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Did early 20th century researchers state why they used E. coli as a model organism?
I am investigating the early uses of E. coli as a model organism. Sadly, many early 20th century papers are not in English. In those that are, I have been unable to find explicit statements as to why a researcher chose to use E. coli as a model organism.
Does anyone know of early literature in which this reasoning is stated? I imagine that prior to the widespread use of E. coli, scientists would have had to argue why they chose to use it to investigate biological phenomena not limited to this bacterium alone.

Nobody justified the organism then, nor did they need to. If they had discovered something that was new then it was publishable. This "model organism" thing is a recent phenomenon driven by medical research funding and political pressure. What is valid in relation to your question is when E. coli started to be used and why. If you can cite any papers you have found do so, irrespective of language. It's only sad for you. Many of us here in Europe speak or read German and French (the most likely languages in this respect) and other European languages.

@user297623, while my answer is given below, I'd be curious to read some of the early 20th century French articles - to which you likely refer, but couldn't get a copy of their text, or find an online copy. If there were online copies: could you add a link?

Historical Fallacies implicit in the Question

“…why a researcher chose to use E. coli as a model organism.”

Researchers did not work with E. coli because they regarded it as a “model organism”. They worked with it because they were bacteriologists and it was a convenient bacterium to use. As Joshua Lederberg wrote in Microbiology Today (2004):

From the beginning, although pathogenic strains were also found, E. coli was used as a representative, harmless bacterium that could be safely and easily cultivated even on synthetic media. On rich media, it will grow with a
  doubling time of 20 minutes; hence readily visible colonies can be seen overnight when it is plated on agar. Specialized media, like MacConkey’s agar,were developed for the selective isolation and identification of E. coli, as this was used as a global indicator for the pollution of water supplies. Hence, during the first half of the twentieth century E. coli was well known to bacteriologists. However, it was rarely, if ever, mentioned in general biology texts, as bacteria were generally regarded as pre-cellular in complexity and devoid of the nuclei and other genetic apparatus of ‘real’ organisms.

Indeed the term ‘model organism’ was not used in this sense until about 1970, as this Google ngram shows.

“I imagine that prior to the widespread use of E. coli, scientists would have had to argue why they chose to use it to investigate biological phenomena not limited to this bacterium alone.”

You imagine wrongly. They were not sitting down and saying “we want to study this biological phenomenon, what bacteria shall we choose?” and certainly not having to justify themselves on publication. In general they published in specialized bacteriological journals where audience and referees would know why they were using E. coli or whatever. Even when Tatum and Lederberg (see below) published a letter on bacterial recombination in the general science journal, Nature, in 1946 they did not waste space on species justification:

No. You are imposing modern attitudes — governed by the contemporary state of science and its funding — upon the science of a completely different era. That is not the way to approach history.
Why did E. coli become the most studied bacterium?
It would seem that the discovery of bacterial recombination in E. coli by Lederberg and Tatum (for which they shared the 1958 Nobel Prize for Physiology or Medicine with George Beadle) was one of the key factors leading to the expansion in the use of E. coli (see Microbiology Today article previously cited). This phenomenon was originally suggested by studies on the transformation pneumococcal bacteria, but its demonstration in the bacterial workhorse, E. coli, opened the doors to the use of a wide range of genetic techniques that could be used for biochemical, as well as molecular biological, studies.

Very interesting question.

Did early 20th century researchers state why they used E. coli as a model organism?

In short: No (at least in the 1920ies). For instance: Werkman 1927: Vitamin Effects in the physiology of microorganisms does not provide any justification.
Similarly, a recent review by Blount, 2015, eLife: The unexhausted potential of E. coli states:

E. coli's meteoric rise and exalted status in biology stem from how
  easy it is to find and work with. Hardy, non-pathogenic, and versatile
  strains that grow quickly on many different nutrients can be isolated
  from virtually any human. These traits made E. coli a mainstay in
  microbiology teaching lab collections. Consequently, when early 20th
  century microbiologists cast about for a model organism, E. coli was
  one of the most widely available choices.

However, when E. coli entered research in the 19th century, and thus a few decades earlier, it wasn't introduced as a tool or model or teaching material. When it entered science it immediately did so as part of one very profound and important discovery about human digestion, as reviewed by Shulman et al., 2007, Clinical Infectious Diseases

Escherich described in detail Bacterium coli commune (the common colon
  bacillus now known as Escherichia coli) and Bacterium lactis aërogenes
  (now known as Klebsiella pneumoniae). He demonstrated their
  fermentation characteristics and the nature of the gas produced during
  fermentation, and he showed that, under anaerobic conditions, growth
  was totally dependent on carbohydrate fermentation. Breaking with
  dogma, Escherich concluded that any role of the intestinal flora in
  nutrition was minor at best.

While only peripheral to your main question: E. coli's second boom during the mid of the 20th century, where it entered the field of genetics (that has been occupied by other organisms before) occurred because of discovery of the ability to exchange DNA between individuals - as reviewed by Telis et al. 2014: A Bibliometrics History of the Journal GENETICS (... which would then promote further discoveries relating to the handling and manipulation of DNA...).

When I read your question the first thing that came to my mind was that Escherichia coli is one of the most common bacteria in human faeces. Of course, the ease of finding and collecting the bacterium (I'm not claiming that the modern source of E. coli is human faeces, I mean not today!) cannot be the only (or the main) factor.
Therefore, I'd like to give you a list of factors — which probably have led the early 20th century researches to choose E. coli as a model — quoting Geoffrey Cooper's "The Cell: A Molecular Approach" (2000).
He starts talking about molecular biology...

E. coli has been especially useful to molecular biologists because of both its relative simplicity and the ease with which it can be propagated and studied in the laboratory. The genome of E. coli, for example, consists of approximately 4.6 million base pairs and encodes about 4000 different proteins. The small size of the E. coli genome provides obvious advantages for genetic analysis, and the sequence of the entire E. coli genome has been determined.

... which is interesting but, of course, not related to your question.
However, in the following paragraphs, he lists a series of characteristics that are pertinent to this question:

Experiments are further facilitated by the rapid growth of E. coli under well-defined laboratory conditions. Depending on the culture conditions, E. coli divide every 20 to 60 minutes.

A clonal population of E. coli, in which all cells are derived by division of a single cell of origin, can be readily isolated as a colony grown on semisolid agar-containing medium.

Because bacterial colonies containing as many as 108 cells can develop overnight, selecting genetic variants of an E. coli strain—for example, mutants that are resistant to an antibiotic, such as penicillin — is easy and rapid.

The nutrient mixtures in which E. coli divide most rapidly include glucose, salts, and various organic compounds, such as amino acids, vitamins, and nucleic acid precursors. However, E. coli can also grow in much simpler media consisting only of salts, a source of nitrogen (such as ammonia), and a source of carbon and energy (such as glucose).

It's also worth mentioning that, despite some pathogenic strains, most of the naturally occurring strains of E. coli are inoffensive.

Source: Cooper, G. (2000). The Cell: A Molecular Approach. Sunderland (MA): Sinauer Associates.


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Why don't humans typically drink human milk after infancy?
Does any human culture routinely do this? Typically taboos have some evolutionary basis. So what would that be? Does any mammal drink the milk of its own species, besides nursing?

I guess your question should be the other way round. Humans I guess are the only species that drinks milk after infancy. We drink cow/buffalo/goat milk. This is an interesting read regarding lactase insufficiency and gene-cultural co-evolution. https://www.americanscientist.org/issues/feature/2010/2/gene-culture-coevolution-and-human-diet/1

I understand about lactose intolerance. And it is interesting that we drink milk from other species. But that is what brought me to the question in the first place.

@KarlKjer As you explained to Polisetty, your question is not about human drinking milk of other species at adult age but in case it is of interest anyway, I want to point to the post Are humans the only species who drink milk as adults?.

Q1: I don't know. Q2: presumably because it's not in the mother's interest to provide direct high-quality nutrition (very energetically expensive) over an extended period of time; additional cost of this parental investment wouldn't pay off in increased total (inclusive) fitness. [HOWEVER: not posting this as an answer because it's speculative/tautological ...] Q3: don't know (but see linked question by @Remi.b)

On might speculate that it's simply a matter of there being a very limited supply.  But it does happen: search "breast milk cheese" for some examples.

The title of your question specifically references humans, but then, in your question body, you mention mammals in general.. which are you most concerned with?

@charles. Humans. Because we have a culture that is often linked to evolution, and everyone reading this is human. The other species just came up as something that might support a universal rationale.

It is only in our modern times that human milk is not consumed. I don't see how you could say for sure that our prehistoric ancestors never consumed human milk as adults.

Giving a woman food for her to inefficiently convert to different food is a waste of time and energy; it only makes sense for infants that can't eat much else (and even there, plenty of people find substitutes so the woman can get back to work).
Turning grass, which people can't eat, into a food people can eat makes a whole lot more sense.

I see your point. But in a capitalist society. if there were profit in it, it should happen. But it doesn't because ...ew... yuck. Why?

@KarlKjer Humans were not capitalist for most of their history, which is the context in which they evolved. Only after thousands, maybe even millions of years under our modern capitalist society can you pose the question you have.

@swbarnes2 Well, it is also inefficient to feed grass to a cow and drink its milk, instead of just growing beans on that meadow and eating those, and yet dairy is a enormous industry.

You don't have to "grow" grass.  It grows on its own with no effort.  Crops take work.  The fact that for millennia people who knew perfectly well how to grow plants did cultivate cows for milk is really good evidence that it really is worth the effort.

