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Which living organisms have antibodies?
I'm wondering if only humans, or only mammals have antibodies and immune system. Obviously humans and dogs have (we vaccinate both) and in my head makes sense since we're so genetically similar to all mammals that we all have antibodies. Do all synapsids, or even amniotes have antibodies as part of their immune system? Do plants have antibodies or insects?

Apparently, cartilagenous fishes are the oldest extant clade that have the true immunoglobulins (antibodies) and the T-cell receptor (Schluter et al., 1997). All extant gnathostomes, incuding cartilagenous fishes, produce antibodies.
However other animals (invertebrates) and even plants have proteins that belong to the immunoglobulin superfamily (to which the classical immunoglobulins/antibodies also belong). Members of this superfamily are structurally related; they are not necessarily involved in immune responses. Hemolin is one immunoglobulin superfamily protein in insects, that is involved in immune function, but not exactly like vertebrate antibodies.

In the animal kingdom adaptive immunity is present in all Gnathostomes.

Agnathostomata (hagfish and lampreys) also have an immune system that is somewhat adaptive, although in many cases it isn't structurally related to the Gnathostome "adaptive immunity".  For example, they have molecules that are analogous to antibodies, including a diversity-generating mechanism, but that are not structurally related to them.  See for example Dual nature of the adaptive immune system in lampreys

@iayork.. I read that too but I as far as I have read they don't produce true antibodies (i.e. immunoglobulins).

@SanjuktaGhosh Yeah I forgot to explicitly state that explicitly but note that adaptive immunity does not really require antibody production as iayork has mentioned.

Definitely not true antibodies (they're structural more like TLRs, as I recall, though I don't recall if they're evolutionarily linked or not) but with surprisingly analogous aspects to them. Lamprey and hagfish immunity is really fascinating, since they share some aspects with Gnathostomes but also have gone in completely different directions in other ways


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"X" in stock solutions
We prepare buffer solutions with concentration in terms of x, for example 50x TAE buffer. How do we come up with x? Is x related to molarity in some sense? And how much can we concentrate the solution. We have 50x TAE but usually 10x TBE buffer, why is it so?

X simply stands for "times" like 50 times concentrated. And there are limits of how much of a certain substance can be dissolved in water. This limits stock concentrations.

Thanks for the comment @Chris. If X stands for "times" as you say, how much is 1 time, i.e, 1x, is it 1M, 0.05M as given here link? And is it same for all solutions?

That depends on your final concentration. If it is 100mM, then 10x is 1M (1000mM), 100x would be 10M.

1x is the final working concentration of the solution (it could be anything depending on the type of the solution). Stock solutions are made at a higher concentration; if it is 10 times more concentrated than the working solution then it is 10x.

Why 50x TAE but 10x TBE?

The salts in TBE precipitate at higher concentrations. In other words, the salts in TBE have lower solubility compared to those of TAE. Therefore stock solutions of TBE are usually 10x or even 5x.

Thanks @WYSIWYG. Can you tell me how do we decide what should be 1x concentration by citing few examples?

@Biginer How to decide the 1x concentration: the first time when someone does that, then they 1. use rational guess 2. use trial and error, and settle on a concentration that is most optimal for the task. Subsequently, others follow it and tweak it when necessary.

Thanks @WYSIWYG. I came to the same conclusion when I discussed it with my peers. Thanks a lot!

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What is difference between breed, variant, subspecies and species?
What is the difference between breed, variant, sub-species and species? Are there any similarities between sub-species and sub-population of a region?

what do you mean by "Are there any similarities between sub-species and sub-population of a region?"?

You may want to add the term strain in you list. @WYSIWYG I would guess that the OP asked between sub-species and sub-population of a region because (s)he has some understanding that species is a term that applies to taxonomy while population is a concept that is used to define a collection of individuals that reproduce and live over a geographical region.

A species is commonly defined as the largest group within which interbreeding produces viable offspring.
A sub-species is a subgroup below the level of a species.  One definition is a group which can interbreed successfully with other subspecies, but does not do so in practice (e.g. due to geographical isolation).  Other terms like variety, form, etc., may be used in some domains to indicate various groupings below the species level.
A breed usually refers to a population of a domestic animal that has been selectively bred for specific characteristics.
A population is a set of individuals within a species that live in the same geographical region.  Depending on rates of gene flow, different populations within a species may eventually differentiate into subspecies or distinct species — this is known as allopatric speciation.

So is there any difference in meaning between population and subspecies? Note that while you are giving the most commonly used definition of species, those definition only apply to lineages that reproduce sexually. I would love to have the definition of the word strain as well in this list. I would tend to think that many of these concepts are poorly defined and are used with different definitions in different field of biology.

@Remi.b These concepts are indeed loosely defined and the accepted definitions vary across different subdomains (e.g. microbiology vs botany vs zoology); this is just an overview.  As for population versus subspecies, population just refers to the members of a taxon in a given region, with no implication of a distinct genetic lineage.

As Remi said, what is strain actually?

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Can the Hebbian theory apply to Inhibitory Neurons
If I understand the basic Hebbian theory, when a neuron fires a pulse to another neuron and this pulse causes the target neuron to fire then the delta energy sent from the initial neuron to the target is increased. (Making it easier to trigger the target cell)
With this in mind is there a way for an inhibitory neuron to increase the delta energy it applies to a target neuron (reducing the excitation level of a target neuron).
If the inhibitory neuron never triggers the target then I would assume it would never increase the decrease in energy it sends to the target.

We now do have mathematical models for LTP. I think Hebbian theory is an oversimplification if we see those models.

≈Yes, it's easy to conceptualize at a simple ganglionic circuit. A really good example is (I believe from Kandel's lab)demonstrated by Aplysia's gill withdrawal reflex. Repeated stimulation causes reduced EPSPs in motor neurons that innervate muscles that cause the withdrawal reflex. However when you apply a electric shock to the tail, the snail will immediately regain withdrawal reflex sensitivity. The tail sensory neuron response activates the serotonergic facilatory interneurons which have multiple IO with sensory and motor neurons.
And don't forget, interneurons can inhibit other interneurons leading to disinhibition.
For most LTP work you're probably ok using Hebbian models. Make sure to keep in mind that in more complex systems like cortical circuits.  there are some modes of communication that don't always play well with Hebb's Laws: gliotransmission, retrograde transmission, neuropeptides/GPCRs, and activation of perisynaptic receptors/receptors on adjacent cells.

Could you elaborate on why neuropeptide/GPCRs may not fall within the Hebbian category ?


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How is DNA Read
Little odd question here. I was told that DNA was read in groups of three.
Assuming this, my question is: Which way would better describe how the DNA is read.
(123)456789 to 123(456)789 to 123456(789)
or
(123)456789 to 1(234)56789 to 12(345)6789
Assuming that the string of numbers 123456789 represents a DNA sequence.

first hit on google: http://learn.genetics.utah.edu/content/molecules/dnacodes/

DNA codes for proteins via codons. A codon is a combination of three nucleotides. As there are 4 different nucleotides available in DNA, there are 64 permutations possible. These 64 codons code for the 20 amino acids and 3 stop codons. Hence, many amino acids are coded by several different codons - the genetic code is said to be redundant.
Typically DNA sequences have a single reading frame (but see @user3790338's answer for an interesting exception to this rule). The reading frame is, basically, defined by the first amino acid of the protein that it decodes. Thereafter, each subsequent triplet is one codon, in a non-overlapping way (123 - 456 - 789 - etc.). Note that DNA sequences contain so-called introns that intervene the coding DNA. These regions are eliminated post-transcriptionally. For clarity-sake I have disregarded them in my answer.
However, one has to realize that this coding of DNA is only important phsyiologically during translation, i.e., when mRNA is being translated into a protein. It is the ribosome that actually reads the codons and stop codons to determines which amino acid is to be incorporated in the growing protein and when to stop translation. Hence, although we read DNA sequences in terms of codons, the cellular machinery doesn't read DNA, it reads mRNA.

Perhaps I misunderstand what you're saying, but stop codons do not terminate transcription.

Not to be pedantic, I also just noticed that you said introns are eliminated post-translationally, which is not true.

"It is the ribosome that actually reads the codons" -- I'd expect the DNA -> mRNA transcription  process  to do that as well, if only to figure out when to stop transcribing the DNA.

@Jan-Dvorak Transcription doesn't involve codons and its termination is by another mechanism. It occurs down stream of the CDS.

Assuming the first coding position is 1, the DNA will be read as: (123)456789 to 123(456)789 to 123456(789). There are fairly few exceptions to this, e.g. some viruses (e.g. http://www.ncbi.nlm.nih.gov/pubmed/1966841), where reading frames overlap like in your second example. This is because the viral genome is much smaller and needs to code all of its proteins into as little nucleic acid as possible. Note that there is more than one way for frames to overlap.


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What causes muscles to generate heat on contraction?
I'm curious what the exact cause is of dramatic heat generation that comes along with muscle activity. Can anybody explain this in understandable language?

does "conservation of energy" count as a valid answer?

@JanDvorak Well, I'm looking for an answer that is understandable with a shallow knowledge of biology/bio-chemistry/bio-physics. An answer consisting out of only this phrase, assumes background knowledge of those scientific areas. It's basically like: "Dad, why does the ball fall down when I throw it? Well, E=MC2, son."

How about the wikipedia article on motor proteins?

... or, rather, the article about muscle contraction?

Short answer: energy transport always has heat loss.

First, it might be helpful to talk briefly about what heat is. It is a form of energy - molecular energy. Basically, heat is the amount of jiggliness of the molecules of a substance or object. When we look at a hot object, it doesn't apear to be moving any more than a cold object, but on a scale much smaller than we can see, it's molecules are moving faster than in a colder object. Read this for more information if you want.
There are at least two things going on in muscle contraction (as well as in other metabolic processes) which produce heat. The first is the chemical reaction that powers muscle contraction. You probably don't want to get into great detail, but basically there is a molecule which your cells use to store power, which we abbreviate as ATP. When our muscles use that power, an exothermic chemical reaction occurs that "burns" ATP, breaking it into two pieces (ADP and phosphate). That reaction releases energy. Some of that energy is used in the actual movement of the muscle. But some of it just "jiggles" the nearby molecules. Again that jiggling is the very definition of heat.
The second source of heat is probably much smaller: friction. In short, just about any time anything moves, nearby molecules get jiggled some more. Imagine trying to walk through a room packed full of harps. Everywhere you move, some of those strings get plucked and vibrate. It's a little bit like that. When your muscle fibers tighten and flex, they rub past each other and jiggle each others atoms. All of that jiggliness is heat, and the jiggling continues until it can transfer to some other medium, as when, sweat evaporates from your skin.

