text:
Why does capsaicin irritate mammals and also kill fungi? Are the two related?
From this article I heard about a study (search "Tewksbury") which concluded that chilies make capsaicin to discourage mammals from eating their seeds, since grinding by mammals' molars render the seeds unable to germinate. Birds, on the other hand, don't break open the seeds and spread the plants far and wide.
But, they also reference a different theory: capsaicin evolved to defend against a certain kind of fungi that infected pepper plants.
My question is: why does the same chemical do these two things? It seems like quite a coincidence, unless capsaicin has some general destructive properties. But Wikipedia's explanation talks about how capsaicin artificially stimulates a certain receptor in our mouths -- which sounds totally unrelated to fungi.

Recent study has shown that capsaicin indeed has antimicrobial properties. For example, see this article:

Two pungent compounds found in Capsicum species (capsaicin and dihydrocapsaicin) were also tested for their anti-microbial effects. The plain and heated extracts were found to exhibit varying degrees of inhibition against Bacillus cereus, Bacillus subtilis, Clostridium sporogenes, Clostridium tetani, and Streptococcus pyogenes.

In one of the attempts to study its mechanism, a study on yeasts suggested that it works in following ways:

Detoxification of capsaicin by a PDR-type ABC
superfamily of multi-drug resistance transporters
Osmotic stress response and damages in membrane
structure caused by the capsaicin treatment
Genotoxicity of capsaicin to yeast cells
The effects of the deletions of the genes those were
induced by the capsaicin treatment
Mechanism of capsaicin in the growth inhbition to
yeast cells:
The DNA microarray analysis of antimicrobial
mechanism of capsaicin shows that capsaicin induced
an osmotic stress element, the key genes for membrane biosynthesis, and the PDR network and repressed the genes for ribosomal components
and cellular growth. The growth characteristics of
deletion strains suggest that PDR5 is important for
the resistance to capsaicin. These observations that
the PDR network may pump out capsaicin from cells
are the first findings. The contribution of the PDR
network also suggests that capsaicin enters to the
cells and capsaicin functions as a toxic substance to
the yeast cells. This toxicity is possibly to the
mebrane structure and/or as osmotic stress.
Full article (PDF) here.

Though in mammals, its mechanism of action is quite different; it acts on ion channels to give a burning sensation. See this article:

The burning and painful sensations associated with capsaicin result from its chemical interaction with sensory neurons. Capsaicin, as a member of the vanilloid family, binds to a receptor called the vanilloid receptor subtype 1 (TRPV1). TRPV1, which can also be stimulated with heat, protons and physical abrasion, permits cations to pass through the cell membrane when activated. The resulting depolarization of the neuron stimulates it to signal the brain. By binding to the TRPV1 receptor, the capsaicin molecule produces similar sensations to those of excessive heat or abrasive damage, explaining why the spiciness of capsaicin is described as a burning sensation.

However, it is toxic for mammals too. Capsaicin is a highly irritant material requiring proper protective goggles, respirators, and proper hazardous material-handling procedures. Capsaicin takes effect upon skin contact (irritant, sensitizer), eye contact (irritant), ingestion, and inhalation (lung irritant, lung sensitizer). The LD50 in mice is 47.2 mg/kg.
Though its mechanisms are different, it performs quite similar functions: protecting the plant from predators and infections i.e. a defense system.
It seems like quite a coincidence, unless capsaicin has some general destructive properties.
It is neither a coincidence nor capsaicin has general destructive properties. In fact, capsaicin is being used as an analgesic too. See this article:

Capsaicin is a chili pepper extract with analgesic properties. Capsaicin is a neuropeptide releasing agent selective for primary sensory peripheral neurons. Used topically, capsaicin aids in controlling peripheral nerve pain. This agent has been used experimentally to manipulate substance P and other tachykinins. In addition, capsaicin may be useful in controlling chemotherapy- and radiotherapy-induced mucositis.

Its mode of action is, seemingly, somewhat similar. See this:

The mechanism of action of topical capsaicin has been ascribed to depletion of substance P. However, experimental and clinical studies show that depletion of substance P from
  nociceptors is only a correlate of capsaicin treatment and has little, if any, causative role in pain relief. Rather, topical capsaicin acts in the skin to attenuate cutaneous hypersensitivity and reduce pain by a process best described as ‘defunctionalization’ of nociceptor fibres. Defunctionalization is due to a number of effects that include temporary loss of membrane potential, inability to transport neurotrophic factors leading to altered phenotype, and reversible retraction of epidermal and dermal nerve fibre terminals. Peripheral neuropathic hypersensitivity is mediated by diverse mechanisms, including altered expression of the
  capsaicin receptor TRPV1 or other key ion channels in affected or intact adjacent peripheral nociceptive nerve fibres, aberrant re-innervation, and collateral sprouting, all of which are
  defunctionalized by topical capsaicin. Evidence suggests that the utility of topical capsaicin may extend beyond painful peripheral neuropathies.

(P.S. substance P is a neuropeptide, a potent vasodilator & iniates expression of almost all known cytokines.)
Pay attention to the last line 'utility of topical capsaicin may extendbeyond painful peripheral neuropathies.' i.e. capsaicin may have more effects on body than known!

So why does the same substance have these different mechanisms of action in different organisms? Is this common in biology?

It is so because of structural complexity of compounds. Many compounds out there and in here are similar in structure; this is the cause of side-effects of drugs, it is the cause of competitive inhibition of enzymes, and so on. It is not very common, but no surprise if we keep finding more such cases.

Capsaicin binds to an ion channel that is fairly well-conserved across metazoa and fungi.  Influencing the activity of an ion channel can have a seemingly small impact on us (e.g. spicy food 'taste') but for a colony of fungus, such activity can cause the individual cells to stop dividing or migrating in a certain direction (fundamentally changing their behavior).  In other words, capsaicin can be lethal or at least make living difficult!  For more information about these channels and the specific mode of action of capsaicin in mammals, see David Julius' lab website.

Interesting, and thanks for the link. Since I don't have a biology background, what is an ion channel and what functions does it perform? Would it be correct or approximately correct to say "Yes, capsaicin does have 'general destructive properties', the property being that it binds to this ion channel which is important in a lot of life forms" ?

see metroplex's tome-like response below.  'destructive' is inaccurate; it's not destructive to birds apparently, and it's not destructive to the plants that produce the compound.


text:
Expression/Mechanism of ROR1 in healthy tissue
ROR1 is currently under investigation as a therapeutic target for cancer (1). A number of studies show different cancers may have their metastatic potential reduced, or become apoptotic through targeting or abrogation of ROR1 (1-3). ROR1 itself is show to have a number interactions (either through crosstalk or interaction) with some known tumorigenic markers; these include c-Met, PI3K, Akt, Wnt5a, EGF, c-Src (4-7). In terms of metastatic potential, interactions with vimentin, Snail/Slug, cadherins, ß-catenin, and CXCR4/CXCL12 were also identified (1, 8). Some of these are via expression of CREB. In terms of ROR1 is tissue, abnormalities that lead to death were noted in newborn mice that has ROR1 knocked down (9). A notable mechanism for ROR1 in development was in neuroprogenitor cells in which ROR1 regulation status determined whether these cells differentiated into neurons or not (10). It's also found that neural, heart, lung and kidney tissue in adults express some form or another of ROR1 (11). More recent studies suggest ROR1 downmodulation may present toxicity for some subsets of normal tissues (12).
The question, now: Are there any empirical studies that illuminate the potential mechanism of ROR1 in healthy, adult tissues? This is from a treatment toxicity standpoint, since the subsets of affected cells seem to be rather slim. I can understand why the effect on metastatic potential can be significant from the fetal neural cortex development (the need to migrate the neurons into position). We also see a truncated version of ROR1 in some instances. If anyone can shed some light, thank you in advance!
References

Cui B. et al. Targeting ROR1 inhibits epithelial-mesenchymal transition and metastasis.      Cancer. Res. 73, 3649–3660 (2012).
Hojjat-Farsangi, M., Ghaemimanesh, F., Daneshmanesh, A. H., Bayat, A. A., Mahmoudian, J., Jeddi-Tehrani, M., … Mellstedt, H. (2013). Inhibition of the Receptor Tyrosine Kinase ROR1 by Anti-ROR1 Monoclonal Antibodies and siRNA Induced Apoptosis of Melanoma Cells. PLoS ONE, 8. doi:10.1371/journal.pone.0061167
Daneshmanesh AH, Hojjat-Farsangi M, Sandin A, Khan AS, Moshfegh A, et al.. (2012) Monoclonal Antibody Against ROR1 In Chronic Lymphocytic Leukemia Cells Induced Apoptosis Via PI3-kinase/AKT/CREB pathway. 54th American Society of hematology (ASH), Atlanta, USA, 8–11 December.
T. Yamaguchi, K. Yanagisawa, R. Sugiyama, Y. Hosono, Y. Shimada, C. Arima, S. Kato, S. Tomida, M. Suzuki, H. Osada, T. Takahashi. NKX2-1/TITF1/TTF-1-induced ROR1 is required to sustain EGFR survival signaling in lung adenocarcinoma. Cancer Cell, 21 (2012), pp. 348–361
Fukuda T, Chen L, Endo T, Tang L, Lu D, Castro JE, Widhopf GF, II, Rassenti LZ, Cantwell MJ, Prussak CE, et al. Antisera induced by infusions of autologous Ad-CD154-leukemia B cells identify ROR1 as an oncofetal antigen and receptor for Wnt5a. Proc Natl Acad Sci USA. 2008;105:3047–3052. doi: 10.1073/pnas.0712148105.
Gentile A, Lazzari L, Benvenuti S, Trusolino L, Comoglio PM. Ror1 is a pseudokinase that is crucial for Met-driven tumorigenesis. Cancer Res 2011;71:3132–41.
Zhang S, Chen L, Cui B, Chuang HY, Yu J, Wang-Rodriguez J, et al. ROR1 is expressed in human breast cancer and associated with enhanced tumor-cell growth. PLoS ONE 2012;7:e31127.
Teicher BA, Fricker SP. CXCL12 (SDF-1)/CXCR4 pathway in cancer. Clin CancerRes. 2010;16(11):2927-31.
Nomi M, Oishi I, Kani S, Suzuki H, Matsuda T, Yoda A, et al. Loss of mRor1 enhances the heart and skeletal abnormalities in mRor2-deficient mice: redundant and pleiotropic functions of mRor1 and mRor2 receptor tyrosine kinases. Mol Cell Biol 2001;21:8329–35.
Endo M, Doi R, Nishita M, Minami Y. Ror family receptor tyrosine kinases regulate the maintenance of neural progenitor cells in the developing neocortex. J Cell Sci 2012;125:2017–29.
Reddy UR, Phatak S, Pleasure D. Human neural tissues express a truncated Ror1 receptor tyrosine kinase, lacking both extracellular and transmembrane domains. Oncogene 1996;13:1555–9.
Linked in text.

