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Recombination between DNA segments question

In the diagram shown above, segments A and C are copies of a repeated DNA sequence, flanking a unique stretch shown as B. A and C are in an inverted orientation relative to each other, as indicated by the arrows. Intramolecular recombination between segments A and C would most likely lead to ...

duplication of segment B only
duplications of segments A, B, and C
inversion of segment B
deletion of segment B only
deletion of segments A, B, and C

I do not understand this question. Or how the answer was arrived it. Can someone provide some light on the subject? Is this related to transposons?

Redraw the diagram so it looks like a horseshoe on its side, such that the two arrows lie parallel, pointing in the same direction. 2. Now draw the 'X' to show the recombination crossover between the homologous segments. 3. Starting at the leftmost end of the DNA (the end with segment 'A' in your drawing, trace the path of the recombinant DNA product after the crossover has occurred. The segment labelled B will have under gone an inversion.

So, apparently the "trick" to this question is in the wording. "between A and B" appears to mean one crossover somewhere in the B segment, which could destroy (delete) a gene in the B sequence if present at the cut.
The answer involving the horseshoe "trick" implies that the chromosome has looped so that the A and C sequences match up, an extremely unlikely condition. Then a crossover occurs while the loop is in place, also an extremely unlikely event.
Another problem is that the horseshoe solution apparently implies that it is a single chromatid that is looping to itself and forming the crossover. That's weird. I could more easily visualize a different solution: One chromatid is aligned tail-to-head with respect to the other chromatid (head-to-tail). This would allow the corresponding A and B segments on the two chromatids to match up, thus allowing a crossover point anywhere (except inside B) to result in an inversion of B. This is also weird.
These two solutions are much weirder and unlikely than a simple crossover inside B: Picture the two chromatids aligned a little off target so that one is cut at the start of B nearest the A segment, and the other chromatid is cut at the other end of B, nearest the C segment. The result is an uncomplicated deletion of the B segment from one of the chromatids and duplication in the other (no inversion). This scenario seems at least as valid as the "correct" choice given in the practice exam.
While I'm glad to have learned the "trick" in this question for when I take the exam, I consider this question "bad".


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From what stage can you speak of an inflammation?
Imagine you hit your foot at a table leg and it hurts a while or you got a tiny graze. Those injuries aren't an infection but could these things still be called an inflammation?
Is it necessary that in both cases cells are damaged to induce a cascade of hormones? Or with other words, is there always an inflammation when cells are damaged or is needed more?

Inflammations are non specific defense reactions instigated on cell injuries.
Inflammation reactions are characterised by certian physical changes that are inturn caused by physiological changes.
The physical changes are:

pain
heat
redness
swelling
loss of function

Here the redness is caused due to vasodilation of the nearby blood vessels (mostly capillaries) which means that the amount of blood passing through the vessel is increased and thus the region appears red. But this doesn't end there, as the vessels dilate their permeability to fluid and leukocytes increase that ooze out into the tissue and cause the region to swell up.
The resident phagocytes (phagocytes present in body tissues including skin) together with these leukocytes  fight against the invading microbes. However microbes that are present all around us, even abundantly on skin get a chance to enter our body through the smallest cut or tissue damage.You can say inflammation is a defense mechanism that the body employs to mitigate any imminent infection.
Now coming to your questions:

Those injuries aren't an infection but could these things still be called an inflammation?

Yes they are inflammations. If they are displaying the classical symptoms then they are inflammations.

Or with other words, is there always an inflammation when cells are damaged or is needed more?

Yes, there's always an inflammation if cells are damaged.

Is it necessary that in both cases cells are damaged to induce a cascade of hormones?

No in none of the cases mentioned by you a cascade of hormones is induced. Rather in both cases; INFECTION and INFLAMMATION a number of immune cells are induced to carry out a cascade of reaction which actually identify the microbes and cause

phagocytosis
neutralisation
agglutinisation or
complement fixation

However an infection can be caused without cell injury, e.g. pathogens entering through nose and mouth.
Note: Phagocytosis etc are complex immune reactions that occur against pathogens and there are chapters dedicated to them in Immunology books . I would suggest you to go through a google search to get a general idea if you are curious enough to know what they are.
Sources:

Kuby Immunology 7th Ed
Wikipedia

DId it help you understand the difference between inflammation and infection?

From PubMed Health:

When a wound swells up, turns red and hurts, it may be a sign of inflammation. Inflammation is – very generally speaking – the body’s immune system’s response to stimulus. This can be bacteria colonizing a wound or a splinter piercing your finger, for example. Inflammation happens when the immune system fights against something that may turn out to be harmful.

So when inflammation occurs, chemicals from the body's white blood cells are released into the blood or affected tissues to protect your body from foreign substances. This release of chemicals increases the blood flow to the area of injury or infection, and may result in redness and warmth. Some of the chemicals cause a leak of fluid into the tissues, resulting in swelling.
Signs of an inflammation :
There are five signs that may indicate an acute inflammation:

Redness
Heat
Swelling
Pain
Loss of function

There is a loss of function, for example, when the inflamed limb can no longer be moved properly or when the sense of smell is worse during a cold.
This means that an inflammation does not start when a wound has been infected by bacteria, festers, or heals poorly, but already as the body is trying to fight against the harmful stimulus or a viral infection.
Not all five signs occur in every inflammation. Some inflammations occur silently and do not cause any symptoms.
So depending on the symptoms we can decide if there is an inflammation or no.

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Why is our voice deeper in the morning?
For most (if not all) people, their voice sounds a lot deeper when they've just woken, compared to how they sound during the day. This effect can easily last for a few hours, like for me today. What are the biological reasons for this? I've heard that it has something to do with relaxation of your muscles during sleep, but I'm not sure how that is supposed to work, and there might be other factors at work.

What is the evidence for this? Are there references to this being a general phenomenon?

@kmm personal experience (n=±20), also, I vaguely remember it being discussed in a pop-science TV show.

Just a guess - higher pitched sounds require more energy than lower pitched sounds (at the same volume). Just after waking up, you are more likely to be tired, so the same effort to speak receives a lower energy input, requiring either the volume or frequency to decrease. For reference, my voice actually switches over to low frequencies when I'm tired as a power-saver feature.

I'm surprised there hasn't been any answer or comments but yes, this is a fairly well known phenomena. It's quite possible that not everyone finds this to be true for them or possible they've never even noticed it. If a person doesn't need to talk for the first 15 minutes to hour, they might not realise their voice is deeper and/or raspier first thing in the morning.
Speech pathologists, voice teachers and professional singers are certainly aware of this. There's been no solid research on why that I know of. After all who's going to fund research into something that's mainly a curiosity with no medical repercussions or profits to be made? Still, there are various thoughts on why this occurs (outside of acid reflux irritating the vocal cords).
During sleep while we're in a horizontal position, a certain amount of fluid collects in our upper body (read from the neck up), so our vocal cords will swell and thicken slightly. It's why our eyes look more puffy first thing when we arise. During the night, we're not using our vocal cords either but while breathing, air is still passing over them. So while the tissues swell a little, their outer membrane dries a little. To counter the drying effect, the body secretes more mucous as a protective coat. This effect is much worse in people who are mouth breathers.
Another possible reason is what voice teachers and singers think happens, too. Vocal cords, being muscles, need to stretch and contract to vary the voice's pitch. Unused through the night, they're nit as limber and can't stretch as well as later. Vocal cords stretch to reach higher pitches. If that idea sounds far-fetched, just remember opera singers and other professional singers need to limber up before performing. They practice hours each day but before a performance, they need their voice to be at its best. Hence they'll practice singing notes up and down the scale.
Supposedly, drinking a cup of lukewarm water first thing in the morning helps, and tea or coffee is supposed to dry out the throat even more. I never drink coffee but, personally, I've found that first hot cup of tea in the morning doesn't just help my voice return to normal but wakes me up.
I've never heard of this effect lasting for a couple of hours though I haven't gone around quizzing people. :) So try either the lukewarm water or a hot drink and see if it makes a difference. You can also try singing or just talking aloud to limber your cords in the morning.
Edited June 14/17
Links (but not scientific studies) where others have noted this phenomena
Why do people's voices sound deeper in the morning? I gave greater credence to the first answer since it comes from an opera singer.
Raspy Voice In The Morning?
And from Music SE Why is my voice lower pitched when I get up in the morning

Can you add references to your answer?

As I said, there's been no real scientific studies done on this (that I know of) but I can include links and will.

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Terrarium Compatibility: Millipedes with Carnivorous Plants?
I have a child that loves his large millipedes (Desert Millipedes) and Venus Fly Traps.  He's also been wanting to get some Sundew Savages.  Given this little collection and his real enjoyment of terrariums, we're curious if we could consolidate his millipedes into a terrarium with these carnivorous plants without causing harm to either of them.
We keep the millipedes fed well with decomposing plant material, but weren't sure if they'd go wild after the fresh plants... and then of course if they would try to do that, could these plants harm the millipedes?
In the end I fear there will be some problems here and wanted to check to see if anyone knows about this compatibility before we dive in and have our hopes dashed.

Millipedes eat decomposing material, not fresh. Carnivorous plants eat very small things like flies, not millipedes. They digest their food using enzymes, just like you and I do - they're not poisonous. You're fine.


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How is green fluorescent protein distributed while inside an organism?
I would like to know a relatively simple thing, but something I wasn't finding the answer to.  When fluorescent protein is used in a relatively large, non-transparent animal, like a mouse, or theoretically a dog or a human, how is the protein generally incorporated into the tissue?  I suppose that it would bind to elastin and otherwise it could be transfected into different cells in and throughout tissue, both around the skin and deeper.  However, wouldn't it only be useful near to the skin, since ultraviolet light and visible light would penetrate a limited distance through tissue?  Then again, a relatively bright light source could possibly produce light from deeper in tissue.  I'm not quite sure.  It's a relatively simple question, but I appreciate it.
(Edit): I may have been a little vague with the question, a more specific version of the question I asked would be; given the brightness of a fluorescent light source that is directed at fluorescent protein filled tissue (with UV assumed to be close to the visible spectrum) and the portion of that light which is converted to visible light, approximately how could you calculate the relative brightness of the protein at a certain depth in the tissue.  Of course it probably is very difficult to get accuracy with that because that would depend on the portion of fat, muscle, collagen, etc in the tissue.  But if there's something rough and general, like the depth of the protein would reduce its relative brightness proportionally to the natural log per millimeter or something, that would be fine.