Aside of an extremely clear explanation on the source of heat, +1 for explaining what heat is and +1 for explaining what friction is. Not that I totally didn't know that, but the way you explained it makes me realize that the heat we feel with our skin receptors is tiny waves, caused by molecules jiggling at a higher rate. Also I get that if you manually push the molecules to jiggle faster, they start producing waves (heat). And that's all there is to conversion of kinetic energy into thermal energy (friction). Your answer explains heat production, heat transfer and my microwave oven. Thanks!

This is oversimplified, but hopefully clear.
When we eat food, metabolic processes break down larger, multi-carbon molecules (like glucose) into smaller molecules. This process is called catabolism, and it releases energy. Here's a simple example of a catabolic reaction:
AB -> A + B + energy

For more on this principle, look at the section on Le Châtelier's Principle on this page from Washington University.
Our body can use the energy released to drive more chemical reactions. Specifically, our cells make a molecule called ATP, which is used all over the cell when energy is needed. However, our cells can't convert 100% of the energy from catabolic processes into chemical energy, some of it is lost as heat (or entropy). When we use ATP, a high energy phosphate group is hydrolyzed (chemically split) from the ATP molecule (ASPU, look at the arrow on the right for energy release):

This releases energy, some of which (during exercise) is used to make muscles contract, but much of it is lost as heat. We heat up when we exercise because the muscles are being used more than at rest, which means more ATP is being used to contract the muscles, which means more heat is being released by the ATP hydrolysis reaction.

Also to be noted that exercise causes increased blood circulation. That also generates heat.

Well explained. Please check if I summarize this correctly: the heat is generated as a side effect of splitting molecules to generate energy needed for muscle contraction.

@WYSIWYG How does blood circulation generate heat? Doesn't it only spread the heat that is generated elsewhere?

I agree with @Alph.Dev - blood circulation in itself generates a negligible amount of energy through friction. Nothing more.

@Alph.Dev Yes you are right that it spreads the heat. Circulation per se can also generate some heat because of movement- it would not be that much. I think that circulation is just correlated with heat and this perhaps has got to do with epinephrine signaling.

@WYSIWYG Yeah, I wouldn't really say high blood circulation causes heat at all. The primary correlation between heat and circulation is really just that the body uses circulation to regulate core temperature. But in fact, when the body has a fever, it increases temperature by decreasing circulation, leaving the extremities cold, and triggering shivers (muscle movement) in order to produce the required heat. You can read more about that here if you want.

Thank you @MarkBailey that point about fever was interesting. I was generally guessing that the hydrodynamics would generate some heat, but it seems that it is insignificant.

@WYSIWYG Well, the friction of blood flow generates some small amount of heat, but assuming blood volume throughput stays the same (which I would expect to correlate approximately to heart rate) I would think that again, decreasing circulation (tightening the blood vessels) would increase friction as the same blood volume is pressing through a smaller, tighter space. Increased heart rate during exercise, on the other hand, would raise temperature a bit. Higher blood flow increases friction a bit, and more significantly - the heart muscle activity generates more heat.

@WYSIWIG Increased blood flow actually helps your body to dissipate heat, this is one of the mechanisms that allows NSAIDs to work as anti-febriles


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Kinesin-5 / cytoplasmic dynein spatial density distribution in neurons
Is there some way to experimentally determine the density distribution of Kinesin and Dynein in a Neuron?
Fluorescence labeling would be impossible(?) as GFP markers would probably alter the motor dynamics.
Any ideas? Or do any studies exist which looked into this topic?

I have next to no knowledge of this area, but I do know that Peter Baas has done extensive studies of Kinesin-5 in neuronal growth cones during development.  I mention that in the off chance that some of his imaging techniques might be helpful to you.

It is possible to tag molecular motors with fluorescent proteins. It may impede with its movement but as this paper describes, a variant can be created that doesn't have cargo binding ability.

Constitutively active kinesin motors can be generated by truncations
  that remove autoinhibitory and cargo-binding regions of the
  polypeptide. For this work, we generated KHC(1-560) (Figure 1A), a
  dimeric motor that has been well characterized in vitro and in vivo
  [16],[18],[19]. KHC(1-560) motors were tagged with three tandem copies
  of monomeric Citrine (mCit), a variant of enhanced yellow fluorescent
  protein (FP) (Figure 1A), and expressed in COS cells (Figure 1B).
  Single Kinesin-1 motors were tracked in live cells using a modified
  TIRF microscope (Figure 1C) in which the angle of illumination was
  varied to enable deeper imaging as described [17]

However, if your objective is just to determine the density distribution of Kinesin and Dynein in a Neuron, you can simply fix the cells and do IHC staining for the motor proteins followed by high resolution imaging.


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RNAs arising from intergenic regions
Which type of RNA molecule is coded for in intergenic regions? I think it must be a non-coding RNA but I'm unsure which type.

The term intergenic is more or less obsolete now. In fact it is ironical to say that a gene, which can give rise to a functional protein or an RNA, is expressed from an intergenic region. However the usage continues for both lncRNAs and miRNAs (other major type of ncRNA in metazoans1 - piRNAs have different classification). lncRNAs are vaguely classified as sense-overlapping (expressed in the same direction as a known gene but not completely overlapping), antisense (expressed from the antisense strand of a known gene) or intergenic; similarly miRNAs are classified as intronic or intergenic.
It is not necessary that the intergenic RNA has to be strictly non-coding, it can be coding as well; a novel protein.
In all these cases the term intergenic means - not overlapping with a known gene. Better nomenclature is necessary as the field of genomics makes more progress.
See this article.
1 Most metazoans.


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Is Thyroxine a hormone?
I have read the phrase 'T3 is three to four times more potent than T4' several times both in books and websites. But isn't T4 a prohormone of T3? Why do then these sources talk about its potency as a hormone(I suppose)?

@AlwaysConfused I didn't find any. But since you pointed out I'll do some research.

It is necessary to distinguish between classical and non-classical actions of thyroid hormones.
Classical action involves nuclear THR (or TR) receptors (TR alpha1, TR beta1, TR beta2). They are activated by T3, 3,5-T2, TRIAC and 3,5-DIAC, and blocked by rT3 and rTRIAC. T4 and TETRAC hardly have an effect on nuclear thyroid hormone receptors, but they are converted in the periphery and in target tissues by deiodinases to T3 and 3,5-T2, and TRIAC and 3,5-DIAC, respectively. From the classical perspective, T4 and TETRAC are therefore prohormones and not hormones in the narrower sense.
Non-classical action denotes binding of thyroid hormones to integrin receptors on the cell membrane. The resulting non-genomic actions may be directly mediated by T4 and TETRAC and don't require deiodination. From the non-classical perspective T4 and TETRAC are hormones sensu stricto.

Figure from Hoermann et al. 2015 (CC BY license)
References

Hoermann R, Midgley JE, Larisch R, Dietrich JW. Homeostatic Control of the
Thyroid-Pituitary Axis: Perspectives for Diagnosis and Treatment. Front
Endocrinol (Lausanne). 2015 Nov 20;6:177. doi: 10.3389/fendo.2015.00177.
eCollection 2015. Review. PMID 26635726
Davis PJ, Goglia F, Leonard JL. Nongenomic actions of thyroid hormone. Nat Rev Endocrinol. 2016 Feb;12(2):111-21. doi: 10.1038/nrendo.2015.205. PMID 26668118.

What do Classical action and Non-classical action mean? I haven't encountered these terms before.

Well, this distinction is a rather new concept. Of course, it wouldn't have made sense before the discovery of non-classical pathways. See the projects page of the THYROID TRANS ACT program for a short overview or paper [2] for a more detailled reference.

THYROID TRANS ACT Projects: http://www.thyroidtransact.de/projects/

Moeller LC, Broecker-Preuss M. Transcriptional regulation by nonclassical action of thyroid hormone. Thyroid Res. 2011 Aug 3;4 Suppl 1:S6. doi: 10.1186/1756-6614-4-S1-S6. PMID 21835053; PMCID PMC3155112 https://www.ncbi.nlm.nih.gov/pubmed/21835053/.

Both T3 and T4 are functional in human body...T3 being only more potent. Both of them fulfill the features of being a hormone, in fact both of them serve the same function in human body. Yes, T4 produces T3 in the peripheral circulation, so you can say it is a pro-hormone of T3, but that dosen't remove it from the hormones. Another example is Angiotensin I which is a pro-hormone (besides itself being a hormone) of Angiotensin II. There are so many other examples.
Following are the references for my answer -
Ganong W F, Review of Medical Physiology, 25th edition, 2016, page- 341
http://press.endocrine.org/doi/abs/10.1210/jcem-36-6-1050?journalCode=jcem
https://www.labome.org/grant/r21/hd/is/thyroxine/is-thyroxine-more-than-a-prohormone--8448119.html
http://thirdworld.nl/l-thyroxine-acts-as-a-hormone-as-well-as-a-prohormone-at-the-cell-membrane

We like people to provide references for scientific assertions. They may well be correct but how can we tell if you don't give the information to check them.

