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Was iron important for the first life on Earth?
Some ions or compounds are thought not to have become involved or important in the metabolism of living organisms until some time after certain mutations took place. For instance, early life is thought to selectively allow calcium ions through its membrane, but eventually also evolved the ability to selectively allow sodium ions, specifically through a mutation that lead to a change in the composition of a channel protein from glutamine to lysine.
Currently, iron is involved in oxidations involving molecular oxygen, such as in cytochromes and clearly holds a key role in modern life, despite that free iron or even ferric compounds are rarely accessible. From my understanding, iron most likely became incorporated into the metabolism of microbes after during/after aerobic organisms had developed, but this does not rule out the possibility that iron was involved earlier on. So, I am wondering if iron was involved in early life, and details on how would be appreciated.

"a mutation in the structure of amino acids to form lysine"? How exactly does a chemical compound mutate? I would stick to your question and avoid unscientific analogies and unprovable remarks about when different amino acids emerged.

@David since most biological compounds used in life are produced through a genetically control process, saying "X mutated" is a common acceptable shorthand for saying "the genes that controls the production of X mutated changing the structure of X".

@John I dont know in what circles is that acceptable, maybe creationists, but if my student wrote something like this on an exam, I would fail him on the spot - and that would be mercy in comparison what my master or phd advisors would do to him. Structure of a chemical compound cannot mutate, period. If you add or remove an atom from the structure of a chemical compound, it becomes a different compound.
Also, the title is misleading. Asking IF iron was important for the first life on earth is not the same thing as asking WHEN did the iron become important.

I am afraid what you write is neither accepted by or acceptable to professional scientists. Nor can a clause evoking a mechanism be shorthand for the simple statement such as “lysine emerged later” — indeed it is a clear violation of Occam’s Razor. It unjustifiably and unnecessarily implies a knowledge of the order of addition of amino acids to the genetic code, the mechanism by which the code expanded, and some sort of ‘purpose’ in relation to ion transport. I have edited your question to make it scientifically acceptable and appropriate to the question.

@david are you not aware cells will modify amino acids, this is how the majority of amino acids are produced after all. Post-translational modification of animo acids is fairly common.

John, I have taken the time to provide a detailed chemical answer to the title of your question (which I did not alter). You might care to direct your attention to that. Do you understand it? Does it seem satisfactory? Have you any comments on it?

I think it's inappropriate for you to make such a large change like that. Life relied on calcium, then selectively included sodium. I wanted to know if the same kind of thing happened with iron and how in order to track the timeline of the incorporation of different elements for microbial evolution, and my original question got me an answer. https://www.ncbi.nlm.nih.gov/pubmed/24517213

The reinsertion of a revised first paragraph is unnecessary, misleading and a poor analogy for your question. First, you are not asking if iron replaced some other metal or system — or if you meant to do so it is not evident in your question. Second you talk about the acquisition of sodium channels from calcium in “early life”, when the paper you refer to talks about the evolution of the channels in eukaryotes. It would be far more pertinent to expend your effort on justifying your assertion of “iron being rarely accessible" — something that my own answer argues was not necessarily true.

I don't think it's misleading at all, I think you're being too technical (if your assertion is even accurate) where it isn't relevant. What I proposed is an example of the kind of phenomena I am referring where life evolved to incorporate another element and in an understandable way, which continued to happen with more elements like molybdenum, copper, iodine and more. The paper talks about life evolving over the scale of billions of years, and Eukaryotes weren't always around, it took a long time for microbes to develop the traits we see today.

If you wish to address comments to individuals other than the person whose contribution you are commenting on you need to add an @joebloggs to alert him to the fact that the comment is addressed to him. All I can say is that it seems to me that your interest isn't in the chemistry or biochemistry of the evolution of iron metabolism, as your question implies, but rather whether it could provide another example of a change of functionality from the change in a single amino acid. A pity, because the question in your title is interesting, but it requires a knowledge of chemistry to address.

It really doesn't require chemistry at this point, it more or less requires a single date or a yes/no with evidence to support it.

Cyanobacteria require iron for photosynthesis and can be found as fossil stromatolites dating back to 3.5 billion years ago.  Stromatolites are layered structures made up of cyanobacteria and sediment.

Source: https://en.wikipedia.org/wiki/Stromatolite
Modern stromatolites can be found at Shark Bay in Australia, Chetumal Bay in Belize, and Laguna Bacalar in the Yucatan Peninsula.
Cyanobacteria are also believed to have evolved into the first microbes to produce oxygen by photosynthesis, which was a catalyst for the Great Oxygenation Event which occurred around 2.45 billion years ago.

So you're saying life nearly started out as cyanobacteria? This would have to be quite a recent development because I've seen multiple sources in the past say cyanobacteria didn't form until around 2.7 BYA.

@John Joe: Sorry, I thought I had provided this source also.  http://www.ucmp.berkeley.edu/bacteria/cyanofr.html

So if that's true, why was it only much later that the atmosphere became oxygenated?

While I largely agree with this answer, I'd point out that as far as I know we have of knowing how similar the metabolism of these ancient organisms was to extant organisms. There's evidence of morphological similarity but morphological similarity does not necessarily imply biochemical similarity.

So if life already had the capacity to harness iron, why didn't life forms release that oxygen earlier?

@JohnJoe This is discussed in the Wikipedia article on the great oxygenation Event: https://en.wikipedia.org/wiki/Great_Oxygenation_Event#Time_lag_theory - it would have been released but was not yet able to build up.

@JohnJoe if you need to ask a separate question I'd post it as such, not add it in the comments; the answer above fully answers what you actually asked in the body of your question (although your title and question body include different questions).

I guess it all makes sense then. I was just surprised that more developed bacteria appeared that early on contrary to what I thought other sources had suggested, but thank you for sharing.

Summary
It has been proposed that iron was indeed important for the first life on earth, specifically in combination with sulphur. This is because conditions are thought to have existed in volcanic hydrothermal vents that would have allowed formation of iron–sulphur complexes which perform oxido-reduction reactions in modern proteins (as well as more sophisticated functions). Some system for oxido-reduction of chemical compounds is required for life to develop, and the inorganic simplicity of Fe–S clusters, together with their ability to interact with the backbone of proteins, argues for their early involvement, rather than the chemically more elaborate NAD and FAD.
The Archaean Environment
One theory suggests that life  originated volcanic hydrothermal conditions in which the oxidation of iron minerals by hydrogen sulphide would have been possible. It has even been suggested that life originated on the surface of iron sulphides (the ‘Iron–sulphur world hypothesis’), although this answer is more modest in its scope.
Iron–Sulphur Metalloclusters
Modern proteins contain a range of iron-sulphur clusters of varying complexity, but it has been argued in a review in Science by Rees and Howard that the simplest of these — the 2Fe:2S cluster in, e.g. ferredoxin — could have evolved in the conditions mentioned above.

[Different FeS clusters. Note that the external yellow sulphur atoms are from cysteine side-chains of the protein. (Adapted from a review by Johnson et al. (2005))]
Interaction of Iron–Sulphur Clusters with Proteins
In some iron-containing proteins, like cytochrome c, the iron is held in place by a sophisticated organic molecule (haem) and interacts with amino acid side-chains. However in simple iron–sulphur clusters interaction with the NH groups of the protein backbone (in special conformations — ‘nests’ and ‘crowns’) can occur. Thus initially they could have been acquired by simpler proteins, which some believe to have preceded the development of those with the side-chains to provide more sophisticated interaction.

[Interaction of FeS clusters with protein backbone NH groups (blue): A. ‘nest’, B. ‘crown’ with the N atoms in space-filling mode.]
Other Contemporary Redox Cofactors
The intellectual appeal of Fe–S cofactors as being evolutionarily most ancient can be seen if one compares them with the structures of other contemporary redox cofactors (images taken from Berg et al.):

It has been argued that the adenine and ribose moieties of these cofactors attest to an ancient origin — in the supposed RNA world — an idea that I, personally, find appealing. Nevertheless, their emergence would require a mechanism for the synthesis of their functional organic components — nicotinamide and flavin, respectively. In contrast, Fe–S clusters come ‘ready made’.
More Complex Iron–Sulphur Clusters
Iron sulphur clusters are also found in the nitrogenase protein, which converts nitrogen gas to ammonia. This must be a very ancient protein, but its greater complexity (the cluster includes molybdenum) suggests it may have arisen later. Another elaboration is proteins, such as aconitase, that have Fe–S clusters linked by more complex organic groups.

[Iron-containing proteins of greater complexity. Haem, the non-sulphur iron prosthetic group of cytochromes etc. is also shown. Adapted from Berg et al.]
Iron in Photosynthesis
As mentioned by @Kurt, iron is a component of photosystem II in contemporary cyanobacteria. However photosystem II is extremely complex and the precise chemical basis of the non-haem iron requirement is currently unclear. Although perhaps necessary if cyanobacterial photosynthesis were responsible for the great oxygenation, this complexity would suggest a relatively late emergence in the pre-aerobic era.

I have expanded my answer, which is now essentially complete, unless anyone requires details of the metabolic pathways aluded to, which I will be happy to provide.

I think if this was hybridized with the first answer it would have made both better, because the first answer showed that the same premise of cellular respiration took place much earlier than thought with direct physical evidence which explains iron and its role but without much theory, whereas you mainly rely on a conjecture of a specific compound and not direct evidence so much. They "can" interact with background proteins, but did that actually make them necessary? Was there actually a mutation back then that lead microbes to incorporate a modern organelle or metabolite from that compound?

Any statement about metabolism in early evolution depends on deduction rather than physical evidence. The argument of @Kurt could be restated as: contemporary cyanobacteria require iron (for PSII); they are thought to have caused the great oxygenation; hence iron must have been used in metabolism before aerobic life. The argument assumes that photosynthesis in ancient cyanobacteria was the same as today. His photo is only evidence for the existence of cyanobacteria even earlier, but if they had the current PSII they would still be far more elaborate than anything in “the first life on earth”.

