text:
How to determine the evolution of a dimension of fitness that has high variability of selection intensity?
How can one determine the evolution of a dimension of fitness that has high variability of selection intensity (low in some generations, high in others) compared to other dimensions of fitness?

Fitness is unidimensional (for an individual, it is a single point, not a matrix). Phenotype and environment are typically highly multidimensional.

The question is unclear to me. Are you talking about analysis of G-matrix (see Arnold et al. 2008 and this post)? Telling us what you've found for the moment would be helpful. Also, if you have a specific application in mind, you can let us know your end goal.

I mean, in a given generation, there may be stronger selection intensity upon an individual's ability to evade predators than upon an individual's ability to find territory.  In another generation, selection on each of these abilities may be more modest.  (I am referring to each of these abilities as a "dimension" of fitness.)  Does this make sense?

Oh ok. That makes sense. I don't think anyone ever referred to the covariance between a given phenotypic trait and fitness (as this is what you are describing I think) as a dimension of fitness. Roff's book, as I recall offers a good semantic on the subject but I don't fully remember it by heart.

I think that a case-study example in your post would be helpful to understanding exactly your goal (I am removing my close vote in the meantime).

This isn't my area of expertise, so excuse my ignorance if necessary, but I feel like your question might be more straightforward if you remove the "dimension of fitness" terminology unless this terminology is standard in the field. Perhaps your question is "How does variability of selection pressures between generations influence the evolution of relevant traits?" I am assuming you are looking for a semi-quantitative comparison of the rates of change in genotypes when selection pressures are variable vs. static across generations.

And it looks like Remi.b beat me to it - I would reiterate that a case study or explanation like in your comment would improve the question and help solicit quality answers.

Thank you, Remi.  Yes Bryan, but not just the selection pressure upon a whole genotype, the selection pressure upon individual traits.

I think a case study will be rather elaborate.  I'll work on it.  Thank you.

When I said genotypes what I really meant was allele frequencies that lead to particular distributions of genotypes in the population, sorry for the imprecise terminology - I think this fits what you are asking.

It's complicated. The classic answer is from Dempster 1955 Cold Spring Harb Symp Quant Biol 1955. 20: 25-32 (doi:10.1101/SQB.1955.020.01.005), which has a whole section on "Selection Intensity Varying With Time".  Summarizing:

An example from Kimura (1954) with a mean selective coefficient of zero: "the variation of selection facilitates the loss or near loss of alleles thus tending, if anything, to decrease rather than maintain genetic heterogeneity".
An example with haploid populations (approximately equal to the diploid case for weak selection) with a time-varying selection coefficient of $s_k$ shows that the behaviour of allele frequencies over time depends on the mean value of $m=\left\langle x_k \right\rangle= \left\langle\ln(1/(1-s_k) \right\rangle$, i.e. the geometric mean of the relative fitness; in general, the geometric mean is smaller than the arithmetic mean (i.e. variation in time would lower the fitness advantage of the more-fit allele). I believe the bottom line here (although it takes quite a bit of work to understand the whole story) is as given in the last sentence of the paper: "Selection pressures variable in space or time could act to maintain genetic variance of fitness ..."

On the other hand, Tănase-Nicola and Nemenman (2011), "Fitness in time-dependent environments includes a geometric phase contribution" (DOI: 10.1098/rsif.2011.0695) say it's still more complex:

the selection coefficient in infinitely slowly changing environments (we call this the adiabatic limit) is given by a time-average of static selection coefficients corresponding to each environment. This time-average is equivalent to the geometric mean result of Dempster [10]. It is independent of the order or the speed with which different environmental states are visited. However, for environments varying at a slow but finite rate, this time-average is not the whole story ...

All of the above is about the evolutionary dynamics of a single allele, not a comparison of the evolution multiple alleles/traits within the same genome.  Things could get (much) more complicated in that case, even in the absence of explicit pleiotropy, linkage, etc. (e.g the Hill-Robertson effect). I doubt there's a simple answer; I would suggest heuristic guesses based on independent dynamics of alleles based on the single-allele phenomena described above, followed by simulation ...

The question does not contain the term "time". Only in one comment did the OP said "in a given generation" and "In another generation" and I would suspect (s)he got lost in between several concepts in trying to clarify the question (but might be wrong). I am not sure the OP was interested about selection pressures varying through time.

fair enough, but what else would "low in some generations, high in others" mean?

I think it was a point where the OP got mixed up with two different concepts when writing his comment. But again, I might be wrong. It will be the OP's job to clarify it. (I am not saying the answer is bad, I just wanted to highlight the point that I find unclear in the post).

I also read the OP's original question to mean variability in time even if this wasn't mentioned explicitly (as opposed to variable pressure on different members of the species) - I think this is the more interesting question because variability across members of the species seems trivial.

Ben Bolker, I thank you very much for that answer.  Remi, this is the kind of analysis I was looking for.  Makes me wonder what you thought I was looking for.  Yes, I'm looking for selection pressures upon a trait varying from generation to generation (though not necessarily varying within a generation).  I've tried reading Dempster's article, but I'm stuck because I don't see how this answer was obtained:  "The change in p in one generation of selection is spq/(1--sq) in the haploid case and spq/(1--2sq) in the diploid."

I haven't looked at it carefully, but this is presumably what you get if you go through the algebraic steps of computing the expected number of each genotype (p^2, q^2, and 2pq in the diploid case or p and q in the haploid case), the relative number of offspring for each genotype, and then scaling by the total number of offspring - i.e. this should be found in any standard population genetics book ...

if this answers your question, you can click on the check-mark to accept it ...

Ben, I sincerely apologize. I did not get notification about your comments.  It actually appears that the formula given (spq/(1-sq)) is the same as the one Remi referenced in this post (http://biology.stackexchange.com/questions/15984/how-do-i-calculate-the-change-in-allele-frequency-in-a-haploid-population-under?rq=1). The derivation is there too. Now I understand it. I appreciate your helpful answer, but I don't feel it answers my question completely (maybe I have to better understand Kimura 1954). If I click the check mark, does it discourage future replies? Do you still get credit?

If you don't feel your question is adequately answered, there's no pressure to accept an answer. However, if you think you can edit your question to clarify what you don't understand, or otherwise try to improve the chances that I or someone else will be able to answer in the future, that would be useful.  You're also welcome to answer your own question, if and when you answer it to your own satisfaction ...


text:
Do transcription factors block transcription entirely?
Transcription factors bind to the DNA to block the transcription of a certain gene, right? But while they are bound to the DNA, do they completely block any transcription of this gene for as long as they stay there or can they also partially block transcription?

Different transcription factors have different effects: they can increase or decrease transcription. Your question is probably too broad, because there are so many different transcription factors which can interact with DNA at different distances from the influenced gene, or interact through protein complexes, etc. See wikipedia for more on the diversity of transcription factors.

Of course it's never 100%. The protein still has a measurable Kd for the DNA, meaning that there's always some part that's not bound (or some time that it's not bound.
Besides that, you're talking about repressors. There are also activators, and they use many different mechanisms. The same regulator protein can even recognize different sequences of DNA and repress one gene more than another. Some can bind and actually recruit a RNA polymerase, some work only while they're binding small molecules.
https://en.wikipedia.org/wiki/Transcription_factor or your molecular biology textbook might be a good place to learn more.

Like Bryan had said in the comments, transcription factors can perform different types of work. Sometimes, binding onto the template DNA strand can cause the RNA polymerase to be activated while sometimes, vice versa.
According to Wikipedia, transcription factors are:
"...protein[s] that binds to DNA and regulates gene expression by promoting or suppressing transcription"
So both promoting and suppressing is possible.
Transcription factors are combinations of multiple types of proteins, therefore it would depend on what protein you mean.

Please add a link to that Wikipedia page and consider adding something from a slightly more reputable source.

source: Stack Exchange

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

sort: votes


text:
Why do we make T4 if we only use T3?
So, recently, I learnt that T4 and T3 are both released into circulation but only T3 is the active form. Why then, do we make T4 in the first place? I read that T4 has a higher half-life, which might be the reason. Also, my professor said that it might be because thyroid peroxidase is not specific enough to control if it adds one Iodine or two. So, what is the actual reason?

T4 also has some biological activity, albeit less than T3. Nevertheless, besides the longer half-life, conversion of T4 to T3 can be regulated at tissue-level. So it adds another layer of control.

It sounds like what you read and what your professor mentioned are different types of causation.
T4 is the primary form produced by the thyroid; T3 is metabolized from T4 in other tissues and more strongly activates thyroid hormone receptors. Metabolism from T4 to T3 then allows tissues to have control over how much active thyroid hormone there is - multiple levels of control are very common to hormones, and other signaling pathways as well.

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


text:
What kind of "size" does SDS-PAGE separate by?
What is the exact property of the protein that affects migration of bands in SDS-PAGE; is it length, volume, or mass?
For example, will GGGGGGGGGG (glycine 10-mer; mw <600) migrate more or less than WWWWW (tryptophan 5-mer; mw >900)?

The protocol for SDS-PAGE uses a solution of sodium dodecyl sulfate (SDS, also known as lauryl sulfate) to solubilize and linearize folded protein molecules and give them a negative charge that is approximately proportional to the length (and more or less to the mass) of the protein, depending on its sequence. Some sequences may bind the SDS more readily, while others may not, so the relationship between charge and mass/length is not perfect.
The linearized (and often reduced, typically with DTT or β-mercaptoethanol) protein solution is separated by polyacrylamide gel electrophoresis (PAGE), wherein the negatively-charged protein(s) migrate though the pores in a gel due to an electrical field applied across the gel. Smaller proteins run faster, and are visualized (by many different methods) nearer to the bottom of the gel, whereas larger proteins are closer to the top. Typically, a standard molecular weight marker is run alongside the samples of interest so that approximate molecular mass can be gauged. A number of situations may cause the samples to not migrate exactly according to their calculated molecular mass, including high levels of glycosylation, phosphorylation, or other post-translational modifications, as well as variable binding to the SDS as discussed above.