I don’t know, but I suspect that T4 was characterized first and fulfils the classic definition of a hormone being secreted by a gland and carried in the blood to its target.
Potency is the measure of some biological or biochemical assay of the effect of these agents in the target tissue, so that you can talk about potency regardless of other attributes of a molecule.
Even when it was established later (I presume) that T4 is converted to T3 in the target tissue, and T3 is very active, the possibility would have existed that this conversion might only be partial (there will presumably always be some T4 present there) and the question arises whether both of these molecules have biological activity and function. The results of measurements of ‘potency’ are part of the argument or consideration as to whether T4 is just a precursor or also an agent in its own right.
I think the thing to bear in mind is although you might read nice clear-cut statements in text books and the like, the observations on which they are based are often not so clear-cut, so authors are being both prudent and scientific in presenting the data to the reader.
Finally, there is the question of semantics. Even if T4 is completely converted to T3 in the target tissue, you could still say that it is a hormone because it is secreted by an endocrine gland, passes in the blood to a target tissue where it has an effect. The fact that its effect requires it to be modified in the tissue doesn’t invalidate its description as a molecule that has an effect on a target tissue. So on that basis you can justify calling it a hormone (as well as a prohormone). I also suspect there may be historical reasons for retaining the description.

Both T3 and T4 are hormones produced by thyroid. The difference between the two is the presence of 3 reps. 4 iodine atoms.
Hormones usually work only on specific cells, by interactions to specific receptors. These receptors may be found on cellular membrane, intracellular, on nuclear membrane or even inside the nucleus.
So, to answer your question, T3 is more potent with reference to T4 hormone for the fact that only T3 can enter the nucleus of the cell. Therefore T4 must be reduced to T3 to generate a nuclear answer.
Lang, Schmidt, Heckman, "Physiologie des Menschen", 31.Auflage


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Does gross production (P) and biomass (B) mean the same?
From fundamentals of ecology, Odum 2005:

... autogenic succession usually begins with an unbalanced community metabolism, where gross production, P, is either greater than or less than community respiration, R, and proceeds towards a more balanced condition, where P=R. The rate of biomass production  (B/P ) increases during sucession until a stabilised system is achieved, in which a maximum of biomass (or high information content) and symbiosis between organisms are maintained per unit of available energy flow.

Isn't gross production (P) same as biomass (B) ? I can't tell them apart, given that Biomass is the amount of matter living organisms (usually of a specific trophic level) of a given area at a specific time is made up of.

Sanjuta, please provide a context in your title. As such hardly anyone would know what it is about without reading your post, and making them do that  is (1) impolite, (2) likely to make them ignore it in the first place.

@David I generally avoid making title too long, i.e. why I haven't put the full forms.

Titles are important for two reasons. 1. As a courtesy to list members so they don't waste their time on posts that are not of interest to them, 2. For indexing of SE Biology so users searching for a topic can find it. Certainly a title should not be longer than necessary, but writing good titles is a discipline a scientist needs to master.

Searching for context from what you wrote, I found this which seems to be an original article later introduced to the textbook you are using. I think this other version is more clear; P refers to photosynthesis, which is also gross production of biomass; B/P is the ratio of standing biomass to new photosynthetic product; rate of biomass production seems wrong unless you expand it to "existing biomass relative to rate of biomass production."
In summary, the correct interpretation should be that P is indeed the gross production, but B/P is simply the ratio of biomass to the gross production. If R is the loss of biomass through respiration and R < P, then both B and B/P will increase (i.e., you will accumulate biomass) until P=R. Probably in this process both P and R also increase, but what is important is that B/P is increasing, which means the new biomass isn't as efficient at new photosynthesis (presumably either because light is a limited resource or because more of the biomass is not held in photosynthetic organisms).
P is in units of mass/time; R is in units of mass/time; B is in units of mass. The equation would be dB/dT = P - R, or another way, B(t1) = B(t0) + (P-R) * (t1-t0), where t1 is some time after t0.

The website seems to quote from an older edition of the book I'm using. I can't agree to P being photosynthesis because in heterotrophic succession the early seres are dominanted by heterotrophs, so there's theoretically no photosynthesis there and also the equation P=R has been used in the broader sense applying to both types of succesion.

Considering autotrophic succession where as you said P= total primary production by plants, what does standing biomass/crop mean? Even when the water is removed the dried biomass will be same as primary produce.

@SanjuktaGhosh I think you are mostly just overthinking the details. By production the author means production in unit time - a great example would be a forest. P might be all the production of new foliage, etc, just this year - B, the total biomass, includes all of the tree trunks, old branches, everything produced in prior years. Maybe think about it like a warehouse storing boxes: P is the new boxes you made. B is the number of boxes in the warehouse. R is number of boxes you sell and remove from the warehouse.

In heterotrophic succession, you are starting with a lot of boxes, but not producing any. R is bigger than P: you are selling boxes faster than producing them. Eventually, one of two things will happen: either you start producing more boxes, so P increases until P = R and now your count of boxes stays steady, or R stays high but P doesn't increase, you sell all your boxes, and now you have no more boxes to sell, now R is 0, P is 0, and R=P.

In autotrophic succession, you start with a fairly empty warehouse, you are making boxes but not selling as many: P is large relative to R. But your warehouse has some carrying capacity, so P can't be large forever without you running out of space. As your B grows, you have to start selling some boxes to make room for all the P coming in, so your R increases. Maybe if you stack too many boxes, the older ones on the bottom get crushed under the weight and you have to remove those boxes as R. Eventually, P = R when you are producing as many boxes (P) as you are selling or crushing (R).

A very important point that you might be getting tripped up on is that neither source is saying that P = R always: they are saying that, over time, as an ecosystem matures after a disruption, P will eventually equal R. You could delay this from happening by constantly introducing new disruptions, but in that context if you just look over a longer period of time you will still see that P ~= R.

Last point - I am wondering, in your mind, what do you think is contributing to "gross production" of biomass if it isn't photosynthesis? What other processes produce biomass? I think the author changed P from photosynthesis to production to allow for more atypical ecosystems like ocean vents where chemical energy isn't coming from the sun.

Back then I had a bit of misconception about heterotrophic succession which lead me think that P is not Photosynthesis. Thank you for the answer.


text:
Which cells release inflammatory mediators?
Wikipedia says

Inflammation is stimulated by chemical factors released by injured cells and serves to establish a physical barrier against the spread of infection, and to promote healing of any damaged tissue following the clearance of pathogens.

then it mentions

The process of acute inflammation is initiated by cells already present in all tissues, mainly resident macrophages, dendritic cells, histiocytes, Kupffer cells, and mastocytes. These cells present receptors contained on the surface or within the cell, named pattern recognition receptors (PRRs), which recognize molecules that are broadly shared by pathogens but distinguishable from host molecules, collectively referred to as pathogen-associated molecular patterns (PAMPs). At the onset of an infection, burn, or other injuries, these cells undergo activation (one of their PRRs recognizes a PAMP) and release inflammatory mediators responsible for the clinical signs of inflammation.

From this we can clearly deduce that the inflammatory mediators are released by Pattern recongintion receptor producing cells. But while studing this topic from different sources some, books on nursing and Pharmacy. They keep repeating that inflammatory mediators are released by injured cells.
What is correct?

There are several kinds of inflammatory mediators. You can broadly classify them as cytokines (including interferons) and chemokines.
Cells which sense antigens (or pathogen associated molecular patterns) do secrete cytokines, as you said but infected cells also secrete some cytokines like interferons- α and β. Infected/injured cells also secrete chemokines that attract leukocytes to the site of infection/injury (Saiman and Freidman, 2012).


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Identification of brown butterfly with orange/black/white spots
These brown butterflies are very frequent at my place now. Two or three can be found quietly sitting with their wings folded everyday, at different locations. It's a transition period between Autumn and Winter here, West Bengal, India.
What species is this?
Why is it taking shelter inside a house? They don't seem to move much, even during the day I've found one sitting quietly by the window. It wasn't flying off even after being disturbed.

I think this is the "Dark Evening Brown" or Melanitis phedima possibly Melanitis phedima bela:

Some further information can be found here (image 1) and here (image 2). If you look close at the second image, you can see the spot on the wing.
Why they are coming into the houses is something I can only speculate about, but probably they are either attracted by light or by warmth.

As to your question why they come into the house: Some butterflies survive winter (hibernate) on a dry, cool but frost-free place such as parts of houses that are not heated. In autumn they actively search for such places. I often find them in a wood stack or on the attic. In Europe, examples are Gonepteryx rhamni, Polygonia c-album and Inachis io. I think the latter two belong to the same family as Melanitis phedima, so it might try to find a place to hibernate. For more info see https://www.britishbutterflies.co.uk/winter.asp

Slight wording issue; For these species (ones with a life history that includes hibernation as adults), it's not that they can survive winter as adults, it's how they survive winter. In most taxa of insects living in temperate regions species survive winter as either eggs, larvae, pupae or adults, or a mixture of hibernation stages.

@fileunderwater You are absolutely right. Improved that in my answer.

How long can these butterflies live?

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Why don't intelligent animals like primates use plastic bags?
I'll be honest here. Although this is a serious question, what made me wonder about it is this comic from Wumo:

This question is not specific to monkeys. It applies to animals that live with or sufficiently close to human dwellings and would be able to observe our habits daily. I'm not referring to training animals.
Even among animals that have an opposable thumb like ours but different HAR regions, the use of tools seems to be too primitive. Chimps have been known to re-use tools and even cumulative cultural evolution is documented. Whales have been hypothesized to have high intelligence (although not necessarily) due to larger brains containing more spindle neurons. But I couldn't find any info on whether whales use tools (Dolphins are said to use sponges though).
On considering if mirror neurons were helping chimps copy each other and use tools, I found that the very existence of mirror neurons in humans is under question.
So if a chimp can use simple tools, what prevents them from looking at us and imitating our use of something as simple as using a plastic bag or a crude tray to carry a bunch of fruits? Is there a gradation of complexity of tool use that various brains can process? A reason that no matter what happens, a chimp would not be able to imitate our use of tools? Could this be compared to how aged people are unable to learn how to use a smartphone or computer no matter how many times it is explained to them (or even how young people fail to understand pointers and recursion)? Perhaps the ability is related to an animal's capability to form new neural connections of a certain type?
Training an animal like Jack the baboon is different from what I'm asking.
Some examples of primates trying to carry many fruits.

Not an expert on this, and it's hard to prove a negative, but the only example I am aware of is that due to the way their vocal apparatus is setup, even the most close relatives to humans cannot exactly reproduce human vocalizations. It seems plausible that the stronger limitations are physical. If an animal has the means to use a tool and its survival depends on that tool's use, I do not see why it shouldn't be able to learn how to use the tool given enough time.

