text:
$F_{ST}$ when considering a multi-allelic locus
Sewall Wright defined the $F_{ST}$ in a metapopulation as being:
$$F_{ST} = \frac{\text{Var}(p)}{\bar p (1-\bar p)}$$
, where $p$ is a vector of frequencies of a given allele and $\bar p$ and $\text{Var}(p)$ are the mean and variance of this vector.
For example, consider a metapopulation made of 4 subpopulations. The allele frequencies in these 4 subpopulations are p=[0.2, 0.5, 0.8, 0.3]. $\bar p$ is the mean of $p$ ($\bar p = 0.45$) and $\text{Var}(p)$ is the variance of $p$ ($\text{Var}(p )=0.07 \space$).
Question
Can we define $F_{ST}$ for a multiple allele locus? Or should $F_{ST}$ be defined for each allele independently?

Can you provide a cite for the idea? The form of these things varies with the source. $F_{ST}$ is a symbol. What is it supposed to stand for, in English?

@daniel $F_{ST}$ is also called fixation index. It is an index used in population genetics in order to describe the population structure (non-random mating throughout the population) of a metapopulation. Here is the wiki page. I think there is only one definition of $F_{ST}$ but several ways to equivalently understand it. There are a bunch of ways to measure and approximate the $F_{ST}$ but this is the matter of another discussion.

@daniel You may also want to have a look to the table and to the slide that follows this table on this video at 31'44''. It gives an explanation of where the definition I wrote in my post comes from. I am personally not really able to give you a good intuitive explanation of what $F_{ST}$ is. I am only able to give the mathematical definition of it. Here is a related question I recently asked that might help a bit!

Short answer: yes, people have formulated ways to estimate $F_{ST}$ for multiallelic loci, e.g. microsatellites. For a review, see here.
Specifically, Nei could define $F_{ST}$ for multiple alleles as
$F_{ST} = \frac{(H_t - H_s)}{H_t}$,
which is to say the proportion of total heterozygosity that is across rather than within populations. This is agnostic to the number of alleles, as it just uses heterozygosity. I believe there are other formulations as well.
There exist alternate statistics such as $G_{ST}$ and $R_{ST}$ (links under each) which are devised specifically for the multiallelic problem, see also the review for further discussion. Basically, microsatellites have high mutation rates such that they deflate the statistic; this will likely be the case for most multiallelic loci.
It's not clear though which statistic works best in practice as far as I can tell.


text:
Does an old growth forest ecosystem produce more oxygen than it consumes?
I would like to consider an old growth forest ecosystem such as a large part of the Amazonian forest. It is common to refer to such beautiful forests as a source of oxygen for the world. For example, the expression Amazon: Lungs of the planet is very common (e.g. this BBC article). I would like to question such an expression.
Questions
My questions are:

Does an old growth forest ecosystem produce more oxygen than it consumes?
Does an old growth forest ecosystem fix more CO$_2$ than it produces?

My Intuition
I understand that such a forest can be an important carbon storage and that if we were to cut the forest down, burn the wood and pour concrete on the soil (to prevent regrowth), then we would definitely release a fair amount of carbon in the atmosphere.
That being said, I am wondering whether, as of today, these forests act as carbon sink or not. It feels to me that while trees accumulate carbon and produce oxygen while growing, this carbon is released when they die and in an old growth forest a tree must die for a new tree to grow. If carbon is being fixed, then it has to go somewhere and I think it is almost by the definition of an old growth forest that there is no more room for more carbon accumulation (competition among trees prevent it). So I would tend to think that calling the Amazonian forest the "lungs of Earth" is very misleading.
Some random WWF article
This WWF article seem to suggest that, contrary to my intuition, the answer to these two questions should be "yes".

great question......

I was referring to your question whether a forest is a carbon sink, I could not see how it was related to the metaphor of forests as lungs. But I’m afraid my comment was not well-thought or funny, I’ll remove it

Does an old growth forest ecosystem fix more CO2 than it produces?

The intergovernmental panel on climate change summarizes some of the data on carbon flux here. For the amazon similar tropical rain forests, it says:

Measurements in pristine, seasonal tropical rain forests in Amazonia indicate NEP of approximately 1.0 t C ha-1 yr-1 (Grace et al., 1995a,b) and approximately 2.0 and 5.9 t C ha-1 yr-1 for dense, moist rain forest (Fan et al., 1990; Malhi et al., 1998, 1999).

NEP is net ecosystem production, which, as I understand it, is essentially the total amount of carbon fixed by the ecosystem.
It seems the tropics, and the Amazon, in particular, are important global carbon sinks. This is also discussed in this more recent article in Nature.
This isn't my field, but as far as I understand it, forests are not closed or steady state systems. They do play a role as a sink in the global carbon cycle. I would assume net carbon fixation must come with increased biomass, so I may have just avoided a key part of your question. All the same, I think the point is that, again, even the amazon rain forest is not at steady state.
As far as oxygen is concerned, the report and article don't address it. I suspect this is because there is no documented problem with global oxygen depletion.

Thanks +1! For oxygen, I would assume that if 1 mol of carbon dioxide is getting fixed, then 1 mol of oxygen is getting freed as per the stochiometry of the photoynthesis and respiration equations. As one mol of carbon dioxide is about 22 times heavier than a mol of oxygen, 1 ton of carbon fixed should lead to the production of 22 tons of molecular oxygen. But I am not sure it is that easy.

@Remi.b I think it probably is that easy, but plants and forests aren't my field. I can pretty confidently say, though, that neither the change in $CO_2$ or $O_2$ are relevant in terms of a direct effect on human respiration on this planet. It's the greenhouse effect of the increase in $CO_2$ that makes this an important issue.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


text:
Dependency graph of life
This is a fascinating paper I read using Bayesian analysis to compare different graph models to genomic data.  Intriguingly, it shows that a dependency graph is a much better fit than a tree model.  However, a tree model is what we'd expect from common descent with variation.  What could make this dependency graph model, instead?
http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2018.3
For those who are worried about site cookies, here is the paper hosted on my Box.net account:
https://app.box.com/s/2mtiwafzr67hsee8o9m7bnfjr7dbmzsv

This paper was discussed by three scientists and the author here: https://discourse.peacefulscience.org/t/winston-ewert-the-dependency-graph-of-life/728. Really interesting paper, but Ewert has not yet made his case.

@Dr.S.JoshuaSwamidass Could you summarize the problems with the paper in an answer?  As a layperson, the tree model is what I've always thought of when it comes to evolution.  It is hard to imagine how common descent could result in anything else.  If you can provide explanation as to how a non-tree could emerge from evolution, that would be very helpful.

It appears the controversy stems from a misunderstanding of what the log Bayes factor in the paper means.  Dr. Swamidass states the D. Graph vs Tree result should be divided by the Tree vs Null result to show the D. Graph only explains the data 1.7% better than the Tree.
However, the author claims the log Bayes factor actually means the D. Graph is $2^{111,823}$ times better than the Tree.  Which clearly shows common descent (Tree) is a vastly inferior explanation for the data than the D. Graph.
The issue is there is an enormous amount of data, which can artificially inflate the log Bayes factor.  However, the proportion should stay stable.  Hence the focus on the 1.7%.  Explained here:
https://discourse.peacefulscience.org/t/uncommon-or-common-descent/776/86

Really?  You ask a question about a paper that doesn't seem to be in Pubmed, and then you give yourself credit for the best answer?

No other answer is forthcoming.  Do you have one?

No way am I giving a click to let some rando site put cookies on my computer. Grown-ups cite Pubmed, so everyone can see that the paper in question is legitimate.

I've hosted it on my box account if you would prefer that: https://app.box.com/s/2mtiwafzr67hsee8o9m7bnfjr7dbmzsv

Kids are curious about the world :)

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Basener's ceiling and evolution
There is a theorem in the Intelligent Design literature called Basener's ceiling.  It states that all evolutionary algorithms that attempt to optimize some fitness function will eventually reach a plateau where complexity no longer increases.  This is seen in practice when engineers and computer scientists try to use algorithmic forms of evolution.

There are a number of standard models for the evolutionary process of
  mutation and selection as a mathematical dynamical system on a fitness
  space. We apply basic topology and dynamical systems results to prove
  that every such evolutionary dynamical system with a finite spatial
  domain is asymp- totic to a recurrent orbit; to an observer the system
  will appear to repeat a known state infinitely often. In a
  mathematical evolutionary dynamical system driven by increasing
  fitness, the system will reach a point after which there is not
  observable increase in fitness.

Biological evolution is the same as an evolutionary algorithm in the relevant aspects.  It is a search to optimize reproductive fitness, where the fitness function is just the fact of survival or lack thereof.
How then is evolution able to make organisms continually increase in complexity, as history shows, despite Basener's ceiling?

Four quick flaws:
1) Environments are always changing. The fitness space is dynamic, and includes both biological and non-biological players, the former which are also ever-changing. Given a sufficiently stable ecosystem, one would expect an equilibrium among species to develop (though it could be cyclical). However even if the environment stays constant, novel mutations could always increase the fitness of a given species, which could then affect the fitness of all the other species. Also, natural selection is not the only factor that influences evolution, and other factors can add dynamic instability.
2) You are conflating genetic algorithms with evolution. Genetic algorithms use selection to solve a minimization problem and are typically bounded within fairly rigid constraints. They are motivated by biology, not models for biology.
3) You are conflating complexity and fitness. Complexity can be more fit or it can be less fit. Evolution only selects for fitness, not for complexity.
4) Do organisms continually increase in complexity? Depending on how you define it, they may not. Thinking about humans as a "goal" of evolution or something like that is a feature of creationism or intelligent design, not biological evolution. Some of the most successful organisms on Earth in terms of number of individuals or even biomass are some of the simplest.
There may be others as well.