Can you also focus on OP's specific example? Assuming that molecules of SDS is proportional to the length, G₁₀ will bind 2x more SDS than W₅. If you calculate m/z then it is higher for W₅. Since the mw of SDS is higher than average amino acid mw, should the binding of SDS basically overwhelm the effect of the peptide's molecular weight thereby making the separation purely length dependent?

@WYSIWYG no problem, I'll try to get to it later today. It's going to be rather hectic at work.


text:
How valid are GO (Gene Ontology) terms?
I'm looking for papers quantifying the validity of ontologies such as GO.
I'm relatively new to using annotation terms, and I often hear things like "annotation is messy" and "GO is good but it's not perfect." So I'd like to find papers that give numbers for just how messy.
I'm looking for answers from any experts that have a sense of the "quality" of GO terms (however you want to quantify it). For example, what fraction of terms are just wrong? The more computational parts of me want to sum up GO (or other ontologies) with a few descriptive validation statistics. e.g. "GO terms have an 80% precision and an R^2 of 0.6."
I'd like to see a few more examples similar to this paper that shows that a good fraction of GO ontology can be rebuilt from the ground up from independent data. That seems like one way to validate GO quality. They include this line about lack of GO validation in general literature: "... problems [with consistency and bias] are difficult to assess due to the lack of any definitive gold standard for the rigorous validation of GO."

for what did you planned to use GO annotation? genes or proteins( maybe enzymes?)

@RickBeeloo Genes or proteins would be good. Although, really, any attempts to quantify bias or precision of annotation terms would be interesting.

There are quite a lot of articles(1,2, etc.) which have investigated this, I think this article did a great job to give a visual representation of the specificity, reliability and coverage:

also this article noticed the following:

Compared to electronic annotations, it is not surprising that curated
  annotations have a considerably lower average coverage (Fig. 8,
  vertical lines). Indeed, the main appeal of electronic annotations is
  precisely that they scale efficiently to large quantities of data. But
  in terms of reliability, and contrary to current beliefs, curated
  annotations that use evidence other than experiments from primary
  literature do not fare better than electronic annotations (Fig. 8,
  horizontal lines, Fig. S9 in Text S1). In fact, we observed a higher reliability for electronic annotations than for curated annotations (0.52 vs. 0.33). the figure blow is figure 8 from the article

I don't know if you are just curious in the reliabilty of GO or if you are searching for an other kind of hierarchical annotation method, but e.g. for enzymes there are also EC numbers.  I can continue citing the article but I would suggest to read the article from which I used the figures ( Quality of Computationally Inferred Gene Ontology Annotations). Secondly this article is more recent and  something similair was done here. Among other things they also compared the computional annotation from 2008 with manual annotation in 2010 for the same set of GO terms:

So I would also recommend to read The what, where, how and why of gene ontology—a primer for bioinformaticians. This article and the previous mentioned article will give you a good insight in GO terms.

No problem, I think the articles will make it clear for you


text:
How to calculate the geometric mean titer (GMT) of titers from a haemagglutination assay (influenza)?
I got a list of Influenza-specific antibody titers from a hemagglutination inhibition assay.
They look like this:

40
640
160
<10

One site says: “The swine influenza HI scale is geometric: 20, 40, 80, 160, 320, 640 (successive values increase by a factor of 2). The geometric scale is logarithmic. It is best to express an average influenza HI titer as a geometric mean. A geometric mean is calculated by averaging the logarithms of the test values and then converting the mean to a real number. This prevents a few obviously high positive values from making the mean unrealistically large.”
What does that mean for my sample? How do I deal with <10 in this calculation? This is surely not rocket science, but honestly I don’t get it right now.

Typically "<10" is converted to a number that is below the limit of detection; often "9".  After that simply following the instructions you have yields a GMT of 77.9.  If you are using spreadsheet apps such as Excel or Google Sheets, they almost certainly offer "GEOMEAN" functions which will give the number directly.


text:
How to build a phylogenetic tree without an outgroup?
I have whole genome aligned sequences of four beetle populations of same species. I wish to construct a phylogenetic tree with the four. However, I am unable to find a suitable outgroup of the species, so I cannot use an outgroup to root the tree. Is there a particular method that one can use to construct a tree without an outgroup? I found that the MEGA software does this well. What is the theory and understanding of constructing a tree without an outgroup? what are the implications of constructing a tree without an outgroup? Ar the distances between trees measured relative to one another?

Isn't a phylogenetic tree without an outgroup just an unrooted tree?

Related.

Most classic phylogeny reconstruction algorithms root the tree a posteriori, based on the outgroup chosen by the user. The tree is actually inferred and internally represented without root.
Therefore, if you use a program that asks you an outgroup, it is likely that you can just choose an arbitrary one and later "de-root" the obtained tree.


text:
Do E. coli produce both cellulose and curli?
I read a paper that describes a specific stain for cellulose and curli (simultaneously) in Salmonella. I think this should work for E. coli but I'm not sure if all strains produce it. If they do, are the tertiary structures similar to those from salmonella?
Real-time optotracing of curli and cellulose in live Salmonella biofilms using luminescent oligothiophenes


text:
How does having spare receptors change ED50 in an irreversible agonist
Competitive antagonists increase the ED50 while the Emax remains the same. Irreversible antagonists do not change the ED50 while decreases the Emax.
Katzung pharmacology, says that the irreversible antagonist may change the ED50 when spare receptors are present. How is that? What difference would it make? Could anyone explain the change graphically?
Spare receptors are said to be present when the Kd (dissociation constant, from the drug-receptor binding curve) is more than the ED50 (from the dose-response curve). This may happen due to

prolonged effect of a drug-receptor interaction or
when the receptors are actually in excess of the drug

ED50 = effective dose at 50% of maximum effect, Kd = Dissociation constant.

Irreversible antagonism is like removing receptors.
If there are spare receptors, maximum effect, or any effect level, can be recovered with more ligand (because displacing the irreversible ligand is not necessary, when there are other sites to fill).
$$K_D = \frac{R*L}{RL}$$
A given effect level corresponds to a given $RL$, but with less receptor $R$ available, more ligand $L$ is needed. That is by definition a change in ED50.
If you have no spare receptor (or there is enough antagonist to prevent full effect even with spare receptors), then maximum effect cannot be recovered. There is a new Emax, lower than without antagonist; but without shifting the dose-response curve to the right.
Here is an example in Rang&Dale (8th ed., p. 12, fig 2.6). Curves are labelled with time of incubation with a given quantity of irreversible inhibitor, that is equivalent to varying concentration of irreversible inhibitor at steady state. First two show the situation with spare receptors, and last two show what happens when the original Emax cannot be reached because there are not enough receptors left to elicit maximum response.


text:
Nomenclature of enzymes involved in synthesis of glutamine
I am considering nitrogen fixation and in my lecture notes, there is the statement

The glutamine synthetase- glutamate synthase system requires use of an ATP molecule as well as reducing power. Although it is energy intensive compared with glutamine synthase, the Km of glutamine synthetase is much lower than that of glutamate dehydrogenase. When NH3 is scarce, the additional ATP investment is worthwhile.

Try as I might, I can't find anything about glutamine synthase. Searches online seem to only return results for glutamine synthetase. I was wondering if this is a mistake in my notes? If so, I can only think that this should be 'glutamate dehydrogenase', in which case the statement is about comparing the method used by animals and fungi (which use glutamate dehydrogenase to fix nitrogen via a Schiff base) compared with plants and other microorganisms  (which use the glutamine synthetase glutamate synthase method).
This is my first exposure to learning about nitrogen fixation, so I would very much are coated any clarification.
Also, I was wondering what the general difference is between a 'synthase' enzyme and 'synthetase', if there is one.

I think you are correct, "glutamine synthase" must be wrong, and "glutamate dehydrogenase" makes sense in the context. Glutamate dehydrogenase does have a much higher Km for ammonia (about 1mM, https://en.wikipedia.org/wiki/Glutamate_dehydrogenase) than glutamine synthetase. Why don't you check with your teacher and then you can answer the question yourself :)

I have changed the question so that it refers to the general topic in the question rather than the mistake in nomenclature. As an original question that was fine, but it has now had all the impact it is likely to have, and by making it more general it — and the answers — will be of more general use.

Probably a mistake in your notes, or in the lecture notes for the class, but not a very important error in either case aside from the confusion it has caused you.
See the wikipedia article on Synthase and on wikipedia article on Ligase for a note on the terminology: historically synthetases use ATP, synthases do not, but this terminology is not adhered to strictly, and the current standard is that the terms are essentially synonymous; in my experience, however, a particular nomenclature dominates the literature even if the synonym is technically correct.

I'll deal with the second question first. There is a difference between synthetases and synthases, but because of the confusion the International Enzyme Commission now discourages the use of the term synthetase. The section on ligases states (my emphasis):

Class 6. Ligases. Ligases are enzymes catalysing the joining together
  of two molecules coupled with the hydrolysis of a diphosphate bond in
  ATP or a similar triphosphate. The systematic names are formed on the
  system X:Y ligase (ADP-forming). In earlier editions of the list the
  term synthetase has been used for the common names. Many authors have
  been confused by the use of the terms synthetase (used only for Group
  6) and synthase (used throughout the list when it is desired to
  emphasis the synthetic nature of the reaction). Consequently NC-IUB
  decided in 1983 to abandon the use of synthetase for common names, and
  to replace them with names of the type X-Y ligase. In a few cases in
  Group 6, where the reaction is more complex or there is a common name
  for the product, a synthase name is used (e.g. EC 6.3.2.11 and EC
  6.3.5.1). It is recommended that if the term synthetase is used by authors, it should continue to be restricted to the ligase group.