What use would a monkey (or a chimp - chimps are not monkeys) have for a plastic bag? Those animals don't typically stockpile or collect foods, they eat on the go.

Where would (wild) chimps see humans using plastic bags?  (Also, I think you are mistaken about older people not being able to learn to use smartphones.  I know many who have.)

Bags are not that useful if your are not human.
Most primates are too small to get any benefit from it, the bags are too large and would drag on the ground or get snagged on branches, even chimps and gorilla don't have enough ground clearance to not have this problem. Primates have been known to play with plastic bags, but they would not provide much benefit. A primate would need to carry the bag around for hours to fill it and wait before they could eat anything from it, all the while dragging it and hoping it did not tear. Upright humans are the only primate built to carry things long distance, a bag would not help other primates much.
Most primates are frugivores, carrying around extra fruit is not actually very helpful, most primates live near their food sources. Not to mention getting fruit in a tree into a bag is rather difficult task. Carrying around fruit is not very helpful because many primates have a different and much better way of storing ripe fruit in other primates AKA food sharing. Most primates will call other primates of the same species to ripe fruit since sharing in this way means they are more likely to have other primates share with them, thats far better food security than carrying around some extra fruit. It is also a lot easier to call many others to you than carry enough for everyone else.
The primates in your pictures are zoo primates which are both extremely bored and often very anti-social due to being raised in isolation. They might get some benefit, but they are not going to do well in the wild, and no zoo in its right mind is going to give its animals plastic bags.

Ok that's logical, but the question isn't really about plastic bags. It's about the thought process of animals going one step further to make more use of tools. I don't think even feral human children brought up by animals have learnt to use tools as well as we do. I know people who prefer using their hands in instead of pliers for better control while soldering, so I guess it's the hyperbolic discounting illusion of better control overriding the technical long-term benefit.

f that is your question you are not clear about it. And you need to define what you mean by "a step further" tool use is quite widespread in animals. also there is no such thing as feral children brought up by animals.

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What biological specimen is this? Seed? Excrement? Fungal form?

Hundreds of these 1-3 mm "seeds" have been found a couple of times this summer on my deck shaded by a large oak tree. But, they are not seeds with typical seed parts.  Too small to be pollen or spores.  I am baffled. They each have one or more deep crevices or slits longitudinally. Structurally, they appear to be composed of tiny (almost microscopic) wood chips. (Though I am sure this is just the appearance they have.) The first time I found them was after a rain and they had absorbed water and swelled to twice or three times their size and had become gooey and almost gelatinous to the touch. Almost looked like hundreds of little piles of brown poop on our deck. This time the weather was dry and they look as pictured in the photo.  I swept up hundreds in a four-foot diameter area.  Another area of the deck had a similar amount.  None on the rest of our deck or any noticed in other areas under the oak tree. My biologist friend was also baffled.  Please help identify

I meant to say "too large to be pollen or spores."

Interesting mystery! How do they behave if you cut/break it? Also, you can edit you post to include your correction.

Caterpillar defecation

All right, I'll say it if nobody else will.  Insect feces.  The "wood chips" you saw are bits of your oak (or some other over-hanging tree) that have graduated from the arthropod digestive tract, so to speak.  The pellets soak up water because the bugs are on a tight water budget and extract all the water before making a deposit.  Never heard of a gall infestation that produced feces like this, but who knows?  Look for dieing, deformed, or discolored leaves.  Look for bugs on the tree and on fallen leaves.  On the 2nd page of the document linked below is a larger specimen of what you are getting.  http://collier.ifas.ufl.edu/CommHort/CommHortPubs/Stained_sidewalks_under_Oaks.pdf

Welcome to Biology.SE! I think you've probably got it. Worth mentioning that insect faeces are normally called 'frass' (not least because Googling 'frass' then identifies a few images of caterpillar frass that look broadly similar; e.g. http://bugguide.net/node/view/842314).

These could be anthers from your oak tree—they look about the right size and shape.
Oaks produce separate male and female flowers. The female flowers become acorns. The male flowers are produced in a bunch on long strands called catkins.
Here's a fresh one.
Here's one where the anthers have opened to release their pollen.
Here's a close-up of a fresh anther.
This has some shriveled anthers still on the catkin.
Take a look to see if any of the catkin strands are on the ground or still on the tree.
(These photos are all from English white oak, so yours may be a little different. All these photos came from here.)

Since these pellets are found under oak trees, I researched further and found a possible answer on the internet in a different location.  Apparently, they are "galls" caused by insects disturbing the leaf structure of the oak trees.
https://ask.extension.org/questions/157218
Not sure, still, what exactly is raining down in the pellets.  Is it just dead plant material or is it something reproductive for the insects?  I am very familiar with the ping pong ball "galls" that sometimes fall from these trees.
Once they get wet and then dry again, they eventually become very powdery and crumble into dust.


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Resource for model organism anatomy/physiology for biological experiments
I'm looking for a resource that best surveys the anatomy and physiology of common genetic model organisms, and how their characteristics are particularly useful for biological experiments.
For example, I'm studying the eyeless Drosophila gene, but it would help to know that species' specific compound eye anatomy and normal development, so that I can weigh the pros and cons of using that particular model organism over another.

I don't think you will find a global DB like that. You will probably need to use flybase, mousebase, dictybase, wormbase etc etc.

In the Bgee database, you can look at gene expression and anatomy of various model species, e.g. Drosophila. This doesn't give you the full anatomy, but at least an ontology of tissues and cell types.


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Since Darwinian times, has there been any striking/notable effects of evolution on humans?
I understand that evolution is constant process that acts on a population in successive generations. Thus, it is obvious that evolution is happening. However, I'm curious as to the  stricking examples of evolution that have occurred since Darwin's publication of the theory.
Essentially, how different are we now from the humans at the time at which evolution was conceived?

Well, "On the origin of species" was published in 1859. If we assume that for humans a generation is approximately 20 years, that means that there have been between seven and eight generations since 1859. That is nowehere near enough time to observe evolutionary changes.
So, in answer to your question, not very different at all.
EDIT:
I think I need to clarify my answer. When we talk about a species evolving or a species being different today than it was X years ago, we are referring to the species as a whole. Of course evolution is an ongoing process, selective pressures are shaping our gene pool constantly. However, in order to say that humans are different today to those of 1859, we would need to show that the prevalence of particular genotypes has changed. That a specific trait (a gene or a mutation in a gene) has become "fixed", or, at the very least, that it has spread to a significant percentage of the population.
@niallhaslam's answer gives a link to a wired.com article about genetic resistance to HIV. This is not something that has recently evolved in response to HIV but is the result of an ancestral mutation. The article itself states that:

Using formulas that estimate how long genetic mutations have been
  around, researchers have discovered that the mutation dates to the
  Middle Ages.

Granted, this could be a good example of selection in action. If, after many, many more generations, this mutation has spread to the majority, or a significant percentage, of the population, we could point to it as an example of how humans have changed under the selective pressure of HIV infection. In order for this to happen, HIV will have to become common enough that having a resistance to is beneficial to a very large subset of humanity. I would expect to see such selective pressure in, for example, countries like South Africa where 12% of the population is HIV positive. Such pressure, however, will be negligible in countries with lower infection rates. In the US, for example, a recent study found HIV incidence among persons aged 13 years and older to be 42,200–54,000. Since the US has ~312 million people, 54,000 represents ~0.02% of the population. This will not provide enough of a selective pressure to observe differences in the short term evolutionary scale.
We do not, in fact, "evolve quickly in response to parasites viruses etc". Pathogens may apply selective pressure yes. But this is not a quick process. In any case, we do not evolve in response to them. Mutations occur, randomly usually, and if they confer an advantage they may be selected for. Said advantage may be because they confer resistance to disease but even then, the original mutation was not "in response" to the pathogen, However, such selection happens over many successive generations and will spread relatively slowly (quickly by evolutionary standards perhaps, but still slow for us, and certainly slower than 7 generations) across the population. The same holds true of epigenetic changes. Even if they can (as now seems likely) be transmitted down the generations, any selective advantage they confer will still act at the generational level.
So, while we are, of course, constantly evolving, there are no significant differences between the humans of today and those of Darwin's times. Sure, some genotypes may exist today that did not then and vice versa. These, however, are not representative of the species' genome. They may become so after many generations but, even if they exist, they have not had time to propagate through the gene pool and cannot be taken as evidence that H. sapiens as a species is "different" today.

In my opinion you are taking a very narrow view of what evolution means. However, with your clarification I have removed my downvote.

I am not expressing an opinion on evolution as such. Simply on what it would take to be able to say that a species has changed (has "evolved" as much as I hate that term in this context) since date X.

I would say that a species has changed as soon as the frequency of some gene has changed. Thus all species are always changing, and no generation is exactly like the previous one.

Even that is hard to define. For a species to have "changed" that change needs to be persistent. Otherwise it may just be a random fluke in a specific generation that will not survive to the next. Unless the frequency of a given mutation remains different over a few successive generations I do not consider that the "species" has changed.

We're constantly evolving resistance to disease, for example HIV.
It's reasonably fair to say this is still a contentious issue, but I think the point is that we still evolve quite quickly in response to parasites, viruses etc.
Another answer, though not strictly Darwinian is our epigenetic response to things.

Yes, the epigenetic, or Lamarckian, response is important +1. The environment - air/water quality, physical activity, availability of energy-dense food, antibiotics and other drugs - have all exerted influences on the epigenome.

But are epigenetic changes evolution?

@Alan Boyd - Epigenetic changes have been tracked across multiple generations, so they are inheritable. Obese mice will sire offspring who weigh more despite given the same diet and exercise as a control mouse. The effect can last for several generations, but that's a good question. I want to say yes, since evolution really just relies on inheritability and selection - but I'm not sure if epigenetic modifications could become permanent.

In this paper the authors identify many human genes that are under recent positive selection pressure, that is to say where natural selection is acting to promote the spread of certain genes.

They are indeed recent. The authors claim that the most recent changes were ≈6,600 years ago. While very recent indeed from an evolutionary point of view, they are still slightly older than Darwin :).