ROR1 knockout mice are unhealthy and die soon. ROR1 knockdown leads to shortened neurites but I guess this should not affect adults much. From this paper: … it is absent within most mature tissues. A low level of ROR1 expression is seen in adipose tissue and to a lesser degree in the pancreas, lung, and a subset of intermediate B cells

Examining the literature it'd seem that the ROR pathways incl. ROR1 and ROR2 are critical for developing tissues in the majority of cases. We also see relevance in the expression of ROR1/2, more specifically ROR2, in cases where taxic cell types are required to migrate, branch, etc. Most of the literature determines much of this occurs through a noncanonical Wnt signaling pathway.
Wnt5a–Ror–Dishevelled signaling constitutes a core developmental pathway that controls tissue morphogenesis
Ror2 Receptor Mediates Wnt11 Ligand Signaling and Affects Convergence and Extension Movements in Zebrafish
Ror2 regulates branching, differentiation, and actin-cytoskeletal dynamics within the mammary epithelium
Notwithstanding the abnormalities we see in neonates with knocked down ROR, is it wrong to assume we'd see developmental defects of branching tissues in developing (or juvenile) organisms such as lung, mammary, neural, glandular tissue, etc.? Some data in that respect would be interesting, but it's also illuminating given the presence of ROR in cancer metastasis and EMT events.

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text:
What Chemical Trigger Causes Ectomycorrhiza To Change From Asexual To Sexual?
I want to know the trigger behind the change of asexual to sexual ectomycorrhiza when symbiosis with a tree root is formed. As ectomycorrhiza attaches itself to a root, it forms a relationship wherein phosphorous to the tree/plant is exchanged for glucose to the fungus. When this symbiosis occurs, the fungus, which is normally asexual, becomes sexual(male/female components) and buds form as a result. Thus I could hypothesize that if glucose is the catalyst, I could saturate the soil and cause this reaction. However, I am not sure what the actual chemical signal is, or if there is an unforeseen factor causing this change. Does anyone have any knowledge on the subject of what the aforementioned catalyst would be?

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text:
What is a starter cell?
I am reading the paper Cooperative Subnetworks of Molecularly Similar
Interneurons in Mouse Neocortex and a term "starter cell" apears there (page 6):

This yielded tissue sections where SOM or
  VIP starter cells carry both nucleus-localized GFP and cytoplasmic mCherry

Does anyone know what a starter cell is?
(I couldn't find it on the web)

Nice question - this terminology isn't referring to a special type of cell or anything, but to a peculiarity of the technique they are using.
They are labeling a subset of cells with rabies virus; rabies then travels in retrograde fashion to presynaptic cells, and labels those as well.
The "starter cells" are those initially infected cells, where the tracing "starts." This reference more explicitly states this terminology, and talks about the technique extensively, I would strongly recommend it for helping to understand the paper you are reading.

I understand now.... I will also read the article you reffer to. Thank you for your clarification!


text:
Breeding Southern Right Whales Genetics
I don't know much about biology. I just like watching David Attenborough videos and this made me curious.
I just watched this video about breeding Southern Right Whales, and these two quotes puzzled me:
Quote 1 occurs at 1:54

"The males barge and jostle one another to reach her"

Quote 2 occurs at 3:51

"One coupling can flush out whatever preceded it, so it may not be the
  first male who succeeded in copulating who becomes a father it
  (will/would?) be the last."

Quote 1 suggests my first assumption.
Males compete to be the first to mate with a female
Quote 2 suggests that a male's chance of being a father is decreased each time a subsequent male copulates with the female. This leads me to my next assumption.
The last male to mate with the female has the best chance of being the father
Beyond what was said in the video, I just have a general assumption that the healthiest male (best genes) will mate first because he's faster, stronger, etc. So here is my third assumption.
The last male to mate is the male carrying the worst genes.
All together, this seems pretty bad for the species. I mean, if the worst genes are the ones most likely to get passed down, wouldn't that make the species evolve in a bad direction? So here is my conclusion.
The breeding habits of southern right whales are bad for the species.
Is this true? If so, does this occur in other species, and does it have a name? If not, where did I go wrong with my logic?
Thanks.

The keyword here is may in "it may not be the first". Most likely the first male will have the highest change. It is unlikely that all his semen is removed by the next and even if so, it might already be to late.


text:
How do I know which molecular structure is glycine's "base state"?
I was looking up the chemical structure of glycine, and I found the following two images:
and
.
My question is, what is the "base state", or the "natural state" of glycine? Under what scenarios does glycine become oxidized/reduced?
Also, I know that amino acids contain a carboxyl group, an amino group, a lone hydrogen atom, and a side chain. What is the formula for the amino group? Is it $\ce{-NH_2}$ or $\ce{-NH_3^+}$?

Both are correct, both are the natural state of glycine and both represent the base state. Amino acids are zwitterions, which switch freely between the two states. Try googling zwitterions.

So, they are just different ways of representing the same thing? Is there a "more correct" diagram?

edited my first comment, try searching for zwitterions.

If you want to be really specific the forms exist in equilibriums, but may be affected by pH. if the ph I very low, glycine is positively charged, neutrally charged around average pK value for the amine and carboxylic acid groups, while negatively charged at high pH.

Wait, so the amino group can be represented as either NH2 or NH3+?

Correct, both are entirely correct. However at physiological pH (6-8), typically the zwitterform with charges are used.

For the sake of completeness: the second molecule should have a negative charge at the -COO group

I really think this should be closed. The poster does not define his question properly — there is no such thing as base state — cannot copy the correct structure of the zwitterion form, and is ultimately asking the most basic of questions the answer to which can be found in any text or web resource. In addition it is ultimately chemistry rather than biology.

Please note that these are acid/base reactions and not oxidation/reduction reactions. If glycine is oxided or reduced its not glycine anymore.

Short Answer: You need to define base state.
Background: The point to keep in mind here is that the base state (as you call it) is not constant. As @jeppenielsen points out in the comments, amino acids are zwitterions. According to Wikipedia:

In chemistry, a zwitterion, formerly called a dipolar ion, is a neutral molecule with both positive and negative electrical charges. (In some cases multiple positive and negative charges may be present.) Zwitterions are sometimes called inner salts. Unlike simple amphoteric compounds that may only form either a cationic or anionic species, a zwitterion simultaneously has both ionic states.

In glycine, the center of positive charge is the -NH2 group while the center of negative charge is the -COOH group. At different pH (acidic, neutral or basic), the structure of the molecule keeps on changing as shown in the image below:
source
Structure of other amino acids also changes similarly. To know why this change occurs, just keep in mind that (in very simple terms) pH is inversely proportional to the concentration of H+ ions in a solution (higher the pH, lower the concentration of H+). The exact formula is $\ce{pH = - log[H_3O^+]}$ (yes, it means that a pH of 4 is 10 times more acidic than pH 5 and so on). Also, as pH changes, so does the formula for the amino group (see the diagram again).

That was a simplification, thats why I also put the formula with it. But I'll change it if it seems incorrect :) seems better now?

or say pH=-log(H+) and do it correctly. ah I see it was added alredy.

@jeppenielsen thanks! There is a post on chemistry.SE (whose link I am unable to find right now) which discusses about why it is better to write $\ce{H_3O^+}$ instead of $\ce{H^+}$ :)

H3O+ only works if you use water as solvent... you could use ammonia as a solvent and H+ would still work. Or you could be in a nonpolar solvent. H+ only fails in heavy water, but then we should be writing pD instead anyways

@jeppenielsen since we're talking about it in biological perspective, we can assume water to be the solvent ;)

Not in the lipid bilayer of the cellmembranes.

@jeppenielsen Do you expect free (polar/charged) glycine to be found in the (hydrophobic) cell membrane? I don't...

Only in extremely low concentration.  But using pH=-log([H3O+]) instead of [H+] is silly especially since we have general notaion for all solvents. Also [H+] is significantly different than [H3O+] in some cases.

Thats why I was talking about that chemistry.SE post. It clearly talks about why we use H3O+ instead of H+. In short, H+ is too unstable to exist and readily reacts with any nearby molecule. Mostly it forms H3O+, but it can also form H5O2+, H7O3+ and even H9O4+. So, once you know what is actually happening at the concerned scale, writing H+ becomes a lot more silly.


text:
Bonding in the primary structure of a protein
My textbook says:

The amino group of an amino acid reacts with the carbonyl group of another amino acid at the end of a polypeptide chain. This condensation reaction forms a peptide bond. ... The precise sequence of amino acids in a polypeptide chain is the primary structure of the protein.