But the old nomenclature dies hard.
As regards your first question, this is an obvious mistake, as others have pointed out. For the record, I post diagrams from my own lectures of the two alternative methods of aminating ketoacids (oxo-acids).

As this question has been reposted (or whatever) for clarification I have given an extensive answer. The shorter answer from Bryan Kause is also correct, so I have given it a vote so this question has at least one approved answer. I suspect the original poster may have lost interest by now.


text:
Neurophotonics vs. Optogenetics
What is the difference between the two? I see them frequently listed together in conference descriptions but can't seem to find anything that clearly explains the difference.

Neurophotonics refers to the use of light to study the brain, including measurement (i.e. microscopy, including the use of fluorescent molecules that allow measurement of ions or voltages in live tissue, but also including histological techniques) and manipulation (using light to activate, inactivate, modulate, etc neural activity).
Optogenetics refers to the use of genetically encoded (whether delivered via virus or in a transgenic animal) constructs that respond to light and are introduced into cells where they are not normally found, often neurons. Neurophotonics is a broad term that would include optogenetics.
In my personal opinion, optogenetics is a fairly specific term that is useful, though it certainly has some popular buzz around it. Neurophotonics is a new buzzword that encompasses a lot of techniques that have been around a long time, and while these techniques are constantly improved upon, the neurophotonics label isn't really necessary (but sounds fun).


text:
Parthenogenesis Induction
I have read about Parthenogenesis induction in a paper : "Hagimori T, Abe Y, Date S, Miura K (2006) The first finding of a Rickettsia bacterium associated
with parthenogenesis induction among insects. Curr Microbiol 52: 97–101 "
I was curious to know what is the evolutionary advantage of parthenogenesis induction for the parasite (in this case Rickettsia bacterium ) ?

This issue is addressed in this review by Cordaux et al, 2011, along with other, similar strategies.
The simple answer is that these types of bacteria are efficiently spread from females of the species they infect to their offspring; by inducing unfertilized eggs to develop into females, they increase their transmission efficacy.


text:
Is excretion always necessary?
I know we defecate or/and urinate to rid ourselves of toxins and excess undigested food. If I was somehow able to get exactly what my body needed to function.
Let's say that I create a pill (or something) that provides the body with literally and exactly the nutrients and hydration it needs, would there still be a reason to carry out excretion?
Do humans or any animal, absolutely have to excrete?

I'm not sure I understand the question because it is slightly unclear as it stands. But I think you're asking about a reasonably interesting and answerable topic; how much of our waste is from processing food and drink. A lot of your feces is bacteria, archaea, yeasts, fungi, viruses, and cells from your body. A fully fleshed out answer for this question could be useful, but we need a few edits!

@James yeah sorry. I have a basic understanding that we pee/poop to remove excess vitamins and toxins, so am just wondering if I have the most perfect diet ever, is there still a need to pee/poop? I'll try and think of how to edit this. I guess most broadly, why do we pee/poop?

Yes; there are byproducts of metabolism and maintaining the body that must be excreted, which has nothing to do with taking in unneeded nutrients. For just a few examples, urea is produced normally as part of the constant building and break down of proteins, but must be excreted, the brown color of feces comes from the breakdown of red blood cells, and a substantial weight of the feces is gut bacteria, some of which are necessary for proper digestion of some of the nutrients you take in.

Hm, that's interesting. So given the fact that I have perfect nutrition thnaks to MiraclePill, would my feces generally be the same amount/weight/etc? You mention substantial weight is due to gut bacteria, so would I expect to poop just as often as now, but just not defecate as much (volume wise)?

"Total parenteral nutrition" is the medical term for full IV feeding - this is not perfected to the "miracle pill" level and typically not used long term, but you can use this to try to find the information you are looking for. I couldn't find an ideal reference for you, in part because patients fed IV are usually quite sick, and in particular they often have serious bowel issues, hence the IV feeding. Just searching around I saw some anecdotes that suggest defecation still occurs but the quantity is reduced - not clear if this is because of frequency or the volume of individual stools.


text:
Protein degeneration/excretion in cell
If I inject a dose of GFP or some other types of protein into a long-living human cell like brain neuron cell. Will these proteins being degenerated or excreted over time?

This paper gives a half-life of 26 hours for wild-type GFP expressed in mouse cells.


text:
Why do an eagle’s feet look ridged?
Why are the knuckles of an eagles toes "ridged"?
(I found these pictures to explain.  One was from PBS and the other is one I found on Pinterest):

I circled the parts of the toes/feet I meant in red (from PBS):

Their DNA made them like that.

I don't really get what you mean by baggy. I can't see any bagginess in eagle talons. Can you be more specific?

Please consider rephrasing your query and hence using alternative terminology -- as of now it is a bit unclear what you are asking.

Those are just scutes.

@kmm you should post that as a brief answer.

@kmm Yeah, you should put it as an answer.  I was able to find information by using that keyword.  Thanks.

The bubbly structures on the dorsal sides of the digits are scutes. Birds retained them from their dinosaurian ancestors. Here is a picture of similar structures on an alligator foot:

What purpose do they serve?


text:
Is the occurrence of a particular enzyme in a given subcellular location a random phenomenon?
Enzymes occur in different subcellular locations. Some are specific to a given subcellular location, whereas others are heterogeneously distributed. What evolutionary decisions influence the occurence of enzymes in particular compartments?. Are the locations species-specific?

Some trace their evolutionary origin in the ancestral organelles (such as mitochondria and plastids) and therefore they are localized in those organelles. Can you add more details to make your question more specific?

I have edited the question above. I wanted to know more about this. Thanks

You have changed your question completely. What's more it is now nonsense: "What evolutionary decisions..." Evolutionary decisions indeed! And If you have to ask about enzyme locations being species-specific I suggest you ask yourself why enzymes are in particular organelles and whether organelles are species-specific. Do some reading about organelles yourself, instead of wasting our time.

Dear David, First of all, you edited my question. I just re-phrased it.This was the same question I was asking from the beginning. I respect your comment. If you don't understand the question, you cannot comment on the question being non-sense. As you know more than me or anyone in this group, I'm just asking you the same question "Why do enzymes occur in specific locations? And What evolutionary decisions influence the occurrence of enzymes in particular compartments?" This may sound a very general question. I just want examples. A review article that explains this question might be useful.

Also, there have been many proteomics studies in related species of bacteria, parasites, etc. where the same enzymes can be found in different subcellular location. I'm just adding to their observation my question as to why they might occur in different locations and also why they are species-specific. If I could not clarify my message still, then its worthy to close this question totally. Thanks.

There are various methods for targetting proteins to subcellular organelles or membrane locations. In general they depend on ‘tagging’ or ‘signal’ sequences in the proteins. Such tags or signals are recognized by specialized proteins that are able to conduct the protein through the membrane barrier to the particular location.
The individual processes for different target locations vary, so I do not think it appropriate to provide details here. You can read a summary of them in this Wikipedia article. For more extensive treatment you can look at the relevant chapters in Lodish et al.  or in Alberts et al. on-line (old edition).
(Please consider donating to Wikipedia, if you use it.)

It might be too broad a topic to be explained here, but you should at least describe some part of it (even if introductory) lest this is too short to be an answer.

@HomoSapien — It may be better to close it as too broad. I looked to see if it were answered previously. I'll add another sentence, but more than that...

Yeah, but that is another point. I meant that just giving some references would be appropriate for a question, especially if its too broad.

@HomoSapien — I think the two book refs are ok. They give a breakdown of the chapters for different locations (nucleus, peroxisome, membrane etc.) That seems to me a good entry point for a novice.

Yeah, they are. +1 for you mentioned donating for wikipedia ;)

Enzymes occur in different subcellular locations. Some are specific to a subcellular location. Some are heterogeneously distributed. Lets take the example of metabolic enzymes. The location of an enzyme in a particular subcellular location may dictate the flow of metabolites through different compartments. I wanted to ask "what evolutionary decisions influence the occurence of enzymes in particular compartments?. Are the locations species-specific?". A review article, book or research article that explains this question might be useful. I'm editing the questions too.


text:
Do Gametes contain mitochondria/chloroplasts from their parent cell?
It has now been established (according to the Cambridge A level text book) that

organisms form a symbiotic
  partnership, typically by one engulfing the other
  – a process known as endosymbiosis. Dramatic
  evolutionary changes result.
  The classic examples, now confirmed by later
  work, were the suggestions that mitochondria and
  chloroplasts were originally free-living bacteria
  (prokaryotes) which invaded the ancestors of modern
  eukaryotic cells (cells with nuclei).

It also states that

It was also discovered in the 1960s that mitochondria
  and chloroplasts contain small, circular DNA molecules,
  also like those found in bacteria

and lastly

The DNA and ribosomes of
  mitochondria and chloroplasts are still active and
  responsible for the coding and synthesis of certain vital
  proteins, but mitochondria and chloroplasts can no longer
  live independently.

So my question is:
Is this DNA found in the mitochondria and chloroplasts coded for in the host's (animal's or plant's) DNA.
If not are there fully formed mitochondria and/or chloroplasts in all gametes (obviously chloroplasts only in the plant gametes) which were transferred directly from the parent who had them transferred directly from their parent and so on?
If so are all the mitochondria and chloroplasts of one type identical in a organism? Are they almost identicle in families (of organisms not the classifictaion Family)?

Is this DNA found in the mitochondria and chloroplasts coded for in the host's (animal's or plant's) DNA.