@terdon: Unless I'm missing something, isn't that 6,600 an estimated average age?  They are discussing several hundred different genes, some may be more recent. Furthermore, as they say, the timeframe is not precise and may only indicate when the gene became common.

I am just pointing out that the time frame here is not of the same order of magnitude. They show no evidence for changes that have become fixed in the last couple of hundred years. I only skimmed the article though, so please let me know if I am wrong.

I agree that they don't appear to produce specific evidence of that any of their examples are in the 200 year time frame. However, I don't think there's anything in the paper that precludes some of them being very recent.

Nor do they offer any evidence that they are very recent so I see no reason to assume that it is true. At least in my experience (in my defense, I did my PhD on comparative genomics), evolutionary changes simply are not observable in the kind of time frame (~7 generations) discussed here.

Fair enough. What would you say the minimum time frame is? Certainly there are plenty of examples of substantial changes happening in less than 100 generations.

Wouldn't presume to offer an opinion :). It is a very complex question that depends on many variables and I doubt there is one answer. It will also change depending on the level of stress (ice ages, disease pandemics and the like) that a species is being subjected to.


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Can diet, supplementation and/or drugs affect sexual dimorphism?
After puberty, can certain diets, exercise, and/or possible drugs affect masculine/feminine dimorphism in adults? We know dimorphism and/or morphology is a product of genes, but to what extent can this be altered through environment? Like, can chewing more give a more masculine jaw shape/angle? Can talking a certain way make a more deep, manlier voice? Can squinting give hunter eyes?
For women, can eating soy-based products increase hip-to-waist ratio? Estradiol?  Feminization of the face, cheeks and etc.? Likewise, in males, can vigorous exercise, drugs/diet and etc. masculinize?
Sexual dimorphism I mean as in how they look and what makes assure genetic/reproductive value.
Aside from genes, basically, what extent can diet, foods, exercise and etc. affect epigenetics, morphology and sexual dimorphism in animals, namely humans? Any evidence/studies/work on this?
This isn't intended to be a medical/personal question thing -- more so, broad on any means a human and/or animal may use their environment to try and improve dimorphism and morphology/phenotype.

Can diet, supplements, drugs or exercise improve masculine appearance in men and feminine appearance in women?
In short, some of the mentioned factors can affect the appearance of the muscles and fat tissue but not the bones, face or genital organs. I'm not discussing about hormonal treatment here.
MUSCLES
Resistant exercise in combination with sufficient calorie and protein intake can significantly increase the muscle mass (Essays in Biochemistry, 2008) in the limbs, torso and neck. You can't realistically expect that chewing or other facial exercises will significantly change the shape of your facial muscles.
FAT
If overweight, a hypocaloric diet can make you lose body fat and thus:

make you look more fit
make your jaw angle more prominent
reduce your breast fat (gynecomastia)
decrease your waist-hip ratio

A diet can result in increase or decrease, but not redistribution, of body fat, which is genetically determined (Diabetologia, 2014).
BONES
There seems to be no natural and healthy way by which you could increase the thickness or length of your bones or change their shape in adulthood.
Bone thickness
Exercise does not significantly increase the thickness of your bones - only 1-2 mm increase was observed in one study in tennis players (American Journal of Sports Medicine, 1994).
High intake of calcium, vitamin D, other nutrients or supplements in adulthood also does not likely visibly increase the diameter of your bones (it may increase bone cortical thickness or bone density, though).
Bone length
I haven't found any studies that would show how exercise or diet could increase bone length or shape in adults.
Jawline
The shape of jawline is mainly determined by the shape of the jaw bone. While the jaw angle can be affected by the genetically determined thickness of the chewing muscles (Scientific Reports, 2018), it does not sound realistic to change the jaw angle by chewing or other exercise.
Shoulder and hip wideness
The shoulder and hip wideness is genetically determined by the length and width of the bones in the shoulder and pelvic girdle and cannot be significantly increased by exercise or diet.
GENITALIA
I'm not aware of any exercise, diet or supplements that would significantly change the shape of genital organs.
VOICE
There are psychological factors, attitudes, conscious effort and exercises that can significantly affect someones voice.

Hormones found in food
Soy and some other foods are high in phytoestrogens that can have some pro-estrogen activity, but do not likely significantly affect the appearance of the muscles or bones.

Nevertheless, the only positive effects of phytoestrogens on bone
  observed so far in post-menopausal women have been small and limited
  to the lumbar vertebrae. (Baillière's Clinical Endocrinology and
  Metabolism, 1998)
Estrogen or soy isoflavones given to postmenopausal women results in a
  small increase in lean tissue mass. (Appl Physiol Nutr Metab.
  2008)

Hormonal drugs
Estrogen, testosterone, corticosteroids and other steroids and growth hormone can affectsome of the following features: the morphology of genitalia, muscle mass, body fat distribution, facial appearance and voice.

There is a slight inaccuracy in your title question. Let's clarify to begin with:
I think you are asking whether environmental factors can affect sexually dimorphic traits. I don't think you are aiming to ask about dimorphism itself (i.e. the presence of apparent differences between the sexes) specifically. You're not interested in whether, say, food will affect sex dimorphism in humans but rather whether it can affect phenotypes which are sex-specific. It's a good correction to start with.

Can diet affect sexual dimorphism?

Of course. This is the case with all sexually dimorphic animals. A good example is nutritional deficiency, sub-optimal calorie intake or ingesting hormones or metabolically-active natural products from food. For instance, a male stag's antlers will not grow very much if the stag does not ingest enough phosphorus or calcium. This has drastic effects on its ability to reproduce, as often antlers are a key element in sexual selection in deer species.
Also, in some nutrient deficiencies, the body's ability to produce sex hormones is affected, which in turn affects secondary sexual characteristics such as jaw shape and the storage of fat. In bulimia and anorexia, periods become irregular due to the body's state of chronic starvation and inability to regulate menstruation with hormone cycles. Thirdly, diet can affect the ethology of disease (diabetes is a good example) which can indirectly affect sexual characteristics. There are many complex examples in which disease has an endocrinological (hormonal) component.
In addition, regular exercise, for instance, is well-demonstrated to affect testosterone levels.
It's important to keep in mind that not all traits which are sexually dimorphic are visible. For instance, smoking has an effect on sperm count, which is something not visible but still constitutes a sex-specific phenotype.

Can supplementation and drug-use affect sexual dimorphism?

Of course. I think taking steroids and hormones is an obvious example. I don't think this one needs explaining - a search engine can help here.

Of course. I think taking steroids and hormones is an obvious example. < But I've seen people -- guys in particular -- who've used steroids and it didn't seem to affect dimorphism of the face. It builds more muscle, but doesn't necessarily create masculine dimorphism face-wise (i.e., stronger jaw; wider face; larger warrior skull; powerful brow ridge and etc.). If this was true then virtually every guy who's used steroids would look/have some kind of highly masculine, dimorphic, cro magnon-esque face, which we know doesn't happen to most male steroid users at least (but female maybe).

I don't think facial features are as 'plastic' in adulthood. Once they are set up, they change relatively little in shape compared to musculature, i.e. overall skeletal shape can't be changed much. The obvious changes that steroids induce are not skeletal, they are most obviously related to connective tissue, muscle, skin, fat storage, etc. Also, transgender individuals who have 'transitioned completely' with the help of sex hormones tend to have distinct facial features that are not typical of their biological sex. You can certainly masculinize or feminize faces artificially with hormones.

Then wouldn't your point be rendered invalid then? If you're a man with bad, non-dimorphic male bone structure and hormones do not make a difference in this way, how would they affect dimorphism then? A non-dimorphic face is bound by bones primarily. How would fat/skin/etc. matter if the overall structure of the hard tissue is what appears non-masculine? In fact you agree yourself with the "distinct facial features that are not typical of their biological sex" part you mentioned. It seems hormone manipulation post-puberty barely affects dimorphism.

You're using the word dimorphic incorrectly. I wouldn't use terms like bad either, it's not clear what you mean. I don't think you appreciate the diversity of things taking place when you introduce steroids. If a man takes estrogen, he will grow soft tissues on his breast region. Breasts are not typical male characteristics. If a woman takes testosterone, she will find an increase in muscle mass, changes in fat storage and a deeper voice. Muscle tone or body shape are very typical indicators of sex-specific traits. Your last statement that hormones barely affect dimorphism is thus incorrect.


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What is difference between light harvesting complex , reaction centre and photosystem
my book says light harvesting Complex are made up of hundred of pigment molecule bound to protein. Is photosystem has all the pigment (except one molecule of chlorophyll A )forming light harvesting complex also called and dinner this pigment help to make photosynthesis more efficient by observing different wavelength of light the single chlorophyll A molecule forms reaction centre.
These things are very confusing for me . I doesn't understand is light harvesting complex is present inside the photosystem or the photosystem is present inside the light harvesting complex.
Is reaction centre not a part of photosystem?


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Would prehistoric humans have been considered negroid or australoid by modern standards?
What are your thoughts about this?
For myself I think that the subject statement is rather obvious isn’t it, since Africans, & especially Australian Aboriginals, have the most archaic features & share the most traits with prehistoric humans & other primates within modern humanity? Africans have neotenized greatly, culminating with the khoisan people, whereas australoids don’t have any neotenous traits which the other races have been developing & don’t lack archaic traits which the other races have devolved.
Which of the great races, the highest general division of humanity, mongoloid, caucasoid, negroid, australoid, etc. would prehistoric humans have been considered both by layman’s perceptions, & classified as more scientifically, by contemporary standards, if the choice had to be made, or at least considered closest to or most resembling?
What we’re probably thinking of then are remains going really far back enough to not be of obvious contemporary racial categories aren’t we?
Since prehistoric humans are said to not resemble any modern race, this question may end up being more about opinions rather than hard answers, might it?
Please explain & fill in details regarding your opinion & knowledge. But please do answer the main question first before adding in more details, even if to explain how this subject statement has no merit!
Not sure how much merit this book holds, but do have a look at the tables in ‘Section II: Traits of Living Populations’ for a nice summary:
https://analyseeconomique.files.wordpress.com/2012/12/richard-d-fuerle-erectus-walks-amongst-us.pdf
Here’s the tables themselves. The site’s in French but you can translate it in google. You can also click on the images & save them:
https://analyseeconomique.wordpress.com/2011/11/20/erectus-walks-amongst-us-richard-d-fuerle-section-2/amp/

Which prehistoric humans? The ones giving rise to modern day Native Australian, Congolese, Han Chinese, ... ?