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Books about human evolution
I want to read some books about human evolution and about other extincted types of humans.
The book "Sapiens: A Brief History of Humankind" writes about history of agricultural and scientific revolution too, which is the part that is not interesting to me as it sounds more like history. However, I want a book about humans living millions years ago up to and before agriculture. I want to know how modern human evolved and what there were besides homo sapiens.

https://www.amazon.com/Humans-Evolved-Seventh-Robert-Boyd/dp/0393614867

It sounds like you are more interested in archaeology and even history than in evolution. This sounds particularly clear as you talk about the scientific revolution. Maybe History.SE would be a good place to ask this question. Note that evolution, in biology, is usually defined as a change in allele frequency over time (a definition that you may or may not understand) and it does not seem to be what you are interested in. I'm voting to close.

@Remi.b By mentioning the scientific revolution in "Sapiens: .... " I meant that I am not interested in this part.

I'm voting to close this question as off-topic because it is about history and archeology and not biology

The Journey of Man is a great book that really dives into the archaeology but also the genetic history of evolution.

I haven't read this, but I see it's published in 2003. If so, it's completely obsolete, missing enormous technical advances since then, completely unaware of the entire Neandertal interbreeding story, preceding the discovery of at least one branch of Homo (denisovans at the least). Would not recommend.

It is good to know that a field could change that much dramatically within 15 years. In Physics it is not so much like that! (of course that depends on the sub field)

I came across 'The Last Ape Standing' by Chip Walter that sounds like it might be something you would be interested in.

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How were we able to determine the age of the first cell?
I heard in episode 20 of Youtube channel CrashCourse's biology series that every living organism descended from a single microorganism 3.8 billion years old. I'm astonished by that figure. Even though it leaves a good 100 million years of wiggle room.
As a mathematician I happen to have a fair background in physics so I have been able to grasp the concept of carbon dating and a few other techniques, none of which seem to me to explain how this was determined. What trace could we possibly have of such an organism ? I can't imagine a team finding a fossilised cell and shouting "We've found the first cell !".
Might it have something to do with a well determined evolutionary rate conjectured to be constant and leading back to that particular time ?

I can't imagine a team finding a fossilised cell and shouting "We've found the first cell !"

Well... not the very first cell, but one old cell, yes!
Most of these very old fossils are microorganisms found in seafloor hydrothermal vent precipitates, in stromatolite or in very old sedimentary rocks typically in Greenland but also in eastern Canada. There were also very old fossils found in sandstone in Australia.

Might it have something to do with a well determined evolutionary rate conjectured to be constant and leading back to that particular time ?

No, that's now how we do. We just look for very old fossils. The reason we can't do such simple regression is three-fold.
As measure of 'evolutionary rate', we would typically use the substitution rate at neutral loci. The method is referred to as "molecular clock". The principle is easy (the stats and detailed implementation are a bit less easy). Consider a diploid population of size $N$. Each generation $2N\mu$ mutations are being created at a given locus, where $\mu$ is the mutation rate at this locus. If those mutations are neutral, then a fraction of $\frac{1}{2N}$ of these mutations are going to fix (fixing means reaching a frequency of 1 in the population). This result can be demontrate with a number of technics (incl. diffusion equations and branching processes) but I am not going to detail that now. This means that $2N\mu \frac{1}{2N} = \mu$ mutations will fix every generation in a population. If each substitutions occur at a new locus, then the number of substitutions accumulated over $t$ generations is $2t\mu$. For the substitution rate at neutral loci to scale with time we need constant mutation rate.

The assumption of constant mutation rate is very likely violated on such time interval.
For very distantly related lineages, substitutions won't always occur at new loci. There are tricks to deal with that but there's a point after which, all substitutions will occur at loci that have already received substitutions and there is no signal left to analyse.
We need two lineages to compare their number of substitutions but there is no reason to think that the oldest forms of life quickly separated in different lineages that would have survived until today

Was it really 3.8 billions years ago?
The date of 3.8 billions years ago that you got from CrashCourse (or that you may have read somewhere) is not as accurate as the Green brothers (authors of CrashCourse) may have made you think it is. There is much more than a 100 million years of wiggle room. The only think we can do is find a very old fossil of something that looked like a living thing, date it and claim that life is at least as old as this fossil is.
We think life appeared after the formation of the ocean (which happened 4.41 billions years ago), so any fossil older than that would be quite an extraordinary discovery. The earth was formed about 4.54 billions years ago, so of course we won't find any fossil older than that.
Papineau et al. (2017) is good read on very old fossil (and potential fossils) that we've found. From their abstract

Here we describe putative fossilized microorganisms that are at least 3,770 million and possibly 4,280 million years old in ferruginous sedimentary rocks, interpreted as seafloor-hydrothermal vent-related precipitates

You will notice that we don't quite know the exact date of when abiogenesis happened. I recommend you having a look at this paper if you want to learn more.

Once again, I am reminded of just how fast (geologically) that life happened after it became possible. I think that this is a good sign that even though planets move in and out of "habitable zones" and some stars have a violent early history, that there is still going to be a lot of life "out there" (at least microbiology).

This article [https://www.sciencedaily.com/releases/2006/07/060721090947.htm] provides a good overview of the kinds of evidence there is for extremely ancient rocks containing traces of once-living cells.  The other half of the question is how to determine when the rocks were formed, trapping those traces.  The answer to that part of the question is not carbon dating (because the half-life of carbon-14 is too short), but radiometric dating of a different sort.  [https://en.wikipedia.org/wiki/Radiometric_dating] does a good job of describing radiometric dating methods that work on the scale of a few billion years.


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Proteins in different organisms
I know that DNA is universal meaning that all organisms have the same 4 base pairs and also that the same codons code for the same amino acid in all organisms. What I am wondering is that say humans and bacteria and rats all have the same gene which codes for the same metabolic enzyme. Will the amino acid sequence of that protein enzyme also be the same in all three of those organisms? And that specific gene segment will also have the exact same base pair sequence in all three organisms too correct?

Welcome to Biology.SE. What do you mean by "same gene", if not "same base pair sequence"?

Before I go into answering your question, I just want to correct some mistake you have. Although DNA nucleotides (bases) are (almost) universal, the genetic code is not - there are organisms that use a slightly different genetic code. See here for example. Moreover, even the mitochondria in humans (and vertebrates in general) uses a slightly different code.
Now, to answer your question, it all comes down to evolution. Humans, rats and bacteria all have a common ancestor somewhere in our evolutionary past. Let's assume that this ancestor had some crucial and universally-useful gene. Since then, human+rat diversified from bacteria and then from each other, but all 3 species kept this gene, since its function was absolutely necessary. However, mutations were acquired along the way in each lineage. These mutations can be random and may not even have an effect on the amino acid results (synonymous), or they can be a result of natural selection and have an effect on the amino acid sequence (non-synonymous). In many cases, the different life styles and selective pressures acting on each species lead to rather different nucleotide and amino acid sequences. So to sum up, you can expect DNA, RNA and protein sequences to be different, although more similar between human and rat than bacteria.
In fact, the concept of the "same gene in different organisms" is somewhat wrong. As I explained, this is not the same gene, but you may say that it is homologous between the species, and more specifically orthologous.

Alright, but say that 2 organisms do have the exact same gene for some protein enzyme. I know there can be mutations and all and this is unlikely, but say that happens. Will those two widely different organisms have the same DNA sequence for that gene and hence the same amino acid sequence, resulting in the same protein? Or can the exact same protein enzyme be coded from different DNA sequences in different organisms? I'm thinking that in order to be the exact same protein, the gene sequence MUST be the exact same as well but I'm not sure.

Just to make sure I understand: you're asking something like "Suppose I see that two organisms produce the exact same protein (same AA sequence), does that mean that the respective DNA sequence is the same?" Is that correct? If so, then the answer is of course not! Take a look at the genetic code table. How many ways are there to code Proline? Glycine? There are numerous way to code the same protein. On top of that, there is splicing, RNA editing, protein processing etc that could be going on and different between the organisms.


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How many generations does it take for one species to become a new one?
First lets consider that a species is a group of individuals that can reproduce by breeding fertile offsprings.
It's usually said that evolution takes a very long time. Lets say that 1000 generations are required for species A to evolve into species B.
Which species would generation 999 belong to, A or B ?
If A then it means that there was no evolution in 999 generations and that the entire evolution is going to happen in a single generation from 999 to 1000.
If B then which specie does generation 998 belong to ?
etc etc
In the end it seems to me that if there is evolution it can only be instantaneous, but that requires many improbable things, one of them being that the spermatozoids and ovules of species A contain DNA of species B !
How does that work ?
EDIT this is not a duplicate I'm not asking what a species is I'm asking what is the genetic process of evolution, how do we move up in the evolution tree.

In short, the concept of species is a subjective one and is not objectively defined. You should have a look at How could humans have interbred with Neanderthals if we're a different species?. While your post is not directly a duplicate of the linked post, your question(s) are being answered in the accepted answer of this other post. I am therefore voting to close as duplicate. If you think your question has not been answered in this other post, please let us know

Btw, the singular of "species" is "species", not "specie".

The observed minimum within animals is three generations. ---- While the question is marked as a duplicate, the answers differ between "How many generations does it take for one specie to become a new one?" and different from  "How could humans have interbred with Neanderthals if we're a different species?"; ------  For the former the answer would be: The observed minimum within animals is:       Three generations. Lamichaney et al. Science, 2018: Rapid hybrid speciation in Darwin’s finches

@tsttst there are plenty of cases of hybrid speciation (single generation) i plants especially.

@Remi.b good point; and there is also at least one synthetic specification in Drosophila; intended to stay close to natural evolution in animals and thus close to the previously linked question - which has an excellent answer about general themes of evolution

The word "species", in the biological sense, is both singular and plural. The  only meaning of the word "specie" that Chambers gives is "coined money". Please edit your question to reflect this so that others do not copy your error.