Distribution of GFP
When used as a reporter usually GFP is expressed by the cells themselves or attached to an antibody and injected. It ends up everywhere, is what I mean.
Localization of GFP
There are three solutions to the hidden-behind-tissue problem for fluorescence.

Use a functionally 2D sample (nematodes, mouse limbs, etc)
Sacrifice the organism(if it's not dead already) and use optical clearing
Cleverness

Of these cleverness is the most interesting. Types of cleverness include time-resolution imaging(Light scatters instantly but most fluorescent proteins take a few nanoseconds to relax) to separate fluorescence from backscatter. Excite a slice of the sample and look at it from a slight angle 3 ns later, and you should see a depth-map. Repeat.
You could also use optical tomography to essentially use computers and many cameras instead of time-delay imaging to solve for the 3d distribution of signal. Computed tomography is much cheaper, mostly because you don't need a nanosecond-scale laser + capture system(those are expensive).


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Download FunCat Database for Programmatic Access
I am enriching RNA-seq data for the fungus Neurospora crassa and would like to be able to search the genome by functional category, determine similarity of genes by category membership, and any other information I find interesting in Python or R. There are many websites that have this information, but the most comprehensive appears to be Pedant.
I would like to download a SQL database, a JSON file, or even a text file that contains the information on these sites without having to use a web interface for everything.
The data I need access to is gene code, gene description, DNA sequence, FunCat category, GO category, and maybe others on the Pedant site.  Is there anyway to to programmatically access these fields or download all of them in bulk?
Note: I have been using the python bioservices module, but it only gives access to KEGG, which is missing information on many of the genes in the N. Crassa genome.

Did you try biomart? I don't think it retrieves FunCat information though. But you can get everything else. It has a python API as well as an R interface (in bioconductor). BTW what do you mean by gene code?

By gene code I meant locus number (NCU#####).  I will look into biomart to see if it has the pathway information I need.


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What is happening in each iteration of PSI-BLAST?
I understand that the first BLAST yields almost the same results as blastp. The second time the iterated blast generates different results as it uses different matrix based on our first result.
But I don't understand how exactly the second matrix is generated.

Addition to previous answers:
PSI-BLAST is a sort of machine learning algorithm which uses the results of the first alignment (PSSM) to score the next iteration of alignment. I would recommend you to refer to the NCBI bookshelf page on PSI-BLAST.
PSI-BLAST adopts a scoring scheme (PSSM) that is built based on a given set of data (the aligned sequences), rather than using a generalized scoring matrix. This improvisation updates the prior knowledge of the homologs and helps to detect similar sequences that were otherwise undetectable. With iterations the PSSM keeps getting updated, thereby, making the BLAST more sensitive in finding homologs.
How PSSM is constructed:
If a position in the alignment is conserved (i.e same residue in many sequences), it receives a high score whereas a position with low conservation gets a low score.
Score is based on relative counts of a residue in a position. If you want to know the details see here.

Hi ! Thanks. Please see the comments to gergana's answer.

Check the link that I mention in the answer. It has some examples too.

I read that this method is much more sensitive for detecting distant relationships. What does this mean ? How using PSSM improve its senstivity ? (Sorry for bugging you so much but am really excited to learn this new(for me!) stuff !)

From Russ Altman (Stanford University) lecture:
Blast takes as an input a sequence, it searches the database, and outputs a set of alignments (a top ranked alignment, followed by a second-top ranked, a third, and so on). Then you take the top scoring sequences (you might use the E-value as a cutoff) and you can create a position-specific scoring matrix (PSSM) based on the occurrences of amino acids in all the columns of these alignments. This is allowed, because there is a high chance that these sequences are homologous to the query sequence and thus looking at the amino acids would give you a good sense of the variability in position that is allowed in the initial query sequence. The next step is to re-search the database for more hits. So now instead of searching with a sequence, you are searching with a profile, and you get another set of hits. You can iterate a few times which would give you a much more sensitive search.

Hi! Thank you so much. So each time we iterate , a new PSSM is formed ?

I also do not understand the significane of using this type of blast instead of standard blast. What specific/new information can i get by doing this type of blasting ? When wud i use this type of blast ?

Yes, each time you iterate a new PSSM is formed. You might want to use it if you would want to identify homologs that are undetectable by simple BLAST.

PSI-BLAST is Position-Specific Iterated BLAST.
I'm probably out of my depth here, but my understanding is that the results of the first, essentially standard, BLAST search are used to create a multiple sequence alignment. This alignment is then converted to a Position Specific Scoring Matrix (PSSM). (The linked Wikipedia entry shows this for DNA sequences, but the principle is exactly the same for protein sequences.) This matrix can then be used as the probe for the next round of BLAST, and the results of that alignment can be used judiciously to improve the matrix, and so on until the results converge.
Here is a link to some slides by Stephen Altschul which go into lots of detail.


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Is reproduction intrinsically part of life?
If all of the characteristics of life are required for something to be defined as living, how can we account people or other life that can not reproduce?

Every species has the ability to reproduce.  Of course, individuals within a species can be born with a mutation that keeps them from reproducing, or lose the ability to reproduce at some point in life.  However, to say that once these individuals fail to meet that criteria they are no longer forms of life would be a fairly absurd semantics argument.  It might be useful to note in an evolutionary sense that those individuals can no longer pass on their genes, which is could select against whatever it was the resulted in that individual being sterile.
You could probably reword the characteristics of life to stress species instead of individuals, but then theres a problem with microbes which have very poorly, or non-existent species.  But in general, this is not something a biologist is going to lose sleep over.


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How do I run each individual record in a multi-fasta file against a database using PSI-Blast?
I'm new to standalone blast+ and the linux terminal.
I set the bash-profile to load the PATH and BLASTDB for my blast already, but I don't know how to use psi-blast yet.
How can I do the search against db with one query sequence? The file has >400 FASTA sequences. I need to checkout every sequence alone against database. Is it possible to run this job automatic in blast+?  (one run in loop for every seq?)

BLAST takes a fasta file with many sequences as a query. Have a look at the BLAST manual. The running in loop question is off-topic since it is about shell scripting.

I agree with @WYSIWYG that the manual should be your first port of call, however it is rather crap. If you're comfortable with ruby, perl or python, consider learning about the respective bio module. They all have great BLAST integration.


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Recent classification for parasitoid (ecological relationships)
I'm about to present an exam about ecological interactions in biological control. Although the position of some groups is clear, in the case of parasitoids they are included sometimes as predators, some others as parasites, while sometimes they are included like an own group. For example, in this paper they
 are included as parasites, but I wanted to know if there is a more recent reference or classification for these groups (Trophic strategies,
animal diversity and body size Kevin D. Lafferty and Armand M. Kuris).

While both parasitism and parasitoidism are both classifications of predation, parasitoids differ from parasites as they [parasitoids] kill their hosts.

A related question I asked some time ago covering why parasites kill their host received some great answers.

I think the wikipedia article defining parasitoids has it right on this one. The term is, and should be flexible and it's definition defined by context. i.e Case by case definitions are made obvious in the literature.

Patently there is no point to trying to draw arbitrary lines of distinction between such vague, and often variable, life histories. In each ecological or ethological study, the terms applied should reflect the facts in the contexts relevant to the matter in question. Such studies need not in all cases use the identical terminology, and there is no reason they should.

This means that you should always describe the life cycle even if you call the organism a parasitoid. There is too much variation between seemingly similar organism life histories to use a strict and specific term.
For those struggling to see the link from the question, they suggest a parasitoid can be measured as a parasite that reduces host fitness to zero:

... they are also quite different from these other parasites,
  in that, similar to a predator, they must kill their host.

A recent (2015) review on Whiteflies refers to Hymenoptera as parasitoids of Whiteflies because the Hymenoptera are parasitoids as larvae as they kill the Whiteflies and then become free-living adults.


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Fst genetic distance: Autosomal vs. mtDNA
As far as I'm aware, mtDNA is only inherited from the mother. Hence, if I compute Fst from autosomal SNPs, then I'll get the actual genetic distance between two human populations.
If I compute the genetic distance Fst between two human populations based on mtDNA sequences, then it alone can't be used to draw conclusions on their genetic distance.
For example, an admixed population will score relatively low Fst value with its maternal ancestral population (assuming the admixture was caused by unisex migration) when computing based on mtDNA sequences. However, the Fst distance based on autosomal SNPs will be relatively higher (depending on proportion of admixture).
Is this correct?

Yes, you are correct.
$F_{ST}$ can vary among specific genetic regions considered. If for example there is a strong influx of females from population A to population B, then the mtDNA and the X chromosome (excluding the pseudo-autosomal region) would show much smaller $F_{ST}$ between the two populations than the Y-chromosome would.
Many other non-demographic processes can affect $F_{ST}$. Background selection (Charlesworth et al., 1993; Matthey-Doret and Whitlock, BioRKiv, 2018), selective sweep (e.g. Chen et al., 2010), heterozygote disadvantage (Ingvarsson and Whitlock, 2000), negative epistasis and other processes can affect $F_{ST}$ as well and cause $F_{ST}$ to differ among genetic regions. Even mutation rate variation (Whitlock and McCauley, 2001) can affect $F_{ST}$ (if the mutation rate for the loci considered is not ridiculously small compared to the migration rate).
For an introduction into the common misunderstandings of how $F_{ST}$ works, Whitlock and McCauley (2001) is a must read!

