. B. T. et al. RNA editing with CRISPR-Cas13. Science (80-. ). 358, 1019–1027 (2017).

CRISPR is a gene system used by bacteria to resist virus invasion/avoid mammalian immune response. Scientists use RNA to guide cas9 nuclease to cut and modify specific genomic sites in a variety of cells, including IPS. The Rudolf jaenisch team injected cas9, te1 and tet2 specific sgRNA into the fertilized eggs of mice, and successfully obtained the homozygous mice with double gene knockout, with the efficiency up to 80%. They co injected cas9/sgRNA with primers with mutated sequences, which can accurately introduce the required point mutations into two genes of mice. In ES cells, they successfully knock out five genes at a time. Compared with ZFN/talen, CRISPR/Cas is easier to operate, more efficient, and easier to obtain homozygous mutants, and can introduce multiple mutations at different sites at the same time. But whether the system has Miss target effect needs further study.

The traditional transgenic and gene targeting technology, due to its stable and mature technology, can modify the genome sequence of mice and rats, and will still be the main technology of model animal construction. If ZFN/talen, especially CRISPR/Cas, can solve the Miss effect, it may be widely used in the preparation and research of mice, rats and other model animals, and become an important supplement to the traditional transgenic and gene targeting technology.


Seeing with one eye, why intensity doesn't get half? Today I just closed one eye(for finding blind spot), and as usual some of the visual field is lost, but I wonder why is not intensity of light(brightness) reduced to half?
Shouldn't it be since our brain is now getting only half impulses?

Does our brain instantly reduces the threshold of rods and cones when one of the eye is closed?

Think of eyes as cameras producing an image at a given framerate. If you have 2 cameras and shut 1 of them off, that doesn't change the amount of light incoming to the other camera.

Your question is one of signal interpretation rather than receiving signals and adding them. Given that the 2 cameras have different perspectives, adding their respective pixels makes no sense. Instead, the dual images (if both cameras are on) are post-processed for spatial reference relevant to perspective.

In the case where a camera is shut off, then the spatial reference becomes a null picture and the post-processing can be skipped.

(For reference, if you took incoming data from both eyes and added them, the result would be an incoherent and largely unusable mess)

Experiment 2

Aim: Effect of intensity on two eyes

Requirement : Two eyes, a dark transparent glass, an object to glance.

Procedure :
1)Sit in a lit room
2)Look at fan with only right eye
3) Look at fan with only left eye through dark glass.
4) Look from both eyes( keep dark glass in front of left eye)

Observation : Brighter in only right eye, darker in only left and medium brightness with both eyes.

Result: Intensity do add when are different. Or more correctly they rather average out.

In your actual experiment, the intensities in two eyes just averaged out, that was mathematicaly equal to single eye.

Theory:

Three principle

  1) Brightness is transferred via frequency principle. Greater the intensity of light, greater the frequency of AP transmitted.

  2) [Action Potential ][1]

Action Potential has a fixed depolarising potential.

  3) Each spatial point, in space, of vision, is represented on a single spatial point in occipital cortex.

Two action potential caused by same image pixel reach their representative point on occipital cortex area 17.

They are then sent to visual associative Area 18 for matching.

  “Fusion” of the Visual Images from
  the Two Eyes

  To make the visual perceptions more meaningful, the
  visual images in the two eyes normally fuse with each
  other on “corresponding points” of the two retinas.
  The visual cortex plays an important role in fusion. It
  was pointed out earlier in the chapter that corresponding points of the two retinas transmit visual signals to
  different neuronal layers of the lateral geniculate
  body, and these signals in turn are relayed to parallel
  neurons in the visual cortex
  Source: Guyton and Hall, chapter 51.

Same impulses from same spatial point are sent to same interneuron.

The action potential cannot rise further.(Principle 1 above)

This fused signal reaches next neuron for further processing. Intensity is judged.

Same amplitude as of one eye reached, so same intensity was percieved by even two eyes.

If fused signal is of intermediate frequency, intermediate brightness is observed.