"Species" is to a considerable extent a human construct.  There are numerous examples of groups which are considered different species because they are reproductively isolated from each other (e.g. the hybrids between native & introduced trout in the Sierra Nevada/Great Basin).  So essentially what makes a new species is a group of biologists agreeing that it is a new species: http://www.bbc.com/news/science-environment-42103058

Your question is like asking about the color spectrum. A wavelength of 530nm is green; a wavelength of 580nm is yellow. So let's say it takes 60nm of wavelength change to go from green to yellow. What color does a wavelength of 579nm have, green or yellow? If it's green, then does the color shift in a single nm difference of wavelengths? If it's yellow, what color is 578nm, etc?
The answer in this case is, 579nm is yellow; so is 578nm. 570nm is more ambiguous; some people might say it's yellow, others think it's greenish-yellow, in some contexts it might look clearly green. And so on along the spectrum; the reality is that there is no hard boundary between "green" and "yellow". There are colors that are clearly green, colors that are clearly yellow, and there is a difference between those two, but there are also plenty of intermediates that are a bit like green and a bit like yellow, and those intermediates are what you go through when you go from green to yellow. There is no definite point everybody can agree on where a single shift happens.
It is the same thing with species. A species is a group of organisms that interbreed to produce fertile offspring, but "interbreeding to produce fertile offspring" isn't a on/off thing. Organisms are more or less fertile. What if organisms from two groups interbreed and produce offspring, and only half of those offspring are fertile? Or they have half as many offspring as couples within the two groups have?
The reason species are an important concept, and can be distinguished visually as being like each other and unlike members of other species, is that within a species there is widespread sharing of genes over the generation, as individuals breed with each other, but they don't share genes with other species. Meaning species will evolve as a unit; changes that happen within a species will spread between individuals of that species, but won't spread outside of it.
But because sharing genes isn't an on/off thing, you could have 100% of genes being shared from one population to another (then they're clearly the same species), or 0% (then they're clearly not), or 90%, or 70%, or 10%... That's where you find the fuzzy boundaries. The races, strains, varieties, sub-species, all those different words to describe populations that are different but aren't outright different species. And the debates on whether different groups are different species or not in the first place, in the cases where it's really ambiguous.
And the same thing is true of evolutionary change in general. You don't have a mammalian carnivore that isn't a cat, and then bam! a cat. You have a mammalian carnivore that isn't a cat (or dog, or weasel... but kind of like any of those in various ways. Like generic carnivore-ish), then a mammalian carnivore that's a bit more like a cat or a dog (and another one next to it that's a bit more like a weasel), then a mammalian carnivore that's even more like a cat (and others that are even more like a dog, and even more like a weasel), then a mammalian carnivore that's clearly feline but isn't a cat, or a lion, or a tiger; it's a different species of feline that doesn't exist today, and also looks more generic-feline-ish than any modern feline. Then there's a feline that's more like a cat (and others around it that are more like a lion, and a tiger), but also clearly isn't a modern cat. Then there are felines that are really like cats but a bit different from modern ones and it's hard to tell, maybe we should extend the definition of "cat" to include them? And then bam! a cat. But that cat isn't clearly a Jungle Cat, or a European Wildcat, or a domestic cat, or any modern species; it's its own "archaic cat" species. And then there are cats that are more like Jungle cats, or more like domestic house cats...
Also don't confuse the creation of new species with evolutionary change in general. Over the long term they are related, because once two groups are different species then they will change through evolution in independent directions, and they will end up looking different from each other as well as from their common ancestor. But over the short term you can have speciation with very little morphological or genetic change (you just need two groups that used to interbreed, to no longer do so), or morphological/genetic change without speciation (if all the change happens within one group).
Both speciation and genetic/morphological change can happen within a single generation, but usually happen over much longer timescales. But there is no hard rule for how long that is; as far as speciation goes, if groups aren't prevented from interbreeding in some way then they will keep breeding with each other and can stay a single species indefinitely (whether individual from generation 10,000 could interbreed with individual from generation 1 is a different question, but it's not like it's a situation that happens). As far as evolutionary change goes, natural selection means species change to adapt to their environment. Once they're adapted to it, if it happens their environment never changes then natural selection will push them to stay the same as they are, again indefinitely. In the real world most environments change over time so organisms do change more often than not, but just to illustrate that the timelines are a product of circumstance, not an intrinsic feature of evolution itself.

Ring species are a great example of how fertility can vary even within a single species, and just how vague the concept of species is. Penguins are another a great example since some species can successfully crossbreed in the wild.

Species is a hard concept to really pin down but your definition is fine for animals and most plants.
If the only distinction we make is their reproductive success, and we know g1000 is the only generation that is part of species B and it is unable to reproduce with g999 then something must have happened when g1000 was born that makes all members of g1000 unable to successfully reproduce with all members of g999. The most likely scenario is geographic or temporal isolation, they must have migrated into another area or their mating season went out of sync with g999. In that case the real speciation happened in one generation, from g999 to g1000.
If on the other hand we know g1000 is species B and g1 is species A, but we haven't decided if g2 through g999 are part of either A or B then the possiblity exists that g2-999 are intermediate populations. Using the temporal isolation example again imagine g1 has mating season from Feb-07 to Feb-16, g100 has mating season Feb-08 to Feb-17 and every hundred generations the mating season shifts one day, then g1000 has mating season Feb-17 to Feb-26. This means there is no way for g1000 to reproduce with g1 simply because they never have sex but g1000 can reproduce with g100 and up. This is the closest explanation we have for speciation, any obvious differences between species come only after many generations of isolation.
Regarding DNA, all species are related and all related species share a lot of their DNA. The closer their relation, the more DNA they share. Even humans and grass both have the genes that allow us to get energy from sugar. So yes, all cells of species B will contain DNA from species A, there is just a tiny difference that is just big enough to keep them from breeding. This could be mating season differences, but also incompatible genitals or one of the species has become allergic to the other, or anything else you can think of.

Welcome. Can you add sources to allow other users to background read on your answer?


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New infectious diseases appear mainly as a result of chance mutations in pathogen genomes?
I am reading the book 'Homo Deus: A breief History of Humankid' by Harari. He mentions the following statement highlighted in the picture below (picture provided for context). I would be appreciated if someone could (1) explain the meaning of it (I have very little background in Biology) and (2) the reason behind it.

Welcome to Biology.SE. The issue is that the text is really not rigorous and phrased in slightly vague term. Also, it is a little unclear what exactly your might be misunderstanding from the highlighted part. I don't think we can answer much else than simply giving you an intro course to evolutionary biology. I am therefore voting to close as too broad but maybe you'll be able to explain better what exactly is unclear to you in these few words.

For an very short and very introductory course, you might want to have a look at Evo101 by UC Berkeley

Mutations happen all the time when DNA is replicated. These random mutations are the building blocks for evolution under natural selection. So when a single nucleotide is changed, (or deleted or added), there are three possible outcomes. 1. the mutation is neutral, so nothing happens. 2. The mutation is lethal or mal-adaptive for the organism, in which case natural selection will remove the individuals carrying the mutation from the population, or 3. the mutation results in some change in function that helps the organism compete under natural selection. This 3rd kind is the rarest, but with pathogenic viruses and bacteria, with huge populations, the evolutionary test pool is much larger because there are so many new mutations being put to the test with every generation. So, for example, a mutation in a pathogen adapted to spread through chickens, could change the pathogen to be better adapted for spreading through humans.

I will be a bit picky and awfully pedantic (sorry) but I think a rigorous phrasing is important here. the mutation results in some change in function that helps the organism compete under natural selection. A) associating change of function with beneficial consequence, not not talking about a change in function in other cases is misleading. Change of function can go both ways. B) summarizing "higher fitness" to "helps the organism compete under natural selection" is misleading because 1) fitness differential does not necessarily require competition 2) NS is not a condition under which ...

competition occurs but the concept of fitness differential (+ heritability) itself. Also, it is clear that population size matters but it is not as easy as your answer might make it think. Also expressions like evolutionary test pool are very much undefined. The expression random mutations can also be very misleading (see the post Are mutations random?)

These random mutations are the building blocks for evolution under natural selection. Mutations are the ultimate source of genetic variance. It fuses evolution whether there is a selective pressure or not.

adapted to spread through chickens, could change the pathogen to be better adapted for spreading through humans I understand that this goes along the example of the text given by the OP but, IMHO, I think it would be good to avoid giving the misrepresentation to the OP that evolution for a pathogen is an event that necessarily allows a pathogen to jump from one host to the other and that all other evolutionary events would be of no interest or even would not be part of evolution.

@Remi.b I'd be glad to discuss this with you.


text:
Gene copies vs. gene paralogs - what's the difference?
I'm trying to get into the theory and practice of gene copy number variation (CNV) analysis, but there is something basic confusing me, which I couldn't yet figure out. Sorry if this is a dumb/trivial question - would appreciate your help anyway.
My confusion is regarding the terms 'gene copy' and 'paralogs'. As far as I understand, paralogs are created when a gene undergoes duplication (never mind by what molecular mechanism), and then starts accumulating mutations as evolution proceeds. So, if gene X was duplicated to create another X, and then X changed to become X', are X and X' considered copies of the same gene, or are they paralogs? Is it a matter of applying some threshold on the sequence similarity between X and X', so they are considered copies up to the point where they diversify enough? Or maybe gene copies are expected to be perfect duplicates? If so, I'd guess that finding such gene pairs is very rare... Maybe it's a matter of function, so once X' gets a different function from X (neo-functionalization), it is considered a paralog? This is a rather complex and difficult to measure definition...
To make things less theoretical and more practical, lets limit the conversation to the context of whole genome sequencing analysis. Let's say that I am annotating a newly-assembled genome, and let's assume that the assembly is good enough so gene copies are not collapsed, but rather are located in their respective genomic positions. How would you look for gene copies and paralogs, and how do you make the classification?
Could anyone clarify this point for me, or refer me to relevant literature?
 Thanks a lot!