Over time organisms have become more complex.  Why is this not obvious?  We start with the simplest single celled organisms and end up with a huge, diverse phylogenetic tree.  It seems weird that this is the point of contention.

@yters I'm referring to local/recent versus long term. Yes clearly there is more complex life now than when life first started. That doesn't mean that evolution is directed towards complexity, just that more complexity than it started with was advantageous for some individuals. Although the phylogenetic tree is huge, most individual organisms on earth and most of the diversity are still single-cellular.

Just because multicellularity took longer to evolve, for example, doesn't mean it is better. Becoming multicellular was good for some organisms, at some time, so the trait was maintained. Most unicellular organisms at the time the first multicellular organisms were originating stayed unicellular, and their descendants stayed unicellular over billions of generations.

The paper says we should not see this complexity increase, regardless of whether greater complexity is more advantageous or not to some individuals.

Well, that's pretty obviously wrong. Note, you are focusing on just one of the weaknesses I pointed out. The others still apply.

Regarding your first point, the equilibrium you mention is the main point in the paper.  Evolution always pushes a group towards equilibrium, at which point change ceases.  If the environment is chaotic, then the paper claims fitness remains constant and cannot increase.  The only way that constant progress can occur is if the environment guides the evolutionary process to the different levels of complexity.

But change doesn't cease, because organisms continue to mutate, which changes their fitness. In the paper you cite, the big flaw is that 1) Fitness is fixed for a given genotype, and 2) Genotypes are limited to just a couple possibilities. Yes, in that circumstance, you will get an equilibrium. Never in nature do those circumstances occur. Organisms aren't limited to X base pairs, evolution can both change and add or delete base pairs.

By the way, that paper is not at all peer reviewed, and just in glancing at a few of the functions it is laughably incomplete and would not make it to any reputable journal.

Let us continue this discussion in chat.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Does evolution violate the data processing inequality?
The data processing inequality (DPI) states that if $X\rightarrow Y \rightarrow Z$ is a Markov process, then $I(X;Y) \geq I(X;Z)$.  We can think of $X$ as a random variable representing some complex functionality that is unrelated to the organism's reproductive fitness, e.g. high intelligence in humans.
If $f(Y) = Z$, and $f$ is a standin for evolution, then evolution can only increase mutual information between $Y$ and $X$ if $f$ contains information about $X$.
However, evolution only contains information related to reproductive fitness.  Therefore, $f$ does not contain information about $X$, since $X$ is unrelated to reproductive fitness.
According to the DPI, $f$ should decrease the mutual information between $Y$ and $X$.
This means that the process of evolution should eliminate all functionality that is not directly related to reproductive fitness.
Yet it seems many organisms have very complex functionality that is not related to reproducing.  Ironically, the higher up the food chain we go the less reproductive the animals become.  So, based on this argument, much of the upper echelons should not exist.  What am I missing here?
UPDATE:
Here is a simple program in python that illustrates the point.

Measure fitness by number of 1s in the bitstring, more 1s the more fit it is.
Set a random bitstring to be a phenotype of interest, P.
Set another random bitstring to be the organism being evolved, O.
Iteratively evolve the organism by flipping a random bit, and then keeping the new bitstring if it is more fit, otherwise rejecting it.

As long as there is no correlation between the phenotype and the fitness function, then evolution cannot turn O into P.

from random import random

P = [int(random() > 0.5) for i in range(100)]
O = [int(random() > 0.5) for i in range(100)]

print "Matches between O from P", sum([o == p for o,p in zip(O,P)])

for i in range(1000):
    j = int(len(O) * random())
    old_fitness = sum(O)
    O[j] = (O[j] + 1) % 2
    new_fitness = sum(O)
    if old_fitness > new_fitness:
        O[j] = (O[j] + 1) % 2

print "Matches between O from P", sum([o == p for o,p in zip(O,P)])

I didn't understand all the maths, however, you have to give examples of "complex functions not related to survival and reproduction" ... All biological functions are either very useful to survival and multiplication, else they are relics of previously apt designs, which are vestigial or modified. ... Also, you will see that mammals can have small bloodcells without DNA nuclei, and small veins, that means they can miniaturize and be metabolically apt. Mammals radiated into bats, whales, moles because of their big "dormant" genome. Birds and lizards, with small genomes and bloodcells, didn't.

Your paragraph beginning "However, evolution is not purposeful" is gibberish. There's no connection between the first sentence and the second. I can't tell if you simply misunderstand evolution or if you've made some logical fallacy in your assumptions, but I suggest you focus on that and explain why you think this makes sense.

@iayork I've attempted to fix the problem paragraph.

You are misinterpreting the meaning of that inequality and confusing information and entropy (there are other logical errors but this one is the first and most obvious, and makes all the others unimportant by comparison).
$I(X;Y) \geq I(X;Z)$
is referring to the mutual information between X and Y compared to the mutual information between X and Z. Essentially "knowing X, how much can I reduce my uncertainty about Y or Z". Those quantities say nothing about the actual magnitude of entropy or complexity in X, Y, or Z, except for placing a lower bound (i.e., you can't have more information about X from Y than the total amount of entropy in X or Y). Entropy in Z could potentially be much greater than entropy in X, but the inequality is just saying you can't get any more information about Z from X than you can from Y.
Interpreting X, Y, and Z as DNA codes, this inequality is perfectly consistent with one part of the evolutionary process that you seem to be thinking about: the introduction of changes into the genetic code (mutation). $I(X;Y)$ in this context would be a measure of how similar the genomes of X and Y are. If Y evolves from X and Z evolves from Y by purely random processes (we are omitting selection and other processes here, which is of course an incredibly important part of evolution as well), then you would expect that inequality to hold: X and Y would be more similar to each other than X to Z. Because evolution is not strictly a random process, however, you could actually get cases where for small parts of the DNA the inequality would not hold. That is because selective pressures do contain information. At the whole genome level this would be probabilistically impossible, however.
You could actually use these measures as a rough way of estimating relatedness (though there are better purpose-built measures for doing so). Essentially, if $I(X;Y) \geq I(X;Z)$ you could conclude that it is likely that X and Y are more closely related species than X and Z.
If you want to view X, Y, and Z as phenotypes, there is really no difference. Decreases in mutual information with X from Y to Z doesn't mean a loss of functionality as you imply, it only means that X and Z are more different than X and Y.

You really misread my answer. To your first comment: "Essentially "knowing Y or Z, how much can I reduce my uncertainty about X" is talking about information theory; there is no directionality to Shannon information. To your second point, you missed the next statement: The information sets a lower bound on the entropy, but that's it. Look at the equation you just wrote: I(X;Y) = H(Y) - H(Y|X). I(X;Y) can be zero even if H(Y) is very large, as long as H(Y|X) is similarly large.

For your third comment, again, I'm not talking about Markov chains or their connection to evolution, I am talking about the inequality the OP was using. I didn't say Markov chains are a good model for evolution, I said that the inequality is consistent with evolution. I open my answer making it clear that I don't intend to dissect all of the logical missteps in the question, but rather I focus on one upon which the rest of it falls apart.

I think that it is a weaker argument to protest that evolution does not follow Markov-like behavior, because that inequality DOES describe evolution in most contexts, it just doesn't mean what OP says it does. The current state of DNA is all you need to predict the probability of the next state of DNA after a mutation. It doesn't matter what the DNA looked like 1000 years ago. That's the part that makes it Markov-like.

Let us continue this discussion in chat.

Thank you for taking a shot at answering my question and illustrating where I went wrong.  My critique of your answer is it misunderstands how I use the variables $X$, $Y$, and $Z$.  Only $Y$ and $Z$ are DNA strands.  $X$ is a phenotype attribute.  So as long as $f$ does not contain information about $X$, then the attribute will be removed by $f$.

@yters You are totally misunderstanding the math here. It isn't that the attribute will be removed by f, it's that the mutual information between X and Z will be less than between X and Y. If you really want to define things the way you are, then the correct interpretation is that when the DNA changes (i.e., goes from Y to Z over evolutionary time) it gives you less information about the phenotype X. This is obvious because in actual biology, it is the DNA Y and Z that gave you the phenotype X. Of course when you change Y to Z then Z will not give you the same X as Y did.

I think this is missing the elephant in the room, namely that you need to have selection (natural or otherwise) for evolution to happen (in a reasonable time). And selection (unlike mutation) is not a local operation on the DNA strands as required by the data processing inequality. Selection tosses out some individuals carrying certain strands in relation to others carrying different strands. The "comparison" performed by selection is not a local post-processing operation (as required by DPE to apply) on a single strand/individual; it takes two or more things to compare them...
The more relevant math for evolution is the Price equation, which partitions the change in fitness in that due to selection and transmission causes (like mutation, recombination etc.) If there's no selection, you're left just with the transmission causes. And in your case the single-individual/strand post-procession would be just mutation. What your math is saying is that not much evolution is likely to happen by mutation alone. (Also, you are taking evolution to mean an increase information/complexity rather than in fitness, but that is a lesser sin. An elephant with 500 legs isn't necessarily the most fit in many environments.)