Later, it states that

The primary structure of a protein is established by covalent bonds ...

Is the primary structure of a protein governed by covalent bonds or peptide bonds? Are peptide bonds a type of covalent bond?
Any help is greatly appreciated.

Peptide bonds (also called amide bonds) are definitely covalent bonds.
This is also mentioned in the first line of wikipedia entry: https://en.wikipedia.org/wiki/Peptide_bond

Yes. Lots of words for the same thing.
Covalent bonds are any bonds where electrons are shared. Polyamide bonds, peptide bond etc.


text:
Mechanism by which water flows through xylem
I was doing a Cambridge iGCSE past paper when I came across the question:

Describe the mechanism by which water flows through the xylem

I thought the correct answer would revolve around the xylem being composed of dead cells, thus allowing water to use capillary action to flow upwards, but it wasn't.
Instead, the mark scheme referred only to transpiration causing tension and so forth, not even mentioning capillary action.
Is capillary action not a valid answer? And if not, why not?
Thanks

See http://www.sparknotes.com/biology/plants/essentialprocesses/section1.rhtml capillary action is just a part of the valid answer.

-
NO,for capillary action 2 things are of importance 1) the radius of capillary tube[R] ,2)the tension force between molecules at surface of liquid [T] (for water=72.8 dynes/cm= 728 X 10^-6 N)
-
height to which the fluid will rise due to cap.effect, H=(2T cosα)÷(ρgR)
-
[ρ=density of liq,here water =1000kg/m³]
-
numer.=constant(for given liq) denomin.=variable R
-
so if capillary was in effect for trees 100s of meters tall the deno. wud have to be small while the ρg is a fixed value here for water = 10000 units the R wud have to be impossibly small

WHAT HAPPENS IS the transpiration of water droplets from the stomata causes a suction as no air can enter to fill in for the water lost the water as to rise up taking more of it from the soil

Could you add sources to your used formulae and reasoning?


text:
Why are humans mostly right-handed?
Most sources I've seen say that about 90% of humans are right handed, and 10% are left handed. Why is this?
My only guess would be that it has something to do with different parts of the brain developing differently and causing right or left "handedness", but this is coming from my very little knowledge of the brain.
Furthermore, about 2/3 of people are right eye dominant, and more people are right ear dominant than left ear dominant.
Why the right side?!?


text:
Why don't we keep evolving until we are super-human?
Humans (homo sapiens) have been on the earth for thousands of generations, and we have kept evolving throughout that time. Why don't we just keep evolving so that, let's say, we live for an average of 300 years? Or why don't we evolve so that we don't need to sleep?
This could also apply to many other species.

This question also has an element of "why isn't evolution all-powerful?". The Understanding Evolution project at UC Berkeley addresses this nicely.

Welcome to Biology.SE!
There are a many misunderstanding of what evolutionary processes are in your post and it is therefore quite hard to answer (hence the current two close votes I guess). You might want to read some introductory textbook on evolutionary biology or other online resources such as the "understanding evolution" project.
The most obvious misunderstanding is that evolution is NOT some kind of forever "improvement" process in a static environment. Evolution is something else! But I can't make a good overview of evolutionary processes in just one post.

[why don't we live on] average of 300 years?

You may want to read about this post concerning the evolution of aging but it would probably be slightly too advanced but you would probably still get something out of the answers.

Why don't we just keep evolving [..]?

Humans, definitely keep evolving. Nothing have stopped. We evolved as we have always and it won't stop until we get extinct! This post may for example help you to understand that evolution keep occurring today in humans.
When you say Humans (homo sapiens) have been on the earth for thousands of generations it sounds a bit like human have came to existence some time ago and have evolved since. It is a terribly misleading point of view, one of the reason is that one cannot date the existence of the first humans without making a very arbitrary decision about what a human is. A more correct way of looking at life on earth is that everything have come to existence about 3.5 billions years ago and everything have kept evolving since. Any single living thing on earth have been evolving for the exact same amount of time. Humans have evolved for 3.5 billions (even if we don't call earlier forms as humans) and unicellular algea have evolved for 3.5 billions years (even if we don't call earlier forms as algea).
Hope that helped!

Natural selection selects for individuals who can leave the most progeny in the next generation. Traits such as longer lifespan do not typically affect fecundity/fertility. So males and females who have the largest families as quickly as possible are providing the raw material for natural selection.

"So males and females who have the largest families as quickly as possible are providing the raw material for natural selection" is a bit misleading. The raw material for natural selection to occur is genetic variance. The males and females having the greatest number of offspring are those contributing the most to the future generations would be more correct. "Traits such as longer lifespan do not typically affect fecundity/fertility" is a bit wrong. Typically traits such as longer lifespan affect fecundity.

For a better understanding of the evolution of aging, have a look at this post

Thank you for correcting these inaccuracies. While I am familiar with classical arguments regarding post-reproductive fitness, for example in social species who may teach their progeny things that aren't hard-wired, I was not aware that post-reproductive life-span was positively correlated with brood-size. Hmmm, maybe I am not using fecund correctly.


text:
Does evolution go only in one direction?
In this video Richard Dawkins talk about intermediate fossils. He describes how the whales were evolved from a common ancestor who lived on land.
But his theory sounds more like a devolution. I thought evolution was coming from the sea to the land and then to the skies. Are there more examples where species evolve back and forth between the ocean and land or skies?

Does evolution go only in one direction?

No, it does not. There is no such thing as a goal of evolution at making things fly or at making things intelligent or whatever. There is no intrinsic directionality.
In short the reasons are 1) Evolution is much more than just natural selection 2) natural selection does not systematically select for a specific trait. Some traits are advantageous under some ocnditions, some other traits are advantageous under other conditions.
I won't talk more about the mechanisms of evolution here as it would take a whole book. Instead I will recommend a source of information for you to further your knowledge.
Source of information
As your question is very introductory and shows misunderstanding, you might want to have a look at an intro course to evolutionary biology such as for example Evo101 by UC Berkeley.
Devolution
Note that this term is rarely used in the scientific literature (actually I think I have never encountered it in the scientific literature). From wikipedia:

In modern biology the term [devolution] is meaningless: evolutionary science deals with selection or adaptation that results in populations of organisms genetically different from their ancestral forms, where evolution has no intrinsic directionality. The discipline makes no general distinction between changes leading to populations of forms less complex or more complex than their ancestors, and in such terms the concept of a primitive species cannot be defined.

The question is a bit unclear
There is a slight issue with the question as it is not that easy to categorize all animals as living strictly in the water, on land or in the sky. Note that almost no living things live strictly in the sky without ever touching the ground. Here are a few examples of limit cases

oysters
dragonflies (larvea live in the water, adult fly)
flying squirrels
Most ducks (spend much time on water but nest on land)

As a consequence the question is very undefined
Examples of potential interest to you
The question is undefined but here are a few examples of cases anyway that will interest you. For simplicity, I will reduce my list to animals only and will not consider similar cases in procaryotes, and non-animal eukaryotes such as plants and fungi.
Whose ancestors were terrestrial

Cetacea (blue whale, orca, dolphins, ...)
Sirenia (dugong and manatees)
Pinnipeds (sea lions, sea leopards, ...)
Monotremes
Marine iguana (and other swimming lizards)
Beavers
Otters

Whose ancestors were flying

Penguins
ratites (Ostrich, emu, kiwi, ...)
dodo
Many birds are able to stay for relatively long period under water when hunting for fish.
Ants and other non-flying hymenopterans.
Ground beetles and other non-flying beetles
water beetle

Again, categorization is not that easy. I just want to highlight the water beetle as example where the ancestor was marine, then terrestrial, then flying, then non-flying and finally living in the water again.
Related post
How many times did terrestrial life emerge from the ocean?

It is still hard for me to believe if I start swimming in the water and all my offspring also they will eventually start growing fins. Down the road, someone will develop something like it. How will that get introduced into their DNA? Shouldn't we be able to see in DNA if changes like evolution are possible in DNA? Mutations do not follow the outside pressures or need but they are just errors in the system.

@Grasper: DNA isn't really as straightforward as you seem to think.  There's not a simple mutation for "fins" vs "feet", but different genes being expressed differently.  Consider phocomelia, a condition where factors like pre-natal exposure to a drug produces flipper-like arms & legs: https://en.wikipedia.org/wiki/Phocomelia  Then any mutations are selected for or against from a population of millions over thousands of generations.

@Grasper You are right to have a hard time to think that your direct offspring will all of sudden and out of the blue grow fins if you swim a lot. But this is not what the evolutionary theory is claiming. I won't give you a whole intro course to evolutionary biology because it takes a lot of time and many other people have already done so.

@Grasper Please just have a look at an intro course to evolutionary biology and you'll understand a little bit of what evolution is about. As recommended above, you might want to have a look at Evo101, a very short and very introductory course to evolution.

Adaption gradually leads to permanent changes...which is evolution. The most favourable,adapted character passes on to the next generation and it leads to evolution. Adaptation and evolution are mutually inclusive events.

You do not seem to fully understand the definitions of evolution and adaptation. In the future, you might want to answer question in the fields in which you have at least some intro knowledge

Is there any reasons for posting two independent answers rather than just expanding on a previous answer? Note that you can use the "edit" button to edit an existing answer.

Oh. Can you help me with that if possible? I'll be really happy to gain some knowledge

@Remi.b  I'm new to stack exchange! Thanks man!

No worries. I'll be happy to take some time to answer a post you may want to open. Asking a clearly defined question can be challenging (and it is not uncommon for new users to see their post getting closed), so it may be good to start with an intro course and build from there. As recommended to Grasper, you may want to have a look at Evo 101. Welcome to Biology.SE (and other SE websites) and Good luck!