The general term "copies" has multiple meaning with reference to genes. In diploid organisms for example, we have two copies of each gene (except those on the Y chromosome). However, these copies are called alleles. Copies that are due to duplication are called parlalogs. There is no distance criterion for differentiating copies or parlalogs. Once duplicated, there are two copies. But the consequences of paralogy would depend on differences, so the question is interesting. At the first generation after duplication, if both copies included all of the upstream regulatory elements, it would be hard to identify which of the copies was the original, since they would both be identical. But over time, if one were to evolve a new function or (more likely) accumulate frameshift substitutions, the altered one would be called the paralogous copy (relative to comparisons across species).


text:
Is there enough evidence in this paper that there is a second (mechanical) layer of information in DNA?
The following commentator writes:

Mechanical cues
  Since the mid 80s it has been hypothesized that there is a second layer of information on top of the genetic code: DNA’s mechanical properties. Each of our cells contains two meters of DNA molecules, so these molecules need to be wrapped up tightly to fit inside a single cell. The way in which DNA is folded, determines how the letters are read out, and therefore which proteins are actually made. In each organ, only relevant parts of the genetic information are read, based on how the DNA is folded. The theory goes that mechanical cues within the DNA structures determine how DNA prefers to fold.

My question is: Is there enough evidence in this paper that there is a second (mechanical) layer of information in DNA?

...isn't your question answered in the paragraph following the one you're citing?

I was trying to work out of this paper had any credentials or not. You’re saying it does?

Ah, it isn't clear from your question that you actually want info about this paper. I suggest you to rephrase it to actually include what you ask in the comment. Something like "Is there enough evidence in this paper that there is a second (mechanical) layer of information in DNA?". In the meanwhile I'll check the paper.

I'm voting to close this question as off-topic because SE Biology does not exist to referee scientific papers.

Biologists already know that transcription can be regulated by winding or unwinding DNA.  (This paper might be informative:http://www.cell.com/trends/parasitology/fulltext/S1471-4922(16)30226-4)
But this is hardly the only method of gene regulation.


text:
Detailed working of the voltage-gated sodium channel
Hodgkin and Huxley formulated the ion currents through the three voltage-gated ion channels Na, K, and L as
$$\sum_{k}I_{k}=g_{\rm Na}\,m^{3}h\,(u-E_{\rm Na})+g_{\rm K}\,n^{4}\,(u-E_{\rm K%
})+g_{L}\,(u-E_{L}).$$
From Gerstner et al, Neuronal Dynamics, 2.2 Hodgkin-Huxley Model
What they probably didn't know - but is known today - is, that the sodium channel possesses four voltage-sensors (S4), opposed to one ball (IFM) which may close the channel and is described by $h$:

From Wikipedia, Ball and chain inactivation
Do I interpret Hodgkin and Huxley correctly, in that they found experimentally that three of the four voltage sensors must be in the up (= open) state for the pore to be open? Does this hold "exactly", or should the exponent in $m^3$ not be taken too "literally"? For example, the four voltage-sensors might be slightly different and have different deviations (when in their resp. up states), and only their "average" deviation counts, which is somehow reflected in the exponent $3$? The question then arises, why the exponent is an integer number. Couldn't it be any real number then?


text:
How much does sprayed water remove bacteria?
I was quite skeptical about some company claiming that their device was able to suppress 99.99 % of bacteria.  Then I read a report testing the germicidal effect of their device, from a large and independant testing laboratory.
The device was tested against a number of bacteria, including Salmonella, Escherichia coli, Staphylococcus aureus, or Listeria.
They incubated contaminated Petri dishes, then used the device, then incubated the Petri dishes again.  It appears that the test samples had a CFU level log-reduced by 4 to 6 (i.e. the number of bacteria is reduced by a factor of 10,000 to 1,000,000) in most cases when compared to control samples, which supports the claim.
However the device implies spraying water, to which the control samples have not been subjected.  I am curious about how much this simple spraying may affect the results.
Would rinsing the dishes with sprayed water significantly reduce the amount of bacteria ?

In which light does that spray? Is it sunlight ?

@JM97 There is no mention of the lighting, but I'd rather guess white fluorescent tubes or bulbs, according to pictures.  It may also be worth mentioning that the water temperature ranges from 20 to 30 °C.

@JM97 Would lighting have a significant effect ?

Uv light kills bacteria, and spraying provides more exposure.

Though conditions are not exactly the same (the water is not sprayed, the duration of water exposition is different, and samples are not Petri dishes ; I am not competent enough in biology to compare methodologies), I found two relevant papers.
Listeria innocua/monocytogenes, pure rinsing
The first paper used Listeria innocua "as a surrogate for L. monocytogenes", while the EMSL report linked in the question tested the latter.
They found the following bacterial log-reduction after rinsing for 15 s under running cold tap water at room temperature and without prior soaking :

on brocoli and lettuce : 1.41 (96.11 %) ;
on apples : 2.01 (99.02 %) ;
on tomatoes : 2.10 (99.21 %).

To be compared to the report from the EMSL which found, after spraying modified water for 10 s on an inoculated Petri dish (which surface is obviously smoother than that of a tomato) :

at 20 °C : 4.24 (99.994 %) ;
at 25 °C : 3.01 (99.903 %) ;
at 30 °C : 3.37 (99.957 %).

Note that although not mentioned, uncertainties on the EMSL numbers must be fairly large since the quantitative counts are below the detection level of the apparatus (but would actually make the numbers conservative…).
Link to the paper : Efficacy of Home Washing Methods in Controlling Surface
Microbial Contamination on Fresh Produce (open access PDF), Agnes Kilonzo-Nthenge, Fur-Chi Chen, Sandria Godwin, Journal of Food Protection, 69, 2, 2006.
(NB : it contains further testing which are out of scope for this question but may be of interest, e.g. soaking, rubbing or wiping with paper towel.)
Escherichia coli O157:H7, rinsing while thoroughly rubbing
The second paper tested Escherichia coli 0157:H7, which has also been tested by the EMSL.
The paper reports the following log-reduction after thoroughly rubbing during 15 s under running tap water (no indication of temperature, but flow of 2.0 L/min ; the values in the abstract seem wrong for tomatoes, here are the in-paper values) :

lettuce leaves (not rubbed ?) : 1.16 (93.08 %) ;
cabbage leaves (not rubbed ?) : 2.02 (99.05 %) ;
lemons : 4.10 (99.99 %) ;
tomatoes : 5.78 (99.9998 %).

Note that the same reduction is reached for tomatoes after only 8 s of washing.
To be compared to the EMSL results (sprayed "modified" water, 10 s rinsing, no rubbing, Petri dish) :

at 20 °C : 5.67 (99.9998 %) ;
at 25 °C : 5.14 (99.9993 %) ;
at 30 °C : 4.88 (99.998 %).

(Same comment about uncertainties applies.)
Interestingly, in this study they also tested the effects of alkaline electrolyzed water, which may not be too far from "ionized water" (I have yet to dig into details), which itself may not be too far from what is supposed to exit the device tested by the EMSL.  And… they found no significant difference with regard to plain tap water.  (Though they did find significant effects with acidic electrolyzed water and by applying both successively — but that's out of the scope of this question.)
Link to the paper : Reduction of Escherichia coli O157:H7 on Produce by Use of Electrolyzed Water under Simulated Food Service Operation Conditions (open access PDF), Pangloli et al, Journal of Food Protection, 72, 9, 2009.


text:
Do women tend to have longer legs and shorter torsos than men?
I've always heard that women tend to have a greater leg length to torso length ration than men, and I think that my anecdotal observations of pedestrians of both sexes tend to confirm that.
However, now I read that is not the case:

If they are the same height, she’s a lot “leggier” than he is. It looks as though women really do have long legs and short upper bodies for their height. (We’ll see later this isn’t the case.)
(...)
This observation is purely anecdotal, though. There are studies which measure the lengths of men’s and women’s legs, arms, upper bodies, and so on. These measurements show that women have shorter legs and longer torsos than men as a proportion of their heights.

So, at least, says a bicycle designer. And I suppose bicycle designers should know anatomy.
I have a cognitive dissonance here, since again, my eyes watching pedestrians tell me otherwise.
So - what is the truth?

I think men look like they have shorter legs because they tend to wear pants that are less form fitting with a lower hanging crotch area for obvious reasons. So this gives the illusion of a longer torso and shorter legs. Women also tend to wear clothes that accentuate the length of the legs to make the legs look longer, like high waisted pants, etc.

We seem to have a preference for proportionally longer legs (see comment here for a good summary around that study).  So when you are observing "pedestrians" they have probably tended to dress and comport themselves to skew your perception of their leg lengths.  Perhaps in your cultural environment females have a greater capacity and/or motivation to alter that perception than do men.
The reality is that adult female legs are on average proportionally shorter than those of men.  See, for example, this detailed 1977 U.S. Army study comparing body proportions in adults by gender.
For readability I would highly recommend this much broader survey of the subject, which contains not only clear illustrations of how proportions are measured but also an extensive survey of cross-cultural and historical variations: Leg Length, Body Proportion, and Health: A Review with a Note on Beauty.


text:
Is it possible to discriminate tetrachromacy using sRGB color?
Hi I'm a physics grad student who has lots of interest on color perception.
I have recently learned that some people (mostly women) have another active cone cell which makes them possible to discriminate more colors than usual people like me.
Is it possible to discriminate tetrachromacy using sRGB color, I mean, is it possible to test it out on computer monitor? I guess so, because even though computer use combination of only 3 colors, it seems possible to make 2 combinations different in which is only perceptible to tetrachromacy. However, I'm not sure about that point because I'm not expert on that.
Anyway, if I'm right, it would not be so hard to make a test which resembles dyschromatopsia test, that can distinguish trichromacy and tetrachromacy. I couldn't find such a thing on internet. Test I could find seemed not valid. Even I could pass all the tests, but I'm not clearly tetrachromatic person.
Can somebody help me?