Given your stated interest in ID, I have the feeling you're dressing up with math a common misconception/argument used by ID proponets, namely that complexity is unlikely to occur via evolution; usually the ID propoents jump to that conclusion by misrepesenting (or misunderstanding) the evolutionary mechanims (as you have done here). Your question reminds of this common ID argument:

Assume that, at each mutational step, there is equally as much chance for it to be good as bad. Thus, the probability for the success of each mutation is assumed to be one out of two, or one-half. Elementary statistical theory shows that the probability of 200 successive mutations being successful is then (½)^200, or one chance out of 10^60. The number 10^60, if written out, would be "one" followed by sixty "zeros." In other words, the chance that a 200-component organism could be formed by mutation and natural selection is less than one chance out of a trillion, trillion, trillion, trillion, trillion! Lest anyone think that a 200-part system is unreasonably complex, it should be noted that even a one-celled plant or animal may have millions of molecular "parts."
The evolutionist might react by saying that even though any one such mutating organism might not be successful, surely some around the world would be, especially in the 10 billion years (or 10^18 seconds) of assumed earth history. Therefore, let us imagine that every one of the earth's 10^14 square feet of surface harbors a billion (i.e., 10^9) mutating systems and that each mutation requires one-half second (actually it would take far more time than this). Each system can thus go through its 200 mutations in 100 seconds and then, if it is unsuccessful, start over for a new try. In 10^18 seconds, there can, therefore, be 10^18/10^2, or 10^16, trials by each mutating system. Multiplying all these numbers together, there would be a total possible number of attempts to develop a 200-component system equal to 10^14 (10^9) (10^16), or 10^39 attempts. Since the probability against the success of any one of them is 10^60, it is obvious that the probability that just one of these 10^39 attempts might be successful is only one out of 10^60/10^39, or 10^21.
All this means that the chance that any kind of a 200-component integrated functioning organism could be developed by mutation and natural selection just once, anywhere in the world, in all the assumed expanse of geologic time, is less than one chance out of a billion trillion. What possible conclusion, therefore, can we derive from such considerations as this except that evolution by mutation and natural selection is mathematically and logically indefensible!

Which has been (easily) debunked before:

This is a rather simplistic attack on evolution by mutation and natural selection. The way that he is calculating the probability actually does not take into account natural selection. What he is calculating is the chance that 200 random beneficial mutations happen sequentially without any bad or neutral mutations happening between the beneficial mutations. Natural selection will select and preserve the beneficial mutations and select against and eliminate the bad mutations. Once a beneficial mutation has become fixed in the population, any offspring produced that changed this would be selected against. His example also has no basis in a known biological system. His model essentially has an organism that reproduces only one offspring and then dies. All biological systems known to me the organisms on average have more than one offspring, allowing multiple chances for unique mutations to happen for selection to act on. Even using his unrealistic model slightly modified to have more than one offspring with adding in Natural Selection and having it take 2000 generations for a single beneficial mutation to fix in the population it would take ((2000 generations) * (200 fixed mutations)) = 400,000 generations to get the 200 fixed mutations, which with a generation time of 0.5 seconds would take about 2.3 days. If we use his numbers of one mutation per generation with a 1/2 probability of being beneficial, which would equal to a fixation rate of beneficial mutations about once every two generations much more generous than my 2000 generations. We do the same calculation with these numbers we get (2 generations) * (200 fixed mutations) = 400 generations, which is about 3 minutes.
tl;dr: The guy is an idiot.

For a more academic discussion of this argument see "There’s plenty of time for evolution". The gist of that paper is

The fact is that with the parallel model, i.e., taking account of natural selection, the number of rounds of mutations that are needed to change the complete genome to its desirable form are only about K log L, instead of the hugely exponential K^L which would result from the serial model.
where L is the length of the genomic “word,” and K is the number of possible “letters” that can occupy any position in the word

For a broader treatment of information theory issues in ID vs evolution see Elsberry and Shallit; an older version of that paper can be found freely on teh interwebz.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
What is the fastest growing bacterium?
E. coli has a generation time of about 20 min, and a single CFU will generate a colony a few millimeters in diameter after 16 hours of incubation.
Is this the upper limit? How much faster can bacteria grow? How much faster can colonies grow?

Depends on the medium

@WYSIWYG Good point, assume the best medium.

made an edit to my response to include the effects on E. coli growth conditions on its growth rate.

E. coli has actually a lot longer generation time outside the laboratory..

The article and published work here and here respectively, reveals that E. coli replication is close to thermodynamic limits of efficiency having modelled this process using mathematical equations. However an interesting article and published work here and here, respectively reports a bacteria (homologous to Thermobrachium celere and Caloramator indicus, which are closely related) with doubling times as short as 10 minutes have been discovered in areas of hot water emissions in Lake Tanganyika.

Small chimneys emitting hot water at temperatures of 66 to 103 degrees Celsius (150 to 217 degrees Fahrenheit) have been discovered at the shallow lake bottom of Lake Tanganyika, East Africa. In a study searching for thermophilic sulfate reducing bacteria in this extreme environment, a spore-forming bacterium was discovered that grew with a doubling time as short as 10 minutes. In theory, a single cell of this bacterium in this environment can multiply to 500 million in less than 5 hours under optimal conditions (60 degrees Celcius).

EDIT: If the question is exclusively about E. coli and it takes into account laboratory conditions then I also came across this references page claiming tha E. coli doubling time is between 4-20 minutes. Based on this paper the page reports that

Internationally renowned researcher Bernhard Palsson and other researchers from the University of California San Diego led a team of scientists from PNNL, the University of Heidelberg, and the German Cancer Research Center to study how E. coli bacteria changed and evolved from one environment to another in a laboratory setting. The team then compared proteomics, genomic, and metabolic data from the study with a computational model for bacterial growth.

The page then goes on to say

Using high-performance liquid chromatography coupled to mass spectrometry, the team gathered data on how the bacteria changed their protein profile as they grew and reproduced in different mediums. The scientists found that the data and model were correlated to a surprising degree (more than 98% in some cases), validating the model's ability to predict the growth of E. coli bacteria under specific conditions.

This confirms the comments above that the growth rate of E. coli depends on the specific conditions in which it is in and furthermore its growth rate under specific conditions can be predicted based on the devised model.

This 2016 Science blog says that the fastest known bacteria doubling time at the time was Vibrio natriegens, at 2x the E. Coli rate (10 minutes): https://www.sciencemag.org/news/2016/06/scientists-want-replace-lab-workhorse-e-coli-world-s-fastest-growing-bacterium
The blog also explains how better characterization work and tooling might be needed to fully replace E. Coli, but there is promise.


text:
Are there any non-mammalian species known that lactate?
Are there any non-mammalian animals that produce milk to feed their young, or are mammals the only milk-producing animals?

The classical definition of a mammal includes production of milk (hence the name). Your question is a bit circular unless you specify your definition of a mammal.

@Superbest: in which case, equivalently, "are mammals a clade?", to which we can reply, "no, because not all common ancestors of pigeons and humans produce milk", or reply "yes, by a No True Scotsman argument" ;-)

Related question: Do any birds beside the family Columbidae (or any reptile or mammal) feed their young "Crop Milk"

one can find pretty detailed examples and a possible explanation in this article

Short answer
Technically, only mammals lactate. To lactate means to produce milk from the mammaries to feed a baby or young animal. Milk, in turn, is defined as the secretions from mammary glands. However, there are animals other than mammals that produce milk-like substances to feed their young.
Background
Both male and female pigeons (Columba livia) possess the ability to produce a nutrient substance, termed pigeon ‘milk’, to feed their young. A similar substance is produced by flamingos and male emperor penguins. The normal function of a crop is a food storage area located between the oesophagus and proventriculus where food is moistened before further break-down and digestion through the gastrointestinal tract (Fig. 1).

Fig. 1. Schematic of the location of the 'milk'-producing crop in a pigeon (left) and a pigeon feeding its chick from its crop (right). Sources: ZME Science and Bird Ecology Study Group
During the process of pigeon ‘lactation’, a curd-like substance is regurgitated from the crop to the chick. The dry-substance of pigeon ‘milk’ is 60% protein, 32-36% fat, 1-3% carbohydrate and some minerals, including calcium. It has been shown that pigeon ‘milk’ contains IgA antibodies, which provides evidence suggestive that it is more than a nutrients alone. The physiological mechanisms governing pigeon ‘milk’ production and delivery are unknown. It is well documented that the pigeon crop is responsive to the lactogenic hormone prolactin. However, the pigeon crop tissue during ‘lactation’ is structurally unrelated to the mammary glands in mammalians, because it is not glandular and secretory processes do not seem to be involved (Gillespie et al, 2011).
The similarity between this process and lactation in mammals is striking, but is a case of convergent evolution, where unrelated species independently evolve similar traits. 'Milk' production is also recorded in some fishes, where it is fed to their young in the form of a mucous secretion on the skin (Buckley, 2010). Certain amphibians shed skin cells that are fed to the young. But the 'milk' of pigeons and doves is thought to be the most highly specialized of any non-mammalian 'milk' (Australian Geographic, September 2011).
References
- Buckley et al., J Exp Biol; 213: 3787-95
- Gillespie et al., BMC Genomics (2011); 12: 452

'Milk'-producing fishes are something I really would not have expected. Cool.
(extra details at http://jeb.biologists.org/content/213/22/i.1.full.pdf+html?sid=82269227-a55f-4c15-982a-9b5f6f5fa6b0 )

Producing milk, per se, is a strictly mammalian phenomenon. There are functionally similar processes in non-mammals (e.g., 'crop milk', produced by some birds), but because these processes evolved independently from the evolution of mammalian milk, they are not considered to truly be milk.


text:
Cosmid genomic library, or genomic cosmid library?
Which usage is better for referring to a "cosmid library of genomic DNA fragments"?

I've always used Cosmid Library but Cosmid Genomic Library is better than Genomic Cosmid Library.