Like I said if there was a way to combine both answers I would be open to it, but it's not mere speculation if we can actually see the imprints of the structure of microorganisms. It does assume the same photosynthesis, but it assumes that because there is consistent material evidence for it, whereas your argument is "well, this compound could have been involved because it could have interacted..." and that's why it's called a "hypothesis."


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How do you culture Cutibacterium acnes?
I've been thinking of culturing Cutibacterium acnes (old name is Propionibacterium acnes) for a thesis topic of mine on the comparison of the efficacy of local antibacterial topical skin care products but I have no idea how to culture it. I haven't encountered any definite instructions on the process in culturing it aside from it being an aerotolerant anaerobe and requring an anaerobic incubator.

Douglas & Gunter (1946) The Taxonomic Position of Corynebacterium acnes. J Bacteriol 52: 15-23.
This is the paper, in which Corynebacterium acnes was proposed to be transferred to the genus Propionibacterium as Propionibacterium acnes, and it contains a detailed description of the cultivation procedure.

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Do antibodies to an arbovirus in a bloodmeal reduce vector competence?
When we conduct mosquito infection studies we typically mix blood and virus rather than using viraemic blood from naturally infected hosts. I'm looking for a paper I read some years ago which demonstrated that virus mixed with blood containing antibodies to that virus (not to mosquito midgut or salivary gland antigens) resulted in a lower proportion of infectious vectors than virus mixed with blood that does not contain those antigens. Unfortunately I don't seem to have kept a copy and now every search I conduct only throws up results to the aforementioned studies of anti-midgut or anti-SG antibodies. The nearest thing I can find is this, which looks at inhibition during intrathoracic inoculation (a completely different route of infection which is not particularly realistic, although we sometimes use it to boost the infection rate).

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Vultures in Germany in the past
I noticed that since the 1970s the bearded vulture , which had disappeared from the Alps due to hunting, has been successfully reintroduced. I have searched for the modern habitats of vultures, but it appears (the wording on the site is a bit imprecise) none occur in Germany beyond the very mountainous regions.
I want to know whether at any point in the past vultures of any species where common across large parts of Germany other than the Alps. I am especially curious about the Middle Ages.
Edit:
This site in German claims that vultures in Medieval Germany followed sheep herds, eating dead, stillborn and afterbirth of cattle. It mentions, beside the Alps, the upper Danube Valley and the Moselle–Rhine region:

Bis dahin hatte es vom Mittelalter ausgehend, auch in deutschen Ländern eine einträgliche Zusammenarbeit gegeben. Geier folgten den wandernden Schafherden, beseitigten verendete Alttiere, totgeborene Junge, die Nachgeburt oder die Knochenreste vom Essen der Schäfer. Geier nisteten im Mosel-Rheingebiet, den Alpen und im oberen Donautal.


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Identify this organism
Can anyone identify this organism please? Often I see it inside my home on the walls moving very slowly.
please click for a better-quality image
some more info:

Geographical location: India (north part)
Image taken recently (March 2018)
Size of organism: about 1 cm in size.

You have to add your geographical location, what the time of year was, the approximate size etc. Also, can't you possibly provide a higher quality picture? This one is kind of grainy.


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Why is the separation of biochemical synthesis pathways safer and more economical?
During our first lecture of plant physiology, our teacher told us that the separation of biochemical synthesis pathways was advantageous because it was safer and more economical. The problem I got, while studying this back at home, was that he didn't explain why it is so.
I can understand why it is safer (for example, a lysosome could break down a lot of major components of the cell if that lysosome was not restricted to its area), but it's quite difficult for me to understand why it's more economical, in terms of energy. Any clear/simple explanation about this would be greatly appreciated.

False Economies?
Goodness knows what the poster’s teacher meant by saying that the separation of biochemical pathway is “more economical”! This is not a term usually applied to metabolism and, anyway, in life people who are economical do not always get value for the money they do spend, never mind obtain a better quality of life.
Most treatments of the separation of biochemical pathways justifiably emphasize the advantages of being able to regulate forward and reverse reaction sequences independently. However let us have a look at the separation of pathways in terms of energy, as the poster requested.
Some basic thermodynamics
The poster also requested the explanation be clear and simple. The following is simple, as long as you are familiar with the some basic ideas of chemical thermodynamics. If you are not, I suggest you read the three pages in  Section 8.2 of Berg et al. online. (Whether it is clear or not I leave others to judge.)

What determines whether a chemical reaction proceeds is the overall
(Gibbs) free energy change (ΔG). If it is negative, the reaction is
thermodynamically favourable.
The actual free energy change depends on ΔG0, the standard
free energy change (reflecting the chemistry of the reaction(s)),
together with the actual concentrations of reactants and products.
Enzymes are necessary to catalyse reactions in living organisms,
but do not affect the position of their equilibrium.

Argument
For simplicity, let us consider a series of reactions interconverting compounds M and P:

M ⇄ N ⇄ O ⇄ P

No separation between pathways
Consider a situation in which the forward (M➞P) and reverse biochemical transformations (P➞M) involve the exact same chemical changes catalysed by the exact same enzymes, i.e. no separation between pathways. In order for this to work the overall ΔG0 must be near zero, otherwise reaction in one direction will be very difficult to achieve (require a very high concentration of starting reactant). For a ΔG0 near zero there will be equilibrium (no net reaction) at equal concentrations of M and P. In order to cause a flow of metabolites, say in the forward direction, there must be an increase the concentration of M relative to P.
There are two problems with this.
First, quite a large ratio of M to P, say, would be required to achieve net flow through the pathway, and this would involve having a large pool of unreacted M. (Section 8.2 of Berg et al., cited above, has some calculations that illustrate this.) This may or may be regarded as economical use of thermodynamic energy, but is not particularly economical in the  use of resources. However, a ‘pathway’ in which it is employed is glucose transport in the liver (actually a single transport process).
Second, the direction of overall reaction is controlled solely by the ratio of M to P, a situation that lacks flexibility.
Separation between pathways
If separate pathways are involved, the first problem of a single pathway mentioned above is overcome in the following way. Each overall reaction can have a high negative ΔG0, so that it does not require such a large pool of reactant and is essentially unidirectional. One might ask how this can be, as the value of ΔG0 for the chemical reaction, M ⇄ P is fixed. The answer is that separate pathways will involve  other reactants, so that the overall forward reaction might be
M + X ➞ P + Y
whereas the reverse reaction might be
P + A ➞ M + B
This is considered for glycolysis and gluconeogenesis in Section 16.3.6 of Berg et al. — with actual equations. The ΔG0, for glycolysis is quoted as – 84 kJ/mol, and that for gluconeogenesis as –38 kJ/mol.
Of course, if both reactions have a thermodynamically favourable values of ΔG0, it is necessary for the cell to prevent the uneconomic cycling of P back to M after it has been formed. However the fact that the pathways are different means that different enzymes will be involved, which are the targets of regulatory molecules that can switch them off and on. These regulatory molecules usual reflect supply and demand, but need not be intermediates in the reaction sequences, and they can act as far more sophisticated ‘switches’ for the enzymes. The particular details of this for glycolysis and gluconeogenesis can be found on the first page of Section 16.4 of Berg et al.
…the price of everything, the value of nothing
So are separated biochemical pathways energetically more economical? The large free energy change that drives these reactions is ‘lost’ as heat, so one could argue that the reverse is actually true. Or, then again, one might say that “you get what you pay for”.

Imagine the enzyme with four different tasks. Its inhibition disrupts four different pathways. Instead, the separation of pathways into a continuous chain of discrete processes carried out by discrete enzymes prevents "catastrophic disruption," and creates a low-energy landscape for the emergence of new pathways.

The concept of modularity in programming (or more specifically in Object Oriented Programming) would be a good analogy.

While the claim is intuitive, it would be good to have a reference for this claim.

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RNA contains Uracil in place of Thymine
Thymine does not present in RNA but DNA containing thymine why


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Why do parasitic amoeba lack a contractile vacuole?
Compared to the other amoeba, most parasitic amoeba lack contractile vacuole. I could not get the correct answer as to why these parasitic amoeba lack contractile vacuole.


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Furry Bug that swarms only certain plant
What is this strange bug?
It swarms only on one certain plant with trumpet-shaped red flowers (in the picture the flowers are all shriveled and the leaves are in the foreground) and totally coats it until the bush dries up. It spreads very rapidly but only to this particular plant - will not touch any other. The bugs don't noticeably move, giving the impression that the whole bush has developed white fur.
Picture taken in Israel:
EDIT:
Here's a closeup of a single specimen (taken from one of the leaves in the foreground):
And it seems the plant is a hibiscus:
http://homeguides.sfgate.com/hibiscus-leaf-87355.html

almost certainly a scale insect (or, less likely, some kind of aphid). Can't seem to get the picture to zoom on my phone, so I can't really see the white fuzz too well...

They are some kind of mealybug.

@Karl Kjer I think you are correct! https://en.wikipedia.org/wiki/Mealybug#/media/File:Mealybugs_feeding_on_hibiscus_plant.jpg

As indicated in @KarlKjer 's comment, this insect is a Pseudococcidae, or commonly known as Mealybugs. The exact species is difficult to find due to picture quality.

Mealybugs are insects in the family Pseudococcidae, unarmored scale insects found in moist, warm climates. Many species are considered pests as they feed on plant juices of greenhouse plants, house plants and subtropical trees and also act as a vector for several plant diseases.
Mealybugs occur in all parts of the world. Most occur naturally only in warmer parts, and get introduced into greenhouses and other buildings in cooler countries. It is unlikely that any live in the Arctic or Antarctic, except perhaps in buildings.

Considering that Mealybugs are found basically anywhere on Earth, it's not a surprise to have found them in Israel.


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Bug species identification
Found this bug in my bed. Don't think it's a bed bug. Pretty small but fat and round and had deep reddish coloring.

That's a bed bug who drunk blood.

Are you sure? I checked my entire mattress and couldn't find any other bugs.

No. That's definitely not a bed bug. See this post for detailed image/description of bed bugs. Among other obvious clues, bed bugs do not have long antennae like the insect in the OP's picture.

@Torqk Please provide information regarding your location and the size of the insect. Without that information, it will be difficult to provide an accurate ID. Thank you.