All the combinations of three sRGB primary colors are distinct for a trichromat. This immediately precludes any way to find out whether you are capable of more: if even a trichromat can distinguish all the colors, tetrachromat even more so.
But in principle, three colors are sufficient to check for tetrachromacy, but they can't be the sRGB primaries. The three colors you need must lie on one line on the chromaticity diagram, so that multiple mixtures of them could appear as the same color to a trichromat. Then a tetrachromat may be able to distinguish the two mixtures, which are metamers to a trichromat.


text:
Mathematical model about the relationship between two animal species
I'd like to relate a mathematical model with  two animal species. This is the model:
$$
\begin{split}
\frac{dN}{dt} & =rN-\frac{rN(N+M)}{k} \\
\frac{dM}{dt} & =r'M-\frac{r'M(N+M)}{k'}
\end{split}
$$
The model means that there is competition within the population of the first species ($N$) and the population is also affected by the population of another animal species ($M$).
Something similar occurs with the population of species $M$.
My question is:

What kind of animals would fit this model?

I was thinking about white sharks as $N$ and whales as $M$. Clearly the first equation would be correct but the second equation would be saying that the population of whales is affected by sharks, which I think is not true. Is it?

Welcome to Biology.SE! I'm not sure if you're asking specifically whether populations of whales are affected by sharks (it would also have to apply vice versa) or more generally what kind of relationship has to exist for this model to apply. Can you clarify? (Personally I think Ben's answer covers the 2nd very well, and I also think that would be the more useful question to ask.)

@arboviral Thanks . At first I wanted to consider a model related with white sharks, but after reading Ben's answer I definitely should not consider the shark-whale example. Now I just need to find something that can be represented by the model. Do you know of any example so I can consider it?

Related question on logistic competition models (that I've answered before), that allows for asymmetrical competition: Stochastic parameters in population growth equations

The model you present here is a special case of the Lotka-Volterra competition equations, where the two species have the same effect on each other (i.e., symmetric competition). Some things to think about in interpreting this:

each species has a negative effect on the other (i.e., increasing the density of either species lowers the other's population growth rate), hence this is a "negative-negative" interaction; it makes more sense for two species that are competing with each other (for resources, space, enemy-free space, etc ...) than for a predator-prey system such as the shark-whale example you give.
In contrast, in predator-prey (or more broadly "enemy-victim") systems, one species (the predator) benefits from the association - its population growth rate increases when the density of the other species (the prey) increases - and the other species (the prey) suffers (its population growth rate goes down when the predator density increases)
the fact that the competition is symmetric (this happens because you are using the sum of the population, $M+N$, and not using a competitive asymmetry parameter, e.g. $M+\alpha_{MN} N$) means that this would be most suited to modeling the competition between species that were very similar to each other (e.g. the same size, resource-gathering ability, etc.)

Thank you for your answer Ben. After reading your answer I agree that the example shark-whale does not work. What could  be a good example ?

Any two similar species of plants or animals (as I said in my answer, "similar" would mean about the same size, living in the same habitat, eating similar diet, using similar resources ... Since this is tagged as homework, I'm not going to come right out and give an example ...

Ok. I think could be jaguars and panthers?

seems reasonable.


text:
How much DNA does a species lose after post-polyploidization genome downsizing?
After whole genome duplication, diploidization takes place, right? A lot of changings in gene organization and expression involving genetic and epigenetic mechanisms (translocations, transpositions, deletion and / or insertion of sequences, additive or non-additive gene action, transposon activation, gene repression or activation, subfunctionalization, neofunctionalization and so on) cause the genome to shrink a little bit before the species karyotype stabilizes and establishes. But how much DNA, in average, is gone in such process? I guess I have read somewhere that the elimination of redundant repetitive DNA families, causes polyploidization to result in a DNA increase of about 1.5x and not doubling. Is it true? I really would like to have some references on this information or similar.. I did look for, but I couldn't find


text:
Do Black Pepper and Black Nightshade share specific characteristics?
In my textbook, I read that two organisms of the same species share specific or fundamental characters. Piper nigrum (Black pepper) and solanum nigrum (Black nightshade) share the same specific epithet despite belonging to different families. Is this because they share common fundamental characters ?

On botanic, the scientific names are: monomial, binomial or trinomial, so having just one word, two words or three words (words attached together, and words attached with a hyphen are calculated as a single word).
So, from top to Genus (inclusive), we use only one word. So names should be unique, and taxa sharing the same name have some common characteristic (or better: a common evolutionary past). Note: there are few cases with same Genus name in botanic and in zoology, for a different genus. [On botanics, with the exception of Genus, looking at suffix of a name, gives you also the rank of such name. If you doesn't recognize and it is not plural, it is a Genus. Else it is unranked clade]
Then there are binomial names, just below Genus to Species. With exception  of species, where is an abbreviation which define the rank between the two names (e.g. subg., sect., ser.). The second name just specify the genus, so e.g. in Solanum nigrum, the nigrum specify which Solanum. Just the word has no meaning.
To be complete, there are also trinomial names (e.g. subspecies, varieties and forms): the first two part are the specie name (so binomial) plus an abbreviation of rank plus the detailed name. Also in this case it has meaning only together with the first two names.
You choose two species with nigrum, and luckily both had black berries. But it is not always so. Helleborus niger (niger is the masculine, nigrum the neutral) has nothing related to black, but if you dig the roots.
Often the specific epithet is about a botanist, and some time just to honour him/her, so there is no common characteristics on such plants sharing the same specific epithet.
Source: The International Code of Nomenclature: http://www.iapt-taxon.org/nomen/main.php?page=title and his companion book: The Code Decoded (where you see such exception and examples, but many of them are put as example directly in the ICN).

Thanks a lot for answering my question using nomenclature! It helped a lot :)

@KavyaChandrasekaran - thanking someone doesn't help; if the answer is helpful - upvote; if the answer sufficiently answers your question - accept it (arrows & check mark on the left of the answers above)

AliceD  thank you for pointing this out to me, I'm new to this site so I didn't know a couple of things. I shall learn from this :)

@KavyaChandrasekaran no worries. I'm just trying to help. Well done and feel welcomed.

Short answer
Nigrum is Latin for 'black'. As you write in your post, it's black pepper and black nightshade. Not until the level of Class and Phylum do they share the same taxonomic classification. Hence, the species suffix nigrum doesn't tell you anything about their kinships, other than their physical appearance (they're both black).
Background
In general, the species part of the linnaeus nomenclature has nothing to do with evolutionary relationships. Instead, it is the higher classifications that denote kinships, for example, as you already suggest, the genus name, that may have various related species in it (Fig. 1). The species you mention are of a different genus.

The Species: Piper nigrum belongs to the Genus Piper, Family: Piperaceae, Order: Piperales, Class: Magnoliopsida, Phylum (Division): Magnoliophyta, Kingdom: Plantae, and Domain: Eukarya
The Species Solanum niger belongs to the Genus Solanum, Family: Solanaceae, Order: Solanales, Class: Magnoliopsida (Dicotyledons), Phylum (Division): Magnoliophyta, Kingdom: Plantae, and Domain: Eukarya.

They share only the same Class (and hence Phylum, Kingdom, Domain). For comparison, in the Kingdom of Animalia, we have the Phylum Chordata (vertebrates), that splits up into the Classes Mammalia (Mammals), Actinopterygii (Bony Fish), Chondrichthyes (Cartilaginous Fish), Aves (Birds), Amphibia (Amphibians) and Reptilia (Reptiles). So your two plant species share as much in common at the taxonomical level, as Mammals and bony fish.
Piper nigrum (or black pepper), is a climbing vine in the Piperaceae (pepper family) native to the Malabar region of southwestern India. Black pepper is grown in various tropical regions, including India, Indonesia, and Brazil, as it is one of the most important spices in the world.
Solanum nigrum (or European black nightshade) is a species in the Solanum genus, native to Eurasia and introduced in the Americas, Australasia, and South Africa. It is also known as black nightshade, duscle, garden nightshade, Indian nightshade, garden huckleberry, hound's berry, petty morel, wonder berry, small-fruited black nightshade, or popolo.

Fig. 1. Linnaeus nomenclature


text:
Can telegony happen in humans like in Telostylinus angusticollis?
Is it possible for a human male to transmit features of his phenotype via non-genetic semen-borne factors to his mate's subsequent offspring sired by another male? As it happens in flies (Crean et al., 2014).

Note that very few authors really use the term of telegony today. When talking about telegony, are you only referring to inheritance of genetic material or do you also refer to non-genetic material? Because the term is rarely used, I would like to invite you to add the definiton you want to sue in the post (by making sure to state wether or not you want to consider non-genetic elements too). You might want to have a look at wikipedia>telegony

Thanks for the edit. The question is clear now +1. I doubt we'll have much data on this. The 2014 paper you refer to does not talk about studies in humans so we very likely don't have any data prior to 2014. Note that as experimental manipulation would be unethical in humans, the question is probably hard to study.

There are also these studies. What do you think of these? https://www.ncbi.nlm.nih.gov/pubmed/29093734 https://www.ncbi.nlm.nih.gov/pubmed/23618818


text:
Does this procedure for extracting DNA from strawberries work?
I wanted to try out this experiment for extracting DNA from strawberries that can be done at home:
https://www.stevespanglerscience.com/lab/experiments/strawberry-dna/
However, while doing a bit of reading, I came across this article:
http://www.ncbe.reading.ac.uk/PRACTICALS/PDF/DNA_isolation.pdf
It states that, "Although these fruits [kiwi fruit, bananas and strawberries] seem to yield copious amounts of DNA, the substance produced is in fact little more than pectin."
Are they right? How could you tell that what you've extracted is actually DNA?