Indeed - comments are better for statements of opinion. In answers, please try to provide reasoning why one phrasing might be better than another.


text:
Why male gametes doesn't go through antipodal cells in chalazogamy
Male gametes in double fertilisation enter the embryo sac through synergid cells even in chalazogamy i.e. when polen tube enters the ovule through chalazal end. Regarding the fact that compatibility reaction has already taken place (i.e. they are the right gametes) after pollination then why male gametes doesn't enter through antipodal cells? Is it just because of filiform apparatus that affiliates the entry of male gametes through only synergid cells or is there something else as a reason?


text:
How do the flowers of Diphylleia grayi become transparent after rain?
Known as the skeleton flower, its flowers turn transparent in rain. How does it do so? How can it gain transparency in rain when water is already present in flower? Or is it because other components present in the rain? Also is there any  advantage of this for the plant? I research using Google, but I couldn't find an answer.

YouTube

I have to hypthesise here:
the white colour you perceive is most likely near-to-full diffusion (or possibly better phrased: reflection with effectively undirected refraction due to multiple reflections) of light by structures on the surface of the petals and/or air space encapsulated in the petals. (This is true for most white flowers, by the way.)
Water fills the structures and/or the air space, which changes the refractive index of the petal surface.
In other words: the flower becomes like water, because the air is driven out.
Edit: seems I was right. SE asked me to add links to my answer, so I asked GoogleScholar about D. grayi and found this: "The inner part of the petal comprises numerous lacunae and intercellular spaces that are filled with air."
(source: Yong et al. (2015). Bioinspired transparent underwater superoleophobic and anti-oil surfaces. Journal of Materials Chemistry A, 3(18), 9379-9384.)

I don't think there's data to support that hypthesis, but then, there's also no data to reject it. (Seriously, though: I can't see why this would be an adaption. Maybe it has an obscure evolutionary advantage, but IDK which that would be. Maybe it just isn't an evolutionary disadvantage. Ecologists, to the research!)


text:
issues with MultiPipMaker
I would like to use MultiPipMaker for testing a genome alignment between two sequences, each sequence is in .fasta format, but the problem is that when I submit the couples of file that I need, the web browser sends an email that the blastz has timed out. Does anybody know why is the that?
The address of the program is:
http://pipmaker.bx.psu.edu/cgi-bin/multipipmaker
thanks

How big are the sequences that you are submitting?

they are 4 Mb each one approximately


text:
Why isn't phosphorus or nitrogen a limiting nutrient for animals?
Nitrogen and Phosphorus are usually the limiting nutrient for plants, especially for algae.  Phosphorus is used for DNA, ATP and phospholipids, and Nitrogen is used for pretty much every protein a cell might want to produce.  That is, their need for biological processes is not tied specifically to photosynthesis: anything that lives is going to need them, pretty much for anything it might want to do.  It would make sense for them to be a limiting nutrient for almost anything that's trying to grow, plant or animal.
Yet for animals the limiting "nutrient" seems to always be energy, ie: food.  Why aren't animals limited by lack of nutrients in the same way that plants are?  Obviously animals need these nutrients, too.  Or to reverse the question, why do plants need so much more phosphorus/nitrogen than animals do?
My best guess is that an animal's digestion of plant material is relatively inefficient energy-wise but relatively efficient nutrient-wise.  So for an animal to eat enough food to have sufficient energy to survive, it's probably eaten more than enough Nitrogen and Phosphorus for its needs.  But I'm just guessing and I can't find any data that would back up that guess.

More a thought: I think it is because plants a bound to one place. They have to take up what the soil in which they grow contains. Animals on the other side do not have this limitation and as they either feed on plants (which then have these subtances in them) or other animals they do not have this problem. For a number of animals salts can be a problem though.

Nice thought, but not all plants are static.  Consider algae, which float in the oceans and get carried by currents.  They're not exactly swimming against the currents, but neither are the zooplankton which feed on them.  Yet I don't think zooplankton is directly nutrient limited in the same way algae clearly is.

Thats right. The question is if algae have this as limitations.

From wikipedia: "Freshwater algal blooms are the result of an excess of nutrients, particularly some phosphates" (http://en.wikipedia.org/wiki/Algal_bloom#Freshwater_algal_blooms).  So yes, algae are nutrient limited in the same way that terrestrial plants are.

Phosphorus
Your suggestion that if we are meeting our calorific requirement we will be getting enough is true for phosphorus.
Most foods contain lots of phosphorus. The maximum dietary requirement occurs during adolescent growth, estimated at 1250 mg per day. Assuming a calorie intake of 2500 kcal we can calculate a 2500 kcal equivalent phosphorus content for various foods:
skimmed milk contains 7,400 mg phosphorus per 2500 kcal
roasted chicken breast contains 7,500 mg phosphorus per 2500 kcal
cooked white rice contains 3840 mg per 2500 kcal
(Calculations are based upon values obtained via this site.)
Nitrogen
Our requirement for nitrogen is met by our protein intake: inadequate protein intake manifests as kwashiorkor which is essentially due to a dietary deficiency of essential amino acids. In other words, the only way to achieve a nitrogen-deficient diet is to not eat protein, and this would not be alleviated by any inorganic source of nitrogen, even if we could consume enough of such a N source.

Thanks!  Numbers always help actually determine what's going on :)  I suppose fundamentally it's a consequence of thermodynamics: matter is conserved during protein synthesis and digestion, but energy is not.  You can't disassemble a protein and get back all (or even most) of the energy required to build it.  But you can get back most of the amino acids used to build it.

As you already mentioned N and P are major components of important biomolecules. In Sterner & Elser, ecological Stoichiometry, 2002, fig 2.2 demonstrates the percentage of N and P in biomolecules. As you can imagine these biomolecules are important and require forms of P and N to be consumed for an organism to function.
Animals are limited by nutrients such as Nitrogen (N) and Phosphorus (P). From an ecological perspective, many aspects of an organism’s life and subsequently their evolution are affected by nutrient limitation. For example, the brood mass of an aquatic snail can be limited by a low amount of dietary P (Tibbets et al., Phosphorus-mediated changes in life history traits of the invasive New Zealand mudsnail (Potamopyrgus antipodarum) 2010). Another example is a riparian crustacean growth limited by a low P treatment (Danger et al., Phosphorus content in detritus controls life-history traits of a detritivore, 2013).
There is even a ratio of the required elements for animals to survive/grow in an environment, threshold elemental ratio. The threshold elemental ratio is often a carbon to nutrient (i.e. N or P) ratio; different clades/species have differing ratios (see figure 2 in Frost et al., Threshold elemental ratios of carbon and phosphorus in aquatic consumers, 2006).
Thinking about animals getting their energy from food is too simple.
Consider this easy example; we, humans, require protein to properly function; a 150 lb adult – who requires about 55 grams of protein a day (these are estimates, I am not an nutritionist). That person can eat about one chicken breast and fulfill that daily requirement or they can eat 25 ounces of potato chips to achieve that. If they only have potato chips available then they have an N limiting diet. Of course, plants and animal have different requirements for energy, but animals are limited by nutrients just as plants are.
https://www.jstor.org/stable/40864578
https://besjournals.onlinelibrary.wiley.com/doi/10.1111/1365-2435.12079?__cf_chl_jschl_tk__=pmd_j7iq6cCQINSFmxVZ.Cvds9jOQmS2OHgpvYjw1t.gTU8-1635260689-0-gqNtZGzNAjujcnBszQvR
https://onlinelibrary.wiley.com/doi/full/10.1111/j.1461-0248.2006.00919.x?__cf_chl_jschl_tk__=pmd_g7eFplMHGUViCzJfN9vFQvHm4vmZabdJLJLo180WrCc-1635260692-0-gqNtZGzNAlCjcnBszQyl

Welcome to Biology.SE. We're looking for long answers that provide some explanation and context. Don't just give a one-line answer; explain why your answer is right. In addition, please include the complete reference information since links can break. One easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information. This is a good example of how to format references. Answers that don't include explanations may be removed.

Thank you that is much better!  ——— If possible, it would be helpful if you added links to online versions of the sources you mention — that will make it easier for other users to follow up.

Off the top of my head:

Plants are photosynthetic so have unlimited access to energy. If an animal had unlimited access to energy it would likely have Nitrogen or Phosphorous or something else as the limiting nutrient.
Animals eat plants and/or each other. Whatever animals eat will have to a greater or lesser degree sufficient protein/fat/nucleic acids etc to satisfy minimum nutritional requirements. As noted in Chris' comment there can be some species-specific limitations like availability of salt in a herbivore diet, or the human requirement of an external source of vitamin C.

Light access can very easily be a limiting agent, though.  Mature forest floors, for instance, have little undergrowth for exactly this reason.  In situations where there's an algae bloom, the top of the water is essentially opaque.  Yet in most ecosystems (certainly temperate/tropical oceans) the total biomass production of producers is not limited by light but by nutrients.  Likewise if animals were energy efficient but nutrient inefficient during digestion, it's conceivable that nutrients would be more limiting than energy.


text:
How quickly can lasers of various wavelengths and powers impair human vision or cause pain in the eyes?
There is a discussion on HackerNews about how self-driving cars might be susceptible to confusion attacks using a cheap laser pointer and a RaspberryPi.
Some people argue that human drivers, too, are susceptible to attacks by laser pointers.
For lasers in the visible spectrum, I'm pretty sure that the human driver can tell he/she is under attack very quickly. But how about lasers outside the visible spectrum? Since you can't see the laser, the only way you can tell something is wrong is if your vision is impaired or you feel pain in your eyes. How quickly can that happen?


text:
Why do animals sleep
Animals spend a good portion of every day doing nothing, and it seems like that time could be better spent hunting, searching for mates, etc. Also, animals are not aware during sleep, so it would be easier for a predator to attack them. Why is sleep required for animals?

different animals have different sleep patterns.. can you clarify which animals are you talking about

In humans, sleep is required for memory consolidation.  You might also be interested in this question (re: the predator question): http://biology.stackexchange.com/questions/7616/do-dolphins-really-sleep

Just to add to this conversation, sleep also has significant influence on the immune system function as discussed in this paper (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3256323/)


text:
How is respiration an unbalanced equation
The equation for respiration is C6H12O6+6O2→6CO2+6H2O+36ATP. The chemical formula for ATP is C10H16N5O13P3. How is this possible, since it violates the law of conservation of mass because it is unbalanced?