That is not a bed bug. The picture is rather poor, which makes an ID difficult, but I think it might be the beetle Ptinus fur (spider beetle), or another species from the same genus. This species is found all over the world, and often indoors (they can e.g. feed on dry foods).
Reasons for this suggestion is the body shape (incl relatively hidden head), color ("reddish"),long legs with thick femurs, long hind legs, and long antenna. The long legs together with the long antenna (the antenna can look similar to a fourth set of legs), as well as the hidden head (so the body look two-segmented) is what makes it look somewhat like a spider .

(picture from bugguide.net)

(from weedimages.com)


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Cattail seeds spring revitalization
There's a genus of plants known as Typha, or cattail.
They have seeds like of dandelion, that form thick heads. Such a head may be cut off from the plant and be used for, say, decorative purpose, but when the spring comes, seeds will spread out their 'hairs' and fly away. It looks like an absolutely dry piece of plant - no life in it - suddenly gets alive.
I suggest that it may be a daytime prolongation of a  that causes it to spread seeds, but I wonder if anyone knows what sort of cellular/biochemical mechanics is at work here.

According to LeRoy G. Holm's World Weeds: Natural Histories and Distribution:

Seeds are protected from germinating in the stalk by the swelling of the pistillodes that are distributed throughout the inflorescence. In humid conditions, they swell and keep the spike intact. They can swell 15 to 20% in 15 min in 100% relative humidity. Upon drying, the pistillodes shrivel, air again reaches the seed, and the perianth hairs spread. Their collective pressure causes the inflorescence to burst, releasing the fruits to the air. If they fall on water, the hairs close and the pericarp releases the seed which then sinks.

So it's all about the humidity!

So the plant should get completely dry to let its seeds free. Wow.


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How to linearize target vector by PCR
In my bio class, we learned that you can use restriction enzyme or PCR to linearize a plasmid. Linearizing by restriction enzyme seemed visual and intuitive but how do one linearize a vector using PCR?
I know how PCR works(at least I believe I do), since I watched couple of videos on YouTube explaining them.
But it is not connecting to me how PCR can be used to linearize a "circular" DNA. I have seen videos where a straight double stranded DNA was separated into single strands and using PCR to produce multiple copies with appropriate primers.
But if a plasmid, the circular DNA is not "straight" or linearized in the first place how do you perform PCR on it? Because if they are in a circular state during PCR the strand would never separate in to linear strands. Wouldn't you just have two sperated strands that are circular? E.g a small ring of single strand DNA and a bigger ring of single strand DNA. They are still in circular state after the strands split from each other. Please correct me if I am spitting out nonsense. I just don't see the visual here.

I like your question. I am not sure if "inverse PCR" means that. But "inverse PCR" also needs restriction enzymes.

If you use PCR, the products from the reaction will be linear pieces of DNA. Yes, you'll have two templates that are circular after the first denaturation, but when you anneal the primers and perform elongation you'll be making linear fragments. The exponential nature of PCR means that these linear fragments will far exceed the template after several cycles.
PCR can also be tuned to be selective for shorter fragments. If you use the proper protocol for PCR of the entire plasmid, your PCR products will be a complete copy of the plasmid that is linear.

Why "when you anneal the primers and perform elongation you'll be making linear fragments"? Can you use some graph to explain?

Not sure how do to graphs in this, so I'll try a more detailed explanation. The plasmid is a circular piece of DNA. When you denature it with heat, you'll have two single stranded, circular, pieces of DNA. If we take one of these circular single stranded DNA pieces, and add a primer, the elongation on that circular piece will continue until it circles around and reaches the primer. The polymerase will not ligate the elongated primer back to itself, which creates a linear copy of the circular plasmid when denatured.


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Sex determination in cephalopod?
I see some source say octopus do not have sex chromosome. So what's the sex determination mechanism for cephalopods?

Welcome to Biology.SE. Can you please link to this source?

Related: Do males of all sexual species have Y chromosomes?

@Remi.b  They may be referencing this 2003 whelk paper: Genetic sex determination, gender identification and pseudohermaphroditism in the knobbed whelk, Busycon carica (Mollusca: Melongenidae)
John C. Avise1, Alan J. Power2 and DeEtte Walker.

Or this 2007 paper trying to find the same answer: Causes of variation in sex ratio and modes of sex determination in the Mollusca—an overview  http://www.bioone.org/doi/abs/10.4003/0740-2783-23.1.89

So far, you're right in that there is no hard method of determining cephalopod sex determiners.  Male and female share the same number of chromosomes, but are morphologically different, with the male developing a special arm for transferring spermitangia and the females often being larger than males (1).
Most research papers seem to focus on just being able to tell the sexes apart by behavior/anatomy (2) and have not yet broached on the How, except to note that they do not seem to have specific markers, which you've already noticed (1).
You can tentatively run with this, and keep an eye out for new research in Google Scholar, and decide that your race uses environmental signaling (3) to determine their sex.  Given how real life nature goes, you'd probably be in the clear as certainly one cephalopod species will use that method to determine sex. It also can segue into sequential hermaphrodism if you're interested in going in that direction.  It would certainly bring a novel element to your sophonts, rather than making an octopus "human". (Hypothetical extrapolation based on the previous version of this question in Worldbuilding.stackexchange)
But, to give you some ideas for environmental factors.  Some species of Daphnia will make parthenogenetic males when three factors meet: a short photoperiod, shortage of food and a high population density (4). The ever popular crocodiles have temperature dependent sex-determiners, with a narrow "sweet spot" to get a 50/50 male/female clutch (5). The green spoonworm determines it's sex as a larvae, if it lands on the seafloor it becomes female, if it lands on a female it becomes male and lives as a parasite inside of her.
Until further research, develop some form of environmental conditions that can be met naturally, or generated by intelligent octopi for what you want this question to answer.
(1) Coe, W. R. (1944). Sexual differentiation in mollusks. II. Gastropods, amphineurans, scaphopods, and cephalopods. The Quarterly Review of Biology, 19(2), 85-97.
(2) Mercer, M. C., Misra, R. K., & Hurley, G. V. (1980). Sex determination of the ommastrephid squid Illex illecebrosus using beak morphometries. Canadian Journal of Fisheries and Aquatic Sciences, 37(2), 283-286.
(3) Rider, C. V., Gorr, T. A., Olmstead, A. W., Wasilak, B. A., & LeBlanc, G. A. (2005). Stress signaling: coregulation of hemoglobin and male sex determination through a terpenoid signaling pathway in a crustacean. Journal of experimental biology, 208(1), 15-23.
(4)Kato, Yasuhiko; Kobayashi, Kaoru; Watanabe, Hajime; Iguchi, Taisen (2011). "Environmental Sex Determination in the Branchiopod Crustacean Daphnia magna: Deep Conservation of a Doublesex Gene in the Sex-Determining Pathway". PLoS Genetics. 7 (3): 1–12. doi:10.1371/journal.pgen.1001345. PMC 3063754 Freely accessible. PMID 21455482.
(5) Janzen, Fredric J.; Krenz, James G. (2004). "Phylogenetics: which was first, TSD or GSD?". In Nicole Valenzuela; Valentine A. Lance. Temperature Dependent Sex Determination in Vertebrates (PDF). Smithsonian Institution. pp. 121–130. ISBN 978-1-58834-203-4.

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How does gene affect organs development in eukaryotic cells?
I'm totally new to biology and apologies if you find this basic. The central dogma insists that genetic information flows in this direction:

DNA -> RNA -> proteins

So far so good, it is very clear to me. The question comes here. How does this flow contributes to creating/developing organisms. I want to zoom out from molecular biology to a bigger picture of an organ.
I want somebody to tell me, how does genetic code in a zygote, results in creating organs just in secreting different proteins by different active genes?

The question is very broad and I think can only be answered in very broad terms.
Proteins have metabolic functions. They do stuff! Their actions include catalyzing metabolic reactions, transporting molecules (incl. transport through the membrane), DNA replication, response to external stimuli and many other functions. Humans synthesize almost 30,000 different proteins Muller et al. (2002). The sum of their action put into a specific environment (such as a womb for mammals) end up building up and maintaining an individual.
Let's consider for example Hox genes. From wikipedia

Hox genes, a subset of homeotic genes, are a group of related genes that control the body plan of an embryo along the head-tail axis. After the embryonic segments have formed, the Hox proteins determine the type of appendages (e.g. legs, antennae, and wings in fruit flies) or the different types of vertebrae (in humans) that will form on a segment. Hox proteins thus confer segmental identity, but do not form the actual segments themselves.

For more information, I would recommend you to have a look at an intro course to developmental biology. You might want to learn about HOX genes


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Do puffin beaks have vertical slits or cracks?
I have seen a photo where puffins seem to have vertical lines on their beaks.  It is uncertain if those are just line or actual slits or cracks in the beaks.  Do puffin beaks have slits or cracks?

Can you add a photo showing what you mean?

an image would be important, puffins shed portions of their bill, have varying thickness, and have color patterns anyone, then there are growth lines and cracks ass possibilities. Any of those could be what you are talking about.

No, as far as I am concerned a healthy puffin hasn't got any slits or cracks in its beak. The lines that you see are literally just that - or little grooves. Obviously, beaks might show signs of wear and tear, so cracks may be observed. However, there are no genes in a puffin's genome that would lead to the expression of slits and cracks in its beak.
I think the photos below might help visualising.

(Photo: Tycho Anker-Nilssen, NINA)

(Photo: Will Nicholls)


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Sucrose inhibits onion root mitosis? Why?
I am doing an experiment about the growth of onion roots.
I put onion plants in different solutions of sucrose in water — 0.1M, 0.2M, 0.3M, 0.4M, 0.5M — with the root touching the water.
Measurements of root growth tells me that the presence of sucrose in the solution inhibits root growth.
Why does this happen? Does sucrose affect the root's mitosis? If so, how?

Have you used the same onion for all the experiments? If not, it could be due to the onions themselves rather than the enviroments they are in.