Evolution helps an organism to be successful in the environment in which it lives. In this case, the organism evolved to suit it's aquatic environment. So there's nothing called devolution. For example, the cave  proteus is blind while it's ancestors weren't. It does not mean that it has devolved. It doesn't require well developed eyes in a dark cave. So it has evolved to suit it's environment. Same case here.

Isn't that called adaptation?

Welcome to Biology.SE! Please add some more details and references in your answer.


text:
What techniques can be used to link environmental conditions to crop yield?
Im interested in how we can determine what are the optimal conditions for crops and how deviations from these optimal conditions affect yield. In the literature I have found two main approaches and I was interested if there were more ways that are used or if anyone can think of a more creative way to test the link.
Approach One
Use a greenhouse experiment to isolate all variables bar one and vary it. Measure the change in yield based on that variable.
But this approach is time consuming and it is difficult to include interactions.
Approach Two
Use a model that relies on some base knowledge of that plant - i.e. the base temperature at which growth is zero, and a rough idea of optimal ranges. But requires this base knowledge already.
Potential Approach Three
Use multiple linear regression in combination with field data to create a linear or polynomial model of each variables effect on yield. Interactions can be included easily. But relationships are unlikely to be linear and without prior knowledge it is hard to decide on non-linear models.
Can anyone think of other ways that could be used to test these links?


text:
Cholesterol and fatty acids role in bile?
The composition of gallbladder bile is 97% water, 0.7% bile salts, 0.2% bilirubin, 0.51% fats (cholesterol, fatty acids and lecithin)1. Bile's role is mainly help for digestion of lipids via bile salts and acids (emulsification) but i dont understand what is cholesterol and fatty acid role in bile. What is cholesterol and fatty acid's function in bile?

What research have you done before asking it here?

First i was studying to biochemistry of lipids generally at Lehninger and i read an information about bile. It says that bile has cholesterol and fatty acids. After i thought there is a mistake and looked to wikipedia (i editted the link) and the same information is writing at wikipedia and i asked here.

extra cholesterol is excreted by the body through bibles and fatty acids are needed to maintain this cholesterol in soluble form otherwise it leads to gall stones.

@JM97 your thought makes sense thank you. Can you find a resource including this information ?

@AhmetÖz see this https://goo.gl/tnE9go.  typo * bile

The main function of bile is to emulsify large fat molecules into small fat droplets. You must have heard about micelle formation by soaps. Well, bile acids perform quite similar function. Bile acids, having both hydrophobic and hydrophilic parts, form micelles and trap fat molecules and form emulsion, hence naming the process emulsification. Similar function might be performed by fatty acids. See this article:

Bile acts to some extent as a surfactant, helping to emulsify the lipids in food. Bile salt anions are hydrophilic on one side and hydrophobic on the other side; consequently, they tend to aggregate around droplets of lipids (triglycerides and phospholipids) to form micelles, with the hydrophobic sides towards the fat and hydrophilic sides facing outwards. The hydrophilic sides are negatively charged, and this charge prevents fat droplets coated with bile from re-aggregating into larger fat particles.

Now lets have a look on bile acids. The principal bile acids are cholic acid, chenodeoxycholic acid, glycocholic acid, taurocholic acid, deoxycholic acid and lithocholic acid, all of which are synthesized from cholesterol (see this). Now this partly explains why a small amount of cholesterol is released along with its derivatives; it might be the 'unprocessed' cholesterol which 'leaked out' from liver. But, in fact, it seems to do a bit more. Actually, cholesterol secretion into bile needs to be carefully controlled; too less secretion may lead to accumulation of cholesterol in blood vessels, leading to cardiovascular diseases (this is why cholesterol secretion is the final stage of elimination of cholesterol from reverse cholesterol transport), while too much secretion into bile may cause gallstones (see this). Hence, cholesterol secretion into bile also serves as a way to maintain cholesterol homeostasis (see this). In fact, bile acids serve as hormones in cholesterol homeostasis in the body. Similar reason may cause fatty acid elimination through bile.
Cholesterol and fats are hydrophobic, so they cannot be released as it is into GI tract. This is why they are released with bile. Bile acids are amphiphatic i.e. have both hydrophilic and hydrophobic parts. Hydrophilic part helps it in dissolving in chyme (containing HCl) while hyrdrophobic part helps it in dissolving fats and cholesterol (and lipids of course) into itself.
source


text:
A suggested ancestor of cyanobacteria consumed manganese. Why not magnesium?
Joseph Kirchvink and others have suggested a theory that a precursor to cyanobacteria consumed manganese (I believe in the form of Mn2+ dissolved in water). Why wouldn't dissolved Mg2+ work equally as well? It was more abundant and is the central ion of the porphyrin ring in chlorophyll.

There is no conclusive proof of why those organisms chose Mn over Mg (for obvious reasons). I'll just give an opinion on how Mn could be beneficial over Mg.
Even in the photosynthetic organisms present today, $Mn^{2+}$ is the ion used for oxidation of water while $Mg^{2+}$ is used to just get electrons by input of photons (from Kirschvink, 2015, if you're talking about this). When electron is removed from $Mg^{2+}$ (from 3s orbital), the formed $Mg^{3+}$ quickly oxidizes $Mn$ in the oxygen evolving complex (see this answer for more details). This suggests that $Mg^{3+}$ is much more unstable than $Mn^{3+}$, maybe too unstable for enzymes to use it to catalytically oxidize water.
Another point could be energy requirement. The third ionization enthalpy of magnesium ($ Mg^{2+} \rightarrow Mg^{3+} + e^-$) is 7732.7 kJ/mol. On the other hand, the third ionization enthalpy of manganese ($Mn^{2+} \rightarrow Mn^{3+} + e^-$) is only 3248 kJ/mol (which is still higher than other elements nearby it in periodic table, but thats another point). Now, though this energy is available today via sunlight for magnesium, it was most probably too large an energy input (keeping in mind the environmental conditions, like low sunlight due to excess sulfur dioxide in atmosphere, Kirschvink, 2015). Thus, manganese may have proved to be more beneficial than magnesium. As time passed, slowly there would have been enough energy available to oxidize magnesium, so it (sort of) took over manganese in the race.
Again, this is just a speculation. The real reason can remain elusive for a long time (until very strong, conclusive evidences are found).


text:
How long could Earth's oxygen supply last if no new oxygen were produced?
I read in an article or heard in some documentary that there's so much oxygen in the atmosphere that even if all photosynthesis stopped, there's already enough to last us a long time.
Is this correct? Why or why not? If so, how long is this 'long time', roughly? I've seen estimates between 15,000 to 150,000 years.

Interesting question (although it may be off-topic as there is not a clear specific answer). Where have you seen those estimates?

@James this isn't Skeptic Stack Exchange, supplying sources for my claims doesnt matter, the question is simple and clear. Everyone else was able to conprehend it just fine.

This isn't skeptics SE, but I am a skeptic. I wanted that reference specifically because it might have provided some objective insight or approach (personally I think the below answers so far are very subjective to what one considers "reasonable estimates"). More generally though, you should support your claims appropriately, not only in your answers but your questions too. Else we end up in this situation.

Disclaimer:
This is going to be a very mathematical answer. Before answering it, I assume that you are only asking about humans, assuming that all other organisms don't require $O_2$ to survive (as it will complicate the answer many many times).
List of variables:
V     = total volume of air on earth (in l)
V'    = total volume of oxygen on earth (in l)
V(1)  = volume of oxygen used by 1 person in whole lifetime (in l)
V(a)  = volume of oxygen used by whole mankind (one generation) in whole lifetime (in l)
V(p)  = percentage of total oxygen used by whole mankind (one generation) in whole lifetime

Method used:
$ \%\hspace{1mm}Volume\hspace{1mm}of\hspace{1mm}O_2\hspace{1mm}used\hspace{1mm}per\hspace{1mm}generation = \underline{\hspace{3mm}Volume\hspace{5mm}of\hspace{5mm}O_2\hspace{5mm}in\hspace{5mm}air\hspace{3mm}}\times\hspace{1mm}100$
$\hspace{83mm}Volume\hspace{1mm}of\hspace{1mm}O_2\hspace{1mm}used\hspace{1mm}by\hspace{1mm}humans$
$Number\hspace{1mm}of\hspace{1mm}years = \underline{\hspace{2mm}Number\hspace{1mm}of\hspace{1mm}years\hspace{1mm}in\hspace{1mm}1\hspace{1mm}generation\hspace{2mm}}$
$\hspace{42mm}\%\hspace{1mm}Volume\hspace{1mm}of\hspace{1mm}O_2\hspace{1mm}used\hspace{1mm}per\hspace{1mm}generation$
Procedure:
Lets first find out the total amount of air on earth.
From this:

The air sphere measures 1999 kilometres across and weighs 5140 trillion tonnes.

From here:

At sea level and at 15 °C air has a density of approximately 1.225 kg/m3

Total volume of air:
$volume = mass \hspace{1mm} / \hspace{1mm} density$
$V = 5140 \times 10^{12} \hspace{1mm} tonnes \hspace{1mm} / \hspace{1mm} 1.225 \hspace{1mm} kg.m^{-3}$
$V = 4195.9 \times 10^3 \times 10^{12} \hspace{1mm} m^3$
$V = 4195.9 \times 10^3 \times 10^{12} \times 10^3 \hspace{1mm} l$
$V = 4195.9 \times 10^{18} \hspace{1mm} l$
Now, from this, 20.95% of this is $O_2$ i.e.
$V' = 4195.9 \times 10^{18} \times 20.95 / 100$
$V' = 87904.489 \times 10^{16}$
$V' = 879.04 \times 10^{18} \hspace{1mm} l$
Moving on to next part, from this:

a human being uses about 550 liters of pure oxygen per day.