The ATP is not actually produced from the respiration. It comes from ADP and free phosphate ions.
The production of ATP in cellular respiration happens in all parts of a series of chain reactions, and you can read more about those here: https://en.wikipedia.org/wiki/Cellular_respiration#Aerobic_respiration


text:
Data analysis of transcriptome sequencing data
I want to learn more about the data analysis and statistics on transcriptome sequencing data. I would like to read some important papers of the field and books and maybe some MOOCS, if they are available.
More precisely I have data of differentially expressed genes across different groups of individuals and I want to test, if the genes are more expressed in one group are the genes also more polymorphic?
Any ideas?

there are several tools available for this analysis. Tophat-Cufflinks is a popular combo that people use.
For analysis, again, there are several tools.

Are you studying a species that currently have its genome sequenced?

No, it does not have a published genome sequence, de novo transcriptome assemly was used and cuffdiff was used to get the information about differentially expressed genes between two treatments. Now I want to statistically test if the genes, that are more expressed in one treatment also exhibit more polymorphism. Also, the data is very overdispersed.

@PiretAvila. You would need different sample isolates (biological replicates) to study polymorphism.

Yes, I have many biological replicates for each treatment. So you see, my problem is not obtaining the data, but analyzing it. I have differential gene expression values for genes that were expressed differently in two treatments (log2(FPKMy/FPKMx)) and I know how many SNPs each of these genes have. I want to know if the genes that were more expressed in one treatment (log2(FPKMy/FPKMx) is positive), are they on average more polymorphic. What would be the best statistical method? I used GLM's (hurdle and zero inflated neg. bin.), since there are a lot of sites with no polymorphism.

Sorry for a late reply. I suggest that you can first see if multiple isoforms exist for the differentially expressed genes that you are interested in. If so then you can find out if there is difference in isoform expression. If the gene has no isoforms then relationship between SNP and expression has to be studied under same experimental conditions.


text:
Are HeLa cells edible?
I'm curious if HeLa cells are intrinsically poisonous or dangerous to ingest.
My understanding is that some of the contamination in HeLa cells such as HPVs are not readily expressed.
I have no plans to do so, but I'm trying to understand why they might or might not be.

..they are cancer cells from a fatal case of cervical cancer and they are favored because they don't stop dividing.  I would not eat them.  I'm sure the experiment has not been done. They are not poisonous, though.  Cultured mammalian cells (not HeLa cells) are being proposed as a way of making meat substitutes.

HeLa can't be as contagious as this dog cancer, but it is transmissible by cells invading the soft tissue of dogs... http://www.sciencemag.org/content/343/6169/437

I think HELA cells are edible, although from moral point of view this would be cannibalism.
Despite they are cancer cells, they are safe for foreign organism, because any ate matter is destroyed. Even if these cells were implanted into another being by surgery, they will be safe since immunity will recognize them as foreign and kill. They are much less cancerous for recipient than just foreign.
Remember, then when we are eating meat, we don't care if cow or pig had cancer. Even if we avoid eating explicit tumors, we can still eat metastatic cells from sick animals. I think this happening all the time and has no consequences.
Simultaneously HELA cells are dangerous for other cell cultures in laboratory. There were several cases, when other cultures were infected by HELA cells and crowd out. HELA cells were traveled by air and on objects unexpectedly. Scientists were not ready for this phenomenon.

I guess I would like the answer to discuss some of the contamination in the line itself. The line itself appears to be contaminated by various pathogens, often mentioned is HPV - although I am not sure if it is actively expressed. For example, if I eat a bunch of HPV contaminated tissue, will I also get HPV? I am not sure if the digestive system is able to deal with all of these pathogens, for example, If I eat a bunch of BSE contaminated tissue I will get mad cow disease.

Of course some pathogens can infect us when eat. But the point is that HELA cells are nothing special in this case. You said it yourself: you can get BSE or HPV in everyday life, you need not eating HELA for this. So, I can get some pathogens from HELA, but unprobably and this definitely won't be a cancer Henrietta died of.

I guess the outstanding question is, if in raw form, they might contain sufficient pathogens to be considered dangerous. I don't consider something that will give you HPV "edible".


text:
Botany related question: liverwort sporophyte
Is perianth part of the sporophyte or gametophyte in liverworts (Marchantiophyta)?

I think it should be a part of the gametophyte because it is formed from the fusion of leaves (which are haploid) and protects the archegonium and the developing capsule.
It also can be logically thought out. Since it develops before the sporophyte forms , it should be part of the gametophyte.

Here it is stated explicitly.


text:
How do you visualize RNA on a gel?
I have run an in vitro transcription reaction and produced some RNA of a single species and definite size. I would like to visualize it to check if the reaction worked.
Can I do this on an agarose gel? Is it sufficient to simply make a 1% TAE-agarose gel with EtBR that you would use for routine DNA electrophoresis, and run this? Is it necessary to take special measures against possible RNAses in the gel or the running buffer?

Include in your agarose gel 4% household bleach to inhibit rnases. It's a much easier alternative to PFA and just as effective.

You have two possibilities: When you only need a quick check if your RNA is ok and you indeed only get one band, you can try a "quick and dirty" method. Heat the sample for 5 minutes at 65°C and then immediately cool it down in an icebath and keep it there until loading. By doing so, you melt up the secondary structure of the RNA and keep it in this state. You will most likely then see only one band.
If this doesn't work or if you want to use a RNA size marker, there is no way around denaturating gel electrophoresis. Here you denature your sample in the loading buffer and then run a denaturating gel in which prevents the secondary structures. There is a good paper about this:

Denaturing RNA electrophoresis in TAE agarose gels

The classical method using formaldehyde (which is more dangerous in handling) is described in the following paper and also in the "Molecular Cloning: A Laboratory Manual" book by Maniatis and colleagues:

RNA molecular weight determinations by gel electrophoresis under
denaturing conditions, a critical reexamination

RNA is amenable to folding, which produces secondary structure and alters its mobility (compare to supercoiled DNA). Therefore, if you don't denature your RNA appropriately, even a single species will produce a smear.
A common strategy is to incorporate denaturing chemicals such as formaldehyde into the procedure. See this Life Technologies protocol.
Apparently, you can also just make a standard DNA gel with some added bleach. I haven't used this technique, but they have some samle results.

I use a 1% nondenaturing agarose gel with ethidium bromide. I use Better Faster Media LB buffer so I can run a high voltage and get my gels done faster. I usually see 2 bands on the gel due to RNA secondary structure, but that can be fixed by heating it to 65C for 5 minutes, followed by chilling on ice for 5 minutes. My RNA may be different from yours, so you might not be able to get a single band with this trick. What I haven't been able to do is run an RNA ladder on nondenaturing gel, but I haven't really tried that hard.


text:
Confusion about mitochondrial electron transport chain Complex I Wikipedia article title
The Wikipedia article title for Complex I (the NADH dehydrogenase enzyme complex) is "NADH dehydrogenase (ubiquinone)". This is confusing to me because this title sounds like ubiquinone is another name for NADH dehydrogenase, but ubiquinone is in fact the Coenzym Q, which is reduced by the hydrogen transferred from NADH through Complex I. What is the reason behind this title? I mean, what is the point of having "ubiquinone" in parentheses in the title?

I've changed the title of the article. The reason for the title was just poor writing (I agree that it seems to imply that the enzyme is ubiquinone) but also the fact that someone had previously tried to change the title to the accepted name tht @xusr has mentioned but they did so incorrectly.


text:
What is a "noninvasive" biomarker for a disease?
What is a "noninvasive" biomarker for a disease? I know what a biomarker is, but what makes it noninvasive?

The term "non-invasive" probably refer to the sampling method rather than the nature of the biomarker. One would probably need the original paper and citation where you found this term in order to answer the question.

There are tons of papers that use this term, and none that I had a look define this term. All those papers as well as Wikipedia assume the readers already know what it is.

A biomarker, or biological marker, generally refers to a measurable indicator of some biological state or condition. - Wikipedia

The presence of certain 'things' (sorry for being vague) in a tissue obtained invasively - via biopsy, for example - are considered biomarkers for, say, a cancer. It could be histopathological - a particular abnormality seen on staining the tissue - or it could be the presence or absence of a membrane receptor, etc.
A non-invasive biomarker is simply one that can be obtained easily and without "harm" to the (patient?), for example, to identify the potential presence of a cancer without the need for a biopsy. (Obviously, this doesn't eliminate the need for invasive methods. It just adds to the arsenal of detection methods.)
That is the usual meaning of non-invasive biomarker in the many, many papers using the term (at least medically), such as the one cited.
Serum microRNAs as non-invasive biomarkers for cancer

Although one could argue that a blood draw is still invasive. I use the term non-invasive to refer to things like the presence of lumps in a cancerous breast (something that can be palpated) or the yellow-tinged eyes and skin correspondent with various diseases of the liver, that sort of thing.

@MattDMo - There are biomarkers that don't involve venipuncture (like exhaled substances), but the literature doesn't use the term like you do, as evidenced by the thousands (literally) of papers about them.