A formula does not identify a compound as many compounds have the same formula. This is an old question but I have edited it to replace the formula with the name of the compound I assume is being referred to.

tl;dr you are using a lot of sucrose. You would need to show us the data, but I'm not surprised if the plant gets confused / dies/ doesn't know what to do when you add so much.
An important aspect of experiments in biology is calibrating the treatment you're applying to the biological system. If you give a plant way more of an important signalling molecule than it would usually expect in nature, it may respond in a way that doesn't make any sense.
1M sucrose would be a 34% solution of sucrose (molar mass of sucrose is 342.3 g / M, in 1 L of solution).
If you look at papers or even at hobbyist forums where people add sucrose to stimulate root growth, they seem to usually be adding a 5% solution or less (50g / 1L ~ 0.16M), which is described as "high". So at the highest level you are adding more than 3X as much sucrose as people usually do.
I'd look at your data and try to understand whether the inhibition happens in a dose responsive fashion, and further whether the dose response is linear or whether it just gets weird at the higher concentrations.
As for the expected response, you will see in published work that sucrose or other sugars tend to encourage, rather than inhibit, root growth in most plants. Here for example is Figure 4 from a paper:

The left panel has no sucrose added and the right panel has 30mM sucrose added. You can clearly see longer roots in the presence of sucrose, at least in these young Arabidopsis seedlings.

tl;dr is not standard English but internet slang. Please replace it.

@David it's common parlance everywhere in SE, which is in turn, in (or on) the internet. https://biology.stackexchange.com/search?tab=votes&q=%22tl%3bdr%22&searchOn=3

@uhoh — Correction it is a text/SMS abbreviation. The fact that computing and IT types on Stack Overflow may be inclined to use it has no relevance to SE Biology, which as a scientific site aims for clear, unambiguous and inclusive communication.

@David part of inclusiveness is tolerance - not insisting things be just the way you personally think they should be. We're all just individual users here. The community has embraced tl;dr, it's here to stay. Also, cf. OED and Merriam-Webster

@uhoh — Could we please refrain from personalizing this, either in suggesting that I am being intolerant and that I am trying to force my views on the site. “Biology Stack Exchange is a question and answer site for biology researchers, academics, and students”, with the aspiration of building a library that will be a valuable resource to its users. One of the ways SE attempts to achieve high standards is by allowing edits of both questions and answers, and it allows comments expressly to suggest improvements in answers. The latter is what I did. I also took the trouble to improve the question.

@uhoh (cont)The common language of the users of this SE is standard English, and using slang etc. that is only understood by a subsection of users is a barrier to those who do not understand it, deters serious scientists who might contribute, and results in the adoption of such undesirable terms by neophytes, to their future professional detriment. This holds whether such terms are textese, non-standard abbreviations or foreign phrases (of which I admit to having been guilty on occasions). The inclusiveness of language is part of SE policy. The embrace of niche slang is not.

@David "tl;dr" is perfectly fine in ALL Stack Exchange sites. There's no basis to go around suggesting here and there that people shouldn't use it. If you'd like to start a new site policy, go to meta and ask "Shall we ban tl;drs in Biology SE?" and see what the rest of the community thinks.

To get back to the topic - surely the problem with the higher concentrations is osmotic effects rather than an inhibition of growth as such.

@uhoh wrote “tl;dr is perfectly fine”… …except that it is unnecessarily incomprehensible to a section of native English-speaking qualified biologists. I have not sought to ban anything, nor would it be within the remit of this site to do so. If I migrated this topic to Meta it would not be to micromanage people’s vocabulary, but to explain my view of the practical implications of the principles already adopted by SE to help them implement them theirselves. I have already made myself clear in this particular case, and SE Biology will not disintegrate if the poster chooses to persist.

@bob1 that's a good point. I'll add something.


text:
To what extent can bacteria actually see?
I found some popular articles (e.g. nbcnews and iflscience) that bacteria can "see," but I highly doubt it's in the same way as people do just from looking at the limitations in the vision of small animals like insects. So what exactly are bacteria capable of "seeing" or what are the limitations of their vision?

Can you please link to some of these articles?

Well I mean google can take care of that, for instance https://www.nbcnews.com/science/science-news/bacteria-have-ability-see-eye-opening-study-finds-n515141
or just http://www.iflscience.com/environment/bacteria-can-actually-see-acting-tiny-eyeballs/

@JohnJoe you are asking people here to help you and then say "google missing information". That is not very nice. Meanwhile, please post a quote that you need help understanding, right now question is unclear.

I'm not asking for people to verify the sources of what I said though. The way the articles phrase it is pop science anyway, not real science, so there's not even a point to referencing that information. However, the general topic is still relevant. Multiple news sources would not all lie about the same scientific subject, it is only that they do not portray it accurately.

Simple answer is that many simple organisms, including bacteria, carry light-sensitive molecules. One example is halorhodopsin (not bacterial but archaeic). This is a molecule, light-gated ion pump, that reacts to light, thus allowing organism to react to photons by changing concentration of certain ions inside the cell.
Study from Stanford described similar molecule found in bacteria.
In conclusion, if by "vision" you understand ability to react to light in the visible part of the spectrum, then a lot of organisms possess such ability. However, they lack other crutial parts of human vision.

I think that makes sense, thank you. So just to be clear, you're saying bacteria have the ability to sense simply "that" there is light in different levels almost like an on-off switch, but not the detail we see in larger animals? Can bacteria in any way distinguish either different frequencies of light, or, any kind of 2D or 3D structure?

@JohnJoe Most likely they don't. The most they can do is differentiate between high and low light. That too not by neural processing, rather by differential activity of light gated ion pumps.

Because bacteria are extremely small, the principles of optics prevent them from having lenses or other organs capable of determining the direction from which light is incident.  On the other hand, an entire spherical bacterium can potentially act as a lens, concentrating light from a given direction onto a corresponding position on the opposite side of the bacterium, and thus forming a very crude image.  Bacteria are certainly capable of responding to the frequency of incident light, if they contain molecules that selectively absorb light in specific frequency ranges.  And, they should be able to respond to the brightness or intensity of incident light, if those molecules return to their normal state shortly after absorbing a photon.  Of course, additional molecular machinery would need to be present in a bacterium to translate absorption of a photon into any sort of meaningful response.

@xusr, that paper makes a pretty convincing case that I was too hasty in rejecting the possibility that a relatively large, spherical bacterium could form enough of an image to "perceive" the direction of light.  The directional response to light described in the paper is, indeed, plausible.

Is there some way to combine both answers? They both have decent points.

I edited the answer accordingly.

Great, the only thing you're missing is credible references.

The reference given by @xusr, Cyanobacteria use micro-optics to sense light direction [https://elifesciences.org/articles/12620] is very good. If bacteria were large and spherical - on the order of a millimeter in diameter- and if their refractive index could be on the order of 2 rather than ~1.4 to ~1.6, then they would be able to form a high-quality image by this means: parallel rays from any given direction would come to a fine focus on the surface on the opposite side of the bacterium.  However, with a refractive index of 1.4, the focus lands far beyond the surface, hence a low res image.

I'm surprised at the focus on light in all these answers! To my knowledge, light is absolutely not the way that some 'bacteria' may be able to see.
Try looking on youtube for a macrophage (white blood cell) chasing down a bacteria.
You can see it actually following the bacteria - it's crazy. How on earth does it know where it is?
Chemical signalling, of course!! Sort of like a neurotransmitter. They secrete chemicals and follow the trail -  it could be really simple, such as, the transmitter converts to something else once it comes into contact with a phospholipid (of course indicating a cell membrane). I haven't researched that bit, but I hope it will allow you to direct your own train of thought/research.
Macrophages also have things called 'Toll-Like Receptor' proteins on their membranes, and they produce these things called 'pseudopods' that are essentially feelers/protrusions of the cell membrane. The Toll Like Receptor proteins recognise antigens by detecting Pathogen Associated Molecular Patterns that are common on the surface of pathogens/non-self objects (funnily enough). This is how your most basic innate immune system works- if the TLR protein on the pseudopod (wavy, baddie-finding arms) comes into contact with something it recognises as 'bad', it binds to it and draws it in for the white blood cell to engulf.
But it doesn't actually destroy/digest it at that point, because the TLR protein isn't perfect and sometimes there's some friendly-fire. A T Cell (I think T-Helper) comes along and 'double checks' that the macrophage hasn't picked up a friendly object. If it HAS picked up a friendly object, the T Cell will actually kill the macrophage for its mistake (usually).
OMG FRED, WHAT HAVE YOU DONE
Or at least that's how I like to imagine it goes down.

Chemical signals aren't exactly vision though, they aren't responding to photons.


text:
Why some seeds are mucilaginous (chia, rucola)?
Why some seeds are mucilaginous (chia, rucola)?
It is not obvious what kind of preferences that can bring to them. What is a role of mucilage in seeds cultivation?
P.S. The cultivation in germination cup shows only "difficulties": more affected by micro-flora, harder consequences after become too dry...


text:
What does this “shell” belong to?
I often find these, what I assume to be shells, during walks along the beach. I haven’t seen any creature or plant alive that has this feature and research attempts haven’t been successful.
There are bright reflective blue streaks along the shell and it is yellow-brown coloured and transparent. I have found these along the Northern Irish coast

I believe it's a Patella pellucida or blue-rayed limpet. They live off seaweed in deeper waters, so it's not a surprise that you wouldn't see many live ones.