Your right, I should have been more specific, since the term prehistoric really means anytime before history. In human evolution terms, that would mean the whole time ranging from when our ancestors split from chimps’ some 6 to 10 million years ago to the eve of civilization some 6,000 years ago, & the current races already seem to have long evolved by then. Let’s take it gradually then, step by step.

I was really being generic & referring to all prehistoric remains not identifiable with modern human races. Let’s discuss gradually, starting from our earliest ancestors, then move on to the earliest identifiable human beings, being Homo Habilis & Erectus, then to our most recent genus cousins like Neanderthals & Florensis, then to the earliest identifiable anatomically modern human remains, currently being Jebel Irhoud, & the earliest outside Africa currently being the Skhul & Qafzeh hominins, then moving to other remains around the world.

The first question to answer might be: Has phenotypic diversity in humans increased or decreased since prehistory?  It might be the case that prehistoric humans were as diverse as modern humans, or more so, since there have been a number of diversity-reducing bottlenecks in our evolution.

https://australianmuseum.net.au/learn/science/human-evolution/how-have-we-changed-since-our-species-first-appeared/ This article might answer your question partly. Nice concise article overall. I thought it was interesting to read them explain in the 6th section that modern humans’ diversity is enormous compared to early Homo Sapiens, who they seem to suggest were all much more similar to each other in physical characteristics?

Still, I’m pretty sure that there would have been fair amounts of variation for most of our’s as well as our genus cousins’ histories, just as there is variation among just about all isolated organisms. Even far traveling bird populations have their physical & genetic isolations & variations within genera & species, so how could one expect terrestrial beings like us to be able to avoid that? You have a good point on how our species has had some bottlenecks. The only studies & information there seems to be available for that is genetics, & not so much about phenotypes.

We don't really know yet what archetypes were like in the paleolithic.
this is your reference: "L’incapacité des noirs à différer la gratification les conduit à louer au lieu d’épargner, à voler au lieu de travailler et d’attendre, et à violer au lieu de courtiser et de séduire. " blacks worship/rent not save, steal not work, rape not seduce? is that your best research? there are many africans with an IQ of 140 and europeans with an IQ of 60, sometimes entier villages of europeans. So he generalizes foolishly.
There probably never was an archetype from any age, there were instead dozens of geographically isolated populations at all times, and the variety of tribes and ethnicities in history is beyond what can be visualized, understood and imagined.
40,000 years ago, there were already chinese looking people, caucasian looking people, african looking people, you would be comparing thousands of different groups at any single time in the paleolithic, and we don't have that information.
The mesolithic, neolithic, bronze and iron ages, are all prehistoric times.
Your timeline is 300,000 years, and your reference compares negro's anthropometrics to orang-utans and gorillas and caucasians. It's a silly old racially biased pseudoscience document. Real science using DNA classes Africans into a dozen ethnicities as different amongst one another as europeans, chinese and australians.
This is a list of human fossils with images: https://en.wikipedia.org/wiki/List_of_human_evolution_fossils#Middle_Paleolithic:300,000%E2%80%93_50,000_years_old
Australians are geographically isolated people so they don't represent an archetype. They are an ethnic group amongst thousands that would have existed prior to boats and horses (3500 years ago), rather than an archetype.
There were probably many dozens of groups of peoples as exotic looking as Australians which have become mixed into todays spectrum of facial types. Nearly all the faces that existed 50,000 and 100,000 years ago have contemporary examples. https://www.bbc.com/news/av/world-14929644/beast-from-the-east-nikolai-valuev-seeks-siberian-yeti

Yes I am aware that the provided article seems to have racist agendas. I haven’t actually read the book & don’t know much about it yet. The agendas are not what I’m interested in however. All I’m interested in the book is the summary tables on the physical characteristics of the races. It’s nice & concise & seems to be accurate for the most part even if only brief & summarized. The tables were probably composed by the author himself, can’t seem to find such summary tables on the races elsewhere, especially considering how this kind of subject is considered politically incorrect in this era

https://www.diffen.com/difference/Ethnicity_vs_Race As quoted from these articles, race should not be equated with ethnicity, which has a sociological meaning. Ethnicity is a self-described category that has three components-ancestry, language, and culture that all have affinities to certain ancestral groups. Race refers to a person's physical characteristics such as bone structure and skin, hair, or eye color. Ethnicity, however, refers to cultural factors, including nationality, regional culture, ancestry, and language. http://www.biologyreference.com/Ar-Bi/Biology-of-Race.html#ixzz5e0Udb5cb

By ‘archetype’ I imagine you mean race by that term? I would agree that is a good way to describe the concept of the major races of humanity. I just hope you understand where the concept of race comes from, that all of human variation can be summed up into 3 or 4 broad but distinct categories phenotypically, & that it’s shown now that these categories don’t overlap with genetics. 40,000 years ago seems to be as far back to when we can trace current races, caucasoid & australoid to be specific, negroid & mongoloid is far newer, so what I’m interested in are the mysterious remains before that.


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Owl identification
This evening I spotted this beautiful owl that had become the centre of concern of my neighbourhood birds. There was a joint commotion of the House crows, Jungle bablers, Bulbuls and Maynas, which is still going on.
I wonder if this is a female Common Barn Owl.

Location: West Bengal, India.
P.S. I couldn't get better pictures.

That appears to be a barn owl, Tyto alba.

Based on the picture, this is a Barn Owl (Tyto alba). There are several subspecies of Barn Owl, 35 in fact. This bird is most likely the subspecies "stertens" also known as the Indian Barn Owl.

As to whether it is a female. It is dependent on the size and a few other features that cannot be determined in these photos.

Females significantly larger than males in body mass, total length, beak length, tarsus length, foot length and width, and wing loading, but not in wing chord or tail length ( Marti 1990a ). Female plumage typically darker than that of males but sexes overlap in this regard.

It's a barn owl. This is probably the most common owl in India and is found in most of peninsular India.


text:
Reason behind formation of positive supercoils during DNA replication/ transcription
When a twist is unwound without cutting the DNA strands or is removed by cutting the strand(s) and resealing, negative supercoils are introduced in the DNA.

From Cell and Molecular Biology -Karp
But strangely enough unwinding of DNA by helicase cause the DNA ahead of the primosome to form positive supercoils. Why is it so?

From: Molecular cell biology -Lodish
My speculations: Underwinding cause the adjacent DNA to overwind and as the DNA overwinds the associated stress developed cause the DNA to form positive supercoils (which would have happened naturally had new twists been introduced in the DNA (Time:1:54) ).
I think removal of twist creates negative supercoils initially but when the unwinding causes too much overwinding of adjacent DNA, the strain developed cause the already negatively supercoiled DNA to form positive supercoils.

It's hard to explain in text, so here's a video:
https://www.youtube.com/watch?v=J4YlcD59-yw
Imagine the shoelaces are two DNA strands in a double helix. They are topologically constrained at each end. As the pen (helicase) moves through the helix, it creates overwound DNA in front of it and underwound DNA behind it.

Does that answer your question?

I didn't follow the notification about this answer. I also found Genome Duplication, pg-12 mention it.


text:
Does one need to perform two Chi-square tests?
A question from my University's Question paper 2016:

A newly identified fruitfly mutant, cyclope eye –large and single in the middle of the head is hypothesised to be autosomal dominant. The experiment started with homozygous wild type females and heterozygous cyclopes males. The data from the F2 generation was 44 wild type males males, 60 wild type females, 110 cyclops males and 150 cyclops females. Does this support or reject the hypothesis$^1$? Use chi square to prove.

I think the following should be a proper approach at solving it:
H0= The proportion of cyclope eyed male and female is not that same,i.e. the gene responsible is not autosomal. $or$ There is an association between the sex of fruitfly and the phenotype.$^2$
H1= The proportion of cyclope eyed male and female is the same, the gene is present on autosome $or$ There is no association between the sex and the phenotype.$^2$
Chi square contingency test with Male and Female (in the columns) and Wildtype and Mutant phenotype (in rows).
Once the H0 is proved wrong (if it is proved wrong), we consider a next Chi-square test, goodness-of fit, where :
H0= The proportion of mutant phenotype is the same as the wildtype i.e. 1:1 ratio is followed
H1=The proportion and the mutant phenotype is greater i.e. the allele responsible is dominant.
When the final H1 is accepted the $^1$hypothesis is correct or else wrong.
$^2$ I'm not sure which one is better / proper.
Is it alright?

The wording of the cited question is strange. Hypothesis testing does not "support" anything, and definitely does not "prove" anything. All you can do is reject the null hypothesis. This means the alternative hypothesis is consistent with the data, but does not prove it. Hypothesis testing is asymmetrical in this sense, and that is very important to grasp.

You should just have 1 chi-square test to test the hypothesis.
Note that the problem is asking about F2 generation, not F1.
H0 in a chi-square test is your prediction based on a model; H1 is that the real outcome differs from what is expected, so you have that a little backwards. H0 should be the expected counts knowing the initial proportions and expecting autosomal dominant inheritance.
Start with your prediction:
F1 generation will be half heterozygous males/females, half WT males/females, so F2 generation has 3 types of mating events:
Cc x Cc occurs 25% of the time, and 75% of offspring are affected
Cc x cc occurs 50% of the time, and 50% of offspring are affected
cc x cc occurs 25% of the time, and 0% of offspring are affected
Multiply these probabilities and you should have 43.75% expressing the phenotype; your prediction for the chi-square test is that you will see this same percentage regardless of sex.
From there, doing a chi-square test is simple and there are many many resources online for this (here is just one).

Is it a two-tailed test? Because the observed data can be significantly more or less than the expected 43.75% i.e 7/16?