So a biomarker in the blood is non-invasive? Hmm. I'll have to chat with my colleagues about that...

@MattDMo - Please do. Serum biomarkers are considered non-invasive when the gold standard is an invasive study. Again, I can cite you papers that use it in this way (see the one cited in my answer, for example.)

No, that's fine, I believe you. I just want to make sure the rest of my team and some of my senior colleagues in the department all think the same way (I'm guessing they do), because I've somehow missed picking up on that in my reading. TIL :)

So even something like a leukopak is non-invasive, but a needle/punch biopsy is invasive? I'm just wondering where the line is. I'm guessing it's whether or not solid tissue is removed...

@MattDMo - Needle biopsy is considered an invasive study. I think the difference is that an invasive study obtains a tissue sample. A buccal swab, however, is considered by many - but not all - as non-invasive, even though tissue is obtained (others call it "minimally invasive".) So, TIL, as well. Thanks. :)


text:
Why are genes expressed as proteins rather than other types of bio-molecules?
I guess, we could infer that the structure of an amino acid has the same functional units as RNA is used to synthesise it. Therefore, from a logical point of view it would make sense that genes are expressed as proteins.
However, why is this the case; why are genes expressed as proteins rather than any other type of bio molecules? Also, from what are other bio molecules expressed if not for genes?

Wow - like a biophilosophy question! The answer lies in in building up the largest diversity with minimal subunits. Efficiency if you will. In this case we are talking about amino acids. We only need 20 of them to approach unfathomable numbers of diversity.
The protein acts as a messenger, as an enzyme, a carrier and it's own building unit. If you wanted that kind of range out of any other known biomolecules, you would need a gene to code for each of them, and itself a gene a completely different mechanism to build them which we can't even fathom. It's so much simpler to code for a protein, which can act as an enzyme to build other biomolecules.
However if you are asking about why the central dogma of molecular biology is the way it is...well then, it seems to be axiomatic.

No, in fact I wasn't intending for it to be a "bio-philosophy" question. I just couldn't think of a better way to explain it, than touching on points that I already know.

No I like it. Don't misinterpret. Life is so complicated though so its a very real possibility that the our central dogma of molecular biology could of been completely different.


text:
Why is this dry pepper fruit still "powered"?
Check out this photo of my pepper plant this cloudy morning: (click for full res)

Usually (and this can be seen on 2 and a half of the 4 fruits in this pic) the fruits are "disconnected" from the plant's juice flow when they're ripe. Then the fruit starts to dry. Yet the middle one in the pic is dry while its "cord" is still green (literally). Why does it not become dry like his fellows do?
There's also another interesting situation going on with the lower right fruit's "cord", which is half-dry. I wonder why it has been like this for a little over a month now without change.
The lighting conditions are pretty poor for this plant, so I use a 40 watt incandescent lamp for it and 4 other plants 24/7.
Please, excuse my poor vocabulary :)

The fruit in the middle had his "cord" completely dried out this week, but the weird lower-right half-powered pepper is still like this. I decided to remove them all and I didn't take a pic, which I regret now. It could have been an interesting visual addition.

probably because of the way sunlight falls on them.. the part that receives more sunlight dries out faster than the others. Please check if the sunlight received is uniform all over.

@TheLastWord  makes sense. The sun is blocked by a few leaves for the left peppers. I suppose it must be the reason.

that is the obvious reason.. might be some   biological processes too, but this could be the major contributor.

It might be a potential reason, but certainly not the obvious reason.


text:
Are there any creatures that will eat their own limbs or body parts to survive?
I'm curious if there are any insects, bacteria or perhaps even large animals who would bite off their own limbs or body pieces to chew on in the desperate times of hunger.

What you're describing is actually a well-documented occurrence in individual cells and single-celled organisms. The phenomenon is called autophagy, and Wikipedia has a page about it here. The basic gist is that when cellular components stop functioning or need to be removed for some other reason, the cell essentially digests those components and reuses their parts to make something else. Cells can also consume themselves to prevent the spread of disease or in the case of extreme starvation, when the extra energy might be needed to keep the organism alive.
Self-cannibalism on the macro scale (larger than single cells) is significantly rarer, but it can and does happen. For example, leopard geckos (and maybe some other lizard species? I'm not sure) regularly eat their own shed skin pieces to conserve energy and nutrients. Sea squirts (a type of marine invertebrates) literally digest their own brains as a part of their life cycle, and apparently, some crickets have been known to consume their own wings. Generally, though, unless the limb in question is already damaged and/or rendered unusable, it would be a waste of energy for its owner to consume it, as the energy spent repairing the damage would likely outweigh the energy gained from its consumption in the first place. That is why it's a relatively rare behavior in multicellular organisms.


text:
What is internal symmetry in membrane proteins?
I have come across the term "internal symmetry" in the context of membrane proteins, but have never found a satisfactory definition.
I'm struggling to figure out exactly what this term means... What plane is this symmetry seen on? Is it dimers that are symmetrical or can a monomer also be internally symmetrical?

Can you please provide the original context? I don't think the concept applies generally...but depending on how weakly one is using the term 'symmetry' it could be in most-any plane and within or across a monomer.

This review paper; Structural Symmetry in Membrane Proteins, made it's way to me soon after I posted the question. It covers the significance of symmetry in membrane proteins. The term is as vague as @Ryan mentioned it could be!

Internal symmetry in this case refers to cases where a part of the protein structure can be superimposed (approximately) on another. It's not a strict mathematical symmetry, more a 'resemblance'
For instance in the 12 transmembrane helix transporters, the first six helices are arranged similarly to the second six, such that if one were to cut the protein in half one would see that the two halves (approximately) superimposed.
Fig 3 of this Nature Micro shows it clearly. http://www.nature.com/articles/nmicrobiol20159 Where the blue helices in 3a could be rotated 180 degrees and then look very similar in arrangment to the yellow helices.


text:
Are all organelle lumens a reducing environment like the cytosol, or nonreducing like the extracellular space and the ER lumen?
I am interested to know if cysteine can form disulphide bridges in proteins within organelles. Typically cysteine will not form disulphide bonds in the reducing environment of the cytosol, but will in nonreducing environments such as the extracellular space.
From the Handbook of Biologically Active Peptides:

The ER is a vastly more common site than the cytosol (which is very rarely the site of disulfide bond formation) because the ER intralumenal environment is more oxidizing than that of the cytosol.

This is fairly intuitive since the ER is where the disulphide bonds will be formed before translocation to the extracellular space. But what about other organelles?
Does this apply to all lumenal spaces as implied in the below picture, or is the ER a special case as a result of its necessity to fold proteins destined for the extracellular space?

I can't speak generally, but I study a lysosomal protein that has many disulfide bonds so, at a minimum, the lysosome isn't reducing and I'd wager the entire endo-lysosomal pathway as well.


text:
Why aren't organelles considered alive?
I'm taking a 3-week Bio I summer course, and my textbook says the cell is the smallest/basic unit of life. I asked my professor why organelles aren't a living unit, and her reply was that they aren't self-sufficient. But it seems that cells in multi-cellular organisms need other cells with different specializations in order to survive. You can't just (or can't always) pluck a cell out of a larger organism and leave it to fend for itself outside of it. Same with an organelle. She said only the entire cell fits all the requirements for life, referring me to the textbook, but I couldn't find an actual description of these requirements. So, what is the relevant difference between an organelle and a cell such that only the entire cell is considered alive?

The definition of life is a controversy in itself, and as it is simply a word that can be understood by everyone however they wish, there is no "correct" definition. It is thus not really possible to give a "correct" answer to your question, but here are a list of things you may want to consider:

Replication of DNA is probably the most agreed common feature to all life on earth. Most organelles do not contain their own DNA but are simply lipid and protein constructs.
Independence is a difficult criterion of life, as parasites require a host for reproduction. However, while the organism may require a host, its cells individually can replicate without a host.
Cells are able to replicate when removed from the body - under the right conditions. (We are getting better and better at culturing all sorts of cell types, for example to avoid having to use animals for research.) Most organelles are not able to replicate under any conditions.
In nature, there are single living cells. In fact, the majority of organisms on earth consist of one cell only. There are no organelles living in nature.

Mitochondria and plastids make a complicated exception to these, as they are originally derived from bacteria themselves. It is indeed debatable whether they could be considered alive, as they possess DNA and it is replicated in order for them to divide, like individual cells do. However, the machinery required is not produced by themselves but rather by their "host" cell, making them subject of a similar argument as viruses.

Neither Mitochondria nor Plasmids could maintain or replicate themselves outside of a cell because both have passed the genes that encode for key proteins over to the host cell.

Which genes exactly are you referring to? As far as I'm aware, mitochondria (I don't know about plastids) replicate their genome themselves and perform a process similar to binary fission themselves as well; but under regulation of the "host" cell.

In human cells, mitochondrial DNA codes for just 37 genes. All other genes required for mitochondrial function have been transfered to the nuclear DNA. Specifically the POLG and POLG2 genes that are involved in mitochondrial DNA replication are now located on chromosomes 15 and 17, so without being present in the host cell they could not replicate. The replication itself occurs in the mitochondria but the proteins needed are synthesised by the host machinery.

So very much alike viruses in regards to their being alive or not then. Thanks :)


text:
Human genetic diversity in Africa in comparison with the rest of the world
Background
The claim ...

Most of the genetic diversity in humans is in Africa

... is quite common. On Biology.SE, it is easy to find posts that make this claim. Consider for example:

Do humans have enough biological differences to be grouped into races or subspecies?
How do we know the human species arose in Africa?
What is the correct classification of population groups of homo sapiens?