Picture from an interesting article: Blue-rayed limpet holds secret for windscreen transparent displays with no internal light source


text:
Fraction of channels open at equilibrium
I found the formula for the fraction of channels open at equilibrium for a three-state mechanism (Colquhoun's paper in the microelectrode book http://www.utdallas.edu/~tres/microelectrode/me.html)

k1 and beta are forward rate constants. k-1 and alpha are backward rate constants.
p1(equilibrium) = (Xa/Ka)(beta/alpha) / (1+ ((Xa/Ka)(1+beta/alpha)))
Can someone show me how to arrive at this by derivation. I tried and I got it wrong (obviously!!!).
Xa is the concentration of the agonist and Ka is the equilibrium constant k1/k-1

The mechanism given by the OP is renowned in the world of pharmacology and drug-receptor interactions, and is due to Castillo and Katz (1957). A very readable review of the history and importance of this mechanism may be found in Colquhoun (2006), published in Trends in Pharmacological Sciences. (For more great papers from the Colquhoun lab, see here)
If A is the agonist, R the vacant receptor, AR an occupied but closed form of the receptor, and AR* the occupied but open form of the receptor, the situation where an agonist must bind before the channel can open may be represented as a three state receptor model (unoccupied, occupied-closed and occupied-open) as follows:
$$\ce{A + R <=>[$k$_1][$k$_{-1}] AR <=>[\beta][\alpha] AR{*} \tag{1}}$$
We need to be more specific here, and define exactly what is meant.  Let $A$ be the concentration of free agonist (ie agonist not bound to receptor), let $AR$ be the concentration of occupied closed receptor, and let  ${AR^*}$ be the concentration of open occupied receptor.  In addition, let $k_1$ be the second-order rate constant for the association of agonist with unoccupied receptor, and let $k_{-1}$ be the first-order rate constant for the dissociation of agonist from the occupied, closed receptor. Finally, let $\beta$ and $\alpha$ be first-order rate constants for the inter-conversion of the occupied receptor between closed and open states, respectively. Rate constants may be thought of simply as constants of proportionality arising from the law of mass action (see below).
The OP asks for a derivation of the following equation,
$$p_1^{(equil)} = \frac{({\chi}_a/{K_a})(\beta/\alpha)}{1 + ({\chi}_a/{K_a})(1+ \beta/\alpha)}\tag{2}$$
where $p_1^{equil}$ is the fraction of channels open at equilibrium, ${\chi}_a$ is the total agonist concentration, ${K_a}$ is the dissociation constant (not the association constant) for the binding of agonist to the closed receptor.
The situation is very nicely illustrated in the following diagram, taken from Colquhoun & Hawkes (1995)

Derivation
Although Eqn(2) looks daunting at first sight, the derivation is surprising simple.
Let $R_t$ be the total receptor concentration. An expression for $p_1^{equil}$ (the fraction of receptor channels open at equilibrium) may now be written as follows:
$$p_1^{(equil)} = \frac{AR^*}{R_t}\tag{3}$$
As
$$R_t = R + AR + AR^*$$
Eqn (3) may be rewritten as follows:
$$p_1^{equil} = \frac{AR^*}{R + AR + AR^*}\tag{4}$$
The problem with Eqn (3) & Eqn (4), of course, is that they are pretty close to useless. The total concentration of receptor is unlikely to be known, and obtaining reliable estimates for $AR$, $R$ and $AR^*$ present almost insurmountable experimental difficulties.
By the law of mass action, which holds that states that the rate of any reaction is proportional to the product of the reactant concentrations (and where rate constants may be considered constants of proportionality), the following may be written assuming the system described by Eqn. (1) is at  equilibrium.
$$ {k_1}. A. R = k_{-1}. AR \tag{5}$$
$$ {\beta}. AR = {\alpha}AR^* \tag{6}$$
Let  ${K_a}$ be the dissociation constant for the binding of agonist to the closed receptor. From Eqn (5), the following may be written.
$$ \frac{A. R}{AR} = \frac{k_{-1}}{k_1} = {K_a} \tag{7}$$
Therefore:
$$ R  = \frac{{K_a} AR}{A} \tag{8}$$
An equation for the total concentration of agonist, ${\chi}_a$, may be written as follows:
$$ {\chi}_a  = A + AR + AR^* \tag{9}$$
The problem with using Eqn (9) to obtain an expression for $A$ (the concentration of free agonist) is that it makes the resulting equations very difficult to solve. As regards the algebra, the situation is make a lot simpler by assuming that the total agonist concentration is equal to the free
agonist concentration, ie by assuming that Eqn (9) may be written as follows:
$$ {\chi}_a  \approx A  \tag{10}$$
When the concentration of agonist is very much greater than that of the receptor, this approximation is justified.
Eqn (8) may be re-written as follows:
$$ R  = \frac{{K_a} AR}{{\chi}_a} \tag{11}$$
From Eqn (6), an expression for $AR^*$ may be obtained.
$$ AR^* = \frac{{\beta}. AR}{{\alpha}}  \tag{12}$$
By substitution for $R$ (using Eqn 11) and  $AR^*$ (using Eqn 12) in Eqn (6), followed by cancellation of the common term ($AR$), the following expression may be obtained:
$$p_1^{(equil)} = \frac{\beta/\alpha}{1 + {\beta/\alpha} + K_a/{\chi_a}}\tag{13}$$
Multiplying Eqn (13) 'above-and-below' by ${\chi_a}/K_a$ gives Eqn (2), the equation requested by the OP.
Comment
Note that when $K_a$  = $\chi_a$ and $\beta/\alpha$ >> 1, almost all of the receptors are open as $p_1^{(equil)}$ is close to 1.  When $K_a$  = $\chi_a$ and $\beta/\alpha$ << 1, almost all of the receptors are closed, as $p_1^{(equil)}$ is very much less than 1.
Note also that $K_a$ is a dissociation constant and is the ratio of a first-order rate constant and a second-order rate constant, and will have dimensions of concentration.
Addendum
It may be of interest that Colquhoun's great book, Lectures on Biostatistics, is (legally) available free of charge (as a pdf) from here
DC's Improbable Science
A great site

Thank you very much. I greatly appreciate the effort you have taken to show me the derivation.


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epigenetic vs. environmental factors
I'm trying to understand the difference between epigenetic and environmental factors. For example, if gene A increases the risk of lung cancer by 50% and smoking increases the risk by another 75% when combined with gene A (just throwing out numbers) person X now has a higher chance of developing lung cancer. However, if for example, certain epigenetic factors are inhibiting the expression of gene A than that 50% higher genetic risk has now decreased because those high-risk genes aren't being fully expressed. The environmental risk factor of smoking still plays a role but it too could be decreased because that 75% increased risk was associated with gene A being fully expressed and not inhibited by epigenetic factors. Am I thinking about this correctly?

If I understand you correctly what you are saying is

There is envrionmental variance and epigenetic variance underlying the phenotypic variance. There can even be a covariance between the envrionment and epigenetics.

Yes, this is true. You might want to have a look at this intro post to quantitative genetics.
Note, there are several definitions of epigenetics. Epigenetic effects are some kind of factors that affect phenotypic variance and that are external to the DNA sequence. Often we think of modification directly on the nucleotides on on the histones (such as a methylation on the histon tail) but we sometimes also extend this context to include all the stuff that is the in the zygote or sometimes even further. In its broadest sense, the term "epigenetics" would be a synonym of "environment".


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Coelom - Bilateria
Coelom is formed of mesoderm. all bilaterians are triplopblastic meaning they have mesoderm. does this mean that ALL of the bilaterians have a coelom?

No. The coelom has been lost multiple times (for example, in Nematodes). Many parasitic bilaterians also lack a coelom, likely due to secondary loss.


text:
Does anyone know if there is a term to describe the following process?
I'm actually currently studying physics but this came up in my textbook (taken from Giancoli 7th edition section 16-10):
The random (thermal) velocities of molecules in a cell affect cloning. When a bacterial cell divides, the two new bacteria have nearly identical DNA. Even if the DNA were perfectly identical, the two new bacteria would not end up behaving in exactly the same way. Long protein, DNA, and RNA molecules get bumped into different shapes, and even the expression of genes can thus be different. Loosely held parts of large molecules such as a methyl group can also be knocked off by a strong collision with another molecule. Hence, cloned organisms are not identical, even if their DNA were identical. Indeed, there can not really be genetic determinism.
I'm aware of different biological processes that can affect gene expression but this is random kinetic motion! Would you call this one of the epigenetic mechanisms that can affect gene expression? If so it would underlie ALL epigenetic mechanisms because all molecules have random kinetic motion.

Eoigenetics requires chemical modificatios. I guess "stochastic" expression will convey the process you are describing but you will have to provide context.

The two terms of main interest to you
Cellular noise

Cellular noise is random variability in quantities arising in cellular biology. For example, cells which are genetically identical, even within the same tissue, are often observed to have different expression levels of proteins, different sizes and structures. These apparently random differences can have important biological and medical consequences
Cellular noise was originally, and is still often, examined in the context of gene expression levels – either the concentration or copy number of the products of genes within and between cells. As gene expression levels are responsible for many fundamental properties in cellular biology, including cells' physical appearance, behaviour in response to stimuli, and ability to process information and control internal processes, the presence of noise in gene expression has profound implications for many processes in cellular biology.

There is also the term developmental noise.

Developmental noise is a concept within developmental biology in which the phenotype varies between individuals even though both the genotypes and the environmental factors are the same for all of them. Contributing factors include stochastic gene expression and other sources of cellular noise.

Developmental noise is often sounds like a synonym of cellular noise, but it is supposed to include more processes that are causing phenotypic variation then cellular noise. For example, it is common to consider "micro-environmental variation" as being part of developmental noise and not of cellular noise.
The way your phrased your question
In your question you describe only sources of cellular noise. However, you end up saying Hence, cloned organisms are not identical, even if their DNA were identical. I just want to highlight that, there are other reasons than cellular noise for which two clones differ. These include micro-environmental variance, physiological noise, epigenetic variance and macro-environmental variance (often just called environmental variance). Note that I had never encountered the term "physiological noise" before, I just made it up but I wanted to highlight that noise also happen in among cells processes, not only within cells processes.
Intro to quantitative genetics
For a short introduction to quantitative genetics and the different sources of phenotypic variance (genetic variance, environmental variance, developmental noise, etc..) and how the concept of heritability fits into this discussion, please have a look at the post Why is a heritability coefficient not an index of how “genetic” something is?

Thank you for the taking the time to provide this detailed answer.

You're welcome. If you think your question has been answered, you can click on the checkmark next to the answer.

Heterogeneous is the term you're looking for I believe.
From Wikipedia,

A material or image that is homogeneous is uniform in composition or character (i.e. color, shape, size, weight, height, distribution, texture, language, income, disease, temperature, radioactivity, architectural design, etc.); one that is heterogeneous is distinctly nonuniform in one of these qualities.

