text:
Identification of a Lepidopteran
I’m afraid the quality of the television picture below isn’t very good, but can anyone identify this moth? It was one of those that invaded the pitch at the Euro Final in Paris on 10th July 2016.

Let me know if my edits translate accurately, to your intentioned meanings

@hello_there_andy — No. Your English was — and is — deficient (intentioned meaning, indeed) and the general edit was poor. If the chatty style offended you and you felt it needed formal time and place I have dealt with this. I commend the revised question to you as an example of succinctness. If you have any further criticism please raise it and I will deal with it or not, but please do not vandalize my English. I am an Oxford educated native speaker.

Noted. And apologies. I enjoy the fact you changed it since :) OP. I will also respect your request to not edit your future work. But believe me, there are certain controls in place to ensure it is not entirely your property. Try deleting some of your answers, to play an example.

@hello_there_andy — I appreciate that questions and answers can be edited by others and understand that they are for the community as a whole. However as I spend considerable time correcting and improving questions from non-native or naive posters, I found your treatment of my question extremely irksome and that of whoever approved the change quite reprehensible.

I really do apologise. I also realise my English might need better practice. You helped me take proactive action to improve it (no sarcasm), TQ.

I didn't watch the game, but from what I've seen on the internet it was the Silver Y (Autographa gamma), drawn there by the lights while migrating http://theconversation.com/moths-expert-match-report-on-ronaldo-insect-encounter-at-euro-2016-final-62314

I couldn't really be completely sure by this picture alone so I did some searching around and turns out it is a Autographa Gamma(Silver Y)

oh, you beat me to it by a second or something!

There is always place for more! Oh and by the way I didn't watch the game either. Was there some kind of "havoc" happening?

i really don't know, all i saw of it was the moth discussions trickling down into my usually sports-free circles.

@Ria — I wouldn't call it havok, but every time the play stopped and the camera zoomed in on a player there seemed to be at least one moth flying round him. And, of course, there was Ronaldo on the ground, in pain, in tears, waiting to be stretchered off, completely oblivious to the moth on his face — unlike the millions watching.

@picapica, actually Ria beat you to it by two mins :) - though, I'm not entirely sure why yours still "won"


text:
BLAST with minimum E-value cutoff
It's easy to set the maximum E-value threshold in a BLAST request. I need to set the minimum E-value. Does anybody have any suggestions?

the only manner (of my knowledge) is to use a script (R, python, java) to do this

There is no such option. You can perform the alignment and filter the hits later. However, I wonder why you really need that. Lower E-value indicates lower chance of an alignment randomly picked from a database, to have a given score.

I'm looking for records that are moderately similar, not highly similar, to my query.

@PhilipHeller As I said, there is no option for that. You have to filter the results. If you have to look for similarity then you should look at percentage similarity/score instead of e-value.

I second WYSIWYG comment, I think it would be the easiest way. Extracting the results and filtering them using scripts could help you out a lot but would need a bit of time if you don't know any scripting langage.

Setting a minimum E-value threshold will result in literally every single entry in the database with E-values above that value, as they will have very large E-values. You will expect a million hits with 1000000 E-value, and as a result you will not get any useful information from the search.
Can you explain why you want to set a minimum E-value?

I'm looking for records that are moderately similar to my query. Normally those records would be at the bottom of the hit list, but there are hundreds of thousands of records that are highly similar to my query and I'm not interested in them.

If you want moderately similar hits can you not just use discontiguous BLAST or blastn with a custom matrix?

A suggestion to get less hits is to take another database, for proteins you could use the PDB database and get orders of magnitude less hits.
Thinking a little bit more about your question: Blasting is probably not the right approach for whatever you want to do. Even if you manage to set a minimum e-value, you'll probably still get huge clusters of similar proteins around that value, and I guess that's what you're trying to avoid.
Blasting is really good to find similar proteins, if you want to get a cross-section of whatever-ases, you need to dig into bioinformatics a lot more.

source: Stack Exchange

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

sort: votes


text:
How Much DNA do Siblings whose Parents are First Cousins Share?
On average, two siblings generally share 50% of their genome. How much does this increase if the siblings' parents are first cousins?

I have edited the title of your question to clarify that you meant siblings who's parents are first cousins. Your original wording implied siblings of first cousins, who would probably be first cousins themselves.

This is going to be a sum on probability. Good one. I'll follow it.