Just to complete this answer, would Fst computed from autosomal SNPs be fully representative of the genetic distance between two populations? Say for the influx of females from A to B, will the autosomal Fst correctly show that the admixed population is between A and B (depends on mixture proportion)?

The difficulty here is in the phrasings fully representative of the genetic distance and correctly show. There is no correct (true) genetic distance among populations, there is only the statistics of genetic distance that one wants to define and those statistics are affected by various processes.
Would an influx of female among populations affect $F_{ST}$ at autosomal loci? Yes. Would this effect be the same than at mtDNA? Not exactly, no. Is the entire parsing of genetic variation among population represented by $F_{ST}$? No, $F_{ST}$ is just a summary statistic (just like a mean or a variance is).
If there is a specific statistic (such as the effective migration rate, the effective population size or the location of loci involved in local adaptation for examples) that you are trying to infer from these $F_{ST}$ calculations, then maybe you should ask whether computing $F_{ST}$ by a specific method would allow you to make good inference of a specific statistic of interest.

Just to complete this answer, would Fst computed from autosomal SNPs be fully representative of the genetic distance between two populations? Say for the influx of females from A to B, will the autosomal Fst correctly show that the admixed population is between A and B (depends on mixture proportion)?

@RudyWinono See edit in my answer to address your comment.

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How do the chromosomes arrange themselves after fertilization in humans?
In human reproduction the male produces sperm containing 23 chromosomes and the female has the oovum containing 23 chromosomes , so after fertilization the zygote contains 46 chromosomes. What I want to know is , how do the chromosomes identify each other and pair up,  fir example say ,how does chromosome '1' of the male pair up with chromosome '1' of the female to make set '1' of the zygote?

I don't understand your question. 23 chromosomes from the mother, 23 from the father and they combined in 23 pairs of chromosomes. What exactly is unclear to you? Maybe you'll want to watch an introductory class about genetics such as e.g. the series of lectures from Khan Academy

Do want to know, how for example the male and female chromosome 1 "find" each other and pair up in the zygote?

Yes that 's right , what I am asking is that after fertilisation how do the chromosomes find each other and pair up.

After fertilization the diploid cells divide by mitosis.  Chromosomes don’t need to pair with their partner during the eukaryotic cell cycle.  After S-phase each chromosome has been duplicated (so there are 46 + 46 = 92).  The two daughter chromosomes resulting from semi-conservative DNA replication are held together at one point: their centromeres. In M-phase two microtubules from opposite poles of the mitotic spindle will attach to the kinetochore that assembles at those centromeres.
Nowhere in this process is the maternal chr1 required to interact with the paternal chr1.
The pairing that you are refering to takes place much later after the new primordial germ cells haved developed into the germline, leading to meiosis.  The molecular details of homolog pairing during meiosis are best understood in the model organism C. elegans where each chromosome has specific cis-acting sequences that are recognized by different trans-acting factors that lead to recognition and then pairing, followed by synapsis, and eventually crossing over.

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What are the structures that make pixel-like patterns in wood?
Some wood seems to have structures that are squarish in cross-section. I've often noticed that these are distributed in arcs or sinusoid shapes on guitar fretboards, for instance.
Here's an example I was able to find online:

Edit: here's a better picture, you can see the pattern as it rotates with respect to the cutting plane I think:

Are they channels or just fibers of a different color? Why are they distributed in this way?

Welcome to Biology.SE. I see a lot of different patterns — I think it could be helpful to indicate (e.g. by adding markings like arrowheads) exactly what structures you are interested in. It also would be clearer if you showed a plain piece of wood (ideally a closeup of a small section of wood) rather than a fretboard, which complicates the issue. Next, if you are using some else's image it should be public domain and properly credited. Finally, have you tried looking up "wood anatomy"? Demonstration of prior effort on your part is one of the site expectations (see: [tour], [ask], and [help]).

I suggest looking for wood cell patterns online. also is that a natural pattern or is a veneer which involves cutting a wood in a rotary slice. https://www.google.com/search?q=wood+grain+patterns+microscope&tbm=isch&chips=q:wood+grain+patterns+microscope,online_chips:forestry:NiLTcVs6464%3D&hl=en&sa=X&ved=2ahUKEwiXw5Pt5_74AhW5rXIEHce0BeQQ4lYoBHoECAEQKQ&biw=1215&bih=571

Wood is composed of a variety of longitudinal cells (those running parallel to the axis of the trunk or limb) and ray cells (those running perpendicular to that axis, from the center of the trunk to the edge).
Longitudinal cells produce the regular ring pattern (you can see them aligned vertically in the fingerboard photo). Rays (also called medullary rays, vascular rays, or pith rays) are producing the darker squiggles.
The ray cells help conduct sap and other materials radially in the trunk, between the center and the bark.
Different types of wood produce more or less prominent rays, with different characteristics. Different cuts of wood also make the rays more or less visible.


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Biological validation of computationally determined gene-gene interaction
How can a computationally determined three-way gene interaction be biologically validated? What kind of assays or tests must be performed using cell/tissue-based and/or mouse models to prove that the three genes may indeed have a joint effect?
Let's say, it is easier to identify and validate gene interactions that involve transcription factors like FOXM1. Consider a three-way gene interaction in Breast cancer - FOXM1-BUB1-CHEK1 - that can be tested for direct interactions via western blot and reporter assays. But such interactions may or may not be interesting - given the fact that transcription factors may be affecting expression levels of other genes. Most computational studies are focussed on identifying gene interactions based on coexpression or co-occurrence. There is literature on computationally identifying AND/OR relationships between interacting genes. I don't have a specific example to provide but, for argument sake, if we did suspect that three genes are interacting in an AND like manner, how do we biologically validate this finding? I'd also appreciate if you may have comments on the usefulness of such findings, particularly, with regard to designing more efficacious combination therapies against a disease".
Thanks

I think that this is an interesting question, and could lead to lots of discussions of strengths and weaknesses of different experimental approaches, etc.  I think, for me, it would be helpful if you could provide either (A.) a specific 3-way interaction—that you have in mind, or (B.) a reference to a scientific publication that reported this type of experimental result (if either os these are possible). Otherwise any potential answers you get might be too general  OR, miss the mark.

Oh also, standard blurb RE: Homework questions would apply here (because this question sure reads like an exam/test), In other words, where is the evidence that you have tried to answer this yourself (and failed)?

Thank you for your feedback, I edited my question to add my "homework".

Hang in there, this answer will grow over time.
Just off the top of my head, I think we could write a small book (or a very long review article) to cover both the depth and the breadth of your question(s).
First, we need to define, and/or clarify, some terms.  The term interaction probably means different things to different authors at different times.  In fact, one author may use this term to mean different things at different times.  So I would like to propose that we make some distinctions.  For example, I would make a distinction between a genetic interaction between two genes (which is typically detected in one of the model organisms, using a genetic test between two loss-of-function alleles) versus a protein-protein interaction (sometimes called a PPI) between the two proteins encoded by those same two genes.  PPIs have been detected classically by co-sedimentation in a sucrose density gradient, or co-immunoprecipitation (co-IP), or by affinity chromatography.  More recently PPIs have been detected by mass spectrometry (MS) (sometimes coupled with affinity chromatography).  PPIs have been inferred by using proxy assays, such as the yeast two hybrid (Y2H) assay.
PPIs can also be detected by surface plasmon resonance (SPR) assays, and there may well be others.
So, when you say gene-gene interactions, what precisely do you mean?

I'm gonna try to cover as many scenarios as I can think of:

Gene interaction ( = co-expression):
This is probably the easiest to validated (e.g. by western blot like you mentioned) but the hardest to interpret. Without further analysis of the genes functions you have no idea what effect their co-occurring activity might have. If the genes are metabolic enzymes or part of a signal cascade it would be a good idea to check both their individual roles in these pathways, but also check for potential synergistic effects. The same is in principal also true for transcription factors, but in that case 'pathways' are often not  equally well understood, instead go for:
Gene interaction ( = on same targets):
In the case of transcription factors (but also e.g. Kinases/Phosphatases) that are co-expressed it might not unreasonable that they also affect the same targets. Here you need to again compare both individual effects (list of up/down regulated genes) with synergistic effects (e.g. geneA prevents normal function of geneB, geneC increases geneB function multifold). For transcription factor analysis you should generally analyse expression on the mRNA level (via qPCR) since the protein level introduces (at least) another layer of regulation.
Protrein interactions:
A good way to prove these experimentally is by using co-IP (immuno-precipitation) experiments: you use an antibody to retain a specific protein and all its (direct) binding partners. Then you show the presence of the partners you're interested in with a western blot.
One caveat for this method with 3-way (or higher order) interactions is that - depending on the binding strength of the proteins -  it can be very hard to prevent anything but direct interaction partners from being co-purified. If you want to absolutely prove that two proteins interact directly a yeast-2-hybrid (y2h) experiment is better suited.

Others have covered a lot more ground but I'll throw in a couple of approaches from the spectroscopy side since I've been looking at them recently.
Bioluminescent resonant energy transer (BRET) shows if proteins bind in vivo: "BRET measures the interaction of proteins using a bioluminescent donor fused to a protein of interest and a fluorescent receptor fused to its binding partner. The bioluminescent donor, usually a luciferase, does not excite the fluorophore using light, but transfers resonance energy through dipole-dipole coupling. To transfer resonance energy, the donor must be within 10nm of the receptor and in the proper orientation making the technique useful for measuring proteins in close proximity." (From https://www.promega.com/resources/pubhub/features/bret-nanoluc-luciferase-and-protein-protein-interactions/)
Surface plasmon resonance (SPR) also shows if proteins bind, but in vitro: "SPR is sensitive to changes in refractive index within about 150 nm from the sensor surface. To study the interaction between two binding partners, one  partner is attached to the surface and the other is passed over the surface in a  continuous flow of sample solution. The SPR response is directly proportional to the change in mass concentration close to the surface. Biacore systems can be used to study interactions involving (in principle) any  kind of molecule, from organic drug candidates to proteins, nucleic acids,  glycoproteins and even viruses and whole cells." (From the Biacore assay handbook)
These are both ways to look at direct interaction, ie binding. Functional interaction is a whole different story.