If you're going to downvote, at least explain why.

Because all living organisms are a heterogeneous mess of proteins, DNA, RNA, lipids, carbohydrates, ions, you name it. The term "stochastic processes" suggested above is closer to the notion referred to in the question.


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moltype controlled vocabulary?
In submitting sequences using tbl2asn to NCBI/GenBank, the documentation states that there is a controlled vocabulary for the key "moltype", but no where on the Internet can I find a full list of that vocabulary.  "mRNA" and "genomic" are given as examples on several pages, and I can see from Sequin documentation what the GUI descriptors of all the vocabulary terms are (e.g., "genomic DNA"), but I can't find the terms themselves.  Any ideas where I can find this list?

Kind of a hassle, but could you download Sequin see what it outputs in the fasta for each molecule type?

I hadn't realized Sequin output fasta files.  I just checked, and it doesn't seem to include any of those descriptors in the FASTA file that will be exported when you use the Export command.

Sorry, I actually don’t know anything about it. Just a thought I had.

It was a good thought.  As you can see, I (perhaps inappropriately) edited my comment because I tested it out, and it didn't seem to work.

There is this "Controlled vocabulary for /mol_type qualifier" page created by the International Nucleotide Sequence Database Collaboration in 2013.  It says the allowed values are:

"genomic DNA", "genomic RNA", "mRNA", "tRNA", "rRNA", "other RNA", "other DNA", "transcribed RNA", "viral cRNA", "unassigned DNA", "unassigned RNA"

I found this as the second result of a Google search on moltype vocabulary.

I found that too.  The issue with this is that in the examples provided by NCBI, "genomic" is one of the valid values "moltype".  "genomic" by itself does not appear on that controlled vocabulary list.

Of course, another possibility is that the other NCBI documentation if invalid, and that this is the controlled vocabulary they use as well.

I just heard back from NCBI.  Even though this controlled vocabulary conflicts with their own documentation (which I suspect is out-of-date), it is the vocabulary they now use.

I've found an archived version of Sequin for Database Submissions and Updates:
A Quick Guide, published by NCBI.

moltype should use one of the following values. Example: [moltype=genomic]

genomic
precursor RNA
mRNA
rRNA
tRNA
snRNA
scRNA
other-genetic
cRNA
snoRNA
transcribed RNA

Great job!   That looks like it is what I need.  Odd that this isn't public.

The other possibility is that the OTHER documentation is out of date, and that the controlled vocabulary the mgkrebbs found is the one NCBI also uses.

@DavidMaddison Yes, it is odd. It may be worth contacting NCBI about it.

Yes, I sent NCBI a note asking about this earlier today.  I will report back!

See my new comment to mgkrebbs answer.


text:
How is it possible for a new species to evolve?
Suppose a new species is created from a random mutation that happened during an instance of reproduction in an existing species. How can that new species survive and flourish if there only exists one of it's kind and therefore it's not able to reproduce? By definition a species can only reproduce with others of the same species, no? It seems to me the only way it could is if a mate is created due to a separate occurance of a similar mutation, and the chances of both mutations occurring at around the same point in timespace must be very close to zero. And even if it were to happen, it seems to me the offspring wouldn't be able to reproduce due to problems with inbreeding.

Your question implies some misunderstandings about what mutation and speciation mean. I recommend https://evolution.berkeley.edu/ - it contains a good short summary of the basics of evolution.

By definition a species can only reproduce with others of the same species, no? No, and this shows a profound misunderstanding of science in general and evolution in particular.  In any case, even if that was true, it applies to "species", not "incipient species". You should read the link that Armatus pointed to to begin to correct your misunderstandings.

Virtually all cats can interbreed. (Lions, Tigers...) So can almost all dogs. Interbreeding is an ancestral condition, lost on a case-by-case condition.

One single mutation won't create a species.  Suppose instead you have an initial population that is separated into groups by geographic barriers - say they're on the Galapagos Islands, for instance.  Then each group will experience random changes, different beneficial ones will be selected for given the different conditions on the islands, and eventually the populations will diverge enough to be considered new species.

"this shows a profound misunderstanding of science in general" thanks @iayork for the hasty generalization / just plain insult.

Suppose a new species is created from a random mutation that happened
  during an instance of reproduction in an existing species.

No honest informed person would define species in this manner.
This is a better analogy

So the key here is that a mutation that contributes to the evolution of a new species doesn't make the recipient of the mutation reproductively incompatible with it's immediate ancestors, but it may make the recipient reproductively incompatible with its ancestors farther up the line due to the cumulative effect of this and previous mutations of ancestors in-between?

Yes.  But also, speciation is not about individuals mutating.  It is about populations changing.  The population, due to mutations, changes so much from the ancestral population that we label it a new species.

When I saw your answer, with this ugly text posted as an image, I was getting ready to complain! Of course, then I read the answer. The analogy is good and simple enough. +1

@Jonah you are still confused about the difference between a definition and reality. There are many different definitions of "species"; you've chosen one of the dozens and are upset because it doesn't cover everything in biology. You're debating semantics that have little to do with science.

@Jonah For more information about the difficulties of the concept of species, you can have a look at this post.

@iayork I'm not upset about anything, I was just asking an honest question. I understand now that a species is not soley defined by reproductive compatibility. Really I already new that it's possible for two different species to have fertile offspring (e.g. Homo sapiens), I just gave an oversimplified definition as a postulate I guess. The confusion I had is more about what makes certain individuals reproductively compatible. My assumption that determining which two animals can reproduce with each other can be done with some hard-and-fast rules like chromosome count is wrong ...

I thought a single mutation would have to "make the jump" between reproductively incompatible groups of animals. Really my question should of asked how any two animals can be rep. comp. if mutating into a new species would always ensure 0 compatible mates. I understand now that reproductive boundaries are not so clear


text:
Are all of our hormones synthesized in the same gland that they are secreted from?
For example, growth hormone is secreted from the anterior pituitary; is it also synthesized there?

For many, yes. But for some, like oxytocin and ADH, which are secreted from posterior pituitary, are synthesised in hypothalamus, the sites are different

Ah, I remember learning about that for those two, for sure. Thank you.

Vitamin D is synthesized in multiple sites though classically it is said that final hydroxylation occurs in the kidneys.

Vitamin D is a hormone the kidneys produce that controls blood calcium concentration and impacts the immune system. It is also known as calcitriol, ergocalciferol, calcidiol and cholecalciferol. Of those, calcidiol is the form doctors most commonly focus on when measuring vitamin D levels in the blood.
The body makes vitamin D in a chemical reaction that occurs when sunlight hits the skin. This reaction produces cholecalciferol, and the liver converts it to calcidiol. The kidneys then convert the substance to calcitriol, which is the active form of the hormone in the body.

https://www.hormone.org/hormones-and-health/hormones/vitamin-d


text:
How many photons are used to make one glucose?
This was a question in a test. The options were
(1) 8
(2) 16
(3) 24
(4) 48
My answer is 30 which was not in options.  Given answer was 48.
12 NADPH
18 ATP for one glucose
12 NADPH and ATP from z scheme where 24 photons are used.
6 ATP more from cyclic where 6 photons are used.
Net 30.
Can someone point out an argument against this?
One explanation for 48 is:
2 electron each hydrogen atom
4 electrons per water molecule
2 water molecules for one oxygen molecule
8 electrons=8 photons for each oxygen,
each glucose 6 oxygen so 8×6 = 48
But what is the mistake in argument for 30?


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Identification of Bird feather, probably from a predatory bird

Found in Berlin,Germany
Area of Charlottenburg
I want to know the species of this bird, someone please tell me.
Approximate size 19 cm

Have you seen this (German) page: http://www.greifvogelhilfe.de/artenbestimmung/gefieder-greifvoegel/ ? That might help to narrow down the number of candidates.

This is a Common Kestrel (Falco tinnunculus) primary wing feather, so it is indeed from a predatory bird. The orange hue suggests that this came from a juvenile and/or female individual. Featherbase provides a good reference here.
For future feather identification questions, you may wish to post them to the Found Feathers project on iNaturalist.

Welcome to Biology.SE! This looks like a good answer, but you are more likely to get a positive response if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. (Note that answers must stand on their own — i.e not require us to follow links.) ——— Please also take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


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Calculating CV for intra-assay ELISA
Sorry if this is in the wrong thread.
I have to calculate CV for intra-assay ELISA sample OD's. My problem is that i'm finding people are using sample standard deviation in their CV formula, though from what i understand as intra-assay CV reflects variability within the same assay run that to me should be considered as a whole data set and therefore population standard deviation should be used.
Am i correct in my assumption or am i missing something?

As far as I am concerned the intra-assay CV is the average of individual CVs found in an assay.
So let's assume you have a data set of 40 samples, and for each sample you have 2 replicates (results), like the one below.

You would first calculate the mean for each sample, so in the sample above that would be: $$\frac{0.132 + 0.128}{2} = 0.130$$
Then you would calculate the standard deviation for each sample, so going back to our example above, the standard deviation for sample 1 would be as follows: $$\sigma=\sqrt{\frac{1}{2} ((0.132-0.130)^2 + (0.128 - 0.130)^2)}=\frac{1}{500}=0.002$$
Next you would calculate the Coefficient of Variation, so in our case:
$$CV = \frac{\sigma}{\bar{x}}\times100=\frac{0.002}{0.130}\times100\approx1.6%$$
Afterwards you would repeat the aforementioned procedure for each sample.
In the end you would calculate the average of all individual CVs, so: $$CV_{intra} = \frac{\sum_{i=1}^{40} CV}{40} \approx 5.2% $$
I have stolen the example from Salimetrics, I think this document explains inter-assay and intra-assay CV very nicely.
Please note: The usefulness of inter and intra-assay CVs are somewhat disputed, as this Wikipedia article mentions.