I have taught that experiment using strawberries as a TA. If I remember right, we used SYBR Gold to detect DNA, though that could have been a different experiment.

The extraction protocol described in the first article is a standard DNA extraction protocol. I've used variations on this method in the lab (with some refinements) on other types of cells at least hundreds, if not thousands, of times. The "strawberry" experiment is very popular for classroom demonstrations, especially at the middle-school and high-school levels, because it's visually interesting and uses commonly available reagents. While these reagents aren't laboratory-grade, they're more than sufficient for a basic extraction of DNA.
I can't think of a scientific basis for why the author in the second article would claim that the extracted substance is "little more than pectin". Since he didn't provide data, or a reference to any data, it's hard to know what he's basing his conclusion on.
It's definitely possible that the DNA is pulling down a certain amount of cellular proteins during the alcohol precipitation step (the final step). This is why in a lab setting you typically perform a few more steps to "clean up" the DNA and remove any co-precipitating proteins. This would be essential if you plan to do further analysis of the DNA, because protein contaminants can interfere with subsequent analyses, making the data unreliable. One exception would be if you're studying protein-DNA interactions, but that's a separate type of experiment.
I'm assuming this experiment will be done for/by beginner level students, as opposed to a college or graduate level class? If so, then for the purposes of a classroom demonstration, those extra purification steps aren't warranted. It's time-consuming, and it would be very boring to watch... As is the case with most labwork. :-) Even if you perform those additional steps, the purified DNA is often precipitated with alcohol again, and it's visually similar to what you saw in the first alcohol precipitation, just a bit less opaque. Probably not something most students would notice or find interesting.
Either way, it's entirely acurate to say that the strawberry experiment is extracting DNA. You could always explain that the DNA might have cellular proteins binding (or "sticking") to it, and that a few other steps would have to be performed if you wanted to analyze the DNA in a lab setting, because the proteins would interfere with DNA analysis. This would also give beginner-level students an introduction to the fact that DNA and proteins interact with each other.
Hope that helps!

Thanks for the info! I was interested in doing the experiment at home for fun, but if it were indeed "little more than pectin", that would have been a bit disappointing.

No problem! Glad you're interested in this! Btw, you can isolate your own DNA (from cheek cells, aka "buccal cells") using a similar method. Here are two protocols. Either one should work fine: https://www.livescience.com/37252-dna-science-experiment.html https://scienceaces.wordpress.com/2015/06/18/biotechies-bucket-biology-on-the-cheap-gatorade-dna-extraction/   I've done this with students before and they seemed to enjoy it. One student was a bit freaked out to see her own DNA in a tube. I told her to just be sure the feds don't get a hold of it or she'll end up in a secret database. ;-)


text:
What order does this bug belong to?
I caught this insect in my house.
It has 6 legs, long antennae, 2 pairs of wings and is dark brown.

Please provide your geographic location. Thanks.

Order Coleoptera, Family Cerambycidae.

You could confirm the family ID by looking at the eyes. They are kidney-bean shaped, with the base of the antennae inserting into the concavity.


text:
If you are 30 degrees, and touch something that is 50 degrees, do you only feel 20?
First off, I don't know if this is the correct site to post this question as it could possibly fit into others? If so, please flag it to be moved as I would appreciate that very much.
Now, if my body was at a temperature of 30 degrees (celcius), I would feel somewhat warm. However if I then dipped my hand into a bowl of water at 50 degrees, would I begin to feel 20 degrees difference?
This seems likely as when I come out of a freezer (at work, don't stress), and wash my hands to "warm myself up", the water feels boiling hot and painful to touch but indeed is only maybe 30-35 degrees. Until it gradually becomes more bearable.
Or you come out of a spa, into a colder pool and you feel freezing cold?
To add some depth to this question, may I ask why this happens, and how your body actually reacts in this situation?

Your sensation of heat is dependent on the change in temperature of your skin, which is roughly proportional to the difference in temperature between skin and material.
However, temperature difference is much less important than the transfer of heat between your skin and an object, which is heavily dependent on the type of material you are touching.
Why does a cold piece of steel feel so much colder than the surrounding air, despite them being in thermal equilibrium? The answer is that steel is a much better conductor of heat, and can therefore draw heat from your hand at a much faster rate than air, which is a poor conductor of heat.
A very interesting study by Lele, Weddell and Williams (1954) [1] demonstrates that the rise in skin temperature is proportional to the rate of heat transfer. The same paper suggests that the sensation of heat is roughly proportional to the rate of heat transfer.
Now for some physics.
Heat transfer along an object of length L and cross-sectional area A is given by:
Q = kAt$\Delta$T / L
where Q is the heat content, t is time, and k is the thermal conductivity.
As you can see, the transfer of heat is proportional to the difference in temperature between the two ends of the object. So a simple interpretation would suggest that your body senses the rate of heat transfer, which is directly proportional to the difference in temperature between your skin and the object you are touching.
However, this neglects the ability of your body to draw heat away from an area (via blood circulation, passive heat conduction etc). Given that your body maintains a core temperature of around 37 degrees Celsius, this complicates matters somewhat, and probably comes into play when you touch a hot/cold object for an extended period of time (e.g. your example of washing your hands to warm up).
So in summary, you are essentially correct, in that your body feels the difference in temperature between your skin and the surroundings, taking into account the thermal conductivity of the surroundings.
[1] Lele PP, Weddell G, Williams CM. The relationship between heat transfer, skin temperature and cutaneous sensibility. J Physiol. 1954;126: 206–234.

Wow! Thankyou very much for this fine answer! Appreciate your time.

My first suggestion would be to try this yourself as an experiment, including the variations you mentioned. In each situation, take a guess at what the temperature of the water is, then write it down, then take a measurement with a thermometer to compare your perception versus the real temperature. Then try comparing it to other situations involving some external factor other than temperature. For example, quick changes between a dark environment versus a bright environment. Or a quiet environment versus a loud environment. These all rely on sensory perception, and the priciples of how the body (particularly the brain) reacts to rapid changes and extremes are similar across most/all of your senses.

Uhh, this doesn't really answer the question. I'm trying to find a somewhat scientific reasoning to this, not perform an experiment. I also don't see how changing light conditions will influence my bodies ability to feel heat? Especially the sound changes, heat is infra-red, not particle vibration...


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Why would I see no bands in DNA gel electrophoresis of red blood cells?

For forensic inspection, you only obtained red blood cells from an individual and amplified for the D1S80 locus in chromosome 1. Twenty nine different alleles of D1S80 have been identified, and 435 allelic combinations are theoretically possible. Approximately 86% of the population is heterozygous at this locus. You set up a PCR reaction for this locus and ran a DNA gel electrophoresis. What would your expected results be based on the described protocol?

A) You would most likely see no bands
B) You would see more than two bands
C) You would see two bands for the heterozygous while one band for the homozygous
D) You would see two bands for the homozygous while two bands for the heterozygous
I thought the answer was C given that heterozygous people would have two bands, one for each allele, and homozygous people would have one band for their one allele. The answer points to choice A for some reason...

Good luck retrieving DNA from erythrocytes...

It is a trick question. Red Blood Cells (RBC) are anucleated in mammals. You are not going to be able to extract anything about chromosome 1 from RBC.
By the way, if you want to know how they got from 29 alleles to 435 possible combinations (in a diploid), you just have to do 29 + 28 + 27 + ... + 1 = 435.

Interesting, I thought the same. But given my miniscule knowledge on RFLP, I was guessing that the answer hid somewhere else in the question. Thanks!


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Is DNA a single molecule or 46 separate pieces (out of 23 chromosome pairs)?
It seems that biology books refer to DNA as 'a' molecule (implying that it is a single continuous uninterrupted double strand) ... but in those same books chromosomes are depicted as 23 separate objects (chromosome pairs) containing DNA. Are these illustrations misleading ? Are chromosomes somehow connected end-to-end or are they disjoint ? Is it a single noodle or is it 46 pieces ?

This is a trivial question the answer to which is in almost any book or article that considers chromosomes. I have voted to close on the basis that it shows insufficient research.

Unbroken strands of DNA are single molecules. So Yes, DNA is a molecule. However, the sequence of nucleotides allow for a near infinite variety. So unlike other molecules, like collagen, or water, they cannot be characterized with a unique descriptive name, other than by their sequence. I think this is the cause for confusion, because in this sense, DNA is a class of molecules, and we don't generally give them names. Each chromosome has two unique DNA molecules in diploid organisms (except in rare cases of highly inbred individuals where the two molecules might be identical). So if you have 23 chromosomes, you have 46 DNA molecules in each cell nucleus.

When a book talks about "the DNA of a cell" it is talking about all the DNA molecules which are contained in the cell.
The DNA in a cell exists as separate objects called chromosomes, each of which is usually described as a single long molecule of DNA.  (The long molecule has two strands, and coils up around many copies of special protein molecules.)
The chromosomes of a cell are separate, and do not have DNA running between them.

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


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Would it be correct to say that viruses are genotoxic?
I know it is an unconventional way to describe viruses, but would it still be technically correct?

From wiki

In genetics, genotoxicity describes the property of chemical agents that damages the genetic information within a cell causing mutations

While some viruses tend to cause mutations, most don't have such a strong mutagenesis effect. As such, they are not really genotoxic. Also, even if a virus is genotoxic, one should definitely not reduce the activity of a virus to its genotoxicity. A virus has a life-cycle and is able to reproduce. It is clearly more than a simple genotoxic chemical agent such as metal chromium.
So, in short

Reducing viruses to their genotoxic effect would be a misrepretentation of what virsues are
Most viruses don't have a strong genotoxic effect and therefore you can not make the claim in the general sense.