@SanjuktaGhosh Chi-square is always one-tailed. It isn't a two-sided distribution like the normal, values that are off to the left are basically just "unexpectedly great fits" like if you flipped a coin 1000 times and got exactly 500. If you look at the math in the calculations they are based on squared differences, so 7/16 and 9/16 are treated exactly the same: if you predicted 8/16 in one case you have 1^2 in the other case you have (-1)^2.


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How to incubate freeze dried culture?
I have a freeze dried culture of staphylococcus aureus; how do I incubate it?
Can I just mix it into Luria broth and just keep it in the incubator?

Yes, it's that easy!

Please don't ask the same question repeatedly. You were already given an answer to your previous question, why did you ask again?

Many micro-organisms do not tolerate freeze drying (you should freeze them using cryo-protectants). Apparently Staphylococcus can tolerate it. You don't directly put the dried cells in the medium. First you have to rehydrate the cells using the medium and then transfer them to the culture vessel. See the following instructions from ATCC:

The preferred method for long-term preservation of bacteria and algae
  is freeze-drying; however, some bacteria do not survive freeze-drying
  well and are frozen instead. For freeze dried cultures, using a single
  tube of the recommended media (5 to 6 mL), withdraw approximately 0.5
  to 1.0 mL with a Pasteur or 1.0 mL pipette. Use this to rehydrate the
  entire pellet, and transfer the entire suspension back into the broth
  tube and mix well. The last few drops of this suspension may also be
  transferred to an agar slant. Alternatively, algal cultures must be
  initiated on agar plates. Please note that anaerobic bacterial
  cultures must be rehydrated in an anaerobic environment; the viability
  of the cells decrease rapidly if the vial is rehydrated in an oxygenic
  environment.
Incubate cultures under the appropriate conditions. Given proper
  treatment and conditions, most freeze-dried cultures will grow out in
  a few days. However, some may exhibit a prolonged lag period and
  should be given twice the normal incubation time before discarding as
  nonviable.

If you had received the cells from some repository or a vendor, you would have also got an instruction manual on how to revive the cells and what media to use. It is best to follow the specific instructions given in the manual.

What is special about the rehydration medium? Like what is it made of?

@user2990508 From ATCC manual it appears that is same as the medium in which you are going to grow the cells. If you are buying from a vendor then follow the specific instructions mentioned by them.


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Do all microRNA isoforms need to be known and sequenced to obtain microRNA expression?
From what I understand, microRNA are short "hairpin" shaped nc structures. When sequencing and counting miRNA, isoform miRNA are "found" which are subsections of varying length and possibly with some mutations or other differences to the "canonical" microRNA. The total counts for a miRNA are the sums of the counts for the isoforms which relate to that miRNA. [Please correct me if this is all wrong]
With regards to Next Gen Sequencing, a 'library' needs to be added which tells it what to sequence. Does this mean only "known" isoforms be read and counted or can "new" sequences (i.e. mutations) also be read and counted which were not known before sequencing started?
With regards to qPCR - does this technique only look for individual isoforms? In which case, if I want to know something about a particular microRNA expression would I need to do qPCR for each known isoform relating to that microRNA. OR, is it in fact easier to sequence microRNA expression with qPCR since sequences can be matched to the main hairpin structure with higher probability. (By easier I mean compared to say wanting to get the expression for a particular isoform since it needs to be matched exactly).

With regards to Next Gen Sequencing, a 'library' needs to be added
which tells it what to sequence. In the context of NGS, the "library" is a pool of molecules which you sequence. You don't have to know their content to get their sequence.

I had worked on a similar problem and I am telling my experience.
First, you have to consider the fact that a mature miRNA can arise from multiple genomic locations i.e. many pre-miRNAs can give rise to same mature miRNA.
As you said there are products of pre-miRNA cleavage with heterogeneity at their ends i.e. there are sequences that do not exactly match the annotated mature region. While products with 3' heterogeneity can be called isoforms, products with 5' heterogeneity are likely to have different targets as the seed sequence is disrupted and hence they are technically different miRNAs (by definition).
Now, the best technique to analyse isoforms is small RNA sequencing (NGS). qPCR would not be a good technique as primers cannot always differentiate highly similar sequences (worsened by the fact that miRNAs are too small). A NGS library is a set of DNA sequences that you obtain from shearing the RNA/DNA followed by adapter ligation (reverse transcription for RNA). Since the adapter sequence is known, the sequencing reaction does not require you to know the sequence of the products. However, you would need to know the reference genome for finding novel miRNAs. This is primarily due to the fact that it is very difficult to sequence pre-miRNAs (low abundance and hairpin structure). You can identify new small RNAs very easily but cannot say that they are miRNAs unless you can map them to a stem-loop precursor (pre-miRNA).
You can very well discover new reads and people have discovered a lot of new miRNAs using NGS. I can tell you the methodology I followed to find atypical products of the same pre-miRNA. I for simplicity I call the 5' heterogeneous products as badseeds (because they have disrupted seed sequence) and 3' heterogeneous products as isomiRs. I used a methodology that is similar to that of a well known program – miRdeep.

Get the pre-miRNA sequences from miRbase
Get mature miRNA sequences from miRbase
Use bowtie-1 to build an index from the pre-miRNA sequences
Remove adapter from your fastq reads and remove low quality reads. There are many tools to do that. You can try Trimmomatic.
Map mature miRNA sequences to pre-miRNA index using bowtie to find the exact location of mature miRNA in pre-miRNA
Map reads to pre-miRNA region. Filter reads that do not map in a pre-defined window around mature region.
Classify the reads as badseed or isomiR

Now, isomiRs and reads that perfectly map to mature miRNA region can be considered as contributors to total miRNA expression. However, badseeds should not be considered as an isoform. You can likewise allow a certain level of mismatch and count these reads. Sequences with mismatch in seed region would again be badseeds. You can additionally have scoring schemes for your reads.
There are not many studies on such analysis. I did not get any publishable result with our data but the methodology is reasonably correct. You can go ahead an apply it for your study.

Ok, at least one answer to the question. The basic point in the answer that's really a comment is worth retaining: the library is the pool of sequences you obtain from NGS, and you sequence all the RNA of a particular size. You identify what you have sequenced in relation to a reference — it could be a reference genome in which the miRNAs are already annotated, or you can try to discover new ones, as you did. And you (or at least I) don't find any pri-miRNAs.


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What are these two insects (or at least one of them)?
I need to catch and identify insects for my biology project, but I cant identify those two bugs.
Can I get the genus and the species (or it can be just general name of what this type of bug is called?)
They were found in Chicago suburban area.

Can you add a short description for their morphology is not very clear to me,especially the second one? Has it got wings?

This question should be splitted, because now you cannot except both right answers.

I the first insect is a cricket, female Fall Field Cricket,Gryllus pennsylvanicus.

It is widespread across much of North America.They are  often found around areas of human habitation.
The the coloration ranges from dark black to dark brown, although some specimens show a slight reddish tint. The black antennae tend to be longer than the body span of the species.

It is a female because it has a long blackish brown ovipositor.

References:

Wikipedia

pbase.com

bugguide

Thanks! I also found the second insect and answered in another answer. I gave you best still..

After tiring hours of research of not knowing what even is the second bug's order I've finally found the second bug as other part of the answer.
The second bug is Slender meadow katydid, Conocephalus fasciatus from order Orthoptera, also a female.

The green abdominal projection is its ovipositor.


text:
How come Logs-Odds Scoring Matrix is symmetric?
I am studying Pevsner's Bioinformatics.
It is stated that Logs-Odds Scoring Matrix is symmetric at page 89.
But with given the equation to calculate the cells of the matrix, I find different scores for from cysteine to leucine and for from leucine to cysteine.
How is this possible?
Do we take the lowest value?
The equation used for constructing Logs-Odds Matrix from a corresponding Pam matrix is : $s_{ij}=10\times\log_{10}(M_{ij}/f_i)$
where $M_{ij}$ is the observed frequency of substitution for each pair aminoacids.
and $f_i$ is the probability of aminoacid residue i occurring in the second sequence by chance.

I'm voting to close this question as off-topic because it is about statistics, not the underlying biology. Please ask at [stats.se].

To answer this will require more information, given that most respondents will not have p. 89 handy. What is the equation you speak of?

Since I do not know what calculations you did. I am going to answer your
"How come Logs-Odds Scoring Matrix is symmetric?".
Let us assume that it is not.
So
\begin{equation}
S_{ij} \neq S_{ji}
\end{equation}
\begin{equation}
M_{ij}*f_j \neq M_{ji}*f_i
\end{equation}
Is this not in contradiction with Bayes theorem?. Yes.
So log odds matrix is symmetric.


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Was the mitochondrion or chloroplast first?
I still don't  know if the mitochondrion or chloroplast was first? I've looked for it on the internet and in various books but haven't found anything. Does anyone have the answer and a theory which backs up this answer?

Mitochondria evolved before chloroplasts.
We know this because Mitochondria form a monophyletic group: e.g. all life with mitochondria traces back to a single common ancestor (source). Since the group with chloroplasts groups within this clade, it must be the case that either (a) chloroplasts were obtained by an organism that already had mitochondria or (b) chloroplasts were independently lost by multiple lineages within the Eukaryotic clade and then many of these lineages re-acquired chloroplasts by secondary endosymbiosis. Since (a) is a (much) more parsimonious explanation it is the one it makes sense to accept.

Straight and convincing.

I do not have a definitive answer but I can argue that mitochondria came into existence before chloroplasts despite the fact that, between their free living ancestors- $\alpha$-proteobacterium and Cyanobacteria, the latter seems to be older in evolution.
I have following points to support this argument:

The organisms that have chloroplasts also have mitochondria but the converse is not true.
There have been events of secondary endosymbiosis (especially in the Chromaveolata) in which organisms that already contained chloroplasts became endosymbiotic organelles in another host.
There is a very recent case of endosymbiosis of a chloroplast like organelle called spheroid bodies in the diatom Rhopallodia gibba which already has a secondary plastid. See this.