No, the DNA contained in these organelles it not a subset of the nuclear genome. However, part of the original genome of the prokaryote has been moved to nuclear DNA. That is why, as you cited, they "can no longer live independently."

If not are there fully formed mitochondria and/or chloroplasts in all gametes (obviously chloroplasts only in the plant gametes) which were transferred directly from the parent who had them transferred directly from their parent and so on?

As the child organism would eventually need these organelles, and they can only be inherited, at least one of the gamete must contain them.
For the chloroplast, the general rule is that only one of the gamete provides it. For example, in gymnosperm it is the male gamete (pollen), in angiosperm, it is the female gamete (ovule). Either it is just not present in the other gamete, or a specific exclusion mechanism makes it mono-parentally inherited.
Mostly the same for the mitochondria, with the caveat that (motile) spermatozoa contain mitochondria for their metabolic functions (energy to move), but these are discarded when forming the zygote, and only the maternal mitochondria are inherited. (In plants, mostly maternal too with exceptions)
This does mean that there is a lineage of organelle on one of the parent's side, up to the most recent common ancestor (approximately, the first individual of the species). In humans, this translates to a presumed Mitochondrial Eve from which all human mitochondrial DNA descends from.

If so are all the mitochondria and chloroplasts of one type identical in a organism? Are they almost identicle in families (of organisms not the classifictaion Family)?

Every mitochondrion of an individual organism comes from the stock of mitochondria of the zygote, through replication. They are thus very similar, except for cell specialization (giving particular morphology to the organelles), and possible mutations. Same for the chloroplast.
Mitochondria (and chloroplasts) are basic components of the eukaryotic cell, providing essential functions  which are highly conserved in a species, let alone related individuals.
However, this does not means the DNA of these organelle is the same for every individual : different sequences may give the same protein, or mutation may affect non-coding segment of the genome. This is the basis for genetic genealogy, retracing family lineage though analysis of DNA, including mitochondrial DNA.

No to your first question. Mitochondrial DNA (m[t]DNA) is individual to the host's DNA- it has it's own DNAs in the organelles itself. The same goes for chloroplasts. The mitochondrial DNA is officially linked to the mother's X-chromosomes, and since the sperm's mitochondria is destroyed and only the maternal egg cell is left, the mother's mtDNA is remained to pass down.
Mitochondria grow, reproduce, and replicate mtDNA by their own - this is another proof that they used to be prokaryotes, not to mention their circular DNA, double-membrance structure, etc..
I am not so sure about the third question of their evolutionary relationships between each other, but you probably have to know that chloroplasts created food by fixing carbon dioxide, while mitochondria broke down sugars to release ATP.


text:
Method for preparation of LB agar plates with Ag+?
I need a method for preparing LB agar plates with 1 mM concentration of AgNO3.
I can not seem to find a method online, does anyone know of one that I could use?
Here are my main questions regarding the method:
a. Do I add the silver before or after I autoclave?
b. do I add the silver in a liquid form for powder?
Thanks.

Why do you want to add silver ions to a agar plate? Besides this: LB medium contains sodium chloride - which will react with the silver ions and form silver chloride which forms an unsoluble precipitate. Additionally silver chloride is light sensitive and will stain the plate black eventually.

Yes, that is true. However, bacteria which are silver sensitive still can not grow on the plate given these conditions. I am in need of growing silver resistant bacteria on an agar plate, and this is the method in which I want to do it. AgCl precipitate will occur, however some Ag ions will still remain in the agar.

If you consider the solubility product of AgCl (which is around 1,88mg/L at 25°C) and the fact that you add 10g/L NaCl, I doubt that there are notable amounts of Ag ions present in the medium. Aren't there any protocols available?

What you could try (and what I did a few times with antibiotics) is to dry the plates and then plate the solution on top of the plate. Then the ions are at least available at the surface layer.

I have done this before. Although the amounts of silver ions available may be minimal, silver sensitive bacteria can not grow on the plates. I have tried concentrations from 1mM - 10mM. The plates were prepared by a different person in my lab. However, I can not currently contact this person for instructions.

Ok, practice beats theory here :-) Can you make a few plates where you add the silver before autoclaving and a few where you plate it on the surface and the compare it?

Sure, here is a picture of what I have seen in the past

Shoot it didn't work, just a sec.

https://docs.google.com/document/d/11qCvylNhwn1XQ_FDEPQZhsojjEmsHmY-6rxG3RJ86q8/edit?usp=sharing

Let us continue this discussion in chat.

You add the silver after autoclaving. Just make sure that you make your stock concentration of silver in sterile water to avoid unwanted contamination. Do it in liquid form; it is easier to dilute from a stock.

Yes, this is what I found to be the standard when working with silver

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


text:
Presence of Aromatase enzyme in males : Result of Natural Selection
Males have increased chances of getting cardiovascular diseases than females ; one of the reasons might be less level of oestrogen ( which decreases deposition of low density lipoprotein LDL in blood vessels).
I know that Aromatase enzyme is produced by sertoli cells in males. It converts androgen into oestrogen.
Now ,
today my teacher said that the presence of Aromatase enzyme in males is the result of natural selection against increased chances of heart attack in males.
My question is-
1. Is the amount of oestrogen produced significant to decrease cardiovascular diseases that it can lead to natural selection?
2. Are there any evidences for the same? please enlist them.
Any help is appreciated.  Thank you!  :)

Estrogen has other functions in males; it is very misleading to attribute the ability in males to synthesize estrogen to effects on heart attack chances. The relationship between estrogen and cardiovascular disease risk is also very complicated, and current guidelines do not suggest estrogen replacement as a preventative treatment for heart disease.
A better explanation for increased male risk of heart attack might be the increased levels of testosterone, but the data on that are mixed as well.

Thanks ! The link you provided was helpful. So basically, it plays role in maturation of sperm?

Wikipedia has a list of functions of estrogen - many of these are not specific to females. On your own, you could also research the effects on males who have a deficiency in aromatase.


text:
How is the beginning of an episodic memory encoded in the brain?
before asking how information is stored, I need to understand

how does episode start and end are determined by the brain ?
how do i remember a movie ?

can you suggest a link to article addressing this issue
thanks

We don't know; it also isn't necessarily true that it is necessary for episodic memories or experiences to actually have any distinct start and end.

thanks. how can the brain recall an episode if it's not bound by some way like start/end "flag" or by special "sub circuit" (hard wired)

If it’s associative memory the chances of ‘multiple recalls’ is high without some boundaries that reduce its ‘fuzzy level’

Two answers to that comment: 1) Think a bit about your own memory. Are you really able to remember your whole life in sequence without interruptions or getting distracted? 2) The 'boundaries' you are talking about can be fairly subtle: just an increase in connectivity that causes an increase in probability of states progressing in the order of the original memory. There is actually a lot of research on just how poor our memories are, as well as how poor our estimates of how good our memories are (we think we remember well when we don't).

We don't have a full understanding of how episodic recall really happens in the brain, but there are theoretical approaches to understanding memory that are supported (but not shown definitively - it is really difficult to design appropriate experiments that are not beyond current technological capabilities) by experimental evidence. These approaches don't require any sort of hard "start" or "end" signal for episodic memory to work. In these approaches, an episodic memory is thought of as a sequence of brain states that correspond to previously experienced states.
The sequence occurs because connectivity promotes the network to progress from State A to State B to State C, etc. Additionally, all of the states consisting of that one "connected" memory are also associated, so that they prime one another.
To recall, you don't need to start at State A - you can start anywhere in the chain, and just recalling State C will prime you to also recall State A and B, so you can mentally "rewind" the memory a bit (we have no idea how exactly this type of conscious control works), even though it progresses most clearly in the A->B->C sequence.
The point of entry that allows you to initially get in to this chain might not be part of that episodic memory, either. For example, maybe you see a cat, and this leads to to an episodic memory of one event you shared with your own cat 5 years ago.
Brains are very dynamic, they do not behave like a feed-forward computation you might implement in a simple computer program. It is possible that there are "start" or "end" signals for episodic memories that we haven't found yet, but they may not be necessary at all.
For some further reading you could look for references on attractor networks, pattern separation and pattern completion, and theories of memory formation.
The book by Dayan and Abbott on theoretical neuroscience is also a good approach to some of the more basic background and includes an introduction to biologically-inspired models of learning and memory.

thank you Bryan. let us assume i have 5 cat's episodes. i might be confused if all are recalled. may be i have 1000 episodes with my family - all are recalled ...i'll be lost :)

You might be interested in reading about "attractor networks" and how they work - TL;DR version is that a network is structured so that there are stable states that are associated with particular memories or concepts. Thermodynamic analogies are appropriate to attractor networks, so the way you would think about it is that the 5 cat episodes are each stable attractors, with a relatively low energy barrier to passing between them.

Could you add some references to your answer? I'm not well enough versed in the area to judge whether or not it's a good answer, so some basic background references, links to wiki pages, good reviews in the literature, etc. would be much appreciated.

@MattDMo I'll try to come up with some basic references at least for further reading...this is the sort of thing people write books about that contain a fair bit of speculation and hand-waving, and far from settled knowledge, so it's a bit difficult to point to a particular authoritative source.

OK, thanks. If the science is totally settled, you probably want to mention that some way in your answer - "One hypothesis is ..." or "Many scientists seem to think that ..." etc.

@MattDMo The first sentence of my answer was "We don't have a full understanding of episodic recall, but let me try to answer from just a theoretical perspective" - by this I meant to convey that we don't have answers as to how episodic recall really happens but there has been a decent amount of educated speculation. I'll try to clarify a bit.