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Where do B cells produce antibodies?
I was recently at a Leukemia and Lymphoma Society conference where a particular oncologist lecturer claimed that all antibodies are created in the bone marrow (I won't mention his name, as he was a great lecturer, and I don't wish to sully his name if he happened to be wrong on this particular point).
Wikipedia seems to indicate that antigens are produced in "Secondary Lymphatic Organs" or occasionally in the bone marrow, but I've been misled by Wikipedia before.  It seems to me that evolution would favor creating antibodies close to the infection, and not far away in the bone marrow or lymphatic organs (how would the antibodies "know" how to get back to the original infection?  It would be very inefficient to send antibodies all over the body if the infection is localized.)
My questions is: Could someone "map out" the travel of a typical B-cell throughout the body from the time the B-cell detects an antigen up to the time it produces antibodies (and if it later stops producing anti-bodies, please include that)?

Related question:  http://biology.stackexchange.com/questions/15390/what-cell-types-produce-immunoglobins-and-where-are-those-cells-found

You are asking multiple questions here. The answer to the first two questions can be found in the post mentioned by @Roland. Please [edit] your post so that it does not contain multiple questions.

I'd be careful drawing conclusions about the location of events in the life of a B-cell from the answer to the question linked above. It's generally good, but has an important error if it is being used to answer this particular question.

The oncologist seems to be incorrect.
Antibodies are created all over the body inside secondary lymphatic organs (lymphatic nodes) or any other mucosal associated lymphatic tissue (MALT).
B cells mature in the bone marrow and finish their maturity in the periphery, then they can live in lymph nodes, MALT, spleen, omentum or other structures and they can create antibodies in all of those structures.
In regard of your localized infection question, you are right. When a pathogen enters the body the B cells closer to it are in the lymph node that is closer to that site and thus there is where the antibody response will take place. That is why when you have a sore throat (throat infection) your tonsils are swollen (they are lymphatic organs too).

While your answer is good, it would be great if you could add some sources to it.


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Which animals live in trees and make noises like rubber ducks at night?
I was recently at night in a public park in Karlsruhe, Germany. I've heard many (at least 10, probably many more - it's hard to tell) animals in the trees making noises similar to that of a rubber duck which is pressed.
What could that be?

It is most likely a Tawny Owl (Strix aluco), or Waldkauz in German, one of the most common owl species in Central Europe. These owls have many different calls, and you can hear them often here in Karlsruhe at night. Particularly their "kewick" call sounds similar to squeezing a rubber duck. It is usally emitted by female individuals during the mating season, but also males can produce it. Juveniles have a similar call as well. But most of the time - as far as I have noticed - you only hear their more common "hoo-hoo" calls (listen here or here).
Photo of a Tawny Owl:

Image Source:
https://commons.wikimedia.org/wiki/File:Waldkauz-Strix_aluco.jpg

Listening to the kewick call and trying to judge whether it really sounds like a rubber duck * ..... mmhh yeah... Ok, that works! +1

@Remi.b well he said "similar", not "exactly like" :)

It sounded exactly like the "kewick" call! Thank you! I'm positively surprised that somebody could identify that with this little information :-)

@MartinThoma Probably because we live in the same town ;)

@adjan Haha, the world ist small. But we don't know each other, do we?

I have lived close by, but our Waldkäuze didn't sound like rubber ducks, or our rubber ducks don't sound like Waldkäuze. Now I am confused.

@MartinThoma No I don't think so.

Where I live near Vancouver Canada, barred owls can sometimes be heard at night. My older son was convinced that some drunk teenagers were making stupid sounds at night. (Too many noisy drunks lived in the area.) When a bonded pair start caterwauling, they cerainly font sound like owls. Animals can make some very surprising sounds for those not familiar with them!


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Identification of Anoles
Can anyone help me identify these anole species? All photos taken on St. Thomas, USVI, in close proximity to one another.
(click to zoom in)

Each photo is a different individual, but the overall similarity makes me think they are likely the same species, although I could easily be wrong about that (the third one especially looks different from the others). They are dull brown overall with fairly subtle patterning, a light line that runs down their spine, bordered by a darker stripe on either side, and a broad band between the eyes. My best guess is that they are either Brown Anoles (A. sagrei) or Crested Anoles (A. cristatellus). Searching images online, there are some images identified for each species that are quite similar to these, but based just on comparison with those images, I really could go either way. Is there a definitive criteria to help narrow down the species?

Note: Usually I'd say that a single question asking for multiple identifications is too broad, but because I think these may be the same species, I felt it was appropriate to group them into one.

If they're not the same species. Whoever answers first, please make it a community wiki.

@canadianer. Looks organised. But they can't be zoomed in, looks like it would require some other markdown.


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Are there any trees that prefer to grow on the floor of water bodies but protrude to the air?
Are there any trees that prefer to grow on the floor of water bodies but protrude to the air? Specifically, those that prefer salt water or grow on shallow sea.

Mangrove swamp trees and shrubs immediately spring to mind. There are many species that fall into this category of trees that grow in intertidal and costal locations. They prefer locations where salt and freshwater mix, known as 'brackish water'.

All roots require oxygen and the species that fall into this category have developed roots that protrude above the surface, called pneumatophores.
Photo from http://www.dutchpickle.com/philippines/palawan/sabang-mangrove-forest-palawan.html
Here is an excellent website with more information
http://www.fao.org/docrep/010/ai387e/AI387E06.htm

Mangrove trees even throw up snorkel roots (Pneumatophores) to get to air.


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Can the brain influence gene expression?
A neuroscientist told me (according to my hazy memory) that the brain/nervous system can have an epigenetic function, ie directly regulate gene expression.
I'm not a biologist, but she talked me through how it worked, and I know enough of the basics to follow along and think it sounded reasonable.  I think the conversation was based on some post-doc research she was doing.
A quick google search (Maybe I don't know enough jargon to get a productive answer) brings up a chap called Bruce Lipton, who completely agrees, but who also, according to wikipedia "remains on the sidelines of conventional discussions of epigenetics, basically ignored by mainstream science".
So what gives?
Are there (a possible chain of) mechanisms by which the subconscious mind can affect gene expression?

It sure does. If you stress up because you have an important appointment, this will impact your sugar concentration in your blood and many other things toward which the body will response by (among other things) modifying gene expression. However, be careful to not misunderstand the term "epigenetics" with "heritable epigenetics" (even though there are definitely variation in stress that affect heritable traits through epigenetics).

Gene expression is regulated all the time. When you learn something, consciously or subconsciously, then your neurons undergo a change in gene expression. Sometimes there can be some epigenetic changes as well (like DNA methylation). However, this doesn't mean that you can think hard and make your muscles grow :P

As has been pointed out in comments, the brain can certainly affect gene expression; but so can anything in our bodies, because the blood stream is super good at carrying stuff around the body to wreak havoc.
But I'm going to take a somewhat uncharitable view of this question1; and assume that what you are asking about is high-level mental processes affecting gene expression throughout the body, which is not a thing that happens.
The basic concept to bring forwards here is that the brain is hell-a layered. The brain is an extremely complicated organ, and while it's not a complete mystery, it's not an organ that we generally can be said to understand, at least not on the level that we can be said to understand in major terms how, say, the liver, kidney or spleen works.
What we do know is this: The brain forms a massive network of neurons; the shape of which informs our personality, memory and cognitive functions. Even our simplest thoughts involve, by necessity, thousands of neurons, and anything more complicated than 'Fire!' involves tens, hundreds or thousands of thousands (millions) of neurons.
At the same time, it's important to understand that our brain does a lot of things that we're not directly cognisant of. For one, our brain controls our breathing. As you're reading this, you'll discover that you take control of your breath, but also that you haven't done so for several hours at the very least, and maybe not for days or weeks, and you haven't died from hypoxia yet. Our brains do these kinds of things all the time, and we hardly ever notice.
Genetics are a very, very, very low-level thing. Way lower of a level than mere breathing, genetics is the engine that drives decision making at a cellular level; which is so far removed from consciousness that it's hardly imaginable.
And this is where layering really comes into play: While recent research indicates that brain cells have hijacked DNA replication techniques to store memories, most of our actual thoughts exist only on levels that are so much higher than the nuts-and-bolts of our brains that the physical structure of our brains don't even come into play.
Essentially, thought as we understand it doesn't exist within individual neurons, but only within the relationship between neurons. When it comes to cognitive or metacognitive processes, things like genetics becomes an implementation detail isolated from the higher-level system as a whole. The underlying physical structures can affect gene expression, but do so not as a response to thoughts or subconscious desires, since these don't exist in the individual neurons; but as a response to primal needs like "more sugar for the brain!" or "more oxygen for the brain!" or "more protein for the brain!".
In other words: While the (sub)conscious mind can affect gene expression, it does so in terms of resource management, not in terms of how body tissues act, because the mind as it is has no physical concept of bodily function.

1: Uncharitable, yes, but it does make the question more illuminating and interesting, IMHO.


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What percentage of human excrement is toxic if ingested?
I have been considering food production, waste management and 3D food printing, particularly during space exploration. This led me to wonder if human excrement could be processed into raw materials for printing healthy food.
What percentage of human excrement is considered toxic to humans if the toxins were ingested in the quantities in which they were excreted? I am referring only to excrement produced by humans not infected with diseases of any kind.

The dose makes the poison. In other words, everything is toxic, which include all the stuff that you can find in human excrements.

You can possibly narrow down to - what components of human faeces are toxic at even lower concentrations that should be removed when faeces are to be recycled.