Thank you for your reply, i have read this. They have 2 result sets, so it's possible to calculate the CV for each individual sample, i generally only have one. It's probably fine to use Sample Standard Deviation in their formula as they are calculating the individual sample CV from a whole data set. As i have only one set to work with i need to calculate the CV from the data set as a whole, which is why i think i should be using Population Standard Deviation in my CV formula rather than Sample Standard Deviation for my scenario instead. Though everyone seams to use Sample SD regardless.

I guess it really depends what you want to measure with the CV. It sounds to me, seeing that you have only one result per sample, that an intra-assay CV is not the measure you are looking for. Going by what you have said it sounds like you simply want to calculate the CV for your entire data set and that seems to make sense. I think it then becomes more of a question what it tells you about your data and that really depends on your study design and what you test for..


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Why does menthol clear a stuffy nose?
I've looked all around online for an answer to this. Some sites say menthol causes blood vessels in the nose to constrict, some sites say it causes blood vessels to expand. Many sites simply say it's a remedy, but with no explanation.
And if it does cause the constriction or expansion of blood vessels, what's that got to do with making the stuffiness go away?

Wow, you aren't kidding about the different answers online.  To add to the confusion here's an answer from the Mayo Clinic saying that menthol tricks the brain into feeling like you are breathing through an unclogged nose.  https://www.mayoclinic.org/diseases-conditions/common-cold/expert-answers/nasal-decongestant/FAQ-20058569

Menthol is stimulating action potential at cells which are inducing thermoception. As far as I have found out it does not have any effect beyond that. The patients only feel like they can breath better while it could not be proven that they actual do.
https://www.ncbi.nlm.nih.gov/m/pubmed/18702906/
The blood vessel thing : In general "cold" is a cause for vasoconstriction - that might lead to the conclusion that menthol is doing the same. I have no experental background on that but - after online research :-D- it seems like that menthol causes vasodilatation.

+1 for the correct answer. Fyi: If menthol caused vasodilation, there would be an increase in stuffiness, which is not the case. One can decrease nasal stuffiness with vasoconstrictors, like phenylephrine hcl. The reverse holds as well.


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Lack of skin in a certain area of the body --- hypo[what]?
Lack of skin in a certain area of the body. How shell I name this?

Hypocutaneousis?
Hypo[somethingElse]?

What is the correct term?

Exactly what are you referring to? A permanent lack of skin in an area sounds like a permanantly open wound to me.

I mean to a partial lack of skin, like when someone has too little skin after bad surgery or after an accident (I'm not aware of diseases that will reduce the amount of three-layers skin).

First, this is not an area where I have any education or experience. However, out of curiosity I consulted google and found two genetic castle diseases that should be relevant to your question:

Epitheliogenesis imperfecta (vetbook.org)
Ectodermal dysplasia

Both diseases are very serious, and Epitheliogenesis imperfecta is fatal (due to infections).
I chose not to include any pictures of the diseases in this answer since they often look quite horrible, and some people might find them unsettling. If you click the links there are pictures of the conditions though.
A "similar" condition in humans might be  Epidermolysis bullosa, which is caused by decreased anchoring between dermis and epidermis, which cause a very fragile skin:

Epidermolysis bullosa (EB) is a group of mainly inherited connective tissue diseases that cause blisters in the skin and mucosal membranes, with an incidence of 20 per million newborns in the United States.[1] It is a result of a defect in anchoring between the epidermis and dermis, resulting in friction and skin fragility. Its severity ranges from mild to lethal.

(Wikipedia)

You can say skin atrophy or just thinning where dermal thickness is reduced.
https://m.iliveok.com/health/skin-atrophy_77524i15941.html

Thinness does not seem to be the same thing as the OP's question about lack of skin.

@kmm what can I say but the question is unclear but being a specialist physician for 40 years my answer is likely correct for most instances.


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Can 2 people give rise to billions? Adam and Eve 2.0
With with the advancement of GMOs the idea of giving rise to humans from 2 people is possible making questions like this invalid?
How many people are required to maintain genetic diversity?
With constant genome engineering to create genetic diversity on each generation of humans before conception how many generations can come from two people with ideal DNA? It is not inbreeding if the DNA is changed enough?

all this is just speculation and I don't think we can provide you an answer on this Stack Exchange website atleast. And I don't even understand what you mean when you say "How many generations of human can come from two people"? We are all descendants of the very first individuals in the homo sapien species.

Also, the picture is really really not in anyway helpful for the post.

I think the question deserves to be close. Yet, I felt like I would attempt to give you some help. I did not down vote but I don't think this is of any importance in the discussion. I don't really understand why this is unfair. In any case, don't worry too much. I wrote bad questions and bad answers before. Sometimes I did not agree with the bad reception I got. Nobody remember those. It is the same for you, people will associate you with your best posts only. And down votes really won't affect your reputation mutation (1 point loss per down vote and you get 2 points from accepting an answer).

@Remi.b how can it be made better?

@Remi.b I didn't down vote either.

The question involves genetics, ecology, sociology and is fundamentally untestable. I do not think it can be edited to become better, it is quite fundamentally not a question that one can give a scientific answer to. Also, "Can genetic diversity be created with technology?" is really broad and really different from the other question, who itself is already quite broad.

Would you feel better if I delete my answer so that you can delete your post (I am not sure you will be allowed to delete your post but maybe...)?

@Remi.b no, the answer is good but feel free to edit my question to fit better.

You do not need any 'editing', in theory it is possible for two people to give rise to 8 billions people. Early generations would suffer from some inbreeding depression but if you somehow get rid of it through 'editing', then you do not even have this trouble for the very first generation but you will have it for the successive generations. It is impossible to tell how important it will be and whether that will prevent this tiny population to survive though. There are ecological and sociological problems that are probably of great importance too. To make it short, it is not easy to survive alone!
For non-recombining DNA, it is necessarily true that we all currently living copies descent from a single individual (see coalescent theory although it will likely be too an advanced topic for you). This is the case of the Y chromosome (excluding the PAR) and of the mtDNA. We refer to these MRCA as Eve-mtDNA (biblical reference) and Y-MRCA, respectively.
Of course, these two individuals did not live alone, did not live together and did not live at the same time or same place. Also, none of these two individual is in anyway a good turning point for considering him/her the first individual of a new species. Y-MRCA is just the MRCA of all modern Y chromosomes and Eve-mtDNA is the MRCA of all modern mtDNA. The reality for the rest of the genome is more complex due to recombination. For your information, Y chromosome and mtDNA put together represent about $\frac{1}{50}$ of the entire genome.

I doubt this answer end up being of much help to you. You should probably just have a look at an intro course to evolutionary biology such as for example evo101.

No this is great. Sometimes just knowing it could be done by today's technology is great. We in theory could start over with less people then it states here. https://worldbuilding.stackexchange.com/questions/3/what-is-the-minimum-human-population-necessary-for-a-sustainable-colony Thanks

Never have I talked about technology in my answer. I just mean to say that there is not fundamental barrier to it. Also, I highlighted that two individuals might not be enough to ensure their own survival but it is impossible to answer this question more precisely in scientific terms because there is no way to empirically test such questions. I think you have misunderstand my answer. Also, you seem to misunderstand the scope of questions that is open to scientific enquiries.

I don't think we should understate the problem of inbreeding depression; sure, once the deleterious genes get selected out it would no longer be a problem, but what are the odds of the population surviving those early generations? If every couple has 20 children it's one thing, if they have two or three it's another. I also don't think we should understate the risks of that level of inbreeding to a population's survival. How many generations would it take to build the genetic diversity back to a point where the whole population doesn't get wiped out by the first epidemic? Thousands, surely?

2 people could give rise to billions?

To be clear the typical pathway for speciation in real biology is not via a 2-member founding group (even if it isn't fully biologically impossible). That's a religious story only.

@BryanKrause Indeed. And, yet again, the two ancestors I mentionned (Y-MRCA and Eve-mtDNA) did not live alone and did not live at the same time or same place and are in no way a good turning point for considering them the first of a new species.

Yeah, I caught the nuance in your answer, but I don't think OP is catching it.


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When doing minipreps, do "good" plasmids produce more DNA than "bad" plasmids?
I've been doing minipreps for close to 10 years using the standard qiagen kits and DH5a e. coli. I typically do 24 minipreps at a time and then identify the good plasmids by enzyme digestion, PCR, sequencing, etc. Something I've noticed is that the good plasmids often seemed to have higher DNA concentrations than the bad plasmids. I thought it was just superstition, but I looked back at a couple of recent miniprep batches and did statistics, and found that the good plasmids had a statistically significantly higher amount of DNA. I don't see this pattern all the time, but I have seen it when using InFusion based cloning and traditional restriction enzyme based cloning. I don't have access to all of my miniprep data, so I can't check everything for statistical significance.

So, why would "good" plasmids have better yields of DNA than "bad" plasmids? Has anyone else noticed this pattern?
As far as I knew, as long as the plasmid carried a working antibiotic resistance gene and the bacteria could replicate it efficiently, then the plasmid should be ok. Could the bad plasmids have been cases where the bacteria manages to ligate the vector backbone together but creates a sequence that doesn't replicate well? Could it be a timing issue, where the bad plasmid doesn't start replicating until later, so that the bacterial growth is delayed? I have not weighed the bacterial pellets, so I can't say anything about bacterial growth vs plasmid yield.


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Is there any non-pathogenic gram negative bacteria?
In the category of Gram-negative bacteria, is there any non-pathogenic species? Is such a list of non-pathogenic gram-negative bacteria's available? Can you give maximum 5 examples of such bacteria which has been proved to be non-pathogenic and is gram-negative?

Well, most of them are not pathogenic. It would be quite a long list.

The most diverse, yet phylogenetically coherent, bacterial phylum is the Proteobacteria, and its members are Gram-negative. If you go through the list of bacterial genera and species belonging to Proteobacteria, and if you look into the papers that describe them, you will always find the information about the source, i.e., the environment from which the bacteria were isolated, and from that you can infer about the pathogenic potential.
http://www.bacterio.net/-classifphyla.html#proteobacteria

Another strategy is to make the list of all pathogenic bacteria, remove them from the list of all bacteria, and exclude Gram-positive ones. You will be left with all Gram-negative bacteria for which pathogenicity is not known.