I want to hypnotize that the “end of memory item” is associate with inhibitor triggered; are there  any supportive evidence ?


text:
why can proteolysis only occur once on a enzyme?
My texbook says that proteolysis can occur once in the lifetime of the enzyme? I know that proteases must cleave the zymogen at more or more specific locations, but why can't the process take place more than once?

Because you mention zymogens, I assume the proteolysis you are referring to is the conversion of the inactive to active form of an enzyme by cleavage. The reason this would only happen once is that there isn't any process to put the two cleaved halves of the protein back together, so once cut in half it stays that way until degradation.
The proteolytic enzyme that is doing the cleavage of the zymogen will repeat this process over and over with multiple copies of the zymogen: it is the zymogen itself, the target, for which this is a once-in-a-lifetime event.
It would certainly be possible for a zymogen to require multiple cleavage events, but each of those events could only happen once.

Just to clarify - proteolysis at a particular site in a zymogen only occurs one in the lifetime of the zymogen. The protease can cleave many many many individual zymogen proteins within its life.

@MattDMo Yes indeed - maybe this is the confusion the question asker had in the first place, I will add to my answer.


text:
Why are two forward and reverse priming sites depicted here? what do they do?
This question is in regard to the baculovirus expression system.

(source: amsbio.com)
Why do we need to generate primers for the polyhedrin promoter and the baculovirus?
Primers are needed to amplify DNA regions of interest.Here, why exactly do we need to amplify these regions? and at which steps?
PS : I am not asking about the need for forward and reverse primers.

what is this slide and why does it have so many typos?

It's just extra information that you don't need to understand the part above. You could use these primers for colony PCR or sequencing when you'd use the plasmid (after transforming to E.coli for example), but they're not absolutely required.
Compare it with this map for example. There are also some primer sites listed, but you don't actually need those primers for anything.

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


text:
Are we naturally born right or left handed or ambidextrous?
Most of you here will be right or left handed. A few might be ambidextrous. But were we born that way?
I'm wondering if everyone was born ambidextrous, but as they grew up became more dependent on one hand, and that hand after more use now has stronger muscles, bones etc. Or were we naturally born with one hand stronger than the other?
I've heard somewhere that it has something to do with the brain, and which side which hemisphere is on. Not sure the validity of this statement. It's also been pointed out that chimps and apes show handedness, so this probably not just a human thing.
So, are we naturally born right or left handed? Or are we all born ambidextrous and does left or right handedness develops later?

Not sure what tags apply here...

When reading up on the subject on the internet, left handedness is described as a preference, as if it were a choice... However, I found this article, which suggests that it is factors such as environment, genetics and chance https://ghr.nlm.nih.gov/primer/traits/handedness

well chimps and gorilla show handedness, take that for consideration.

Good question. I think the fact most people are right-handed suggests a genetic mechanism. Otherwise the choice should be random, and I would expect left/right to be equally common.  This article might be a starting point:  https://www.scientificamerican.com/article/why-are-more-people-right/

I think you are born left or right handed and I think the following experiment 'proves' it. In the Netherlands in the 1950s (and probably many other countries), left handedness was considered bad at schools they 'taught' children to be right handed. They all had to write with their right hand. It didn't help, left handed children remained left handed. Some still write with there right hand, but do everything else with their left hand.

tl;dr
Yes!
Is handedness determined before birth?
Without thinking of whether handedness is genetically or environmentally defined (see below), is handedness decided before birth?
Hepper et al. 1991 and DeVries et al. 2001 show that handedness can be inferred from from fetal position and hand usage. Typically, looking at what thumb is used for sucking is good indication of handedness.
Is handedness heritable?
The question

[A]re we naturally born right or left handed?

can sometimes be understood as

Is handedness genetically determined?

or in more concrete terms as

Is handedness heritable in humans?

If it is not obvious to you that this is your question, then you probably don't understand the concept of heritability! Then you should have a look at Why is a heritability coefficient not an index of how “genetic” something is? first and then come back here to read the results.
There have been a large number of studies on the question, unfortunately most of them were very small studies with small sample size. Medland et al. 2008 is pretty large scale twin study which report a heritability of 0.24.
In other words, yes handedness is heritable. To be more accurate, 24% of the total variance in handedness is explain by additive genetic variance. Yet again in other words.
The cooperation-competition hypothesis
On the evolution of the handedness in he human population you might want to hear about the cooperation-competition hypothesis. For that, you should have a look at this TED-ed video. As you watch this video, you'll probably be interested in reading the wikipedia article on frequency-dependent selection.
Thanks to @Mockingbird for pointing out to this video.

I understand heritability but that wasn't really my question. Sure, I get that you  an inherit the handedness of your parents, but as your answer shows, this doesn't happen very often. I'm asking whether or not we are born with the hand we use most often, or whether we aren't born with a particular handedness and it develops over time.

Ted-Ed has an interestjng video on this subject.

@BeastlyGerbil I understand. Please see edit.

Ah that's a lot better. Thanks. The hand used for sucking a thumb is a particularly interesting point...


text:
What bacteria results in a Gram +ve cocci and catalase +ve? What test comes next?
Results so far.
We are trying to determine unknown microorganisms in intro to microbiology course. I first did gram stain and they were all cocci morphology, purple color and clumped together  (actually I'm not so sure if clumped is right word, but they definitely were not in chains and I didn't see any isolated coccus, so if that's qualifies as clumped then they were clumped.
So I have a gram+ here.
Next I did catalase test and got bubbles on slide; I put thick chunk of the unknown on slide and dropped 2-3 drops of ${H}_{2}{O}_2$; instant bubbling.
Next test.
So now I will test for coagulase but I'm uncertain what a positive or negative result will tell me about he organism and whether this is the terminal test (for ID-ing organism I mean)
My notes say that positive for coagulase indicates S. aureus.
But does that mean that it is unnecessary to do the Mannitol test at that point then? Or is Mannitol used as a confirmation test?
Further, if unknown tests negative for coagulase, my notes say that if its also novobiocin sensitive (pos) then it is S. epidermidis.
But my same question then is, is it necessary to still do the mannitol test?

Hi there and welcome to Bio.SE! I've made some edits to make the question fit the site format better (a specific title, a more attractive format etc). Feel free to roll back, or make a further edit. I like the spirit of the question and hope to see more like this on the site generally!

At this point you have staph, you can use this flow chart (from here) to figure out what staph exactly.
If the test comes back as coagulase positive be very careful as Staph aureus is pathogenic.


text:
Can we use cancer cells to generate blood vessels?
Is there any possibility to use cancer cells, which generate blood vessels, to generate our blood vessels when we are wounded or when we have varicose veins in our legs?
Thanks for your answer in advance.

Great question, it's hard to control cancer, this approach is harder than the elimination, so I think controlling it is a level higher than destroying it.

Using cancer cells in this manner would be far too dangerous, as there is nothing to prevent the cells from implanting and forming new tumors. Fortunately, we already know a great deal about angiogenesis, which is the process by which new blood vessels are formed or grown out of existing ones. If you want more details on how the process works, the article I linked to goes into a good amount of detail regarding the key players and how they interact.
It would be much easier (and safer) to use our knowledge of the cytokines and growth factors responsible for blood vessel formation to develop biological therapies that could potentially be used to treat varicose veins. However, current therapies can be quite successful, and there may not be a large enough market to justify the quite large expense required to develop angiogenesis-based therapies.
Unless a patient has some sort of genetic or other issue, angiogenesis is already involved in wound healing. As new tissue grows back, capillaries and perhaps slightly larger blood vessels expand out from the nearest sufficient vein/artery pair to vascularize the new cells. There may be issues with patients who are taking angiogenesis inhibitors as part of a therapy plan for cancer, for example, in which case compromises would have to be made if necessary.

It is also worth noting that although angiogenesis occurs in many cancer cells, the blood vessels formed are not as structurally sound as normal blood vessels, they are 'friable' and as such have a tendancy to bleed. In some tumours for example this can lead to major haemorrhage.

@Spinorial that is correct. This is due in large part to the inherent dysregulation of tumor signaling pathways and lack of "proper" angiogenesis as one would see in growth or wound healing, for example. To anthropomorphize, tumors are only interested in getting nutrients to support growth, not in building a proper, sustainable blood vessel scaffold that will last. A tumor is evolving as it grows, responding to its current environment, and doesn't have a genetically-set evolutionary "plan" like normal cells and whole organisms do.


text:
Why might the chirality of gastopods be dominantly dextral?
This wikipedia page on gastropods provides a definition of chirality, and briefly describes the genetic mechanisms behind why a shell is wound left (sinistral) or right (dextral) handed. It also mentions the fact that there are more species of gastropods that are dextrally wound than sinistral. What the page does not offer is why this might be so with regards to evolutionary pressures.
Does anyone have an explanation of why gastopod species have wound up dominantly dextral?
This question relates to my question about a specific species of gastopod that is found in equal proportion of both chiralities, and both in the question and answer there are suggestions of a chiral relationship between predator and prey and perhaps ease of mating. But it really doesn't answer my general question.
If it's a predator-prey pressure then is there any evidence across a larger sample of species that supports this explanation? Or of the left and right handed species of gastropods, anatomical evidence across a large number of species that shows mating advantages? Or likewise any other explanations that offer evidence?

Possible duplicate of Does the species of snake that eats Amphidromous inversus have chiral dimorphism?

I don't think the question per se is a duplicate, but @Remi.b's answer covers this nicely.


text:
Do all chromosomes in one human body contains same genome?
As I understand it, each nucleus of a cell contains multiple chromosomes. Each chromosome has multiple DNAs. Each DNA contains some specific gene sequences. That sequence is called Genome.
My question, do all chromosomes in cells in a human body contain same types of genomes (i.e. gene sequences)?