From this:

71 years was the average life expectancy at birth of the global population in 2013.

$V_1 = 550 \hspace{1mm} l.day^{-1}.person^{-1} \times 25915 \hspace{1mm} days$
$V_1= 142.53 \times 10^5 \hspace{1mm} l.person^{-1}$
From this:

The world population (the total number of living humans on Earth) was 7.349 billion as of July 1, 2015.

So
$V_{a} = 142.53 \times 10^5 \hspace{1mm} l.person^{-1} \times 7.349 \times 10^9 people$
$V_{a} = 1047.452 \times 10^{14} \hspace{1mm} l$
Finally
$V_p = V_a / V' \times 100$
$V_p = (1047.452 \times 10^{14}) / (879.04 \times 10^{18}) \times 100$
$V_p = 1.191 \times 10^{-2}$
$V_p = 0.0191 \hspace{1mm} \% $
This gives the percentage of total $O_2$ in air used by one human generation. From this, we can find the number of years for which $O_2$ will last, as I have done below:
$25,915 \hspace{1mm} days = 71 \hspace{1mm} years$
$71 \hspace{1mm} years = 0.0191 \hspace{1mm} \%$
$1 \hspace{1mm} \% = 71 / 0.0191 \hspace{1mm} years$
$100 \hspace{1mm} \% = 3717.277 \times 100 \hspace{1mm} years$
$\hspace{13mm} = 371,727.748 \hspace{1mm} years$
Conclusion:
So, yes at least humans can live for a very long time without plants doing any photosynthesis (ideally). 371,727 years seems too large a period of time, but it is just based on ideal assumptions, this number would come down (maybe into your specified range) when more variables are added.
For example:
To show extent of deviation by addition of factors, I add a very general, but complex factor in the expression: air pollution.
How much $CO_2$ is released per year can be estimated from this:

In 2011, utility coal plants in the United States emitted a total of 1.7 billion tons of CO2

And with the contribution of countries like China, India, Europe, etc. that number should rise up to at least 2.5 million tonnes (its just that I couldn't find the worldwide data on it).
Now:
$1 \hspace{1mm} C + 1 \hspace{1mm} O_2 \rightarrow 1 \hspace{1mm} CO_2$
$2.5 \times 10^9 \hspace{1mm} kg \hspace{1mm} CO_2 \Rightarrow 2.5 \times 10^9 \hspace{1mm} kg \hspace{1mm} O_2$
So, 2.5 million tonnes more $O_2$ is being used each year from the environment. But, there is another twist in this. From this:

WHO reports that in 2012 around 7 million people died - one in eight of total global deaths – as a result of air pollution exposure.

It means that 7 million people less will consume $O_2$ each year i.e.
$Net \hspace{1mm} population = 7349 \times 10^6 - 7 \times 10^6$
$\hspace{32mm} = 7.342 \times 10^9$
$V_{a} = 142.53 \times 10^5 \times 7.342 \times 10^9$
$V_{a} = 1046.455 \times 10^{14} \hspace{1mm} l$
$V_p = V_a / V' \times 100$
$V_p = (1046.455 \times 10^{14}) / (879.04 \times 10^{18}) \times 100$
$V_p = 1.1904 \times 10^{-2}$
$V_p = 0.01904 \hspace{1mm} \% $
$25,915 \hspace{1mm} days = 71 \hspace{1mm} years$
$71 \hspace{1mm} years = 0.01904 \hspace{1mm} \%$
$1 \hspace{1mm} \% = 71 / 0.01904 \hspace{1mm} years$
$100 \hspace{1mm} \% = 3728.991 \times 100 \hspace{1mm} years$
$\hspace{13mm} = 372,899.159 \hspace{1mm} years$
So, overall number increases instead of decreasing. This example was just to show how adding more factors to the equation would deviate the overall answer, and how large that deviation can be.

an average of 30'000 days = 82 years, is way too high to be seen as an accurate estimation. According the the WHO it is more around 71 years/ or 25'915 days

@JordiZambrino it was just an assumption that I heard about in a TV show. Its just that I couldn't find an appropriate reference for this, but thanks for telling that :)

Average age is just a guess. We can change it and won't change answer much. Main thing is to include stochastic factors - especially pollution and I would like to know how much it will skew the answers

@TalhaIrfan as I said in the answer, adding such factors would complicate the situation to a large extent, but I don't think that polluting gases would have any effect on the amount of O2 in the environment, yeah but burning of fuels would surely do. Anyways, I'll try to add it in the answer :)

@TalhaIrfan I hope this helps. I wouldn't be shocked to see you shocked with the answer because I am already shocked by the answer, I mean just see how shocking is that ;)

My first response was: I don't want to live on this planet anymore ;) Man!! What a research and effort you put behind this answer. I am shocked this answer hasn't got the upvotes yet it deserved. One of the best answers I saw on this website in these 2 years. Awesome!

10/10 for effort. Am I right in pointing out that two critical assumptions undermine the estimate? 1.everything else stops besides humans, 2.the population stays the same.

@James yes you are correct. I am not good in calculus, so I solved it by using these assumptions and as I said in answer, such variables would deviate the answer to a large extent (I don't even know if it can be solved using calculus also). Did you give the downvote BTW?

@another'Homosapien' It was my vote :( (but you shouldn't really ask specifically as it probably isn't the person that comments). I think that whilst you do make a real effort to point out the deviation, there are too many unreasonable assumptions for the answer to be useful. The most valuable part of the answer is "Who knows?" not "372,899.159 years". Note I voted to close the question because it inevitably demands answers that make a lot of assumptions that are subjectively "reasonable".

@James thanks for pointing it out, I just wanted to give OP an idea about large or small this value can get, how hard it might get to find exact value, and how OP can calculate a much more accurate value by themselves (in vacations ;)

The answer above gives a nice calculation how much oxygen there is, and how much we use. There are some BIG other factors that warrant a second answer IMO.
Starting at 371 thousand years (above).

Animals: according to http://xkcd.com/1338/ (probably sourced somewhere reliable) humans make up only ~20% of the walking biomass, so we would burn through the oxygen supply 5 times faster.
Fuels: my guess for an average fuel consumption would be around 5 metric tons per annum (http://data.worldbank.org/indicator/EN.ATM.CO2E.PC/countries, 17 metric tons of CO2 per annum for the USA, 1,7 for India). To get 5 tons of CO2 we need 3,6 tons of O2. From the above calculation I calculate that we use 245 kg per year of O2, so for our fuel we need 15 times more oxygen than for breathing.

That leaves us with around 5000 years to live. However, from http://www.engineeringtoolbox.com/co2-comfort-level-d_1024.html I guesstimate that above something like 1-5% CO2 is not survivable on the long term, leaving us with only 250-1250 years to leave before we slowly suffocate.
Of course we would die long before that from starvation.

You can't go on burning fuels when the oxygen content of the air drops below a certain percentage. I haven't got a reference for that, but I would guess that around 15%, rather than 20%, oxygen concentration, it would be pretty hard to ignite hydrocarbons.

Didn't think of that (but it's the same with breathing of course). With methane you'd need only 12% oxygen: https://en.wikipedia.org/wiki/Limiting_oxygen_concentration


text:
Why does getting soap in your eyes cause redness and irritation?
I am wondering why do eyes become red after getting soap in them. What is the cause behind it?

This is because of the soaps chemical nature. They are alkaline agents and human eyes have a very low tolerance for alkalinity. Human eyes are roughly neutral with a pH of around 7, and soaps are around 7.5 to 9.
The eye can't handle the alkaline object as it is potentially harmful to the eye so it will start watering to get rid of the alien substance. Blood vessels then enlarge, coming closer to the surface of the eye, making them appear red.
Most soaps are tested before released to make sure if they come into contact with eyes they are non-toxic. Baby soaps have a lower pH as well to make sure that the baby doesn't come to harm.
Either way, its probably best not to put it in your eyes.
See here for more information.

Seriously, the page you link looks (in general) as realiable as yahoo answers.

@TomášZato looks can be deceiving

This does not answer the question. Yes, soap/shampoo has different pH values from the standard eye environment, but that is not a really surprising answer. Why do different pH values cause redness? If we could make a "soap" that contains almost the same ingredients as actual soap but has its pH fixed to 7 still cause red eyes? Will any other substance that is wildly different from water but has ph=7 also cause red eyes? What is the function of the redness (if it has any except to tell us that we rather not put that stuff into our eyes). Etc.

@AnoE I don't think its a function, more a reaction

Yeah... take my longer comment up there as an incentive to enlarge the answer to the (rather interesting) question. But if it is just a nonfunctional, arbitrary reaction, it would be at least nice to see details about the actual way it comes to pass (i.e., why does the eye get red, why does it not just start watering profusely to dilute the substance down to usual pH values).

@AnoE if I understand right, the red is simply blood vessels having grown larger and come closer to the surface, which is why we can see the red colour.

Anecdotally, "tear free" shampoo still hurts my eyes.

Basically, the eye would react to anything that is not similar (w.r.t osmolarity and pH) to the solution that covers it. Eye will react to neutral substances too. Tap water (without chlorine or other such chemicals) would also hurt in the beginning.

So how do red eyes help to get rid of that pH change?

When soap gets into the eye, Our immune system reacts to the foreign substance, it releases a chemical known as histamine as a part of the inflammatory response.
Now as result of this, blood vessels in the eyes become enlarged, dilated or swollen.
It leads to redness in eyes.

Source

XXX has chemicals is not a way to start an answer on scientific page.

Why so much downvotes, Any reason.

What is the mistake in the answer. Is it scientifically incorrect ?