Do you think that would make it more likely people would look at the question or answer? Only 23 views so far. :/


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Can any animal ejaculate at will without physical contact?

Note: In this question, I'm asking about animals that have a penis that functions very similarly to humans. I've read some animals have dramatically different methods of copulation and physiologies, so for simplicity I'm only asking about males with reproductive systems very similar to mammals, birds, etc. However, if you feel a certain species deserves special note, please tell me about it.

Are there any animals that can ejaculate at will, while awake, without any form of physical contact with the sexual organs?
I read that a Muscovy drake everts his penis in about a third of a second and the accompanying video shows ejaculation once eversion is complete. This is so fast that I wondered how the male could aim accurately into a female's cloaca. I began wondering if the process was voluntary or involuntary, since a voluntary process seemingly would allow greater accuracy.
So, this led me to wonder are any animals capable of ejaculating at will without any form of physical stimulation to the penis or body?

Can humans ejaculate at will in your opinion? If not, you should clarify what you mean by "at will".

@Remi.b Ah! I had not thought of it that way. Thank you. I'll clarify.

There are literally oceans of animals who fertilize their eggs outside their body, I bet most of them don't require physical contact.

@swbarnes2 that's correct. Perhaps you should post it as an answer with some elaboration.


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How did mitochondria make energy long ago?
I've learned that mitochondria is thought to have been eaten by a larger cell, resulting the mitochondria to be part of a bigger cell. Well, here's my Q. If you look at how mitochondria works, you find that in order to initiate the TCA cycle, you need to have pyruvate acid.
Then does this mean that when mitochondria was all by itself, there were pyruvate acid around it? I mean, isn't pyruvate acid a complex molecule, therefore, cannot be abundant??? How could this be?
Furthermore, if cell A swallowed a mitochondria, then that cell A should provide mitochondria with NADH and pyruvate acid. How could this be? Did ancient cells produce NADH and pyruvate??

Actually it is acetyl CoA that is required for the TCA cycle, not pyruvate. The acetyl CoA can come from other sources, e.g. fatty acids. I agree this doesn't alter the substance of your question. You might do better to wait until you have assimilated more of your course material before posting questions about evolution of metabolism. If you haven't covered photosynthesis yet you can't even start thinking about it.

Umm sorry... What I mean was, you need acetyl CoA for TCA, but that acetyl CoA is made from pyruvate acid, which

Must be entered from outside the mitochondria. In other words, you need pyruvate acid to make mitochondria work.

No. As I said, acetyl CoA can come from the breakdown of fatty acids without any involvement of pyruvate. It can come from other intermediates as well. I assume you haven't met these areas of metabolism yet.

@David Though the OP mentioned pyruvate in specific, there is no real contradiction on it being a substrate. Just that it is not the only substrate. I would rather call Ac-CoA as a reactive intermediate and not a substrate. Organic acids like fatty acids and pyruvic acid (alpha keto acids) are substrates. I see your point but that is not really the central idea of the question. IMO, the idea is where did the ancient mitochondrion obtain its substrates from. An edit would resolve this confusion.

@DannyHan Perhaps you would want to edit your question.

You are asking a very interesting question.
As you correctly mention, the substrates of mitochondrial metabolism (TCA or Krebs Cycle) are pyruvate and NADH, and, through oxidative reactions, ATP is produced. Indeed, it seems unrealistic that when the "mitochondria" were by themselves there was pyruvate and NADH in the environment. Let's take a step back.
In the 1970s, Dr. Lynn Margulis proposed the extracellular origin of mitochondria. What does this mean? Margulis suggested that, due to the bacteria-like characteristics of mitochondria (e.g. circular DNA), it is plausible that the first mitochondrion was in fact a bacterial cell that had been introduced into another cell by endocytosis. Therefore, we cannot really describe mitochondria as having been "by themselves", since originally they were (most likely) bacteria. (I am emphasizing this because in your statement it seems like perhaps there is some misunderstanding with this point.)
Where were we? Ah, yes, so we have a bacterium (pre-mitochondrion) inside another (host) bacterium. Consider that the combination of one bacterium inside another works and, voilà!, we have symbiosis and, more precisely, endosymbiosis. This means that the two bacteria collaborate to survive, they benefit from interacting with each other (symbiosis) and one of them is inside another (endo-).
But, of course, the combination is not optimal: the two bacteria have common steps in their metabolism and this is a waste of energy. And evolution does not like that. Evolution encourages organisms to minimize their energy expenditure through natural selection: those organisms that manage to make the most out of their energy supplies will survive and thrive. This means that the pairs of endosymbiont bacteria that manage to use less energy to carry out the same actions will be positively selected for.
Indeed, what this possibly lead to was the host bacterium keeping its basic glucose metabolism (glycolysis), and the "inside"-bacterium exclusively keeping its TCA metabolism, effectively becoming a mitochondrion. Hence, the current arrangement of glycolysis in the cytosol and respiration in the mitochondria.
In short, it is important to look at the bigger picture: were there ever really "free" mitochondria? No, according to Margulis' Endosymbiosis Theory there mitochondria-precursors, which were bacteria. Once these bacteria were introduced into the cytoplasm of another cell, their metabolism degenerated and was reduced to the minimum necessary. This is a success story: the mitochondria are evolved bacteria that have managed to survive and thrive, and have made themselves fundamental for survival of many lifeforms, including humans.
I hope this is a useful answer to your question. Feel free to ask for clarifications in case I did not describe something well enough :)

As a fun fact, mitochondrial DNA has an extremely low mutation rate, estimated to be one base pair per 7884 years... crazy!
Source: http://www.genetics.org/content/156/1/297.full

I have a further question... Bacteria originally had 1 cell membrane, 1 cell wall, and 1 capsule. So then the cell wall and capsule was degenerated while the membrane didn't??

It is thought that a primitive nucleated eukaryote acquired the proteobacterium that gave rise to the mitochondrion — not another bacterium. The later makes little sense and would still have to evolve a nucleus and other features of eukaryotes, lose its cell wall etc. Your answer would be better if you cut 95% out and left the key fact (or hypothesis) that mitochondria were bacteria acquired by primitive eukaryotes that lacked aerobic metabolism.

@rlluc Since the nature of the ancient eukaryotic ancestor (the host cell) is not really known, you should refrain from calling it a bacteria. Just simply call it a host. This propagates a wrong notion. Unfortunately, there are even some articles that are propagating this unreferenced claim as a statement (not even as a speculation). Perhaps you may also add a reference (a book or wikpedia would do) for the endosymbiotic theory. Everything else is fine :)

@DannyHan If you have additional questions then you may post them separately. Look at other Q&As on this subject, in this site or some basic resources elsewhere (like wikipedia) before asking a question; we appreciate some research effort from your side.

@David It is fine to ask someone to remove the 95% of the answer if that was really irrelevant. I don't think that is the case here.

@WYSIWYG Thanks for your comment! I appreciate the knowledge, I was not aware of the uncertainty about the "host".

@David I also appreciate you letting me know about the possibility of a proteobacterium being acquired and not another bacterium. However, you can spread knowledge without being condescendent.

@rlluc proteobacteria is a class of bacteria and extant α-proteobacteria and mitochondria fall under the same phylogenetic group (clade). Therefore it is believed that the ancient mitochondrial ancestor would have been a bacteria of the α-proteobacteria group. The details of how this happened are still unknown.

@WYSIWYG — What will you take then? 90%, 85%? I'm afraid that  "Where were we? Ah, yes…" in an answer is a flag that it is verbose (and can I say self-indulgent). This turns out to he the case. The answer spends so long in unnecessarily describing the history of the idea that it ends up with the nonsensical suggestion that one bacterium engulfed another. When this attracts four up-votes, somebody has to point out that the emperor is naked. One would hope that the feedback will help the answerer improve and thus help improve the site as a whole.


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Does DNA helicase or topoisomerase actually "unwind" DNA?
I am reading through my textbook (Genetics, Brooker 4th edition) and the summary it gives seems imprecise for the functionality of helicase and topoisomerase.
The following is an exerpt:
At each replication fork, DNA helicase unwinds the DNA and topisomerase alleviates positive supercoiling.
Is it proper to say that helicase "unwinds" DNA? In other places in the book, it says the function of helicase is to separate the two strands of DNA, and topoisomerase "relieves the supercoiling" caused by the strand separation activity of helicase.
Pardon my ignorance, but it seems rather like helicase actually induces more winding, and topoisomerase (gyrase) actually unwinds DNA.
Is this just a case of poor wording, or does helicase actually somehow unwind (untwist) DNA? I am finding this particularly frustrating because virtually every resource I can find says that helicase unwinds DNA, but based on the mechanisms they offer, it definitely does not "unwind".

It would be pretty difficult to separate the strands without unwinding them. As you pull the strands apart, the adjacent regions will either have to rotate (unwind) to accomodate this or break.

Why wouldn't the replication complex just rotate (spiral) along the double helix?

The strands must be separated so the incoming nucleotides for the newly fabricating strand can be base-paired to the template strand. The other (antisense) strand must be moved out of the way for this to occur.

I mean, I get that they're separated but how do they "unwind"?

Got a short piece of three stranded rope handy? (I don't think they make two stranded rope.) Hold the rope firmly in each hand about 5 cm apart. Twist in the direction opposite the winding. The strands of the rope will separate in the region between your hands. The unwinding and the separation of the strands are, um, inseparable from one another. You can't separate the strands without unwinding.
The heilcase unwinding is merely straightening out the double helix in a very local area. This separates the strands such that one strand can serve as a template for transcription or replication.
But a consequence of the unwinding in the local region where the strands are being separated, is that other nearby regions get more tightly wound. This occurs because the DNA is far too long for the ends to spin around to accomodate this unwinding. These more tightly wound areas are what is refered to as supercoiling. The topoisomerase alleviates this stressful coiling. https://en.wikipedia.org/wiki/Topoisomerase
So, the answer is both helicase and topoisomerase result in the unwinding of DNA.