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Why don't self pollinated crops show inbreeding depression?
Being continuously self pollinated means the fusion of same/similar genes from time to time, then why don't they show such a decrease in productivity?

Yes, self pollination does lead to inbreeding depression:

However, we found substantial inbreeding depression, with seeds per fruit, progeny survival and progeny growth being lower after self- than after cross-pollination. Progeny arising from self-pollination also had a higher frequency of certain traits ... which were associated with lower rates of survival. ... high inbreeding depression has also been reported in other self-compatible trees ...

--Self-pollination and inbreeding depression in Acacia dealbata: Can selfing promote invasion in trees?

Inbreeding depression is one of the leading factors preventing the evolution of self-fertilization in plants.

--Inbreeding depression in self-incompatible and self-compatible populations of Leavenworthia alabamica.

The strategy for breeding F1 hybrid squash is to develop parental lines through self-pollination. However, it increases plant mean homozygosis, which is not the natural genetic state of a cross-pollinated species, and can cause "inbreeding depression".

--Depression by inbreeding after four sucessive self-pollination squash generations
So why don't all crops that self-pollinate show decreases in productivity? In part, they do, but the reduction in productivity caused by inbreeding is outweighed by the increases in productivity caused by inbreeding (i.e. selection for productive traits via inbreeding leads to both positive and negative results, and the total outcome is the sum of the positive and negative effects).
And partly because the deleterious effects of inbreeding can be partially overcome through "purging". The negative genes that lead to inbreeding depression when homozygous can be removed from a population as the affected individuals die (or fail to breed) and take their negative genes with them. Purging is most common when a population has a moderate degree of inbreeding over a longish time, which is what you'd expect with a crop that typically self-pollinates. It's an effect in many but not all common crops:

Several plant species, E. g alfalfa (M. sativa) carrot (D. carota) , hayfield, tarweed etc show very high inbreeding depression. ... Many crops species, such as maize, jowar, bajara etc. shows moderate inbreeding depression. ... Several crop plants, E. g onion (A. cepa), many cucurbits, rye (S. cereale), sunflower (Hannus), hemp etc show only a small degree of inbreeding depression. Only a small proportion of the plants show lethal or subvital characteristics. The loss in vigour and fertility is small; rarely a line cannot be maintained due to poor fertility. The reduction in yield due to inbreeding is small or absent. Some of the inbreds lines may yields as much as the open pollinated varieties from which they were developed.

--Degree of Inbreeding Depression

Interesting question, but the answer might not be very simple. I'm not a big expert, but will try to give some clues.
So, first of all in many cases there is inbreeding depression. For example, some crops that are highly inbred (like tomato for instance) have a big problem of genetic diversity, which is very low among cultivated variants. This is sometimes solved by introducing introgressions from wild relative species. Otherwise you end up with crops that suffer from low biotic and abiotic stress tolerance.
Also note that in some cases, the seeds that are sown by farmers are not inbred lines, but rather the F1 result of a cross between two inbred lines. This is common for instance in maize, where all commercial cultivars sold by seed companies are hybrids. This leads to a phenomenon called Heterosis or Hybrid vigor, in which the progeny of the cross (the hybrids) have improved phenotypes over the parental lines.


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Are these 3.5B year old fossils the oldest on earth?
The following commentator writes:

Researchers at UCLA and the University of Wisconsin–Madison have confirmed that microscopic fossils discovered in a nearly 3.5 billion-year-old piece of rock in Western Australia are the oldest fossils ever found and indeed the earliest direct evidence of life on Earth.

It seems strange that this would come up recently. I thought there might be something older.
My question is: Are these 3.5B year old fossils the oldest on earth?

Your question seems to directly challenge qualified and peer reviewed researchers from highly esteemed U.S. universities who have confirmed that they are oldest. How is it that an answer from a website, answered by grad students goofing off in their spare time would convince you?

I wasn’t aware of their credentials, I was hoping someone could point out whether the paper is the real thing or not.

I'm voting to close this question as off-topic because it appears to be about archeology not biology.

@David This is not archeology (which is about humans). It is about paleobiology.

@KarlKjer — OK, that sort of thing. But hardly SE Biology.

Oldest found so far?  Yes, according to the evidence. Oldest on Earth? Possibly not, because we haven't looked everywhere yet.

Yes, the study was peer reviewed and published less than a month ago (Dec 18, 2017) in PNAS, among the most prestigious journals in science by qualified experts. They could be wrong of course, like all science. But there is no reason I can see to doubt their work.


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Why does UVA penetrate deeper than UVB, though it's weaker?
Even though UVA radiation ranges in longer wavelengths (315–400 nm) than UVB (280–315 nm) and thus is less energetic, UVA is able to penetrate deeper into the skin and even reach the dermis. Why is there such a discrepancy?

Melanin itself may absorb more UVB? I speculate...

It's not simply a matter of energy, otherwise we wouldn't see different colors of transparent materials.  Different molecules &c preferrentially absorb different wavelenghts.  Probably there's nothing in the skin that absorbs UVA, just as lighter-skinned people don't have much that absorbs visible light.

This answer may be pertinent: Interaction of radiation with the body.

Our skin contains quite a lot of water and I think this is answers the question: The absorption of UV light by this water goes drastically up when you shift to shorter wavelengts with a minimum absorption in the UV-A spectrum.
See this figure (from here):

So water has a very low absorption around 340-350nm (UV-A) and a very high absorption at shorter wavelength (UV-B and UV-C). This also explains why we get a lot more UV-A through the atmosphere than for harder UV-Radiation.


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Is it possible to sort droplets inside an oil phase with a FACS
In a nutshell, is it possible to FACS a sample that is in oil rather than in a buffer (water based solution)?
I would greatly appreciate any help with this.
Thank you

Not sure about FACS, but what you describe is similar to droplet digital PCR (ddPCR). The samples are still in an aqueous buffer, but they are emulsified in oil, creating many microscopic droplets that each contain some sample and are isolated from each other. BioRad makes a machine that does this, but whatever you are detecting would have to produce a fluorescent signal.

Thanks ndusek, yes it seems detection of fluorescence is possible inside oil. Its only a question if a FACS could achieve the same.

It's possible that there's some specialized modified machine that can do it, but conventional flow cytometry machines can't do it. This article suggests one possible approach:

Unfortunately, FACS instruments are incompatible with nonaqueous suspensions, so to sort a water-in-oil emulsion, it is necessary to carry out a further emulsification to produce a water-in-oil-in-water double emulsion. The resulting sample, now dispersed in an aqueous phase, is amenable to FACS sorting.

--One in a Million: Flow Cytometric Sorting of Single Cell-Lysate Assays in Monodisperse Picolitre Double Emulsion Droplets for Directed Evolution
There are also microfluidics machines that might be able to do it, but I think you'd have to build your own rather than being able to buy a solution (which would be expensive in any case, I think).


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What happens when I pop my ears?
What happens when my ears are popped?
I understand it increases the air inside there which makes my volume louder, what happens after that, do my ears gradually readjust back to the air pressure that they were before?
What causes ears to (need to) be pressurized/depressurized?

To whoever downvoted, please comment your problem with my question.

The downvote probably comes from the fact your question is an anecdotal report and a self help question, both essentially being off topic here.

The outer ear canal ends at the eardrum, and beyond that is the middle ear.  The middle ear is normally a closed chamber, but can be connected to the outside world by flexing the jaw or muscles related to.  The flexing opens the Eustachian tube, which runs from the middle ear to the back of the nose and mouth.

Hearing is best when the air pressure in the middle ear is the same as the pressure of the outside air.  If it is different, the ear drum is forced to bend outwards or inwards depending on whether the pressure is higher or lower in the middle ear.  In either case the ears senses less sound, and the volume is reduced more for some frequencies than others.
When you pop your ears, the Eustachian tubes open enough to allow your middle ears to equalize pressure with the outside world.  This restores the ear drum to its normal position and your hearing returns to your normal, optimal state which is louder and more balanced than the previous condition.  As time passes, your brain adapts to the new sound sensing state and you no longer notice any unusual loudness. The pressure in the middle ear doesn't change as your Eustachian tubes usually remain closed, and so the ear continues to hear well (as long as the outside air pressure remains little changed).


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Bistability vs bimodelity
In a systematic viewpoint, bistability refers to the existence of two stable equilibriums for a biological system. But, I don't understand the difference between bistability and bimodality. In both cases, the system should have two different behaviors, so I guess bistability is a specific case of bimodality, in which either of the system's behaviors might not be stable. Is this a valid distinction between these terms?

I am not a big system biologist, so I am not really used to the terms used in this discippline. In statistics bimodality simply refers to the existence of two peaks in the frequency distribution of a variable. Do you think you could add a quote just so that we have a context in which those terms are being used?

Bistability referrers to two coexisting stable conditions (if you disrupt they will tend to restore to one of those two areas) and has a slightly broader application it can also involve chemical stability for instance. Bistability includes the element of stability (obvious in the name) if disrupted bistable condition tend to return to one of two stable configurations. Enzyme stable configurations could be another. Galapagos finch beak shape during wet years is the one I think of but that could also be argued as tri-stable. to go really simple you can even think of a clicky pen, fully clicked is stable and unclicked is stable but anything else immediately moves to one of the other states.
Bimodal just means the distribution has two peaks, they may or may not be stable, many are only temporary. It is a much simpler concept.
Another way to consider it is bimodal is purely descriptive while bistability has a predictive quality.