This is a scientific page. You're free to chose whatever formulation you like for an answer, but you should also include references.

@Tensor_Product, the downvotes are likely because you do not answer the question. You are more or less reformulating the question with a few more words.

Do you have a source that histamine is released in response to irritants, rather than allergens?


text:
Purpose of the conversion of 3-PGA to G3P in the calvin cycle?
3-PGA ($\ce{C_6H_7O_7P}$) is converted to G3P ($\ce{C_6H_7O_6P}$) before it is able to be made into glucose, with an expansion of 6 ATP and 6 NADPH. My question is why this process is needed and why the loss of 1 oxygen atom decides whether a sugar molecule can be synthesized into glucose. My take on this matter is that if they incorporate 3-PGA directly into glucose, they can save time and also energy in the form of ATP and NADPH.

Obviously not a complete answer, but I wonder if it's partially because NADP+ is needed to absorb the electrons and protons at the end of the ETC at PS-I to avoid a surplus of NADPH and H+, resulting in a dangerously acidic environment.  Good question, btw.

@rotaredom — Please observe the text that appears in the comment box: "Use comments to ask for more information or suggest improvements Avoid answering questions in comments." Comments are not for answers, complete or incomplete.

Please refer to chemical compounds by their names as well as their abbreviations for clarity and indexing. 2. This is a question of chemistry which is covered in any biochemistry text. Your naive remark about "saving time and energy" and your emphasis on irrelevant chemical compositions suggests that you should consult such a text before posting. I suggest Berg et al. online Chapter 20. This wouldn't be a homework question by any chance?

Although I liked answering this question, it did not take me more than 5 minutes to gather all the required stuff for this answer. From next time, @user35897, please show some research effort before asking a question. As of now, I am voting to close this question.

Nice question! To see what trouble that extra oxygen can cause, lets get to the core of the reaction i.e. Calvin-Benson cycle; one step at a time. To start with, have a look at the detailed Calvin-Benson cycle (following image taken from here):

As becomes quite clear from this image, the actual use of Glyceraldehyde-3-phosphate is at the step of formation of Fructose-1,6-bisphosphate. Yet, we don't know why we cannot use 3-Phosphoglycerate instead at this step. For that, lets go a step further and see how the concerned enzyme, fructose-1,6-bisphosphate aldolase/phosphatase (aka aldolase), works.
Since the full article is behind a paywall, lets get a sneak peak into it. See this image1:

Pay attention to the steps where G3P enters i.e. steps between b and c. Even without entering into details of the mechanism, we get two factors which can prevent 3PGA from being utilized in this reaction:

Steric Hindrance: replace the terminal -H with -OH of G3P in the first image in your mind. You can clearly see that this would cause some steric hindrance and prevent formation of covalent bond between DHAP and G3P.
Formation of Geminal Diol: again, replace the terminal -H with -OH, but this time in the second image, in your mind. You get geminal diol in the resultant molecule, which is famous for its reactivity and instability. Thus, by adding 3-PGA instead of G3P in the reaction, we might end up with unstable molecules that cleave themselves up. I hope this is what you were looking for.

Reference: Juan Du, Rafael F. Say, Wei Lü, Georg Fuchs, Oliver Einsle Active-site remodelling in the bifunctional fructose-1,6-bisphosphate aldolase/phosphatase Nature 478, pages 534–537 (27 October 2011)
doi:10.1038/nature10458

Hi sorry I missed your answer. So just to clarify, the reasons are 1)NADP+ is needed to absorb the electrons and protons at the end of the photosystem 1 electron transport chain,  or else it would result in an acidic environment in the chloroplast.
2)It will prevent covalent bonding between the DHAP and G3P, causing steric hindrance.
3)An unstable molecule (Geminal Diol) would be formed, which will cleave itself much like the intermediate 6-carbon molecule which was formed after carbon fixation.

are there any more reasons or holes in the above summary?

The first point seems to come from @xusr's answer, so I cant be so sure about it. The other two points seem just fine though (sorry for being late, I really cant get time to access this site)

Thanks for the help! Much appreciated. I tried researching on this myself actually but I couldn't find anything useful

Anytime, mate! Thats what we're here for ;)


text:
What does it mean to "write an image and GIF into the DNA of bacteria"?
BBC News recently published an article saying that:

An image and short film has been encoded in DNA, using the units of inheritance as a medium for storing information ...
  The team sequenced the bacterial DNA to retrieve the gif and the image, verifying that the microbes had indeed incorporated the data as intended.

The news article shows an image of a hand (shown above) and a short film (not shown here) of a horse rider that was encoded into the DNA "using a genome editing tool known as Crispr [sic]".
My question is, what does this mean? Did the scientists break down an image into 0's and 1's and (install?) it into bacteria?  How does a scientist (download?) an image into bacteria and then (redownload?) the image later?  How does DNA hold information of a picture that can be (downloaded)?

I'm just going to migrate this to [biology.se], I believe you'll get a better answer there. By the way - the BBC article links to the Nature journal article in which this work was published. That's the first place you should start trying to read from (although I wouldn't blame you if you didn't understand it).

It's refreshing to see the actual CRISPR part of the CRISPR-Cas system being used.

"Did the scientists break down an image into 0's and 1's" Digital images are already 0s and 1s. No need to "break down" anything.

Just an off-topic note: Stating a "short movie of a riding horse" I think its probably the first movie made in history "Race Horse" which actually was just were several stringed pictures. https://movies.stackexchange.com/a/42182/20039

Just to add what might have been missing in the beautiful answer by @iayork. I just want to give a more simple picture of the encoding done in the E. coli DNA.

First for the rigid strategy in which 4 pixel colors were each specified by a different base, suppose we have a sequence:
AAGCCCTGGTCAGCT
Ignore the first AAG and start with C. Now, each base of DNA can represent a 2-digit binary number, and each number then corresponds to a color, like:
C = 00
T = 01
A = 10
G = 11
With this strategy in mind, the sequence CCCT would give 00000001 pixet (or pixel set), and so on as the sequence grows. This pixet would define the color of four pixels in the image. Thus, each base corresponds to a pixel in the image, and the base defines the color of the pixel in a 4-color image.
Now, lets come to the flexible strategy. To begin with, see the table again:

Here we are using standard 3-base codons. From the predefined value for each color (1 to 21), we can find the color using the codon. For example, from the same sequence:
AAGCCCTGGTCAGCT
Ignore AAG again and start with CCC. From the table, CCC encodes a value of 1. Move to next, TGG encodes a value of 16, TCA encodes 10 and GCT encodes 7, and so on for longer sequences. So, now we get an image with 4 pixels i.e. 2 x 2 with the pixels having color code 1, 16, 10, 7. In this way, each pixel can have a color from predefined values. On extracting this data, the image comes out as (from gizmodo):

The above part talked mostly about the single image of a hand. Now, talking about the horse-riding GIF, the process is almost the same. Here, we have to encode 5 images instead of one. Scientists encoded these 5 images in 5 different cells. After culturing them for some generations, they extracted the information of all images (using standard bioinformatics tools) and compiled them to get the GIF back. The initial and final GIFs look like this (from wired.com):

What do these rigid and flexible mean?
In this technique, the terms rigid and flexible are more about individual base rather than the codon. In the rigid strategy, the value of each base is fixed i.e. rigid. For example, in any sequence, C will encode the value '00', whatever the next or previous base is. This means that in both CCCT and GGTC, C has its rigid value '00'. So, for a 4-color image, where each base rigidly corresponds to the color of a pixel, we get as many pixels as the bases in the sequence.
On the other hand, in the flexible strategy, the individual bases do not have a fixed value, and the overall value of a pixet is defined by all the bases encoding that pixet. For example, TCC encodes a value of 6 while CCC encodes 1. The value of individual base is degenerate (or flexible), hence the name flexible strategy.
Thus, in a nutshell, while the rigid strategy is more efficient since one pixel is defined by one base (whereas in flexible strategy, one pixel is defined by one codon), the flexible strategy is better suited for getting more colored images since you get more color options by increasing the number of bases in a codon (whereas you only get 4 colors in rigid strategy, defined by 4 bases).
Why are we ignoring AAG?
As @canadianer points out in their answer, AAG is a PAM i.e. Protospacer Adjacent Motif. According to Wikipedia:

Protospacer adjacent motif (PAM) is a 2-6 base pair DNA sequence immediately following the DNA sequence targeted by the Cas9 nuclease in the CRISPR bacterial adaptive immune system. PAM is a component of the invading virus or plasmid, but is not a component of the bacterial CRISPR locus.

In simple terms (avoiding technical details), PAM is required for the CRISPR to function, but is not a part of the sequence itself. Much like a punctuation, it is necessary for proper functioning of CRISPR, but it is not to be read for encoding/decoding purpose. For the Cas9 found in E. coli (and is the most popular one), the sequence AAG serves as a PAM and is thus not used for encoding purpose here. Scientists also avoided to use AAG in their pixets so that there wouldn't be more than one recognition site for integration (ignore this point if you're unaware of the working of CRISPR).
Reference: Shipman, S., Nivala, J., Macklis, J. and Church, G. (2017). CRISPR-Cas encoding of a digital movie into the genomes of a population of living bacteria. Nature. http://dx.doi.org/10.1038/nature23017

Just a note: The AAG sequence is a PAM for a specific Cas protein. There are Cas proteins from different bacterial species and they have different PAMs.

Why doesn't CAS9 read AAG?

Nice addition, but there is no Cas9 in BL21. In this paper, PAM recognition for protospacer acquisition is mediated solely by the heterologous Cas1-Cas2 complex. Internal AAG is avoided so that there isn't more than one recognition site for integration.

You might also mention the benefits of a degenerate code that are discussed in the paper, especially avoiding repeats and internal PAMs.