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Improving transformation efficiencies- induce supercoiling?
From my limited knowledge of science, I know transformation can be one of the hardest step in cloning, and that a large amount of research/trial and error has been done to improve on this step. I've heard electroporation is the most efficient technique, though I have no reference, and of course the cell, media and duration all have vital parts to play in the process.
However, I've never heard of supercoiling as an important factor. Size of the plasmid plays a large part in transformation, so intuitively it makes me think supercoiling the plasmid prior to transformation would improve the efficiency. I thought transformation was simply DNA diffusing through holes, but are parts of the plasmid required to bind/interact with the host?
Why aren't we suggested we supercoil prior to transformation? I have several thoughts but I'm just guessing:

Is it because gyrase can disrupt the integrity of DNA?
Or is it that it's just an expensive enzyme and the gain isn't worth it?
Or perhaps supercoiling reduces efficiency of subsequent plasmid preps/transcription (though wouldn't the host's natural enzymes supercoil anyway?)

Two comments on this from my lab experience with transforming bacteria: Making cells competent (I usually use chemical competent cells since we have no electroporator in our lab) is not a hard thing to do. Transformation effeciency isn't usually a problem either (with good competent cells you easily get 5x10^8 transformants (and more) per ug of DNA. So my guess, why nobody bothers to use an additional step (besides the time and money it costs for the enzyme), is that the methods we have are simply good enough.

Here is a report that shows significant increase in transformation efficiency for large plasmids (transformation was by electroporation. However the paper has been cited fewer than ten times so clearly the technique did not catch on.

Zhixing, Y and Nahon, J-L (1995) DNA gyrase improves DNA transformation of E.coli cells with large recombinant plasmids. Nucleic Acids Res. 23:3353-3354

Thank you, interesting to know in case of any problems with transformations that this might actually work!

The paper predates bluelight and sybr safe, which improve the efficiency by several orders of magnitude, so they were definitely ahead of their times.
The reason why nobody does it is that from what I can tell they use Micrococcus luteus gyrase because they had it. Sigma sells Eco gyrase but at £500 I am not sure who would try it —I myself am working with epPCR libraries with a big plasmid yet I wouldn't spend that much.

Correction. (NEB)[https://www.neb.com/products/m0306-dna-gyrase-e-coli] sells it for USD70 —for 100 0.5 µg rxns. That makes it worth a shot...


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Literature about putative epigenetic state changes in mammal sequences after cloning steps in Escherichia coli
I would like you to point me out some literature about putative epigenetic state changes in mouse/mammal sequences after cloning steps in Escherichia coli.
This are the last search details I used in NCBI PubMed:

"epigenomics"[MeSH Terms] AND "cloning, molecular"[MeSH Terms] OR
  "molecular cloning"[All Fields] AND "sequence"[All Fields] AND
  ("escherichia coli"[All Fields] OR "e. coli"[All Fields])

Where do these epigenetic changes happen? while cloning a mammal DNA in E.coli?

I am interested in finding any record of epigenetic changes while cloning mammal DNA via E. coli (so, the initial DNA would have its epigenetic state, the purified plasmidic DNA after the molecular cloning would have another, possibly different, epigenetic state). By the way, any paper suggesting conservation in the epigenetic state through the cloning steps is also welcome, as it would provide evidence of the lack of changes.

I think you can narrow it down to DNA-methylation since bacteria don't have histones.

This is mostly true, but in principle I would like to include any possible bookmarking event.

E.coli strains that have dam or dcm methylases can methylate plasmid at adenines or cytosines respectively. See here — It is a NEB web page but has links to the cited references.
DH5α has both the methylases- dam+ dcm+ , BL21 is dam+ dcm− and ET12567 is dam− dcm−


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Diet of free-range herbivores
Giving minimal credence to estimates in popular media of the average biomass of  insects/arachnids, etc. in an acre of land, it seems that a "free-range" cow (I don't mean to pick on cows) might be something of an omnivore. Is there any evidence that herbivores derive essential parts of their diet from sources other than cellulose? Or that they do not?

Cellulose alone is just a sugar source. Plants do contain minerals and vitamins. They also contain protein, though the amount can be extremely low - thus the need for a lot of grassland to feed cattle. I'd expect the amount of protein intake from hapless bugs and spiders would be low, though, compared to the overall intake from plant sources.

As a fraction of diet it must be low, yes.

Deer have been known to eat bird eggs or young birds possibly to supplement calcium for antler growth.  I can't image it's a large part of their diet though.

@RioRaider: interesting, do you have a source for that?

@nico Here is an article in National Geographic.  Here is an interesting YouTube video of a deer eating a bird.  Here are two USGS webpages, 1st and 2nd, that discusses nest predation by ungulates.  Also, take a look at this Journal of Zoology article.

Animals lick salt deposits. It's an important part of there diet for plant eating animals.

One key nutrient worth thinking about in the context of this question is vitamin B12. Herbivores such as cows and sheep will derive this directly from the bacteria in their rumen. Rabbits produce two types of feces - soft and hard - and they eat the soft variety, rich in gut bacteria, as a source of nutrients like vitamin B12. Gorillas are primarily herbivores, but are thought to derive their vitamin B12 from insects, eaten purposefully or inadvertently.
So yes, herbivores derive this particular nutrient from non-plant sources.


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Can oil be used instead of water in preparing wet mounts for microscopy?
Is there a reason that oil (e.g., vegetable or clear mineral) is not used to make wet mounts in microscopy? I am not referring to oil immersion technique but substituting oil for water in wet mounts in bright field microscopy.
The question is mostly about moss or mold, things that appear plantlike on a slide. The optical properties may be good and the viscosity, as with glycerine, gives a little depth to the slide. Maybe it causes some sort of distortion? I don't see this listed as a suggestion on microscopy sites.
Thanks.

One thing is that the slide must be viewed quickly, otherwise spores tend to bunch up adhere to other structures. FWIW.

Typically wet mounts are used to observe the mobility and behavior of microorganisms. A classical use for a wet mount would be to study something like pond water were you could see all the different organisms swimming around like they would in their natural environment. Oils are more viscus and would impede mobility and might impact behavior or even be toxic to the microorganisms.
If you were an olive oil manufacturer, and you thought you had some odd microbial contamination of your olive oil you might look at a drop of your olive oil between a slide and cover slip thus using an oil based wet mount like you are describing. You might also do this if you were studying the microbiology of an oil spill in water.
There is nothing saying you could not suspend a sample in oil. There may even be a unknown benefit of using this method in certain circumstances, that is waiting to be discovered.

Have you looked at a mold under the microscope using vegetable or mineral oil?

Can't say that I have. I may not be understanding your question. You mention depth of the slide... If you are trying to view them in more of a 3-D environment then a wet mount might be helpful. Try it with oil and see.


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Advantages of pain sensation?
The hazards of congenital insensitivity to pain (CIP) are well-known.
This question is about the obverse: what selective advantage, if any, does the normal sensation of pain confer? I'm thinking of severe pain such as that associated with back injury, burns, and some intestinal problems in which the pain seems to serve no function other than to incapacitate.
A related question is whether there is a spectrum of sensitivity to pain, ranging from CIP to heightened sensitivity, what the distribution looks like, and whether this is a genetically plastic trait (like color perception)? If the distribution were sensitive to selective pressure then naively I would guess it serves our needs well, but we spend a lot of our collective time trying to dial it back, hence my question.

Yes a range of pain exists. This can be seen probably in your friends who all probably have a completely different threshold for pain. When doctors ask patients to rate their pain it's usually to establish a baseline so after treatment we can see if there's a decrease. The different thresholds have so many factors from general health to receptors to brain activity to emotional state. You name it! Often just focussing on a pain makes it more painful.
It's definitely an unpleasant sensation pain but it's our way of our body saying "hey, you need to pay attention". Usually the response required is rest or to identify what might be there causing the pain. For example pain means we will withdraw very quickly from a hot surface. Doesn't even require the brain as it is a reflex arc which minimises the time we spend burning that part of our body. And as it continues to hurt we use the arm less letting it recover and protecting it from infection by doing so.
As these hazards of being cut, burnt, bit, knocked, fractured are very common there is a survival advantage to be the individual that is alerted to these hazards and take the necessary actions. Particularly in children where pain is necessary as it makes the baby know it needs to eat (or the mother) or that something isn't a good idea (putting hands on something hot).
However as you say there are times when the pain itself is more crippling than anything else and in that situation we have a problem. Childbirth, backache and in cancer or in tension headaches are just some examples. As being able to feel pain is pretty much required for a long life, the disadvantage of having pains like the above is less and doesn't outweigh the benefits. Pain is always going to be necessary. They also usually don't interfere with reproduction and so genes are passed on.

+1 but we could imagine a world in which a much higher threshold (lower sensitivity) was an advantage. You agree that there is a a range--do we know anything about the distribution? Has it been quantized? Does it change in response to selective pressures?

Don't think of the whole world's threshold changing, think smaller. Boxers and fighters are likely a population which represent those with a higher threshold as a selective pressure exists. I've seen a distribution curve somewhere, I don't know where though.

In terms of inflammation, the purpose of pain is to force the organism to rest the area that is inflamed. Thus promoting healing. In terms of chronic pain, this is the same thing. However I think that if the pain will not cease regardless of protection of the affected area, and say if the underlying cause of the pain is ultimately fatal, then the pain is subordinate. The phenotype is already being selected out.
I think the concept shows a lot of parallel to the underlying concept of hypersensitivity (allergy).
Remember that over generations as all different things that can cause and prevent pain in our bodies are evolving, So too is the pain mechanism itself evolving.