About your first paragraph, a correct phrasing would be "Each nucleus contains multiple chromosomes, each chromosome contains 2 strands of DNA (although it depends on the timing in the life-cycle). The genetic information is in the sequence of amino acids that make up the DNA. DNA. The genome is the entire genetic sequence of an individual."

@Remi.b, where does the gene stand in your description?

A gene is a vaguely defined functional unit of the genome :). It corresponds to a given locus (position on the genome) and often contain a coding region (a coding region is a sequence which is translated and transcribed into protein). Have a look at wikipedia for more definitions. As everyone can see the comments, I edited your post to remove your copy-paste of my comment.

@Remi.b, how is my question a duplicate here? I couldn't figure it out !!!!????

You are correct, the post I linked is not a duplicate. Sorry about that, I'm removing it.

Yes, all cells contains the same genome. This is because, for a given individual, all of its cells comes from the zygote, a singular cell formed after fecondation of the maternal ovum and paternal spermatozoa, through repeated cell division (mitosis). This is a process which replicates quite exactly the genome that will be passed to the newly formed cells.
There are some exceptions however, such as :

Red blood cells, and platelets : these cells lack a nucleus, and don't contain DNA at all.
Cells bearing mutation(s) : even though the replication machinery try to make an exact copy of the DNA, error(s) may happens.
Gametes : ovum and spermatozoa are produced through meiosis, a specific replication mechanism that keeps only half the genome, and may produce new sequences through recombination.
Lymphocytes undergo V(D)J recombination and somatic hypermutation which alters their DNA, a process that is necessary to the working of our immune system.


text:
How are the words taxa and taxons used interchangeably? When are they different?
I am confused about the terms "taxa" and "taxon". In one video lecture it is said that

Dolphins represent taxa at a very low level, while fish has a litter higher level of taxa than dolphins and once again animals are at higher level of taxa.

Dolphins exist in forms of various sizes so it will represent taxa. I have considered taxa to be the taxonomic group when it combines together.
In the definition of taxonomy, why is this taxa a suitable word for this while not taxon in both the statements?

Welcome to Biology.SE. I did not read the whole post as I got bored midway through by the format. Can you please capitalize your "i" and use correct spacing (space after comas, dots and interrogation marks but not before). I don't get all your "Sir" in your question. Is it to be polite? It is likely that a woman would answer the question. Do not use all these please and sir. Don't beg for us to answer. Just ask your question straight. Also please use paragraphs. You can have a look at other posts in this website to take example for the format.

It is indeed very off-putting to see sir so many times. Ultimately though, I have no idea what the question is (and I did read it to the end)! This is beyond editorial help.

Do thorough google search or read an introductory Zoology book to form a clear concept of taxonomy.

@GH05T seems to have made a very good effort at editing the question! Well done, but it seems that the question is merely about semantics, and would still be considered off topic in most cases.

Taxa is the plural form of taxon.

From wikipedia

In biology, a taxon (plural taxa; back-formation from taxonomy) is a group of one or more populations of an organism or organisms seen by taxonomists to form a unit

So, in short

Taxon is a synonym of taxonomic group
Taxa is the plural of taxon. Therefore, taxa is a synonym of taxonomic groups

You say one taxon but two taxa. While most words in english takes an s in plural, some have an irregular plural. Here are some examples drawn form the field of biology (and data science in general):
Regular plural

adaptation / adaptations
finger / fingers
cell / cells
flower / flowers

Irregular plural

nucleus / nuclei
cactus / cacti
stimulus / stimuli
fungus / fungi
analysis / analyses
diagnosis / diagnoses
hypothesis / hypotheses
louse / lice
mouse / mice
bacterium / bacteria
genus / genera
offspring / offspring
tooth / teeth
gouse / geese
vertebra / vertebrae
taxon / taxa

The video you linked
I had a very quick look at the video and I understand you are getting confused.
From 1:50 to 3:30 the author of the video repeatedly makes the false statement that dolphins are fish! No, dolphins are not fishes!! Also, the author of the video seems to be very confused about the difference between the terms taxon and clade. It is probably the worst educative video I have ever seen! Please don't trust them.
For more information about related terms, please have a look at What is the difference between these terms: clade, monophyletic group and taxon?.

Besides I would like to add that Original Poster should look up wikipedia when stuck with anything instead of watching youtube lectures with are seldom faultless. @RKhan

Excellent answer. I use to give Greek and Latin classes to my biology students, and they were always amazed when I said that in Greek we can have up to 15 different plurals (5 cases, 3 declinations, giving 53) and that in Latin we can have up to 30 different plurals (6 cases, 5 declinations, giving 65). Curiously, in Greek, taxis (row, order, arrangement) has the nominative plural taxeis. Very different from "taxon"/"taxa".


text:
Can anyone identify this bug?
Spotted in Czech Republic. Our office was hit with cockroach infestation, so I'm afraid if I haven't carried one home.

Looks quite like a cockroach. Did you damage it somehow?

From my experiments with cockroaches as a kid (and crickets, mouses. frogs, ants, gecko's) this cilinder definately reminds me of their egg sac.
(English is not my primary language, forgive any mistakes)

It is German cockroach (Blattella germanica) with two dark parallel streaks on it's pronotum.
The one in your picture is a lady laying her ootheca.

It is a pest.
Here's it in different stages of life cycle.
Things you might like to know:

Blattella germanica occurs widely in human buildings, but is particularly associated with restaurants, food processing facilities, hotels, and institutional establishments such as nursing homes.
German cockroaches are omnivorous scavengers. They are attracted particularly to meats, starches, sugars, and fatty foods. Where a shortage of foodstuffs exists, they may eat household items such as soap, glue, and toothpaste.
The German cockroach reproduces faster than any other residential cockroach, growing from egg to reproductive adult in approximately 50 – 60 days.

Source: Wikipedia and different pest service websites.

Finally found it!


text:
Why do women mature (physically) earlier than men?
All sources I've read (the first page) states that the fact that women mature (in the sense of physical maturing) earlier than man is caused by the earlier selective prunning in brain. Though, this is an explanation just for the mechanism, not for the cause.
So what is the real evolutionary reason women mature earlier (though, probably slower) than men?

When asking for "evoluitonary reason", always be careful to not fall into the pit of the panselectionist view of evolution (as briefly explained in the second paragraph of this answer). This is just a warning but your question is fine!

What do you mean by "no chance in the concurence"? Otherwise, good question regarding ultimate versus proximate causes.

A quick look at "All sources I've read" suggests that the "maturing" here is entirely psychological, and quite subjective.  (And on a personal note, I've done quite well for some decades now by refusing to either "grow up" or "act my age" :-))

I have found many claims that women are in average 3 years ahead of men, when it comes to maturity, but I haven't found any study done to support this claim. However, it may appear true, and it actually does seem like this in reality (my own observation of peoples behaviors, just in general), There are also men who mature before women, and some women who mature late. Point being, that it could very well be genetic, but it could also be a psychological variable that is affected by ones environment, life situations and indoctrination.

I would like to add to my previous comment, regarding life situations... What is it that separates girls from boys in relation to passing time, when not in school (or at work?)... Basically during their free time, while growing up. Some people are required to be an adult at an early age too, an example because of the loss of a parent/guardian, thus they have to inherit some of the tasks of their lost one, so that the other parent/guardian isn't overwhelmed.

When you say all sources I've read, have you really read all  9,920,000 results? You might want to be more specific about what you read.

What kind of maturing are you asking about? Reproductive (sexual) maturity - the ability to ovulate and carry a pregnancy? Social maturity - acting like a "grown-up", not constantly making jokes centered around the physical elimination of waste, ability to maintain a polite conversation, ability to handle responsibilities and make appropriate decisions? Emotional maturity - the ability to recognize, validate, and control one's emotions in a socially-responsible manner? Physical maturity - achieving one's final height, full development of secondary sex characteristics, full set of teeth, etc.?

How about religious maturity - the ability to fully participate in all rituals and practices of your chosen religion or belief system? My point is, the word "maturity" on its own is vague and misleading. Your question is unclear, and needs to be edited to reflect exactly what you are asking about. You might also want to research a bit more than just glancing at the first page of a single vague Google search.

My guess is that the reproductive age of women is shorter and therefore they invest into the earlier development, unlike men that would have no chance in the concurence of all the men up to 70. This sentence makes absolutely zero sense to me. Please rewrite it in a grammatically correct and informative fashion. We don't have any clue what you're talking about or what point you're trying to get across. If you are having a difficult time expressing yourself in English, get a more fluent colleague, friend, or associate to help you.

@Remi.b The first page

@MattDMo All kinds of "maturities" are tightly bind together, just as I wrote, the mental maturity (religious, personality) is connected with the blood level of the hormones which is the key thing for the reproductive maturity.

@Probably your final paragraph in italics is fundamentally flawed. You seem to think that mating (and reproducing) is a zero-sum game, which it absolutely is not. First, you completely overlook the possibility of multiple partners. Second, your hypothesis that women are somehow automatically attracted to older men is just wrong, if you take 2 seconds to think about it. You block "older men" into a single group, and there's certainly a significant difference between an 18-year-old woman and a 30-year-old man vs. that same woman and a 70-yo man. Also, some women like younger men - just ask them.

@Probably "men don't affect the reproductive fitness of the offspring as much [as women]" Do you have any evidence whatsoever to support that statement? "older men have better chances to succeed between the girls because they're better physically developed" When was the last time you actually looked at an 18-yo standing next to a 50-yo man? Which one is more fit and "physically developed"? How do you know that older people have fewer parasites? It would be just as likely for them to have more, because they've lived longer and accumulated more.