Does darker skin color make it easier to live under sun? I have always thought darker colors absorb more heat from the sun, so if you are wearing a white T-shirt you will be cooler under sun than wearing a darker T-shirt, or a black piece of steel will be hotter under the sun than a shiny silvery one.

If this is true, then why is the same not applicable to skin color? It seems to me like the more sun in an area the darker the people's skin has become, isn't that the case?

It isn't about heat but ultraviolet light. Melanin is the pigment that makes our skin colour whatever it is and in darker skin there's more melanin. Melanin dissipates UV, which otherwise would cause skin cancer as it introduces mutations into DNA. Melanin production is stimulated by UV so that's why tanning beds work, our body senses the danger and responds by making our skin darker. Yes this makes us hotter but that's a small price to pay, melanin needs to be dark to do its job well.

to answer your question from years ago maybe to better inform any new readers that read this. yes and no. we have melanin in more areas than just our skin, it's in our nervous system, in our eyes, and etc and we should also ask what "information" we obsorb in those areas. having melanin does make it easier to absorb all wavelengths on the electromagnetic spectrum, but not everyone with dark and lighter skin can live easily under the sun. also consider what i call "inorganic" or "chemical" EMF/wavelengths highly melanated beings are receiving from computers and other man made devices which there are links to cancer and other issues in the body from those unnatural EMF.  Research has shown that most bodies whether light or darker can't survive past 104F because the thermoregulatory system shuts down. now if it 120f outside does this mean that your body is the same temp,,, i don't feel so after being exposed to such weather. i have light skin, but can develop melanin rapidly with minimal damage or sunburn occurrences. but my auntie who is darker than me, who has lupus, cannot be in the sun. this is on an individual basis, but having more melanin or active melanin in general to protect you may be more in your favor, especially this 2017 and upcoming years. the color white is said to block the UV rays, but not absorb most of it. this poses the question to cancer caused by over exposure to the sun and the hue you are as man, if you are of darker hue and do not have any sun exposure, you will or may have more health problems, little to no active melanin or light skin, you may or may not have more health problems in the sun or certain longitudes and latitudes. this is good to consider whether you are aligned in a place where you are getting the correct amount of sun exposure, or consider if you are getting the incorrect amount of sun exposure. again, this answer can only be answered on an individual basis.


What is the difference between a circular and a cat's-eye (slit) pupil? I've been to local zoo the other day and one lizard caught my attention: its pupils are circular, which, I thought, is not usual for reptiles. Turns out it is, but now I can't find any explanation on why some animals have one kind of pupil and others have the other. Lizards can have both, and so can snakes. The only difference I have found is that circular pupil can't shrink quite as much as a cat's-eye pupil, but that hardly explains why circular pupil even evolved in the first place as I don't see any advantage to it.

Ideas?

P. S. Fish only have circular pupils so that shape is older, right?..

Circular pupils are always functionally superior to vertical pupils; a slit does not correctly focus light from all directions whereas a circular pupil does. If you observe cats when they're hunting at dawn and dusk*, they have big, circular pupils; it's only when they're in bright light that the pupil shrinks to a slit. So why have vertical pupils at all? Because, as you mention they're capable of letting a more controlled range of light into the eye.

Thus vertical slits let you be active in a wider range of light conditions at the cost of poorer vision in bright light; whilst circular pupils continue to function well in brighter light but at the cost of not allowing such a large range of control over the amount of light entering the eye.

It is then easy to see why you get both kinds of pupil: circular pupils are favoured by animals that are typically active in bright light and need good vision under these circumstances; vertical pupils are favoured by animals that are primarily active in low light but need some ability to see in bright light.

*- it's often stated that cats are nocturnal, this is untrue; cats are crepuscular - that is they are most active at dawn and dusk.