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Electrodes in the brain and 'repetitive orgasms'
The advent of chlorpromazine in 1955 put an end to one of the more bizarre chapters in American psychiatry.$^1$ Dr. Robert Heath implanted wires or delivered injections of acetylcholine (a neurotransmitter) deep into the 'septal regions' of the brains of men and women with various physical and mental disorders. His discovery of the brain's 'pleasure center' actually preceded the discovery of the same center in rats by about 20 years [Baumeister, below, at 272].
In one of his papers$^2$ Heath describes intense orgasmic experiences on the part of his patients in response to his treatments, which he dutifully records on EEGs.
His description of Patient b-5 is especially interesting. He relates: "The patient became more attuned to her environment, answered questions more rapidly and accurately, and solved simple mathematical problems with more ease...and in most instances, within another 5 to 10 minutes, this [heightened attunement] culminated in repetitive orgasms." [Heath, below, at 12].
In addition to refreshing my interest in solving simple mathematical problems, this article made me wonder whether this area of research had been resumed in some form. Many of the ethical and technical problems discussed in Maumeister's article seem surmountable, especially in light of computer-aided visualization of brain structures. Not to mention that a kindred treatment, ECT (electroshock), which can still actually be done involuntarily, has seen something of a comeback in the U.S. since the 1940s. ECT is basically controlled destruction of brain tissue, which seems to cast Heath's work in a kinder light.
So my question is whether this thread has been taken up or whether, as one VIP put it, the absence of evidence is evidence of absence. I was unable to turn anything up.
Thanks for any enlightenment.
$^1$ Baumeister, The Tulane Electrical Brain Stimulation Program: A Historical Case Study in Medical Ethics (2000), J. of the History of the Neurosciences 9 (3): 262-78. See page 270.
$^2$Heath, Pleasure and Brain Activity in Man, (1972) Journal of Nervous and Mental Disease 154 (1): 3-17.

This question belongs to Cogsci.


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What is the mass of a human retina?
I'm struggling to find a reference for the mass or density of a human (monkey or rabbit would also work) retina.
I'd appreciate any help!

I did some research and I found this site : https://www.covance.com/content/dam/covance/assetLibrary/posters/StrubleEVER14.pdf
It has the weight for ocular tissues for different kinds of animals ( rabbit , human  etc. ).
I also found that the area of a retina is 1094 mm² and the thickness is 0,12 mm , so if you can find the density you can find the mass.
(found on this site https://faculty.washington.edu/chudler/facts.html#sensory )

Are you sure that the referenced value of 2500 mm^2 is not the surface area? Because there is no way that the retina is 5 cm x 5 cm.

I'm sorry . I did some more research and you are right. The actual area of the retina that i found is  1,094 mm^2 (Link that i used https://www.ncbi.nlm.nih.gov/books/NBK11556/ )


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What is the distinction between the terms detrivores, decomposers, saprotrophs and saprozoic organisms?
All of them feed on dead and decaying matter (detritus). Detrivores and decomposers are distinct, as it says on Wikipedia, in the fact detrivores consume macroscopic clumps of detritus while decomposers metabolise detritus on a microscopic scale. Are detrivores and decomposers both types of saprotrophs? Also, what exactly does the term "saprozoic" mean, and how is it distinct from saprotroph and decomposer?

Detritivores consume (eat) detritus.
Saprotrophs feed on dead organic matter by the means of extracellular digestion.
Saprozoic organisms are protozoans that are saprotrophs. This actually comes from an obsolete classification of plants and animals where bacteria and fungi were grouped with plants and were therefore called saprophytes if they are saprotrophic. Protozoans were considered animals; so saprozoic.
Decomposer is a broad class including both detritivores and saprotrophs.
Scavengers also consume dead organisms. They are distinct from detritivores because the former consumes a relatively larger amount of dead matter. Often, scavengers are the first to consume dead organisms; the leftovers are processed by decomposers.

I could not find any authoritative source for these definitions. A peer-reviewed article by Getz (2010) attempts to classify organisms based on their eating habits.

How do we define decomposes then? The definition that I have come by mostly is that they are organisms that  break down complex organic molecules into simpler ones, in heterotrophs at any level digestion does the same. So why a new term 'decomposers'? (I'm definitely missing out something).

Also scavengers? They too eat dead organisms(part of detritus)?

@SanjuktaGhosh Decomposers is a very general term and can be considered as a colloquial term. As I mentioned in the answer these organisms enable breakdown of the dead matter. Of course they are heterotrophs but they are different from other kind of heterotrophic interactions such as predation and parasitism. Other heterotrophs are not very efficient at turning over a large mass of organic matter like the decomposers.

I tried to find out what do human beings excrete, as obvious the excreta is rich is macromolecules(undigested). I read somewhere that the 'excreta' of microbes is rather formed of inorganic molecules (something that can directly be absorbed by plants?- is this what makes this group of heterotrophs decomposers?)

The bulk of a decomposers diet is non-living organic matter or dead organisms,  things that do not fight back in any way. Comparing decomposers and detritivores are like comparing predator and carnivore, they are extrememly close in meaning but one is more focused on how they eat the other on what they eat.

@SanjuktaGhosh I have added some information about scavengers.

Decomposers are responsible for the "decay" of dead organisms (carcasses), dropped plant matter, and animal wastes (fecal matter) by externally breaking down the organic material and then absorbing the resulting "nutrients."  This typifies the approaches taken by many fungi and bacteria.  Detrivores actually feed on or consume decaying material, including the decomposers themselves, and/or other detrivores.


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Understanding DNA supercoiling
While trying to understand DNA supercoiling, I came across these lines in the book Genetics by Ursula Goodenough :

All natural DNA is superhelical. The axis of the duplex itself follows
  a helical path in space. For virtually all DNA, the sense of the
  superhelical turns is opposite to that of duplex, thereofer, they are
  negative supertwists.

I am unable to understand these lines. Specially, the second one.

It means that the direction in which the normal double-strand is wound up (which is also helical) and the direction on which the double helix itself is twited to reach the supercoils are opposite to each other. Have a look at this image from the Wikipedia, I think it makes this clearer:

The first show a DNA ring with the normal helix-coiling. The second show the supercoiling of the coiled ring molecule. Imagine a rubber band. This you can twist around its band axis to get the coiling and around its vertical axis to get the supercoiling.
For linear DNA molecules, this looks like this (taken from here):

The rubber band example was awesome !


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Molecular biology - fundamental questions
Basic Gene, Chromosome, Genome, Protein - how are they ordered?
Genes make up Chromosome, and Chromosomes make up a Genome...
So, where does Protein come into play?
What do you call Genes that are spliced together to form something new?
What do you call a variable inside a Gene?
Thanks.

Welcome to SE! At Biology SE we appreciate some evidence of personal effort of the PO to answer the question. Without it, we may put the question on hold, giving you the chance to add some background information.

I have zero biology education and I am asking because the people that write stuff about such things are very verbose (needlessly so, just like writers for other things) when I just need a quick answer. I am in a circumstance where I must/should get this right. If you have a "for dummies" simple introduction link/answer that can answer the questions, then please post it.

Makes sense. Hope my answer helps.

where does Protein come into play?

A Gene codes a protein.
DNA is transcibed into messenger RNA (mRNA). mRNA is translated into protein.

What do you call Genes that are spliced together to form something new?

Genes are not spliced together. One single gene can consist of introns (intervening sequences) and exons (expressed sequences). Transcribed introns in the RNA are spliced out and the exons glued together to form a functional mRNA.

What do you call a variable inside a Gene?

Genes are made up of DNA. DNA is made up of nucleotides.

+1 Just an interesting note (definitely an exception to the rule), in some organisms, exons from different primary transcripts from different genes can be ligated. This is known as trans-splicing.


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Explanation of the meaning of high-throughput
Almost all of the papers about bioinformatics, I faced with the high-throughput word, but I could not find any explanation about it (I think it is so easy to understand and that's why anyone explains it but I could not do it ) . Is there anyone who can explain me what do they mean by high-throughput ? Thanks in advance.

It's not necessarily a biological term. http://www.merriam-webster.com/dictionary/throughput

Ha! So throughput is just reversed “put through”! @canadianer

High-throughput sequencing specifically refers to sequencing techniques like Illumina that allow you to sequence massive amounts of DNA at once (hundreds of thousands of strands), as opposed to older techniques such as cloning the cDNA in plasmids, followed by sequencing.

Shotgun sequencing uses Sanger sequencing protocol.

Yes, yes it does. I was not implying that shotgun sequencing is a high-throughput method. I'll edit my answer to reflect that

Sorry. I got confused. Clear now. But still Sanger sequencing is not really low throughput. It is still high-throughput but not as efficient as Illumina.

Thanks, what would be a good example of a low throughput technique then?

PCR, western blots, ELISA, Bradford assay etc are all low throughput techniques.

You should edit the answer to remove Shotgun sequencing as an example of low throughput technique because even Illumina uses the "shotgun" approach. Low throughput sequencing would include cloning a gene into plasmids followed by sequencing.

High-throughput, as indicated by canadianer in their comments refers to amount of data that is processed by the system. Though the answer by CactusWoman would be correct for the case of DNA sequencing, high-throughput is not really confined to that domain.
Any high-throughput technique tries to measure several variables simultaneously. The examples include, other than the Next Gen DNA sequencing, RNA sequencing, protein identification and quantification by mass spectrometry (LC-MS), lipid profiling by GC-MS etc.
There are also medium-throughput techniques that can measure several variables but much less than high-throughput techniques. Many low-throughput techniques can be converted to medium-throughput by some level of automation and experimental planning. Example would include real-time PCR.

There is nothing particular about the bioinformatic use of this term; it is normal English not specialised jargon. 'Throughput' simply means the rate at which something can be processed. A high throughput system is one which handles things at a high rate, and it could be equally applied to genome sequencing, a city transit network, the ticketing gates at a football match, a factory processing potatoes into chips (fries), or the processor in your computer.
In biology, though, throughput usually refers to the rate at which samples can be processed. A 'low' throughput method is therefore one that can takes a longer time to carry out, can only be applied to a few samples, or needs to be repeated in order to obtain a full set of measurements of different factors. A 'high' throughput method is simply a faster method, which allows a greater number of samples to be processed in the same, or less, time. This can be achieved by working faster, processing multiple samples at once, or simultaneously handling multiple aspects of the same sample.
Note that there is no definition of when something becomes 'high throughput'; it is simply 'high' relative to earlier methods, although you would usually expect it only to be applied when the new method is many times faster than the existing method, not a small incremental improvement.