Before I actually answer your question, let us clear up some problems in your assumptions. The fact that you expect 50% similarity in siblings is a full of several assumptions.
Imagine a case of a simple diploid organism with 2 traits. To restate your assumption, if both the parents are heterozygous in either of the two traits, and the alleles present in either parent for each trait are different (four different alleles possible for each trait), then the probability of getting two children who share 50% of the same alleles is more than any other percentage sharing.
Let us break this down. We'll gradually add complications.
For the 2-trait organisms, let us assume the genotype of the parents to be $\text{AB,EF}$ and $\text{CD, GH}$ where $\text{A,B,C,D}$ are the alleles controlling trait 1. Hence, for their first child, the possible genotypes are $\text{ACEG, BCEG, ADEG, BDEG, }$ and so on.... Since there was no allele match in the parents, each of these genotypes is equally likely.
For the second child, the same possibilities with equal probabilities exist. Now, I computed a matrix which has each possible genotype for child 1 as rows, that of child 2 as columns and the values are the proportion of alleles shared (i.e. common between the two). .
So, all proportions of the sharing is possible between the two kids. But, to find out the most probable configuration, we plot another kind of plot.
Technical note: Although the barplot has frequencies of appearing in the above similarity-matrix, it is equivalent to the probabilities since each genotype was equally likely.
Hence, the case with the two siblings sharing 50% of the genome is most likely for this case. Now, if we expand to 3 alleles, here's the corresponding plot.
It shows, that even if we increase the number of traits (as we gradually approach the human case), the maximum likelihood still includes the sibling-organisms sharing 50% of the genome.
Now, what if the parents already shared some genome? Let us say, the 2 trait organisms already shared 50% of the genome. It is equivalent to say that in the genotypes elucidated above, $\text{A=C, E=G}$. With this assumption, I ran the same kind of simulation to get the following graph.
Another technical note: Although the plot still shows frequencies of appearing in the matrix,the repeats of the same genotype along rows/columns in proportion to their probability of forming will make these frequencies equivalent to probabilities.
So now, the siblings with 75% similarities are the most likely outcome.
Let us now ask, for the 2 trait organisms we are working with, that if the grandparents had zero genomic similarities, and their two kids in-breed, what will their two kids share? For this, we take the probabilities of the first generation (children of the grandparents, sorry for the semantic mashup) for each %overlap, and multiply it with the probabilities of their kids having the various overlaps and plot a final graph.

This shows that they will most likely share 50% or 75% of their genome.
Limitations of this analysis:
 It does not account for linkage of genes. It assumes totally independent assortment of the alleles. It models all similarities to be in alleles of different traits initially and then allows for same diploid pairs, i.e. it does not allow for the observed probabilities of forming a same diploid pair, i.e. case where the similarity (genomic sharing) between two individuals is because of two same alleles for the same trait. It is also blind to any parental imprinting. Homozygosity is not yet incorporated in the simulation, will do in a while.
Below is the two-generation probability simulation for an organism with 4 and 5 traits.
The maximum likelihood of %similarities in genome, as you can appreciate, for a large number of traits would be somewhere around 63-64%.
I shall post the R code in a while, after I format it properly. For computations for greater than 5 traits, I shall write a better engine in a day. Sorry for the improper formatting of the question. Shall rectify in a while.

Note that this analysis is only looking at areas which differ between the two parents.  More than 99% of the genome is identical between all humans.

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


text:
How long can an infant human hold his/her breath as part of the "dive reflex"?
Various other questions on the site have talked about the Diving Reflex, which is also known as the Mammalian Diving Reflex. This reflex is observed in mammals of various species, but also in human adults and infants. A number of studies have been done examining the diving reflex (e.g. Advances in Physiologic Education).
If you've ever observed an infant submerged in water (e.g. at a swimming pool) who has this reflex it seems so amazing because the baby will spontaneously hold his/her breath while submerged.
Are there any estimates of long an infant will hold his/her breath as part of the dive reflex?
Obviously this is dangerous to try and test this in the real world, but I'm wondering if anyone has any idea. This reflex seems so remarkable to me because unlike the adult human who knows they shouldn't breath in water, I would think that the baby doesn't know that at such a young age.

It's life threatening because water enters the stomach of infant.

@JM97 what is life threatening about water entering in the stomach? I'm not following what you're saying.

The infant will drown , and it doesn't know how to swim.

when my 3 month old son was in swimming lessons he would spontaneously hold his breath and go underneath the water just fine... actually 10-15 times in a 30-45 min time frame...and he's doing just fine - do you have a particular source that you get your information on this?

The glottis is spontaneously sealed off and the water entering the upper respiratory tract is diverted down the esophagus into the stomach.   ( https://en.m.wikipedia.org/wiki/Infant_swimming#Infant_swimming_or_diving_reflex )

@JM97 correct, but that doesn't mean the infant will drown just because some water enters the upper GI tract


text:
Is this in vivo or ex vivo?
This question has probably been asked a few times but I get the concept I just dont know how to apply it for this paticular experiment
I aim to use cherry tomatoes and determine its glutamate content after drying for varying amounts of time.
This would involve putting the tomatoes into the centrifuge to extract its juice.
Due to this, I am 'preparing' the tomatoes in vivo (I think need clarification) but I am observing the Glutamate content outside of the organism (ex vivo)
I dont know how I should be classifying this experiment (between in vivo and ex vivo)
Help will be greatly appreciated !!!
Thank you!!