Question

Is the claim true?
What fraction of the total genetic diversity is present in Africa?

I understand that the term genetic diversity is often used in a vague sense. Please make sure to explain what statistics has been considered in the study you would refer to when giving estimates of what fraction of the genetic diversity is found in Africa. Note that I am not asking "why is it true?" but only "is it true"?

I would love to know the source for this claim. My money is on it not being true.

Here is a tree based on mitochondrial DNA variations in human populations.
van Oven M, Kayser M.  Hum Mutat. 2009 Feb;30(2):E386-94.
Updated comprehensive phylogenetic tree of global human mitochondrial DNA variation.

Looking at genetic distance between populations via mitochondria DNA, all nonafricans are descended from a founder in one mtDNA group (L3).  All the other L groups are African populations: L0 is the San people, L1 is Mbenga pygmies, L5 is Mbuti pygmies, and the others are other African groups.
If one considers each L haplogroup to represent genetic variation then 5/6 (83%) of human genetic variation is from African populations.
From a different source looking at genetics differently   A map of human genome variation from population scale sequencing Nature. 2010 Oct 28; 467(7319): 1061–1073

Populations with African ancestry contributed the largest number of
  variants and contained the highest fraction of novel variants,
  reflecting the greater diversity in African populations. For example,
  63% of novel SNPs in the low coverage project and 76% in the exon
  project were discovered in the African populations, compared to 20%
  and 33% in the European ancestry populations for the exon and low
  coverage projects respectively.

I've found two papers that provide some information on this, but no definitive answer.
The 1000 Genomes Project Consortium (2015) analysed whole genomes and found that "28% of novel variants" were found in African individuals. Novel variants were mostly (>99.9%) single nucleotide polymorphisms or short indels. This table has full count of all variants. However, 26% of the genomes were African, while African's make up ~16% of the world population, so these numbers cannot be extrapolated to the whole world. Another problem is that the samples were not taken from geographically dispersed people (figure 1).

Figure 1. Proportion of genetic variations shared in different populations.
Evidence for greater African genetic diversity is presented by Stephens et al (2001), though they look at North Americans from different ethnic groups which isn't ideal. They found many more unique SNPs in African-Americans than other ethnic groups.

Figure 2. SNPs in Americans of different ethnic groups.Population codes are AF, African-American; AS, Asian; CA, Caucasian; and HL, Hispanic-Latino.
I haven't been able to find the claim that most human genetic variation exists in Africa being made in the literature, though Africa is characterised as having high genetic diversity, e.g. here. I'm sure I've heard this claim outside of Stackexchange though.
My review of the literature definitely isn't comprehensive, so if anyone finds anything else feel free to add it.

Thanks that was already helpful. I had to check the original paper to make sure this weird 3D, Excel look alike graph was indeed from a peer-reviewed journal (journal: Science)!

Two new studies, the result of the human genome project, examined the genetic diversity of over 1,000 individuals from 51 population groups all over the world.6, 7 As in previous studies, peoples of Africa were the most genetically diverse. However, these studies also determined that those from the Middle East were the second most genetically diverse.
  difficult to interpret

http://www.godandscience.org/apologetics/humans_out_of_africa.html
I think it means that Africa contains 150,000-500k years of human heritage in a wide base of population, whereas the base for the rest of the world is narrower... same as if you had 10 colors of cats in one enclosure, and only 3 colors of cats moved into the park across the road and bred there.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4067985/
Consistent with the “Out of Africa” model of modern human origins, analyses of genetic data indicate that Africans have higher levels of genetic diversity than non-Africans (Cann et al. 1987, 2002; Tishkoff et al. 1998; Marth et al. 2004).


text:
Why 20 amino acids instead of 64?
This question got me thinking about amino acids and the ambiguity in the genetic code. With 4 nucleotides in RNA and 3 per codon, there are 64 codons. However, these 64 codons only code for 20 amino acids (or 22 if you include selenocysteine and pyrrolysine), so many of the amino acids are coded by multiple codons.
Is there any hypothesis as to why there are only 22 amino acids and not 64? Is it possible that there were 64 (or at least more than 22) at an earlier time?

It seems more likely that once there were fewer than 16 amino acids and codons were 2 nucleotides.  In earliest form, codons may have been 1-to-1 with nucleotides, with three or four amino acids used.  The redundancy in the present code may simply have remained in place after the extension of 2-nucleotide codons into 3-nucleotide codons.

@mgkrebbs Do you have any reference for that idea? It seems exceedingly unlikely to me. From tRNA to the ribosome, every part of protein translation seems to be adapted to triple nucleotide codons.

@MadScientist, No, this was pure speculation on my part.  Indeed present mechanisms are highly oriented to triple nucleotide codons.   Smaller codons would only have occurred back in the RNA world, before DNA was used.  The pattern of redundancy in the code is compatible with the 2-nucleotide idea, but could also be explained in other ways, such as selective pressure for synonymous translations of single-base mutations.

A quick look for literature doesn't show much, but this review paper shows that the idea of two-nucleotide codons is not unknown: "It is usually assumed that the primitive genetic code was simpler (for instance with a two-nucleotide codon and less amino acids) and expanded in the course of evolution."

@J.M. selenocysteine is in no way restricted to microbes. In fact, all animals except a few insects encode selenocysteine.

Remember also that there are plenty of non-proteinogenic amino acids, such as hydroxyproline, which are nevertheless found in proteins despite not being encoded in the genetic code.

@MadScientist: Certain functions require every single one of these 20 amino acids. However, in isolated cases a selected subset of amino acids might very well lead to an active protein.

well you need at least one STOP codon so at max you could have 63.

Brian Hayes wrote a very interesting article from a mathematical point of view:
http://www.americanscientist.org/issues/pub/the-invention-of-the-genetic-code
especially the "Reality intrudes" section. Basically people had created fancy mathematical reasons why it has to be exactly 20. Nature, being nature, does not follow the reasoning, but has its own ideas. In other words there was nothing especially special about 20. In fact there seems to be a slow grafting of a 21st amino acid, selenocysteine using the codon UGA. Also pyrrolysine is considered the 22nd. The last section suggests that the code was originally doublet, so coded for <16 amino acids. This can partly explain why the third base in each codon is not as discriminating.
So perhaps in the year 2002012 someone will be asking on biology.stackexchange why there are only 40 amino acids.

There is no evidence of selenocysteine being "grafted" in. Much the opposite actually, it has even been suggested that "UGA was originally a codon for Sec in the
anaerobic world, perhaps two to three billion years ago, and after introduction of oxygen
into biosphere this highly oxidizable amino acid could be maintained only in anaerobic
organisms or in aerobic systems which evolved special protective mechanisms". If anything it is cysteine that has been taking over.

The first position of the anti-codon, the "Wobble" position, forms hydrogen bonds less well than do the second two.  This means that the last position of the codon has less coding potential than the first two.  The reason is that the anticodon is at the bottom of the anticodon loop of the tRNA, and so there backbone of the tRNA is bending back to pair with itself.  The nucleotides do not hold their bases flat and regular in relation to each other.
Here is a picture of the anticodon loop.  In this case 5'-CAU-3' is the anticodon for 5'-AUG-3', so it would be the C, right at the sharpest part of the bend in the anticodon loop, that would pair poorest.
Here is an interactive model where you can spin the tRNA/mRNA around and see that not all the hydrogen bonds are equal length, nor are all the bases coplanar.

I am not convinced that is a cause, as much as a consequence of the redundancy. It could be that cells used to have a lower number of aa (<16), that could then be coded with only 2 nucleotides. As new aa entered the game, a triplet system developed, but this introduced (unharmful) redundancy in the code, which did not put any selective pressure towards having a strong bond in the 3rd position.

The first link is dead.

There are two other ideas to throw in here.
1) just to add to KAM's thoughtful answer.  There was also a thought that the last base also gives a lot of flexibility for GC content which responds to some
2) lets not forget that redundancy in the genetic code helps give some resistance to mutations which might be disruptive.  the amino acids less disruptive to a typical protein fold are more common in the code. (we have some idea of this from studying mutations of protein structures.)
3) some biochemists have proposed that there is a sense that the 20 amino acids we have are a fairly stable set - that adding other amino acids don't help create better proteins.  Peter Schultz learned some of this as his group really wanted to add extra, human synthesized amino acids into native proteins.
 I was at a talk where he noted that attempts to make cysteine with a longer side chain caused the amino acid to cyclize to form a thioolactone.
Thinking along these lines adding another CH2 group to proline might not make packing better.  There is probably some value, but just not enough to disrupt all the sensitive machinery for making and realizing the genetic code.

thanks, fixed -its been a while since i did any organic chemistry.


text:
Can fruit tissue be cultured and grown independent from the plant?
Can fruit tissue be grown in a tissue culture as is done to other plant tissues? From the answer to this question, I learned that fruit is alive. Could it be possible to manufacture fruit products without plants, using this method?