I see one possible advantage to round pupils. A slit pupil gives higher visual acuity vertically than horizontally because of diffraction and when a slit pupil is very nearly shut, there's high diffraction in the horizontal direction giving poor horizontal visual acuity. A round pupil on the other hand gives a creature the highest visual acuity in all directions for a given area of pupil. A smaller pupil is better for reducing chromatic aberration but chromatic aberration can be pretty much neglected because for any creature with evolutionary pressure for sharp vision in all directions, good accomodation will ensure at least one wavelength of light focuses onto the retina forming a sharp image because the sun emits a continuous range of wavelengths.


Why are there three stop codons but only one start codon? I was wondering whether there is any specific reason that there are three stop codons but only one start codon in prokaryotic and eukaryotic cytoplasmic mRNAs.

Disclaimer

It is important to realize that it is not possible to answer questions of this sort (the evolution of translation)  in anything other than a speculative manner. Please bear this in mind, especially if you find the speculation below persuasive.

Summary

It is suggested that the redundancy of termination codons is largely similar to that for ‘elongation codons’ decoded at the A-site of the ribosome, although protection against suppressor tRNAs may also be a factor. The consideration here is, therefore, mainly focussed on the question why there is only a single codon for methionine (initiation and elongation), and I suggest this may have been a combination of the late appearance and infrequent usage of methionine, together with the particular requirements for an initiation tRNA at the P-site of the ribosome, where standard wobble is apparently not possible.

Disposing of a Red Herring

Although alternative initiation codons are sometimes used, this usage differs in prokaryotes and eukaryotes, is very limited, and is not seen with the use of methionine in elongation. I would therefore consider this does not invalidate the question, but perhaps rephrase it as:

  “Why does the genetic code have only one codon assigned to methionine,
  the initiation codon, whereas other amino acids and termination have
  generally more than one?”

Time of appearance of and extent of use of Methionine

It is generally thought that genetic code initially encoded a small number of amino acids, and that this number increased over time. Methionine is one of the most complex (and energetically expensive) to synthesize (see Wikipedia entry), so is likely to have appeared late. One can argue that most of the codons would have been ‘taken’ (assigned) by that time. This argument is consistent with the situation for tryptophan, the other amino acid which has only a single codon, and which is also synthetically complex. Furthermore, these are the two least abundant amino acids so on can argue that their number of codons reflects their relative usage.

Admittedly, there need only be one stop codon per protein, but it is possible that the mechanism of termination evolved before that of methionine-specific initiation. (Initiation might originally have been from the 5′-end of the mRNA.) There is also the question of protection against suppressor tRNAs, but I shall delay discussion of this until the end.

The unique features of the initiator tRNA

Elongation involves several dozen amino acyl-tRNAs being recognized by an elongation factor which binds them to the A-site of the ribosome, at which 3′-codon wobble occurs where the redundancy of the genetic code allows and the anticodon of the tRNA has evolved appropriately.

In contrast initiation involves exclusive recognition of a special tRNA by initiation factors but not elongation factors, and subsequent binding at the P-site The tRNA has unique structural features that allows it to be N-formylated — structural features that are retained in eukaryotic initiator tRNA, even though there is no transformylase in eukaryotes. (see this SE Question]

This uniqueness may explain why there is only one tRNA for initiation. However one might ask why there is a not a group of methionine codons (e.g. AUA as well as AUG) recognized by the same initiator tRNA through wobble. The reason for this would seem to be that the P-site does not allow third position wobble (as I explain in the answer to a related question), so the initiation met-tRNA would be codon-specific.

Loose Ends

Although perhaps straying a little from the question, one might still ask why there are not alternative elongation codons for Met — e.g. AUA, which could have been ‘stolen’ from Ile, which already has AUU and AUC. In fact in mammalian mitochondria this codon reassignment has happened, but unfortunately does not help explain things. In mitochondria there is only one tRNAmet for both these codons, consistent with the simplification of tRNAs for the small mammalian mitochondrial genome. Initiation requires the formylation of the methionine.