A digital picture has many pixels on different sections. But is there any way to locate pixels of specific location of a picture on this method. Or the scientists designated different bacterias for different sections?

@mockingbird AFAIK the only way is to count. Nope, scientists encoded one full image in one cell, only different images were incorporated in different cell. As for your first question, Cas9 does read AAG, but its more of a signal, so we don't take the risk of using it as pixet. See canadianer's first comment.

@Mockingbird I think they just wholesale sequenced the entire CRISPR locus, which is really not overly interesting. To me, the neatest part of this research is how they used CRISPR to integrate the information into the genome.

I don't understand what you mean by "wholesale sequenced the entire CRISPR locus". Do you mean that the entire CRISPR locus is encoded for one image? But an image has many pixels. How did they maintain the order?

@Another Can you include a link to a paper regarding this phenomenon which is not behind paywall?

@another'Homosapien' Yes, just finished ;)

you write - Now, each base of DNA can represent a 2-digit binary number. Why 2-digit? why not 1 or 3 digit?

@user1993 because there are only 4 bases, too many for 1 digit (2) and too few for 3 digits (8)

But what is not clarified in the answer was the use of the word "GIF" - did the researchers actually encode the image in the CompuServe Graphics Interchange Format, or is "GIF" being used intentionally as a misnomer because it's a more familiar way of saying "animated image"?

@oldmud0 I won't consider it either. They just broke the GIF (i.e. a group of images) into individual images and encoded it. Later, they extracted the data for individual images and merged it to get the GIF back. So, its neither being encoded in the GIF format, nor is GIF a misnomer. It does seem perfectly fine to me :)

@another'Homosapien' Then, it would be more professional and correct to refer to a an animated image not as a GIF, but rather as an animated image, no? A GIF itself was not written to the DNA, nor is the format of the animated image important ("graphics interchange format") in the experiment.

Frankly, yes it should be so. But people not so familiar with computers and formats often fail to understand the term 'animated image' since this is what they refer to by the term 'GIF' (ironic, I know, but I've seen this many times)

@oldmud0 Without reading the paper again, I guess the correct description would be that they transcoded a GIF into their novel DNA code.

The image was not in the DNA as such, only as an abstract representation that could be converted into an image from knowledge of the code.  Briefly, they encoded the image into DNA, using a couple of different strategies in which DNA represented pixels -- either with a single DNA base representing a pixel, or with a triplet representing a pixel.  Knowing the code they used, they could then extract the information and turn it back into an image.
Quoting from the original article, CRISPR–Cas encoding of a digital movie into the genomes of a population of living bacteria:

We began with an image and stored pixel values in a nucleotide code ... We first encoded images of a human hand using two different pixel-value-encoding strategies: a rigid strategy, in which 4 pixel colours were each specified by a different base; and a flexible strategy, in which 21 possible pixel colours were specified by a degenerate nucleotide triplet table ...  To distribute the information across multiple protospacers, we gave each protospacer a barcode that defined which pixel set (denoted as ‘pixet’) was encoded by the nucleotides in that spacer. Four nucleotides define each pixet, and the pixels of a given pixet are distributed across the image ...

Their 21-color strategy is outlined in this figure:

Note: The paper isn't open-access. If you want a full-access version, Church often puts freely accessible versions of his papers on his web site; this paper, #441 on his list, is still shown as "in press" there, but check back at intervals and maybe it will be available there

For clarification, if I had a square image of lets say 9 pixels (3x3), I would assign "arbitrary" bases to each pixel lets say, line1: [G A T], line 2: [T A C], and line 3: [A A A].  And I make an arbitrary rule stating this 3 line code of bases is equivalent to this 9 pixel picture. I then install this code using CRISPR method into bacteria and read it back. Simply put, is this what the scientists did?

Just to be clear to the OP, this isn't conceptually any different than encoding images in binary, except there are 4 possible states instead of just 2. Effectively, each base in DNA is 2 bits.

@PiratePi  conceptually that's pretty much right. You describe arbitrary encoding for a full image, they did it using arbitrary (but consistent) encoding per pixel, but that's the only difference.

Just to add an explanation of one point that may not be clear (and might usefully be incorporated into the answer). GIF is a format for colour images that allows images of up to 256 red-green-blue colours (2^8). A colour table defines what colour corresponds to each of the 256 number values. The genetic code will only allow a maximum of 64 colours to be defined from a DNA sequence. These 64 colours can still be interpreted by software that can interpret GIF image encoding — the fact that the other 192 possibilities are not used is irrelevant. Likewise for 21, rather than 64.

Though there's nothing stopping them from using 4-base "codons" to get 256 colours.

@canadianer Indeed; for this purpose there is nothing any more special about using 3-base codons than there is using 8-bit bytes.

Is there a reason that AAG doesn't map to a number?

"The image was not in the DNA as such, only as an abstract representation that could be converted into an image from knowledge of the code" Right, which is what encoding means. The image absolutely was "in the DNA" ... and the subsequent faithful extraction proves it.

@AndrewPiliser This would be a great, separate question. AAG is the PAM used by E. coli which is necessary for protospacer acquisition, or at least greatly increases acquisition efficiency.

What's exactly a protospacer?

"Four nucleotides define each pixet, and the pixels of a given pixet are distributed across the image" Are these 4 nucleotides are the 1st base of a triplet codon?

The mentioned paper isn't free accessible.

@Konrad Rudolph they did both.  "a rigid strategy, in which 4 pixel colours were each specified by a different base; and a flexible strategy, in which 21 possible pixel colours were specified by a degenerate nucleotide triplet table"

@Mockingbird The four-nucleotide approach was a different, simpler but less flexible, strategy from the triplet strategy.

@iayork Thanks for the clarification, turns out I misread the comment that that [the comment that I criticised] was replying to.

I hate to pile on with more comments here, but I should correct my previous statement that there is "nothing stopping them from using 4-base codons". In fact, I see in the paper that they were already concerned about the cost of synthesizing all of these oligonucleotides.

@LightnessRacesinOrbit I'd suppose if the image was encoded in the DNA, then the bacteria would be able to construct some protein which would look like that image. Alas, it wasn't, even remotely. Instead, it's just that the DNA was used as a medium for storage of image data, which is much less exciting.

Since a few people asked why the AAG triplet is avoided in the code, I thought I'd add this in addition to the other answers. The interesting part of this research is not necessarily the image encoding but rather how they utilized the CRISPR system to integrate the encoding DNA into the genome. It may be a surprise to some that the image is not encoded in one long string but rather, due to the nature of the type I CRISPR system of E. coli, in 33 base pair chunks called protospacers (of which 27 bases are used for the actual encoding, which gives 9 pixels per spacer). Thus the entire 30x30 pixel image required stable integration of 100 protospacers (though not necessarily in a single cell). These protospacers (oligonucleotides) were chemically synthesized and then introduced into cells by electroporation.
Integration of these protospacers into the genomic CRISPR locus utilized overexpression of heterologous Cas1 and Cas2 endonucleases. These proteins recognize exogenous DNA preferentially when it is flanked by a protospacer associated motif (PAM), which in the case of the CRISPR system in question is AAG. The complex recognizes the PAM and cleaves the exogenous DNA to form the 33 bp spacer which is inserted into the genome. Simplistically, it could be pictured something like this:

However, consider a situation where AAG is used to encode a pixel:

This creates an internal PAM that could lead to loss of information, depending on which PAM is recognized. Actually, the major benefits of having a degenerate code is to avoid certain triplet combinations that lead to internal PAMs or sequence repeats (which are error prone in replication).

References/Further Reading:
Amitai G, Sorek R. 2016. CRISPR-Cas adaptation: insights into the mechanism of action. Nat Rev Microbiol 14:67-76.
Shipman SL, Nivala J, Macklis JD, Church GM. 2017. CRISPR-Cas encoding of a digital movie into the genomes of a population of living bacteria. Nature.
Wang J, Li J, Zhao H, Sheng G, Wang M, Yin M, Wang Y. 2015. Structural and mechanistic basis of PAM-dependent spacer acquisition in CRISPR-Cas systems. Cell 163:840-853
PS: For anyone that cares, those images are not technically correct but, at the moment, I don't feel like changing them. In reality, the PAM is not part of the processed spacer.

Good enough, +1! Yet I feel you should expand the second paragraph a bit :P

@another'Homosapien' I tried to avoid too much mechanistic detail since I expect a lot of the people interested in this question are not extremely well versed in the intricacies of CRISPR-Cas (and neither am I, for that matter). I'm open to suggestions, though.

Without a little jargon, how is anyone supposed to assess the credibility? ;)


text:
In reconstructions, how are various shapes of facial features determined from skull only?
I have seen reconstructions (with skin, eyes, muscles etc) of some first humans based on skulls and skeletons. But how can the shape of nose (protruding part), shape of eyelids, shape of eyebrow, hairline be determined base on the skull only?
Examples of these reconstructions:

Disclaimer: I am an evolutionary geneticist. I know nothing about anatomy and forensic methods....
You should just have a look at wikipedia > forensic facial recognition. There are a number of different facial reconstruction methods, one of which is the so-called Manchester method (see a review of the Machester method in Wilkinson 2010).
In any method of facial reconstruction, there is some part of artistic representation to fill the gap of what we fail to infer from the tissues available. It is typically not so uncommon esp. for recent(-ish) fossils to have remains of soft tissues as well. In absence of such soft tissue, the morphology of the mouth and ears are typically left to artistic interpretation.

'artistic interpretation' sounds rather subjective and so says Wikipedia. But that means that the reconstruction does not necessarily represent the original

Yes, that's what it means. It means that there are things we don't know and we just go with our feeling.


text:
Can fever cure Ebola disease?
Why is ebola disease does not cured on elevating body temperature by body defense system?
Can we cure it either by elevating or reducing body temperature (in ice bath) and creating hostile environment for virus?