Plants are not a strong suit for me, but in general the answer is yes.  What I know mostly comes from animal tissue, so someone may have a better answer than I...
Botanists have been cloning plants from cuttings for thousands of years.  More recently, propagation from cell lines around for much longer than for animals.  Entire plants can often be grown from a plate of cells.  So you can grow roots or an entire plant from cells right now, but I can't find any mention of anyone trying to grow fruit without the rest of the plant, and there might not be any research for this.  Let me explain why this may be...
Bioengineering animal tissue and organ growth has been an intensive area of research for the past 15 years or so.  In some cases, such as the growth of skin or liver, the technology has proven to be exceptionally valuable and useful.
Using plastics with biological growth factors attached and 3D printing, even more complex organs such as bladders and tracheas can be grown from the patients own cells, which avoids the problems of rejection and the complexities of donor matching.
More recently growing muscle tissue in an animal free culture has been tried, which would relieve some of the environmental and ethical problems of raising meat animals.
All this has been driven by a strong cost-benefit payoff.  A transplanted organ is highly valuable and improving that process and making organs more broadly available for patients has a high economic value.  The more often the structure is related to the tissue around, the more structurally complex, the more difficult it is to imagine growing that organ independently of the host organism (brain and eyes come to mind).  Other transplant worthy tissue cultures look quite promising.
Right now, it seems as if plant fruit like an apple or a kiwi might be difficult/expensive to grow in the lab as opposed to just picking them off the tree.  I think that growing a banana pulp or an apple sauce might be possible, though.  Who knows what we might be doing in 50 years or more though?


text:
Evolution of long necks in giraffes
In this question, the OP uses giraffe necks as a supportive example of evolution. Is the mechanism described in this post accurate? At some point, I thought I remember hearing that giraffes did not evolve long necks to reach higher food resources, but instead longer, stronger necks gave some sort of mating advantage (male competition perhaps?).
Is there a consensus in the scientific community as to evolutionary mechanism(s) that contributed most to the evolution of long necks in giraffes?

That was Lamark's postulate: http://evolution.berkeley.edu/evolibrary/article/history_09

There seems to consensus that it is not competition for tall food.  Giraffes actually often feed on resources that are lower than their maximum possible height.    See:
Simmons, R. E. & Scheepers, L. 1996. Winning by a Neck: Sexual Selection in the Evolution of Giraffe. The American Naturalist 148: 771–786
This paper put forth the idea that sexual selection is the reason behind long necks.  The idea is that longer necked males are dominant.  But this  theory has also been questioned.  See:
G. Mitchell, S. J. Van Sittert, J. D. Skinner. 2009.Sexual selection is not the origin of long necks in giraffes. Journal of Zoology 278, Issue 4: 281–286
So in the end there's no clear consensus.  Some papers have returned to the theory of competition for research in the past few years.To put it simply, no there is no consensus.

Competition for research? Giraffes must be more advanced than I've been giving them credit for!

Lol, yeah, that's awkwardly worded I suppose.  I meant returned to the theory of competition as a topic of research :)

Long neck might have started for food gathering... but once necks became long enough, it would have been useful for males to fight with. Hence the selection pressure on the neck changed.


text:
Human metabolic pathways involving particular proteins
I am currently working on a project that involves analyzing the pathways in which certain proteins are involved. I have compiled a list of proteins, and I am keen to explore the pathways they participate in within the context of human biology.
In this regard, I am in need of a reliable and comprehensive website or database that catalogs pathways in humans. I am particularly interested in a resource that allows me to input a list of proteins and retrieve information about the pathways in which they are known to be involved.
Could you please suggest a website or database that meets these criteria? Your recommendation would be immensely helpful in advancing my research objectives.

we would need to know which sort of pathways you are looking at there are about 1,000 different databases out there with various bioinformatic resources. Try the NAR database summary for the extent.

The Problem
There may well be a web facility that allows input of a simple list of enzyme names and outputs a list of associated pathways. However there are two main reasons why this may be hard to find. The first is that most databases relating to metabolic pathways are not established from the standpoint of enzymes: their focus tends to be the pathways themselves, metabolites (because of the advent of the field of metabolomics) and gene sequences (because they are abundantly available). The second is the anarchy of enzyme nomenclature: the Enzyme Classification (EC) system allows several different enzymes under a single category, and there are generally several names for a particular enzyme (see, for example, the situation for hexokinase).
KEGG
One of the major databases of metabolic pathways with a web interface is KEGG (https://www.kegg.jp).
This is searchable using their specific enzyme nomenclature, rather than a protein name or EC number.
However, one can also apparently search on the basis of the amino acid sequence of the protein, as described in: Kanehisa, M.; Enzyme annotation and metabolic reconstruction using KEGG. Methods Mol. Biol. 1611, 135-145 (2017). This is available here, but requires a (e.g. institutional) subscription for access.
[KEGG contains information on many organisms, but one can filter by Homo sapiens etc.]
MetaCyc
The other major database of metabolic pathways is MetaCyc, which I merely mention as its use now requires a subscription (after a trial period). It is certainly possible to search MetaCyc interactively for a particular enzyme name like hexokinase, but I do not know whether bulk searches are possible and how flexible it is regarding nomenclature.


text:
Oxygen requirement of Eschericia coli
What is a good DO% range for E. coli cultivation (BL21(DE3), recombinant protein expression). 30%? At what point is a culture oxygen-limited, or 'highly aerated'? If DO% is relative to reactor conditions, how can we compared values?

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works. As usual with these sorts of question, the homework poicly applies - so tell us what you have found in the literature.

Wow, I really mis-typed "policy" there

@bob1 LOL... happens to all of us humans... Just FYI, even after 5 minutes, if no one has responded to your comment, you can simply delete your comment and repost it with your error(s) fixed. (Technically, you can do that even if someone has responded, but that gets confusing.)

@EndAntisemiticHate I am aware of that, just couldn't be bothered retyping.

@bob1 Ah, I thought you were perhaps copy and pasting your comment (or using a script), given it includes a lot of text plus several links.


text:
Mechanism of random assortment of chromosomes
How does the random assortment of chromosomes during meiosis occur?
I am a mathematician, not a biologist, and I am surprised that it is difficult to find an answer to this question online (AI chatbots are also clueless). If I were human or a computer, I would use a random generator (coin flips, dice, pretty sophisticated algorithms in the case of a computer) to perform the random assortment.
How does this work during meiosis? What random generator mechanics are being used? It is not sufficient to say the assortment is random. Randomness needs to be accomplished by a mechanism.

We don't post duplicates on purpose, and we close them when we find them. If there's something you didn't understand about the answer posted there, could you either leave a comment on the answer  to see if the author can help - or you can post a bounty on the question so it receives more attention. You'll be able to place bounties on things when you've sufficient reputation. Alternatively, you could [edit] to clarify how this is different from that one.

Would you consider https://en.wikipedia.org/wiki/Brownian_motion to be a "mechanism"? That's generally what one means when talking about randomness in chemical reactions. It's a bit weird to ask what the mechanism of randomness should be; in most of the physical world, randomness is the "null hypothesis", and the interesting stuff is that which happens not-completely-randomly. So, biologists would study why there are "hot spots" or places where recombination is more common than elsewhere, rather than why it doesn't always happen in the same exact place.

Randomness is hard in computing; it's not hard in the real world.

Quite true, computers generate pseudo-random numbers, the more sophisticated the algorithms, the more random. Electronic engineers use thermodynamics and the behavior of individual electrons in "hot" components to generate actual random numbers.

Does this answer your question? How random is genetic recombination?

@John, that question is about recombination. This question is about assortment, which is a distinct (though procedurally related) process. Recombination is about how recombinant segments form chromosomes, assortment is about how chromosomes end up in gametes.

@JiminyCricket I would argue that this is a distinct question (see comment to John). Independent assortment and recombination are distinct processes.

@MaximilianPress vote to close retracted, your problem is indepentant assortment can refer to both.  I would assume a mechanism would be needed to prevent random assortment of chrmosomes, since chromosomes are not grouped or organized by cells.

OK, @MaximilianPress I'll abide - not being overly familiar with the topic I'll not flag.

keep in mind mathmatically random and scientifically random do not mean the same thing. a mutation is random even if we know all the causes and can predict them. Random is often synonimous with sufficently random to be difficult to predict in biology.

@John: understood, I think of recombination as specifically the process by which crossovers occur chromosomes and of independent assortment as specifically the mechanism by which individual alleles/chromosomes are inherited (e.g. here), but I guess all of these concepts get fuzzy, especially from person to person. When I get some time I will try to edit the question to carve out the two concepts and also try to answer.

Welcome to SE Biology. Our subject may lack mathematical precision, but we try to use precise and complete descriptions when we are communicating our ideas. You will notice I have edited your original question to make it clear you are talking about chromosomes, and maintained the words “random” and “assortment” rather than indulging in the “elegant variation” of “independent” and “segregation”, which is confusing to the non-expert who  cannot be sure you are referring to the same thing. I also stated your title with a capital letter — we like to maintain standards on our site.

God does play dice! And I am not aware that he needs to invoke his powers to ensure that there is a one-in-six chance of throwing a six.
So I don’t accept the unsubstantiated assertion in the question. Is there a mechanism to determine which atom of radioactive carbon-14 in a population is the one that decays? And radioactive decay — a zeroth order process — is surely random.

David, I think the question poster would consider carbon-14 decay to be a mechanism, and thus be the answer he is seeking (although probably desiring further explanation about how radioactive decay controls the selection).  The fact that our understanding of that quantum process indicates it is not predictable would not be relevant to its being a 'mechanism'.  I presume you don't believe it is in fact based on decay but rather believe it is based on the thermodynamic unpredictability of ...

(Cont'd)... molecular motions in the cellular environment.  I suppose you jumped to a quantum mechanism rather than the actual thermodynamic one is for rhetorical impact since the thermodynamics are predictable in theory (though not in practice), while quantum theory indicates it is simply not predictable.  Since the poster considers coin flipping a mechanism (though "theoretically predictable"), he should also consider thermodynamic disorder a mechanism.

@mgkrebbs — I had considered discussing this. I would consider throwing dice the end as well as (or rather than) the "mechanism" the poster invokes. Likewise for chromosome segregation. And, though not qualified to say more, I assume randomness in nature is a fundamental consequence of the physics of matter. I would say that randomness needs no justification — it is non-randomness that does. Were the dice loaded?