@Probably "men are in principle fertile till death" Umm, no. That's just plain wrong. How many 60- or 70-yo new fathers do you know? "there's no reason of spending resources on the physicall development (maturing) in the age when they have no chance of succeeding between the other men (i.e., before 15 years)" Again, what does this even mean? Of course someone who has not hit puberty doesn't have a chance of "succeeding" because they're not even playing the game! Afterwards, it's pretty much an equal playing field. Male and female adults exist in equal numbers, so all get a chance.

@Probably "All kinds of "maturities" are tightly bind together, just as I wrote, the mental maturity (religious, personality) is connected with the blood level of the hormones which is the key thing for the reproductive maturity." No, I beg to differ. Sexual maturity has nothing to do with emotional or social maturity. Just because you can doesn't mean you should, as the saying goes. There are plenty of teen parents who don't have as much social maturity as my 11-yo son.

@Probably Your entire question is a string of unsupported opinions tenuously connected together to give a completely unreasonable conclusion. You still haven't defined what you mean by "maturity", so it is impossible to know what you're asking about or to give a clear answer. Your "facts" are either misinterpreted or just wrong, and you clearly don't seem to understand evolution very well. I'd suggest taking the brief class Understanding Evolution from the University of California, Berkeley, then delving deeper into some topics.

@MattDMo: WRT 60-70 year old new fathers, you could probably find about as many as have the resources,  financial and otherwise, to attract women of childbearing age - and these days, of course, the desire to become fathers.  And for fitness, I know a number of 50+ individuals who are in far better shape than a lot of 18 year old couch potatos.  There's a lot more individual variation than you seem to think.

@jamesqf I was speaking (well, writing) there in generalities about populations, which is why I didn't bring up individual variation. Yes, of course there can be vast differences between individuals. Perhaps I should have said "average 18-yo vs. an average 50-yo". Women individually also have vastly different preferences for men. My overall point is that the OP has not thought through the question very carefully, and has made a lot of unsubstantiated claims, a number of which are simply incorrect.

@MattDMo Ok, thank you for your corrections. Just one basic thing: You don't a selective pressure to apply universally on the whole population, all you need it is just to be more stronger on individuals with some common trait. Apart from that I didn't mean "older men" as "elderly", I meant "more developed, mature" men.

As I said, of course men aren't fertile literally till death, the important thing is that the age is much longer than women's. Of course not everyone who is physically mature is as well sexually (I assume you mean maturity that consists of the awareness of your sexual identity, otherwise it's physical maturity) and mentally mature. I don't want to offend anyon but clearly, these things usually go along.

I've read it and there's nothing new for me. Please select the individual mistakes if you want to discuss them. I just find it obvious that there's much bigger difference between older women and young women than between young and older men.

@MattDMo: I agree on the lack of thinking through.  As I said earlier, most of the "maturity" seems to be purely subjective.  As for fathers in their 60s, my neighbor - 102 last birthday - has a daughter in her 40s, so it can be done.

@jamesqf I totally agree. Some family friends had an "oops" pregnancy when he was in his late 50s (she's probably 10-15 years younger than him), so it's definitely possible. All I'm saying is that it's rather rare.

@MattDMo: Sure, but I think the rarity is due less to physical inability, than to relatively few older men having the financial resources to attract women of childbearing age.

@MattDMo Ok, I've removed the part what I think, please don't consider it in your potential answer

I'm fine to delete any unfair comments from the list. The question can have two interpretations, it is a bit ambiguous: Why is there a gender difference in the age of maturation, growth and fertility in humans? One interpretation is biochemical reasons, and the other is human ecology and evolutionary reasons. The biochemical ones are subject to evolutionary pressure, as all neoteny is, so i understood the evolutionary pressures as being the driving factor for the reason of the difference. It's a very good quesiton that requires proper phrasing.

The problem with the question is that you refer to an article that talks about mental maturity, and you are instead querying about the entire process of different gender maturation time in males and females. what are the reasons for the earlier growth, physical and mental maturation of human males and females, and illustrate the query with a good summary of the ages males and females get different morphological and mental changes.

The tags you use are not related to the question.

@comprehensible Well all the sources were connecting the fact with the intensity of the selective prunning so I don't know why should it be so crutial to seperate mental and physical maturity but I'm asking primarily about the physical because I understand that such effects can be partially a work of society habits.

This is a question about Neoteny and Heterochrony.
The closest field of study which will have specialists of this kind of topic is the study of the late maturation of humans compared to other species, which has had some research: 5-7 years ago there were some papers measuring the different bone growth rates of humans compared to chimpanzees and exploring the notion of natural selection through preference of immature traits: being attracted to girls with child like faces, smaller nose, large eyes, small voice, babyish, with various causes for example allowing for later brain pruning and longer brain development.
If you research in google publications you can find some research on the topic, for example:
Heterochrony in human evolution: the case for neoteny reconsidered
Sexual selection, physical attractiveness, and facial neoteny: cross-cultural evidence and implications (1995)
The origins of sex differences in human behavior: Evolved dispositions versus social roles.
It's all about evolutionary selection due to survival fitness. A complex age dynamic is at work in human evolution due to our extended lifetime, memory and brain size, amidst heavily variable social patterns (mate selection, monogamy, tribe size, bride rights, patriarchal/matriarchal systems) in paleolithic humans.
Bonobos mature at roughly the same time: 9 years, and female bonobos have a baby at 11 to 13 years. I think that illustrates the flexibility of maturation age according to the role of the adults.
Human females can have babies in between 9 and 15 years for the most part, some of them at 7, so maturation age is an evolutionary trait rapidly changeable according to fitness of the resulting offspring, so it is entirely fine tuned by survival performance.
EDIT: I wrote this answer to be helpful, but apparently my lack of sources and "errors?" deserve a mark down. so here is an additional text:
"They found that Paleolithic girls arrived at menarche - the first occurrence of menstruation - between seven and 13 years. This is a similar age to modern girls, which suggests that this is the evolutionarily determined age of puberty in girls.
'This would have matched the degree of psychosocial maturation necessary to function as an adult in Paleolithic society based on small groups of hunter-gatherers,' they write.
Disease and poor nutrition became more common as humans settled, causing puberty to be delayed. Modern hygiene, nutrition and medicine have allowed the age of menarche to fall to its original range.
However, today there is a mismatch between sexual maturity and psychosocial maturity, with sexual maturity occurring much earlier. This mismatch is a result of society becoming vastly more complex, with psychosocial maturity therefore taking longer to reach."
Note that they are talking about female adult paleolithic maturity and tasks at that age. Females compete for mates by attractiveness and fitness, and some research suggests that males compete for females by other mechanisms, even force or threat.(ref)
There is clearly a reason for which men are available to make and care for their offspring later than females. Females prefer older males by at least a couple of years with moderate adult muscle mass(ref), and in our species males of 17 to 35 years are biologically the strongest and wisest. Nature would have it that 11 /13 year old fathers clearly are counter productive to the survival of their partner and child in an ordinary setting of hunter gatherers, because of the very long gestation and complexity of human survival tasks.
The human mental maturation range has a wide variety of deviation, and between the age of 8 and 25, we are pre-programmed to be in an intense task of learning and physical adventure. Physical coordination of the male can reach an optimal level as late as the age of 22, 3/4 years after his bones have finished growing and his muscles and reflexes have had time to increase and adapt to his new frame, which is why athletes are at their physical peak between the ages of 18-27, and the "mental pruning" article suggests that their mind continues to re-organize itself well beyond the age of 30. During that stage, a human male is programmed to learn a wide array of advanced skills: flint knapping, tool making, botanic knowledge, hunting skills, clothes making, landscape exploration, orientation, memorization of food places, wells, tree climbing, metal work, net weaving, pottery, pigments, weapons, blow darts, wild animal experience (game, lions, rhinos, birds, rodents, traps, stalking, poisons, frogs) etc... All that time based survival experience reinforces the notion that a male reaches his functional optimum as a provider and protector of his family well after his sexual maturation age.
Females have a less physically intensive role to play in human society. While they can learn all the hunting/survival skills of the male, their central role is to be nourished and provide for the child(ref). Their parenting tasks rely less on individual memory because they stay socially at home more (papua new gineans, africans, aborigines, yanomami). Their task can be less intense physically, require less physical training, and can be less intensive on memory and adventure (being nourished, childcare, craftwork, leadership of the group at home and less in exploration and precarious tasks). Both the human male and female memory has a very important role for guiding the group. A female can provide guidance up till the age of 50-90 in a natural setting.
Females are generally less expendable and adventurous than males, because a male can potentially have 3 offspring every day, he is limited by the number of females, and she can only have 1 offspring every 9 months, she is more precious to the multiplication of the group.
Add to that the function of memory, hunter gatherer fitness, and social acumen, absorption of mental and survival skills
Other great apes have gestation periods arount 8.5 months compared to our 9.
Because of the difficulty to assess the paleolithic social and environmental pressures that caused the sex age maturation difference, it's a question that theorists would be unwise to wade into to any great depth, in an academically competetive field. A good anthropologist should be able to list all the predominant selection factors.

This doesn't answer the question, and is really just a bunch of hand-waving without much in the way of supporting citations. "It is well-known that females prefer older males with young adult muscle mass in almost all species" Actually, it isn't. Citation needed. "maturation age is an evolutionary trait entirely tuneable according to fitness of the resulting offspring, so it is entirely fine tuned by survival performance." Again, citation needed. Finally, your last sentence basically says "I read the first results from a Google search and don't actually know what I'm talking about."

Onset of menarche at 9 years old is a very recent phenomenon due to significantly increased environmental exposure to estrogen and its analogs, as well as some other as-yet-unagreed-upon causes. Historically, girls living in 6th to 15th century Europe, for example, began menstruating at an average age of 14.