As Canadianer already mentioned in the comments, the majority of bacteria (this includes gram-negative bacteria) are non-pathogenic.
I think a prime example is the human gut flora. You can find loads of bacterial species living in your gut without doing you any harm, if anything they are doing you a favour by breaking down food.
Here some examples of gram-negative genera:

Bacteroides
Escherichia

Most species within those genera are non-pathogenic, however, there are exceptions.

So bacteroides vulgatus is gram-negative and non-pathogenic?

It would appear so.. Here is a study (http://jb.asm.org/content/193/15/4025.full) that refers to Bacteroides vulgatus as one of "the most commonly isolated microbes from the human gastrointestinal tract, and it has been found to constitute part of the core gut microbiota in healthy humans".

I should add, however, that infections may have been reported for said organism. This happens when they grow in environments where they shouldn't be growing. The questions of pathogenicity isn't always as black and white as we would like it to be. Generally, Bacteroides vulgatus is considered commensal.

There are more than 15,758 named bacterial species, and the majority of them are Gram-negative, and most of them are non-pathogenic.

the document is password protected, how to open ?

The password for "Bacteria I. Taxonomy: Genera and Species" is: 1


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What absorbs light at 380 nm in a sample of DNA oligonucleotide extracted from a PAGE gel?
I have extracted DNA oligonucleotide of size 77 bp from a crushed 10% PAGE gel using 3 rounds of $\ce{LiClO4}$ in water. The extracted elute was dried down in a vacuum centrifuge to a certain volume and then precipitated with 5 volumes of Ethanol before taking a spec on a NanoDrop. I do have a significant peak, characteristic of a DNA oligonucleotide, at 260 nm with a $A260/A280 ≃ 1.75$.
However, I also get a peak at 380 nm. I used to get this since a long time but I could not understand what it meant (did not find any literature reference). I do not want to worry about it too much, as long as I have my oligo, but I would like to know what it is. A colleague of mine also got the same peak, though not very prominent, who did not do a PAGE purification but direct UV Spec after Phenol/Chloroform extraction and $\ce{LiClO4}$ in acetone precipitation.
What would you suggest?
[Note: For your information, I have already asked this question here on ResearchGate. Out of all the answers, Paul's seem to be quite rational. However, I wanted to see if anyone has any other opinions]
Thanks a lot for your answers.

I did not understand what was the edit that you made @kmm?

I was fixing some of the mathjax formatting.

I guess I would like to close this question. I have already got answers on the ResearchGate forum. Thank you!


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Can gut flora affect what we can eat and what we cannot?
Back many years ago, I've read a mushroom guidebook, which I don't have anymore. I was unable to find the name of a particular mushroom. The book comprises listing of edible and poisonous mushroom species. One particular mushroom was said to be "poisonous to some people". the effect is not allergy-based, but rather straightforward poisoning. What drew my attention was the phrase:

If you haven't tasted it before, do so in small doses first. Each family member has to do it regardless of how other family members responded, because the condition is not genetic

This has lead me to think, that if condition is not genetic, then it may depend on which gut flora you have. Gut flora is very helpful in digesting many substances in our food, and possibly even toxins. This has lead me to ask the question Can a human be inoculated with gut flora from another animal and thus be able to eat food otherwise poisonous to humans?
Supporting evidence:

I have read that pronghorns can browse on sagebrush, a herb that is poisonous to ordinary cattle. The toxins kill the cattle's gut flora, that is supposed to aid in their digestion. It is not, however toxic to the pronghorn's gut flora, which can digest the toxins.
Changing your diet abruptly may result in embarrassing stomach upsets. These upsets are transient, however. This may reflect a change in the ratio of bacterial species which reflects optimal adaptation.

Putting that theory to the test:

Attempting to inoculate Pronghorn's gut flora to cattle -- Will the cattle be able to feed on sagebrush?
Diversity of gut flora in humans: One may expect some difference in gut flora between that of city dwellers, such as in Europe, and that of tribes in the rain forests of the Amazon and Africa. Can a city dweller in Europe eat anything the forest dweller may eat? Does he/she need some bacteria inoculation to adapt to certain foods?

Limitations
Not all poisoning cases may be avoided by introducing gut flora that is supposed to digest the toxins. Failures to avoid poisoning may include:

Poisons that are absorbed by the body and the animal eating the plant or mushroom is not affected by it. Floral gut from the animal will not avoid that type of poisoning in a human eating the plant/mushroom.
Poisons that are digested by the animal's own digestive enzymes.
Environmental incompatibility: The introduced bacteria must be compatible to the type of food the host feeds on, as well as the chemical environment of the guts. For humans, this limits us to gut flora extracted from animals with diet similar to ours (Not counting processed food and cooked food). Ruminants and predators are out, Omnivores are in.
Poisons that an animal avoids by excreting it rather than absorbing it, and the bacteria does nothing in digesting it.
Host compatibility: The introduced gut flora must do its job in the guts, and not turn against its host. In turn, the host's immune system must "leave it alone".

DISCLAIMER -- a somewhat-related breakthrough research is underway at the Weizmann Institute of sciences. Conditions such as diabetes, Krohn's disease, obesity, resistance to infections, behavioral and psychiatric tendencies among others were once considered issues on their own, and unrelated to gut flora diversity (or lack of). This research shows otherwise. The research even includes a custom diet which is unlike common diets. Rather than counting calories, your diet is tailored to suit the type of gut flora you have. You may assume that some bacteria may secrete toxins which cause organ damage, such as kidney, liver or pancreatic failure. The healthy gut flora may keep those harmful bacteria in check. On the other hand, it is possible gut flora may digest some of these toxins before they are absorbed by the body.


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DNA code and codon
I work as a highschool teacher and I believe that in most highschool textbooks in my country there is a lost-in-translation problem involving some molecular biology basics. It has spread to the point one starts to doubt his basic knowledge, so here it goes:
For example, let's say that a triplet in mRNA is:
5' AUG 3'
That triplet is named CODON. (no problem there)
The DNA that corresponds to it has two strand.
One is coding or sense strand and contains the corresponding triplet 5' ATG 3'
The other is non-coding or antisense strand and contains the triplet 3' TAC 5'
Highschool textbooks in my country say that the triplet 3' TAC 5' , therefore the non-coding strand, is the CODE.
It makes no sense to me whatsoever, but I'd like to check it out since in English literature the term code is rarely used anyway and genetic code is usually presented as codons. Sometimes, when the list of DNA triplets is given (and it's always in 5'->3' direction since the information is read that way) it says "DNA codons".
So, to sum it up - is the DNA CODE equal to triplets in the coding or the non-coding strand?
Thanx in advance!

I wonder why you put in parenthesis: "(and it's always in 5'->3' direction since the information is read that way)". Do you mean: even if might as well be the other direction that wouldn't answer the question?

The non-coding strand is indeed not the coding strand as the name suggests. It is the template strand. The template strand serves as the strand from where the mRNA is constructed upon. The mRNA contains the complement of the template strand, and is ,in fact, the actual codon. This is also the reason why the other strand is called the coding strand, it's the complement of the template strand, which makes it essentially the same as the mRNA, except uracil is replaced by thymine.
DNA Strand section:
5'---A-T-G---3' => coding strand
     : : :
3'---T-A-C---5' => template strand

mRNA formation:
5'---A-U-G---3' => mRNA strand
     : : :
3'---T-A-C---5' => template strand

are the coding strand and template strand synonyms?

@BenHughes Nope, but they are complementary to each other. It's both of those strands that make up DNA. During transcription, the two strands split and the mRNA strand forms taking one of them as a template (hence it's name template strand). The other one doesn't do anything, but has the same base pairs (T replacing U) as the mRNA, hence called the coding strand.

In the English literature, a sequence like your 3' TAC 5' (when considered as the complement to a 5' ATG 3' or 5' AUG 3' codon) is typically called an anticodon.  Most often this is in the context of a tRNA having an anticodon to a codon on an mRNA.  See, for example, this page from Molecular Biology of the Cell or, similarly, this page from Berg's Biochemistry
Generally, code is used in molecular biology to refer to the conceptual mapping from a codon sequence to an amino acid (or meta function like STOP), or collectively to the whole set of such mappings.  The latter kind of reference is more likely to use the longer name the genetic code.

Very helpful you "bring up" anticodon. Are you sure that this term is not exclusively used in mentioned context of transfer-(t)-RNA? The question seems to be on coding/negative "strand" relating/corresponding to "template"/transcribing(cp. related answer by David) "strand". In that sense, the anti-codon of a t-RNA doesn't appear to be a "strand".

@PeterBernhard, I disagree with you about what the question is asking, which is exactly why I added my answer after Twisted Genes' answer, which does a fine job of explaining strands. The OP mentions strands only as a point of reference for the actual question, which occurs in the last large paragraph.  I believe he is asking about the names for triplets, and in English they are 'codon' and 'anticodon', and not about strands.  (I also discuss the usage of 'code' which is another aspect of the question.)  'Anticodon' is not used much, and probably does appear primarily in the context of tRNA.

Maybe "Anti-" ought to be (trying some irony) opposed to the wording of the question "...the non-coding strand, is the CODE. " As I found with David quoted above, it's very well a matter of linguistics, too. As you  say in your second part of your answer, "Crick's CODE" refers to that eminent fact that the proteins of life are made from amino acids which there is THE code for, hence - to my mind - "coding" for what IS the code, and not for that template fabricating. Your second part is the answer, question not on difference codon/anticodon (you made me emphasize). Will read all your reference.

Would you agree with  "anticodon" in a wider sense being in use for any sequence that complements what has been defined as codon? -  One more example I suggest is "interfering" RNA that matches m-RNA which may be named "non-coding anti-codon"? -  Is non-coding, i.e. are anti-codons always read from `3 to '5, even when, as genes, are found on the 5' to 3' -codon strand? Thank you.

Albert, The cell you quote, says, defining: "anticodon - Sequence of three nucleotides in a transfer RNA molecule that is complementary to a three-nucleotide codon in a messenger RNA molecule". In fact, the term seems to be restricted to the context of tRNA.