Usually a cell has many mitochondria but fewer chloroplasts. Though this doesn't say much about the evolutionary age but higher number allows more organelle to nuclear gene transfer, considering the limited transfer window hypothesis. More the transfer, more "dependent" will the organelle become on the host.
Even though I claim in the first paragraph that Cyanobacteria is older than $\alpha$-proteobacterium (In fact I dont have a strong reason to support that claim), it doesn't mean that photosynthesis has an older origin. Chemosynthetic pathway and membrane bioenergetics have evolved very early on. Coupling of light to assist these processes, most likely came later when organisms surfaced to the limnetic zone.

The use of molecular oxygen as an electron acceptor evolved some time after photosynthetic processes had made molecular oxygen abundant in the earth's atmosphere. So I think you can make the argument that photosynthesis has an older origin compared to the oxygen dependent metabolism that is performed by mitochondria.

Point taken. But oxygen is not the only electron acceptor... Mitochondria which use $Fe^{3+}$ also exist (one of the $e^-$ acceptors other than Oxygen). So yes, photosynthesis is older than aerobic respiration but ATP-synthase is older than both :)

@WYSIWYG: your third argument doesn't seem very strong.

@har-wradim yes that's the weakest of all :) I mentioned it because it is likely that mitochondria are numerous because they became associated early on. Also considering the limited transfer window hypothesis, the chance of mitochondria to nuclear transfer of genes is easier because of its higher number. Although, one can argue that $\alpha$-proteobacterium was inherently fast dividing than Cyanobacteria and therefore the higher numbers in the cell.

I think you mean "descendants", not "ancestors", and even then, this is probably incorrect. The original endosymiont is probably in a sister clade to the extant bacteria. I also think the single origin of both endosymbionts is the strongest argument, anyway.

According to my knowledge, this was the molecular and cellular evolutionary path of life.

Synthesis of essential building blocks (fatty acids, aminoacids, cofactors...)
Condensation of building blocks
First RNA replicase; RNA genomes (differentiation between genomic and
functional RNA, primitive metabolism)
Ribosomes and first matrix dependent translational machinery
Copying RNA into DNK (rNDP reductase, reverse transcriptase)
PROGENOTES (DNA genome, introns in genes, slow growth, anaerobic
heterotrophs)

From here you have two main branches, organisms with branched lipids, and with unbranched lipids (the first will become archaea, and the latter urkaryotes and Bacteria)
In the Urkaryotes, you have selection of complexity. Their growths is inefficient, and they tolerate extra DNA. Bacteria favored efficient growth, autotrophy and loss of extra DNA.
At this point the endosymbiosis occurred (presumably), and the bacteria became a very specialized parasite. Mitochondria as you probably know, have their own genome which replicates independently from the nuclear genome. Cells and mitochondria became permanently linked when the mitochondria "decided" to relocate parts of it's genome to the nucleus, incorporating it's genome in the host's.
Now we have the first Eukaryotic organisms that are similar to today's. They were heterotrophic, but one more event of endosymbiosis occurred. That was the formation of chloroplasts.
Many people think that autotrophy is more primitive compared to heterotrophy. That simply isn't true. The conditions when these organisms arose were quite different. Building blocks were readily available and plentiful, so the organisms were all "friends" with each other. It is when food became scarce that selective pressure started nudging species into different directions (autotrophy).

Why would a mitochonrion be of any advantage in a world without oxygen?
Chloroplasts evolved to fill the atmosphere with oxygen then mito's exploited that situation.

Welcome. You may have an interesting point, but without sources it's more of a comment than an answer. The more so as your answer seems to contradict the existing answers above. You will need some reputation to place answers, but if you could improve your answer with some more evidence and sources to allow other users to background read on your answer, that would be great.

Chloroplasts did not evolve to fill the air with oxygen, but were acquired symbiotically to allow plants to obtain energy from photosynthesis. This had already evolved in cyanobacteria, which were responsible for the great oxygenation — not chloroplasts in plants. We welcome new users to SE Biology but, please respect other members. Given the detailed and academic responses already received for this question, you might have considered that the previous contributors to this question had some knowledge of this area.


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Microbial Fuel Cell Reaction
I found a formula online which explained the reaction which occurred in the anode chamber of a microbial fuel cell but there was a typo
$\small NADH + Ferredoxin_{(ox)} (NADH-Ferredoxin\ Oxidoreductase) \longrightarrow NAD^+ + Ferredoxin_{(red)}\ \
Ferredoxin_{(red)} (Hydrogenase)\#61614;Ferredoxin_{(ox)} + 2H^+ + 2e^-$
I attempted to correct it but I'm not sure if I'm right could you check this and see if it's correct?
$\small NADH-Ferredoxin\ Oxidoreductase \longrightarrow NAD^+ + Ferredoxin_{(red)}$
$\small Ferredoxin_{(red)} \longrightarrow Hydrogenase + Ferredoxin_{(ox)} + 2H^+ + 2e^-$

This the page? http://www.altenergymag.com/emagazine.php?issue_number=07.04.01&article=haldia

Anode reaction,
$\small Glucose + 2NAD^+ (Embden-Meyerhof pathway) \leftrightharpoons 2 Pyruvate + 2NADH$
$\small Pyruvate + Ferredoxin_{(ox)} (Pyruvate-ferredoxin Oxidoreductase) \leftrightharpoons Acetyl-CoA + CO_2 + Ferredoxin_{(red)}$
$\small NADH + Ferredoxin _{(ox)} (NADH-Ferredoxin Oxidoreductase) \leftrightharpoons NAD^+ + Ferredoxin_{(red)}$
$Ferredoxin_{(red)} (Hydrogenase)\leftrightharpoons Ferredoxin_{(ox)} + 2H^+ + 2e^-$
[Last one: http://en.wikipedia.org/wiki/Ferredoxin_hydrogenase]
Cathode reaction,
$4 H^+  + 4e^- + O_2 \leftrightharpoons H_2O$
$C_6H_{12}O_6 + 6O_2 \leftrightharpoons 6 CO_2 + 6 H_2O, DG° = - 2870 kj$
Full paper: http://www.altenergymag.com/emagazine.php?issue_number=07.04.01&article=haldia


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Why does Taq polymerase add 3' adenine overhangs?
Is there a mechanism for the preference of Taq polymerase to add a non-templated 3' adenine (overhang) instead of other bases?

Non-templated terminal addition by certain DNA polymerases is apparently dependent on the base stacking between the incoming base and the existing duplex (Fiala et al., 2007*). This was verified by using a non-base-pairing (but better stacking) nucleotide analogue called deoxyribo pyrene nucleoside triphosphate (dPTP). Adenine seems to have a higher efficiency of base stacking compared to other three bases:  A (1.0), G (0.7), T (0.6), and C (0.5)
It was also verified that the preference for dATP did not depend much on the terminal base-pair of the duplex with the incorporation probabilities being:
79% dATP 16% dTTP, 3% dCTP, and 2% dGTP when the last base pair is A-T (A is 3'), and
81% dATP, 8% dTTP, 8% dCTP, and 2% dGTP when the last base pair is G-C

Fiala, Kevin A., et al. "Mechanism of template-independent nucleotide incorporation catalyzed by a template-dependent DNA polymerase." Journal of Molecular Biology 365.3 (2007): 590-602.
*They had used the Dpo4 polymerase from Sulfolobus solfataricus as a model because it is a known lesion bypass polymerase and its kinetics and structure are well studied.


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What is the charge on oligonucleotide 5' pGpGpApCpT 3' at pH 7.00?
What is the charge on the nucleotide 5'pGpGpApCpT 3' @ pH 7.00?
I thought adenine has 1 NH group and Guanine has NH and OH groups and cytosine and thymine  has OH groups on it and phosphate at 5' end an OH at 3' end .so at pH 2.00-3.00 OH will give away an electron and becomes negatively charged.so is it +2+2-1-1-1 which is -1? please explain?

Does gp mean group? Also, atoms don't become negatively charged by giving away electrons.

@canadianer GGACT are the nucleotides and the p stands for the phosphate backbone I presume..

@TheLastWord No I was referring to something  else that was present before the post was edited.

@canadianer k..

I didn't quite understand where you're getting all your OH groups, maybe from the enol tuatomers of the nucleotides. I tried to look up the pKa's for the keto tautomers of the nucleotides on Wikipedia1,2,3,4.

In general, if pH is below a functional group's pKa, that group will be protonated, and if pH is above pKa, it will be deprotonated, though this is an equilibrium.
If we assume pH of 7 and assume I have the pKas right ( these values are for the free nucleic acids, no deoxyribose attached ), then the primary amines on A, G, and C will be protonated NH3 groups with positive charges.The amides on G and T should remain deprotonated and uncharged.
So with the sequence GGACT, we have 4 primary amines, so 4 positive charges. However, we also have 5 phosphates, each carrying a negative charge, so +4 plus -5 is -1.
Of course all of this goes out the window once we bind that oligonucleotide to another oligonucleotide, I assume the hydrogen bonding will alter the pKas and charges. For all I know, simply attaching the nucleic acids to a deoxyribose and stacking them together changes the pKas.

we also have -ve charge at 3' oh end right?

I don't think the OH group on the 3' terminal deoxyribose would deprotonate, hydroxyl groups don't usually deprotonate at neutral pH unless something is pulling electrons away to stabilize the negative charge, such as the carbonyl in carboxylic acids. For example phenol has pKa of 9.99, while benzoic acid has pKa of 4.2.

There is no positive charge on the bases at pH 7, but there are 4 phosphodiester bonds which have -1 charge on each phosphate so total -4 also the terminal Phosphate at 5' end is free so it has a charge of -2.
Thus the overall charge of the oligonucleotide is -4-2=-6 (determined by number of phosphate groups)

There is no positive charge on the bases at pH 7, thus the overall charge of the oligonucleotide is -4 (determined by number of phosphate groups)... See details here: https://books.google.cz/books?id=v9HL5VyRmZcC&lpg=PA204&ots=DQYKZ9PxXg&dq=why%20amino%20group%20of%20nucleo%20bases%20protonated&pg=PA204#v=onepage&q=why%20amino%20group%20of%20nucleo%20bases%20protonated&f=false

It's unclear which text you are referencing in the linked book.  Can you quote the relevant portion?

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