I'm not an expert on Ebola in particular but as far as I know its eclipse period is independent on the body temperature (well, of course, if the entire metabolism of the body slows due to hypothermia I guess its replication would also slow as a consequence), so it just don't make any sense trying to "kill" it by that. I would advice you to read up more on the Ebola replication cycle and our attempt at devising a vaccine for it. This will be more helpful finding a way to "kill" it, then replying on ice baths.

Fever, in and of itself, doesn't really cure any disease.  It does help, though.

Short Answer: Fever cannot cure Ebola simply because the virus is not temperature-sensitive.
Background: Fever is a defense mechanism of the body which is specific to temperature-sensitive virus and bacteria. It is so because high temperature induces stronger immune response and makes the body hostile for the pathogen1. Ebola virus, on the other hand, is not affected by this mechanism because it can survive over a much broader range of temperature. Ebola virus is moderately temperature-sensitive, and can survive in temperatures as low as 4°C2 and as high as 60°C3 (at least for half an hour). So, in practical sense, it is not possible to cure ebola disease by heating or cooling the body, either naturally or artificially. But, if we ignore practicality, then Yes, you can cure ebola disease if you take an ice bath or a steam bath for hours so that your core body temperature drops to 4°C (in former case) or 60°C (in latter case). However, it wouldn't be a very nice idea as your body would become hostile for yourself before becoming hostile for the virus.

Having cleared the point about making body hostile for the virus, we are now left with another option: inducing stronger immune response. However, this will not work either because of a peculiar, but dangerous, property of such viruses: they use our defense system against us. Ebola virus, coming under the category of Filoviridae4, attacks host's immune cells, specifically monocytes and macrophages, to replicate inside them. This serves dual purpose; first, the virus has its work done, and second, it kills the host's immune cells. Although how ebola enters into immune cells is not understood, but it has been shown that the virus is helped by the host's antibodies in entering into immune cells5 (quite ironic). Ebola virus can also accomplish this through a process known as macropinocytosis6 (a form of endocytosis). You can refer to this page for its life cycle as well as the diagram of the ebola virion which I've used above, or just have a look at the diagram below from here:

References:

What is the benefit of fever during infections? - Biology Stack Exchange
Okware SI, Omaswa FG, Zaramba S, Opio A, Lutwama JJ, Kamugisha J, et al. An outbreak of Ebola in Uganda. Trop Med Int Health. 2002;7:1068–75. doi: 10.1046/j.1365-3156.2002.00944.x
Mitchell SW, McCormick JB. Physicochemical inactivation of Lassa, Ebola, and Marburg viruses and effect on clinical laboratory analyses. J Clin Microbiol. 1984;20:486–9
Wikipedia contributors. "Filoviridae." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 24 Sep. 2016. Web. 5 Apr. 2017.
Takada, A. & Kawaoka, Y. Antibody-dependent enhancement of viral infection: molecular mechanisms and in vivo implications. Rev. Med. Virol. 13, 387–398 (2003).
Hunt, C. L., Kolokoltsov, A. A., Davey, R. A. & Maury, W. The Tyro3 receptor kinase Axl enhances macropinocytosis of Zaire ebolavirus. J. Virol. 85, 334–347 (2011).

Fair enough +1.

I really like a nice answer like this being posted in a controlled, well communicated,  and top notch style like this.

I want to upvote your answer but I am not currently (will do later) , as it may lead the script of Biology SE to detect this serial voting (I already have voted 3 of your answer in last 15min, all are very nice), and I don't want you to lose that reputation that you deserve.

@jaideepkhare I don't know how to tell you this...but those upvotes didn't add to my reputation :( I had already reacjed my daily repo limit, so your upvotes would only add to the displayed score. Anyways, even that would help, thanks for appreciation :')


text:
Will you stop sweating if you exercise in a cold enough room?
It's common knowledge that you will sweat from being in a very warm room. And you will also sweat from exercise, presumably because it raises your body temperature.
But if you exercise in a cold enough room, which magically adjusts its temperature to counteract your body temperature, will you then not sweat at all? And is it therefore possible to exercise without sweating... And not even have to take a shower afterwards?

Well, if you define "cold enough room" as outdoors in the winter, and the exercise is cross-country skiing, then it is perfectly possible, as long as you adjust your clothing layers appropriately.  Indeed, you do not want to sweat much - enough to wet your clothing - as that exposes you to a risk of hypothermia when you stop.

Apparently you can sweat even in a cold enough room, without even doing exercise! The main causes of sweating include, among exercise and high body temperature, stress and anxiety. This condition is called cold sweating. See this article:

The body normally produces sweat as a way to help keep cool. Sweating normally occurs with exertion such as when exercising or in high temperatures. However, there are other reasons for sweating. Sweating can be triggered by fear or anxiety, and this is often referred to as a cold sweat. It comes on suddenly and results in cool, damp skin. It is the body's reaction to stress as part of the "fight or flight" response that helps us to react in a dangerous situation.

So, even if you just think about doing heavy exercise, you might get sweat in hands or feet.
But cold sweating is not the only cause. It may also be caused by a more severe condition known as hyperhidrosis. See this article:

Normally, your sweat glands produce perspiration that’s carried to the skin’s surface when the air temperature rises, you develop a fever, you’re exercising, or you’re feeling anxious, nervous, or under stress. When those factors are no longer an issue, the nerves that signal sweating are put on hold. For the 2% to 3% of the population who have hyperhidrosis, however, the sweat glands don't shut off. They sweat even when the circumstances don’t call for it: when they’re in air conditioning, or while they’re sitting and watching television. Some people even tell their doctors that they sweat in a swimming pool.

So, one might start sweating even in a cold enough room, if not because of body heat, then because of anxiety, hormones or medical conditions. Also, this condition does not work the way you are speculating. When the surrounding environment is very cold, the body prefers to shut off blood supply to skin than to cool it down through skin i.e. sensing cold environment, the body shuts off blood supply to skin and diverts it to core of the body. This is what causes more urination in cold environment and is called cold diuresis. Have a look at this answer for more information on this point.

Why the downvote? Anything I missed or said wrong?

I believe many at times people would have experienced this. I have had sweat drops even on a very chilling evening.

It wasn't me, but it might have been because you didn't actually provide OP with the information they were looking for. At least, according to the way I read the question. You go into other things that can trigger sweat to conclude "it is possible to sweat in the cold," but "Is it possible to sweat in the cold?" isn't the question that I see, rather it is "I start sweating when I exercise, but would that still happen if I exercised in a cold room?" Read: all other things being equal, am I likely to sweat... not is it possible to sweat. Note the "Is it possible to exercise without sweating"

... However, an answer about people who have a condition that makes them unable to sweat likewise would not answer the question, even despite the "Is it possible to exercise without sweating," as the context is (again) "Normally I sweat when I exercise. Could doing it in the cold stop the sweating." Still, interesting information and relevant to the topic, even if it doesn't get OP to precisely what they were after.

@another'Homosapien' I do understand your perspective, and your answer was a good read. And if you try to pick out a single sentence from the question and answer it directly, and you pick the part that says "is it possible to exercise without sweating", then your post has answered that very directly, and quite well. I'm merely responding to your (1.5yr old) comment asking for criticism because of a down-vote. Although you have answered one of the specific questions contained within OP's post, I would suggest OP did not get the info they specifically were after based on the question's context.

That is, it appears that the asker is interested in avoiding sweating while exercising. If you set aside the specific words the asker used, and just look at what their end goal is, the answer you provided hasn't helped them with that. At least, if my assumption about the asker's intent is correct. This is one of the issues with the format of StackExchange... if the asker asks the wrong question, even a perfect answer might not help them. And we aren't supposed to have a lengthy discussion about it.

@aaron oh I get your point now! I will surely try to make some edits to make the answer better

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


text:
What amount of protein comprises the feces of a domestic cat?
I've heard it said that the fecal excrement of cats, Felis catus, contains adequate amounts of protein so as to attract the interest of other animals e.g. dogs (Canis familiaris).
However, I am unable to locate any studies which reported the composition of a cat's feces as compared to those of any other animal with regards to a controlled quantity of proteins in the diet.  I do see a lot of people on the internet making claims one way or the other, but never a citation to be seen.
Would anyone be interested in citing some references here so as to provide a more reputable resolution to this oft–repeated “fact”?
Unlikely as that would be, I'll post an answer here next time I check the university library.


text:
correction of read counts for spikes
I have 4 RNA-seq samples (1st is control and the other 3 are treatments) and 5 spikes. I used different concentrations for 5 spikes but over different samples, I used similar concentration. for example I used similar concentration for spike1 in 4 samples. and this is the case for the rest of spikes. I am trying to normalize the read counts for the spike. do you guys know how to do that?
this is what I have done so far:
I counted the spikes in different samples and and got the ration of them (treatments compared to the control for all spikes). the ratio is as expected (looking at the concentration of spikes).
one thing that I can do to correct the read counts for spikes is to multiply by the ratio between samples. but I am not sure if that is the right way.

The most common and simplest normalization method for spikes is the Total Count Normalization. It's actually what you're doing here, so what you're doing here is correct. TCM is a useful algorithm for normalizing sequencing depth, that includes your spike amounts.

https://academic.oup.com/bib/article-lookup/doi/10.1093/bib/bbs046

has reference on the TCM normalization.

Gene counts are divided by the total number of mapped reads (or library size) associated with their lane and multiplied by the mean total count across all the samples of the dataset.

The paper doesn't talk about spike-in controls, but the idea is the same. We'd use the spike-in controls for estimating the difference in sequence depth (instead of the whole data set).