I will finish by returning to the question of multiple termination codons, which are not really consistent with my suggestion that the extent of redundancy reflects usage. Although termination codons, like elongation codons, are recognized at the A-site they are recognized by protein release factors rather than tRNAs. This means that they will be affected differently by a mutation in a tRNA that alters the anticodon. For an amino acid codon, an altered non-cognate tRNA would only cause some misreading and an altered cognate tRNA might be neutralized by wobble or by duplicate or redundant tRNA genes. AS termination codons are not normally decoded by tRNAs, a suppressor tRNA would cause read-through at all the suppressed codons. The presence of two alternatives means that termination would be likely to occur within about 30 codons 3′ to the original termination codon. Variation in the length of the N- and C-termini of proteins is common among related species, and thus need not be deleterious to the cell.

Related SE Questions

‘Wobble’ in Initiation and Elongation — I have contributed an answer to this.
Why is AUG the Initiation Codon? — I will respond to this presently.
Redundancy of the Genetic Code — I have contributed an answer to this.
Initiator and Elongator tRNAs in Translation — I have contributed an answer to this.

Somewhat obvious, there's weaker selection on the stop codons than on the start codons:

  The selection affecting stop codons is relatively weak. In particular, comparison of the strength of purifying selection to that on start codons indicates that purifying selection on UAA is slightly lower than that on GUG and UUG start codons and much weaker than purifying selection on AUG, the primary start codon.

The reasons for this difference are a bit more difficult to grasp... but even for stop codons...

  UAA is the optimal stop codon based on its higher proportion in highly expressed genes

On the other hand there's drift ("switches") in the stop codons

  Fast-evolving genes generally accrue more stop codon switches than slow-evolving genes, suggesting that the higher evolutionary rate involves also the stop codons.

So come back in a few billion years with the same question on the stop codons.

On the other hand it's fairly well-established that

  In prokaryotes, the start codon is one of the major translation initiation determinants: replacement of AUG with an alternative start codon, such as GUG, typically leads to a several-fold drop in the translation efficiency

As for the stop codons:

  The causes of the observed preference for UAA as the stop codon, particularly in highly expressed, slow-evolving genes remain unknown. One potentially plausible possibility is that UAA is less prone to formation of stable secondary structures in RNA molecules than UAG or UGA which facilitates the release factor access and is likely to be particularly relevant for highly expressed genes. Furthermore, the frequency of readthrough differs for the different stop codons and is the highest for UGA, at least, in E. coli. Because the deleterious effect of readthrough is the greatest for abundant proteins, the difference in readthrough frequencies could, in part, explain the strong preference for UAA in genes encoding such proteins.

So, in summary, the selection reason for the start codon is fairly well understood, but the reason for the observed preference for UAA as an optimal stop codon (in highly expressed genes) is more speculative, which goes hand in hand with its purifying selection not being as strong as that for the AUG start codon.


Can a mathematical function be assigned to ECG diagram? This is a 12 lead electeocardiogram of a 26 year old male:

This is the graph of function $5sin(7x)sin(.5x)cos(3.25x)$
 This graph look quite similar to the ECG diagram.After sketching this graph, I thought whether ECG diagram could be assigned roughly to a mathematical function.

Question: Has anyone ever tried to even roughly assign the diagram to a mathematical function? Is it even possible?


How does one maintain balance sleepwalking? Anectodal. Feel free to shoot it down.

Walking is an acquired skill; As far as I'm concerned exhaustion causes disorientation. Even after waking up it sometimes takes a second or so to get balanced.

How is it sleepwalkers don't stumble around when walking?

Balance is mediated by 3 things: the cerebellum, vision and the ear via the semicircular canal + vestibular nerve (i.e. the ear).

Sleepwalkers lack the visual feedback, but they have a functional cerebellum and semicircular system which is sufficient.

As for waking up and feeling disorientated, if that's when you get up fast that's because your semicircular system hasn't yet reset (as well as your blood pressure has just dipped).

The part of the brain that maintains balance acts subconsciously, and so while you are sleeping in the behavioral sense, you part of your brain (the cerebellum) do not necessarily have to be asleep. And so it can still maintain balance.