High-throughput sequencing specifically refers to sequencing techniques like Illumina that allow you to sequence massive amounts of DNA at once means hundreds of thousands of strands.
Producing multitude of data sequence simultaneously.

can you add a reference?


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Nucleosome wrapping direction
Does anyone know which direction the nucleosomes are wrapped? I wonder:

Relative to the B-DNA double helix twist direction (right-hand)
Relative to the neighbor nucleosomes. Do they alternate to prevent supercoiling?

B-form DNA is wrapped around histones in a left-handed manner resulting in a left-handed solenoidal superhelix (see that, that and this). The reason for this wrapping is that it reduces the helical tension. This post has more information about DNA helical tension. Also note that exceptions exist (i.e. right-ended direction) especially for histone at the centromere as described in this paper.
For your second question, the exact way nucleosomes are then arranged to produce the chromatin fiber is, as far as I know, still not fully understood but the most accepted model is a zigzag arrangement (Woodcock CL & Ghosh RP, 2010 and Grigoryev SA & Woodcock CL).


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Importance of fate maps
I did some normal google.book search and found the two importance of fate maps-
1. They helped establish the idea that communication between different parts of an embryo leads to the formation of new cell types and have thus helped discover different signalling pathways.

2. They enable us to interpret experiments in which cells of the embryo are exposed to conditions that may alter their developmental fate.

I really don't know where to look for the experiments that support these merits of fate maps. So is my question,what are some experiments that support these merits?

A good place to begin is with the experiments of Hans Speymann and Hilde Mangold, done in the 1920s. They transplanted a piece of the dorsal lip in a newt gastrual to the ventral side of another newt gastrula with different pigmentation. Because of this transplant, a "secondary" embryo formed, on what would have been the belly, in addition to the standard embryo expected. (Some picture show this to be rather like a second head.) Use of differently pigmented embryos allowed the researchers to note that the transplanted dorsal lip material developed into a second notochord. But the interesting facet is the newly developing notochord induced the development of a new neural tube in the adjacent cells which were otherwise destined to become "belly stuff".
My appologies for not finding a great reference with diagrams, my source is the 7th edition of Biology, Campbell and Reece. Here's a very thorough reference, with diagrams, if you're up for it.
https://app.shoreline.edu/kwennstrom/spemannmangold.pdf
This work contributed to a Noble Prize for Speymann. The bottom line here is that tissues receive information from adjacent tissues that influence their developmental fate.
Later experiments showed that the inducing agent was chemical in nature


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How does UV light damage the DNA when the chromosomes are deep inside the cell?
When UV light falls on the skin it has to go through the cell membrane and the nuclear membrane to reach the chromosomes. So it looks like that the DNA is protected but it probably isn't. Won't membranes be damaged first and the so that the cell dies before the DNA is affected and is replicating wrongly (if it is damaged too)? Or is DNA just really much more vulnerable than cell membrane?

UV Rays kill the cells by damaging the DNA. UV lights do not disrupt the cell membrane. If a cell is exposed to UV light, it creates THYMINE dimers (bond). Thymine dimers are the actual disruption in the kinks of DNA. UV exposure to skin is proportional to the cell damage.
P53 is a gene product which takes care of fixing cell damage. However it has a tolerance. If the damage is less, P53 sends damage repair machinery. If it's non-fixable, then P53 directs the cell to programmed death.
More UV exposure, more thymine dimers causing more cells to die (cell death). If the damage is not extensive, then that may cause cancerous cells (Result of cell damage).

It sounds like it is better to get a lot of uv rays than a bit to much....

Please cite your sources

When UV light is on your skin it has to go through the cell membrane
  and to the membrane of the core. So it looks like that the DNA is
  protected.

I don't understand what you mean by membrane of the core (perhaps nuclear membrane) but yes there is cell membrane and other cytosolic components. You should, however note that not all cells are spherical; some cells like skin cells are flat and along the thickness axis the DNA is much "less buried".
However, UV light does get attenuated by different cellular components. Melanin (which gives the skin a tan), for instance, absorbs UV and protects the DNA.
In spite of all this UV can reach the DNA. Furthermore, DNA (basically the bases) can absorb UV because of the nature of their chemical structure. After absorbing UV they reach an excited state and can become reactive. Reactions such as pyrimidine dimerization happens because of UV absorption. Note that this kind of an effect is elicited only by high energy UV (200–300 nm) (Durbeej and Eriksson, 2002; Svobodová et al., 2012).
Low energy UV (UVA) does not damage the DNA directly but can do that indirectly by generating free radicals. These free radicals are generated when other cellular components absorb UV and become reactive. Lipids are also affected by UVA and UVB; lipid peroxidation happens in the presence of UV and these peroxides are a source of free radicals (Morliere et al., 1995). So, the membrane is indeed "damaged".
It is also interesting to note that UVA is the most available to the skin cells because UVC and UVB are filtered to a great extent by the ozone layer and also scattered/absorbed by skin components (What is the relationship between UV wavelength and penetration depth into human skin?).
To summarize, DNA is more vulnerable to certain UV ranges but the damage frequently happens indirectly by other free radicals generated in the cytosol.


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How fast can our skin recuperate from sunlight?
Imagine that you get burned in the sun after half an hour. But a quarter and another quarter is also a half hour. So if you go into the sun 15 minutes and after one hour another 15 minutes do you get equally burned? Or what in case you pause half an hour etc. Is there a kind of schedule for recuperation times/pauses?

It depends a lot on skin type. Pale skin has higher sensitivity to sunlight and is burnt relatively more easily than dark skin.


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Does a queen wasp sting also have poison?
Last night I got sting by a wasp and because of the time of the year I suppose it is a queen. But usually it swells and hurts for a day after it, but this time nothing happened only that I woke up of the sting which hurt a little for a short time, but in the morning I couldn't find any signs of the sting.
Now is this because of the poison is worked out because it could be a pretty 'old'  new wasp queen and her enzymes like histamines and aptoxine are got too old? Or do queen wasps not use/have poison or less? Or is it my body that just reacted different?

A good read.

Ok interesting, so higher levels of spiroacetyls in the worker venom are more harmful than the acetamide in the queens.

I'm voting to close this question as off-topic because question is based on an anecdotal example.

@AliceD although I agree the bulk of the question is based around an anecdotal experience, the root of the question is both on-topic and interesting. I'm voting to keep open. Marijn, perhaps you could edit this a bit to reflect more on the biology and less on the personal experience.

Yes, all female wasps are expected to have venom. In the case of social wasps, which I am inferring is what stung you, all female wasps are equally potent as they're morphologically the same. [This opens the question of how could you say this was a queen wasp.] The only difference between a wasp worker and a queen is that a worker is forced to fly around and forage by the queen so it doesn't have the time and energy to invest into laying eggs.
The following paper discusses this: http://dx.doi.org/10.1590/S1519-566X2008000600011
However, not all individuals are the same, both wasps and people, so you may have been stung by a rather weakened wasp/species to which you're not particularly sensitive.
I'd like to recommend the following paper which isn't about wasps, but discusses fundamental venom composition differences between fire ant workers and queens.
Fire Ant Queen Venom is Fire Ants' Secret Weapon
This is the DOI reference: http://dx.doi.org/10.1016/j.toxicon.2018.11.428
(Free Version)
This is the DOI reference: https://doi.org/10.1101/454637
Contrary to wasps, most species of ants present a marked caste specialisation, meaning queens are quite different from workers. However, they still produce (and deliver) venom.
Thanks for your account!


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What's the difference between reaction norms and phenotypic plasticity?
I'm trying to understand better these two concepts, but I cannot see a clear difference yet.
Reaction norm: "set of phenotypes that can be produced by an individual genotype when exposed to different environmental conditions"
Phenotypic plasticity: "ability of individual genotypes to produce different phenotypes when exposed to different environmental conditions"
Are phenotypic plasticity changes temporary changes in genes; are they an extension of the reaction norm?

You should cite the sources from which you are quoting these definitions.

I think it's a little simpler than what you describe- phenotypic plasticity is the abstract property of phenotypes differing with respect to environment, whereas a reaction norm is a particular environmental response.
So you might make an argument like this:
"Daphnia show extensive phenotypic plasticity in their morphology. For example, see the attached figure showing head morphology norms of reaction (y axis) of two Daphnia strains with respect to food richness (x axis)."

This is figure 9 from Woltereck's original publication on reaction norms. It shows that as you grow Daphnia with denser cultures of algae (their food), more individuals in the population show a distinctive head morphology. It shows further that the shape of the curve is similar between two Daphnia strains (solid and dotted lines). Each curve is what Woltereck called a norm of reaction.
Hope that helps.

Phenotypic plasticity, as you define in your question, is an ability or a property of the organism (a given genotype) to manifest different phenotypes in different environments (Pigliucci et al., 2006).
Reaction norm is an analysis of the pattern of phenotypes exhibited in different environments. In other words it is an analysis of the phenotypic plasticity.

I'd pick on this a little. A norm of reaction (at least as originally defined by Woltereck 1909) is the pattern. It is the specific biological phenomenon expressed as differences in phenotype with respect to some environmental variable.

@MaximilianPress usually people represent these patterns as graphs/curves etc and that's what I meant by analysis. Some sources just defined it as a "curve". So I just used the term "analysis" because it appears like a post experiment analysis.

I agree that the representation is normally in the form of some quantitative visualization - but I think it's important to separate the phenomenon (a particular phenotypic response) from the analysis or visualization of the phenomenon (e.g. an ANOVA plot). See also my answer.