Finally, your last sentence basically says "I read the first results from a Google search and don't actually know what I'm talking about" ... No it sais your markdown is idiotic. I search science publications for 30 minutes and find that the topic, which is conjectural, has virtually no precedent, I publish here what precedent there is in related fields. I'm not inclined to argue with someone who speaks nonsense and who has no better answer than I do. You are an example of a negative forum contributor with low experience in biological academia. Use established measurements from extant tribes.

They found that Paleolithic girls arrived at menarche - the first occurrence of menstruation - between seven and 13 years. This is a similar age to modern girls, which suggests that this is the evolutionarily determined age of puberty in girls. That's not just one factual accuracy of my text. you may as well consider the entire text as relatively well informed... and learn... because you are not informed, and yet you act as if you were. listen and learn. i'm certainly not a very good biologist in this field but i am effortlessly less misguided than yourself.

Much of the information contained in this post requires additional references. Please [edit] to add citations to reliable sources that support the assertions made here. Unsourced material may be disputed or deleted. I don't care if your statements are correct or not, they still need to be supported by peer-reviewed literature. Scientists understand that. I'm not going to address your personal attacks, as they only reflect negatively on yourself. You don't know me, so don't make assumptions.

I never mark down other users except if they provide negative imput to the forum, because i have regard and empathy for their efforts. your first comment contains a flat personal critique, and your second comment contains a falsehood. clearly you are not wise enough to interact with the page, citing false information as you do. I've added references for everything, because i didn't stray into inexperience as you did in you second comment, oxford and cambridge zoology. botany, human sciences, and ecology departments dont provide a narrow base of culture: read a single book on human sciences.


text:
Why do we have the tibia and fibula (a 2nd bone) in the lower leg?
Does fibula participate in rotational movement of ankle or not (just like the radius in forearm)? If not, what is the purpose of that bone?

The Tibia is just like the Radius bone in the forearm, which combined with the biceps, enables the hand to rotate. Could there be a similarity?

the Tibia is just like the Ulna.

@GlebVoronchikhin - The tibia is not really like the ulna. If you take a closer look at the articulation of the tibia/fibula with the talus, you'll see that the fibula allows a nice fit with stability.

@anongoodnurse so the fibula's main function is not rotation of the foot?

Two bones in lower limb (forearm or leg) is the ancestral condition for mammals. But, depending on size, there can be some degree of fusion between the two bones. Mammoth and rhino skeletons can show this. The hypothesized biomechanical trade-off is stability on uneven terrain (so, joint flexibilty is useful) vs weight support (robust limb is useful). Need to hunt down appropriate refs and skeleton images, though.

It does function in the rotation and stabilization of the foot, but that is not why we have it, even species in which it serves no function still have it. A bone does not necessarily have to have a purpose in an organism, instead it can have on in its ancestors.
We have this arrangement becasue we inherited the basic limb bone arrangement from our fishy ancestors. Basically all tetrapods share the same pattern of bones in their limbs, one bone, two bones, many small bones, followed by several groups of long thing bones. this goes for front and hind limbs.

tetrapod evolution


text:
Are these principles worth being validated?

Odunayo's principle of inhalation states that provided a given amount of water is ingested, inhalation through the nostrils will be excluded due to the presence of oxygen in the water.

From the above theory, I was drinking water and it suddenly hits me that when drinking water, it'll be impossible to breathe. So.....
Q1. My principle is based on the fact that why it's impossible to breathe while drinking water is because of the presence of oxygen in the water, Is this true?

Odunayo's principle of immortality states that provided the injuries to the heart and brain remain excluded, an organism will be unable to experience immediate blackout with the aid of determination by that organism although weakness and other symptoms related to it may persist.

I actually came up with this principle when wondering if when a person is shot apart from the heart or brain, will be able to survive much longer than how an ordinary person would due to that person determination to stay alive.
Q2. Is that true or is it simply due to the place the person was shot,(still, apart from the brain and heart and when no treatment is involved in such scenario)
Q3. If the second principle given above is true, could it also be applicable to animals?
Q4. Which of the principles given above is worth being validated and how can it be improved, if there is any room for improvement?

I know this question is a bit primarily opinion-based, but i'm not sure where to post this question except from here, since it's a biology related question.

Odunayo is actually my late colleague's name, I named the principle from him. And the principle was made up by me,(a 16yr old kid)

No matter how much an individual wants to live, an untreated traumatic injury that is causing loss of blood will lead to loss of consciousness and eventual death unless something is done to treat the condition. A body (human or otherwise) requires a certain amount of oxygen to be delivered to the brain per minute in order to survive. Go lower than that limit, and the brain shuts down. Stay lower than that limit for a certain amount of time, and recovery is impossible. It's as simple as that. You need to stop watching quite so many movies and crack open a few books.

Additionally, it's not very scientific (I understand you're only 16) to make up pompous-sounding "principles" just to ask about them on a website. If you have a question, ask it, according to the rules discussing what is on-topic and what is not. Pay attention to the advice given in How to Ask a Good Question as well. We encourage curiosity, but not lying.

I don't know who this Odunayo is, but the reason you can't breathe while drinking water (or swallowing anything else for that matter) is that your epiglottis closes off your trachea to make sure you don't aspirate the food/drink which could cause infection or drowning. This has absolutely nothing to do with the oxygen content of either.
Other organisms that do not use the same orifice to eat/drink and breathe, such as invertebrates with a trachea or book lung system would not be subject to these limitations; you could say the same for the gills of fish.
These "principles" sound meaningless from any scientific standpoint, though there are some studies that support a true effect of "will to live" in some terminal patients, though it's hard to separate cause and effect and impossible to do a true randomized experiment. There is no evidence that "will to live" has any effect on outcomes related to acute trauma like a gunshot - these studies are mainly focused on elderly patients with chronic illnesses.

Thanks for your answer, so, I guess you've shown to me that my first principle doesn't actually have a scientific background. What of the second principle, from your answer, you clarified that the second principle could be supported in some cases(that is, 50% proved)

I never said anything was 50% proved, I said there is some support that terminal patients who have a strong will to live may possibly live longer than others who don't. The biological explanations for this are very unlikely to involve any sort of "mental power" but maybe something more along the lines of differences in cortisol levels. This isn't the same thing as surviving a severe trauma - the Hollywood "just stay with me!" refrain, for example, is totally bogus. If EMTs ask patients something like that they are just trying to judge their level of injury, not actually provide treatment.

@BryanKrause as far as I know, the whole "will to live" thing applies to people late in life who still want to do things, remain active, be involved in family, community, and decisions about their care, etc. etc. These active participants tend to live longer than neglected elders in nursing homes with little to know family or social interaction, often previously-deceased spouses or significant others, and little desire to remain in this world. You might want to clarify that a bit in your answer. I've never read of, for example, gunshot victims who just want to [...]

[...] hold on for little Jonny back home, and have the will to live, vs. a depressed gunshot victim who welcomes the circumstance and just wants to die in peace. That sounds 100% Hollywood. An injury is an injury, and while there is certainly medical evidence of some people being able to control certain aspects of their physiology, including heart rate/blood flow, breathing, body temperature, etc., two in other ways identical average Joes who get the same traumatic injury will die pretty much at the same time, regardless of the "will to live" of one over the other.

@MattDMo yes I think in my comment I made that clear, and in the answer I said terminal patients. Even in those cases, the science is a bit unclear. There are clear statistical trends for increased death rates following holidays, for example, but it isn't really known if that is because people are "holding on" for the holidays or if there are stresses caused by the holidays that hasten death in the following days to weeks. Nonetheless, I will clarify my answer a bit.


text:
What does “energy transfer in cells” mean?
"ADP and ATP are involved in energy transfer in cells."
I know what is ATP and I know how ADP is formed, but I don’t understand what “energy transfer in cells” means.

Cells require a constant supply of energy to generate and maintain the biological order that keeps them alive. This energy is derived from the chemical bond energy in food molecules, which thereby serve as fuel for cells.
Cellular nutrients (components in foods that an organism uses to survive and grow) come in many forms, including sugars and fats, so food molecules are rich sources of energy for cells because much of the energy used to form these molecules is literally stored within the chemical bonds that hold them together.
Cells release the energy stored in their food molecules through a series of oxidation reactions. Oxidation describes a type of chemical reaction in which electrons are transferred from one molecule to another, changing the composition and energy content of both the donor and acceptor molecules. Food molecules act as electron donors. During each oxidation reaction involved in food breakdown, the product of the reaction has a lower energy content than the donor molecule that preceded it in the pathway. At the same time, electron acceptor molecules capture some of the energy lost from the food molecule during each oxidation reaction and store it for later use. Eventually, when the carbon atoms from a complex organic food molecule are fully oxidized at the end of the reaction chain, they are released as waste in the form of carbon dioxide.
They (Cells) do not use the energy from oxidation reactions as soon as it is released. Instead, they convert it into small, energy-rich molecules such as ATP and nicotinamide adenine dinucleotide (NADH), which can be used throughout the cell to power metabolism and construct new cellular components.
Sources :

How Cells Obtain Energy from Food ?
Cell Energy and Cell Functions

For more informations :

What Are Nutrients ? - Definition & Examples
Cellular energy production

Lets imagine the energy budget of a cell as the economy.
Using this analogy a glucose molecule is like a 5kg bar of silver. It is very valuable, but it is hardly convenient if you want to pay for chocolate milk or buy a cup of coffee. What you need is an exchange that will break that silver bar into smaller units of currency like a stack of $1 dollar bills. The smallest and most common currency of energy in a cell is ATP.
Most (but not all) chemical reaction in a cells that requires an input of energy uses ATP. This is why ATP is said to be used in energy transfer within the cell.
Glucose is a 5kg bar of silver.
The mitochondria and the TCA cycle is the exchange.
ATP is a $1 dollar note.