It is a little unclear to me the distribution of what has two peaks. That's why I think we would need a specific quote to discuss. Also, talking about bi-stability and sex. The variable to the system could be sex-ratio typically, in which, such systems typically have a single stable equilibrium at 0.5.

For the sex thing sure it all in how you describe it, as a variable in a population it is bistable but it can of course also be described as a ratio, or in a number of other ways. I t will just add confusion so I will delete it.  As I said bistability is Not a purely a statistical term unike bimodal. biochemical stability can be a good example as many enzymes will have two stable configurations with all the inbetween configurations being unstable.

To expand on what you said, bistability in the dynamics of a system can result in bimodality of the distribution of whatever the system does or makes.


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Estimation of the amount of bacteria
For my first research project in microbiology I've chosen to determine the effectiveness of sanitizers and soaps in killing bacteria from our hands, however, after putting the bacteria on agar plates using cotton swabs, why do we incubate them? Won't their numbers increase and give us the wrong results?

This is a very standard method. The idea is that you have a culture of bacteria on an agar plate. During the incubation each bacteria forms a colony. After a few hours of growing the colonies grow and become visible for human eyes. So you can easily count them.
Then you can compare the number of colonies before and after washing your hands with the sanitizers and soaps and find which method has the lower amount of colonies on average and therefore whihc one is the most efficient one.

Keyword: colony-forming unit (CFU).

Should I use only EMB plates then, so I can identify the bacteria?

Well, there are many options from many providers. It all depends on what you are trying to identify, the cost and your budget!

When you swab the agar plate with your sample, what you're doing is spreading out all the bacteria in your sample so that each cell is able to grow separately from the other cells and form an isolated colony.
Since bacteria are microscopic and you can't actually see them directly in your sample, you need to allow them to grow a little until they form a colony and you can actually see them with your eyes. The assumption we make when we use this method to "count" bacteria is that a single cell gives rise to a single colony on the plate. That's why we call the cells "Colony Forming Units".
This might be of some help: https://en.wikipedia.org/wiki/Colony-forming_unit


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How do I look for pathogen in water with a microscope? Is it possible?
I am a 9th grade student from Manila and we're currently working on an investigatory project. We want to know how effective SODIS or solar water disinfection is. The purification method claims to be able to kill pathogen. We've just finished our methodology; we have not done to experiment yet.
There's one thing that concerns us: is it even possible to see pathogen in water using a microscope? We raised our concern to our teacher and at first she believes it is possible. However, she said that she was not sure because she mentioned that some stuff (I forgot what) are "cultured" before checking for pathogen like  bacteria.

Yes your teacher is right. In a microscope you can see microorganisms. Now the question is to identify them as pathogens.
I guess what your teacher has in mind is to use specific culture mediums for different pathogens and see if anything is growing there, then you have a positive.
You could also do a PCR. This is extracting the DNA and amplify specific genes that you know belongs to pathogens.
But the most currently trendy analysis is metagenomics. Basically, you exctract the genetic material from the sample, then sequence and compare against public databases. This methodology allows the identification of everything that is there pathogens and non-pathogens.

Thanks for the reply. I'll be honest, my members and I aren't really in to biology nor science itself so we chose a simple project but we really didn't think about how to look for pathogen.

I don't quite understand the two mentioned methods however I think metagenomics might be the easiest to do? Is it as simple as taking a sample of the water, putting it on a petri dish, observing on a microscope, and comparing it to existing microscope images of pathogen?

No it's not that simple. You need to buy for culture media. Different ones for each pathogen you want to identify. You need to find the right protocol for what you are trying to do. In the following link there are several things you can do. Maybe there are some useful hints for you: https://www.nap.edu/read/9595/chapter/11#189

If I'm not mistaken, are the "Assay Methods for Waterborne Pathogens" the methods for confirming pathogen in water?
I was not able to read the chapter entirely but I at least scanned it. Please confirm if my understanding is correct:
To detect pathogen in water, it involves three steps: (1) recovery and concentration, (2) purification, and (3) assaying.
Does recovery and concentration mean the "getting of pathogen" in the water? Does purification mean "the removal of unrelated particles in the pathogen?" Does assaying mean the "identification and detection of pathogen?"

I apologize for the swarm of questions but for a group of high school students, what do you think is the simplest method to do this?

Possibly, the simplest test one can analyse a water sample for micro-organisms is a visual analysis using a light microscope (perhaps appropriate for secondary level school inquiry), then proceed to conduct the more complex chemical analyses (usually done in tertiary level school labs) like genetic surveys mentioned earlier. Prepare the water sample in a test tube by centrifuge to cast most if not all elements, bio- and non-bio, to the bottom of the test tube. Using a dropper, obtain a sample from the bottom of the test tube and drop a liquid onto a glass slide, then put a cover glass. Liquid stains are usually applied to the margins of the cover glass using a dropper to aid visualization of the unicellular and multicellular micro-organisms in the water sample. Visual identification of organisms should point the researcher on the next steps to take to obtain a more accurate analysis of the water sample. a good simple protocol for the experiment, as mentioned earlier, should be able to narrow the complex findings of this inquiry.

Consider adding references to help the reader


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How to cite a herbarium specimen
How do I cite a herbarium specimen that I have used to prepare a botanical description? Do I use the collector's name and number or the herbarium code and accession number? What if there is no record of the collector's name or number?

In general, the "how to cite", depends on the journal you publish. Check on their website (hot to submit) or check common journal used in your field, and copy the style used in articles.


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EVOLUTION OF MAN QUESTION
I have a few questions concerning man's origins
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Man has 10  vital Organs and support systems. yes or no? Man needs all 10 of his vital Organs or he dies. yes or no?
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Either those 10 vital organs evolved together all at once, or they evolved separately.. yes or no?
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If they "Evolved" Separately they must have had an order of evolution. yes or no?
Can anyone provide a plausible order of evolution of vital organs from microbe to microbiologist? (TOE)
Stomach Skin Heart Lungs Brain Upper Intestine Liver Lower
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Intestine Pancreas Kidneys
which one(s) could have been the first, second, third etc..?
If UCA for all flora and fauna (Evolution) were to somehow be true, and If we slowly go back in time, Our "Ancestor(s)" would, at some point, have 9 Interdependent vital organs, then 8, then 7, then 6 5 4 3 2... Yes? or no?
A Microbe has ZERO interdependent interlocked VITAL Organs and their support systems. A Microbiologist has TEN interdependent. interlocked. VITAL Organs and their support systems.  Yes? or No?

Comments are not for extended discussion; this conversation has been moved to chat.

Two problems:

You have a fundamental misunderstanding of evolution by natural selection.
You appear to be wanting to pick a fight. Its obvious no answer that refutes creationism would satisfy you.

In fact your issues have been addressed over 150 years ago in Darwin's Origins. Many wonderful books exist today expanding upon it.
I suggest you pick up a text, watch a video, or read an article on the fundamentals of evolutionary theory. Google is a good place to start.

I agree, but this is not an answer, it is a comment. The poster will not take your advice and will be happy that you have written something he can argue with. There is a golden rule here: "Don't feed the trolls".

Good point David.. Instead of trying to answer the question, he just insults me (ANYONE can do that) and simply DODGES the question..  So should I not ask questions?  If my 1question cant be answered, wouldnt it be more honest to just say so and admit that the Methodological Microbes to Microbiologist Myth is merely q Science Fiction Tale about "Long ago and far away" that people believe in ONLY because of it's IMPLICATIONS?

You can ask questions, of course! That is what this site is for. However, it is not a debate forum. If you actually want to understand something, and have a question about it then ask. If you want to try and persuade people about creationism, then I would say - do you really think that will work?

So It appears painfully obvious that the answer to my question is a resounding NO!

MamaTank
"1.You have a fundamental misunderstanding of evolution by natural selection."
2.You appear to be wanting to pick a fight. Its obvious no answer that refutes creationism would satisfy you.
In fact your issues have been addressed over 150 years ago in Darwin's Origins. Many wonderful books exist today expanding upon it.
I suggest you pick up a text, watch a video, or read an article on the fundamentals of evolutionary theory. Google is a good place to start.

MamaTank
"1.You have a fundamental misunderstanding of evolution by natural selection." .....  That is merely a baseless assertion.. you don't know me, you don't know what I do or do not know, This is what is called an "Ad Hom" logical fallacy and is Irrelevant to my question which is "Can anyone provide a plausible order of the 10 Vital Organs from microbe to microbiologist"?  Yes or No.. If the answer is Yes, please provide the order  1 through 10  Thank you

MamaTank  "2.You appear to be wanting to pick a fight. Its obvious no answer that refutes creationism would satisfy you."    Wrong.. I only want the truth.. If Evolution is true, I want to know it.. Presenting a plausible order (1-10) of Vital Organs from microbe to microbiologist would clearly demonstrate that Creationism is not the only Valid explanation for Man's origins..

MamaTank  "In fact your issues have been addressed over 150 years ago in Darwin's Origins. Many wonderful books exist today expanding upon it." Wrong again..If you believe this, you did not understand the question at all because if you did, you would surely already know that my question has NOT been addressed anywhere in ANY of those books. If it was, I surely would have had it shown to me by someone by now remember we need to see an Order 1 2 3 4 5 6 7 8 9 10..   Thanks anyway, but clearly you cannot answer my question or know anyone who can..

MamaTank  "Many wonderful books exist today expanding upon it. I suggest you pick up a text, watch a video, or read an article on the fundamentals of evolutionary theory. Google is a good place to start." Sorry, been there and done that.. Just because people ask questions doesn't mean that they are low IQ or Ignorant or haven't studied the topic  I am quite certain I know quite a bit more about the topic of Origins then anyone that you know.. I only asked the question to get people to think instead of simply parroting the propaganda that they have been brainwashed into believing.. Good Luck JT