This would all be in vitro work. See my comment below the (incorrect) answer. This may also be helpful.

Personal opinion: nevermind. Provided it is clear from the your experimental description what you actually did, who cares what to call it in latin ... As the below answers and discussion shows, there is no real consensus on exactly what these old latin terms mean nowadays, and I really think most people just include them in journal articles to appear sophisticated ;-)  Just describe your experiments as clearly as possible when writing your paper, so the reader to can judge for him/herself how relevant the data is to the organism you study.

The classification usually applies to the experimental conditions. Are the experimental conditions applied to an organism, or to a less than whole organism (cells culture --> all the way to test tube chemistry reactions)?
This is somewhat subjective, but in your case, since the experimental conditions are drying time of the pretty much whole organism (the tomato), I would call it an in-vivo experiment.
Think of it this way, if you treat animals with X and examine Y, this is an in-vivo experiment regardless of whether you are isolating proteins, DNA, RNA etc... to examine afterward to characterize the change in Y.
Now if you isolated cells first from mice and plated them to grow in cell-culture, and then treated with X to examine the same endpoint, this has become more ex-vivo.
In-vitro would be to isolate a single enzyme from mouse cells, put into a test tube, and examine its ability to reduce some substrate after X treatment.
In your case, if you isolated enzymes from tomatoes and then used them in a test-tube to reduce some agent and measure activity before and after a given treatment, this would be more ex-vivo and have gone all the way to in-vitro.
EDITED: Matt pointed out I had confused in-vitro and ex-vivo on my continuum and he was correct.

This is completely incorrect. You're mistaking ex vivo ("out of life") with in vitro ("in glass", referring to old-fashioned Petri dishes). An in vivo experiment is performed in an experimental organism, such as giving a mouse cancer. Ex vivo refers to taking samples from that organism and processing them separately - surgical or post-mortem removal of the tumor for analysis of the cells and structure. Creating a cell line from the cells and culturing them would be in vitro.

@MattDMo In vitro studies are performed with microorganisms, cells or biological molecules outside their normal biological context.    In science, ex vivo refers to experimentation or measurements done in or on tissue from an organism in an external environment with minimal alteration of natural conditions. Ex vivo conditions allow experimentation on an organisms cells or tissue under more controlled conditions than is possible in in vivo experiments (in the intact organism), at the expense of altering the "natural" environment.  I'll change my test tube example but rest is correct.

@MattDMo In response to : Ex vivo refers to taking samples from that organism and processing them separately.  This is not correct. Ex vivo also means that experimental conditions are applied after taking samples from the animals. No room above, but links to ex vivo and in vivo definitions here: https://en.wikipedia.org/wiki/Ex_vivo and https://en.wikipedia.org/wiki/In_vivo  The distinction is where the experimental conditions are applied, to the whole organism or to parts isolated from it, not the processing as you stated.

@MattDMo To add, I routinely process mouse tissue taken from experimental mice in order to determine their protein/RNA expression levels. I would definitely consider these in vivo experiments.

It depends upon your field, and its proximity to native specimen. In practice, in-vivo and ex-vivo are used to stress a relative difference.

If you are biochemist in a field / research area that usually uses purified components and reconstitution: in-vivo
If you are biochemist in a field / research area that usually measures glutamate within undried tomatoes: ex-vivo
If you are a cell biologist: ex-vivo
If you are a developmental biologist: ex-vivo

(Similarly cell culture is usually considered in-vivo by a cell biologist, but ex-vivo by a developmental biologist).


text:
Why cancer disease is named after sun signs ?
I googled it, It didn't helped me a lot.
So Why cancer disease is named after sun signs ?

duplicate of http://biology.stackexchange.com/q/26086/3340

It isn't. The name of the constellation/zodiac sign and of the malignant cell diseases comes from the Latin word "cancer", which means "crab".
This name for the disease dates back to the Greeks and Hippocrates, who used the word "karkinos" (the Greek equivalent) because the veins around the tumors they observed made the disease look like a crab 3.

The word "cancer" comes from the Latin cancer, meaning "crab". Both the Latin cancer and the Greek karkinos (hence "carcinoma"), that also means crab, come from the proto-Indo-European "qark", meaning "to be hard (like a crab)".
Historically, tumours have been called this way because the similarity of some tumours with a crab. According to "Etymology Online":

Greek physicians Hippocrates and Galen, among others, noted similarity of crabs to some tumors with swollen veins.

Out of curiosity, can you post any photos of tumors that look like crabs?

Personally, despite having seen countless carcinomas (I'm not a physician, but a biology teacher), I've never seen one that, for me, looks like a crab.

The ancients just had such a vivid imagination! Or maybe crabs looked different back then. :)

From personal experience... I had two poor bunnies with mammal tumours. They grow in a roughly crab-shaped way, you can feel them being encapsulated in this shape under their skin. You can even move them back and forth a little. If the old greeks got their first idea of tumours from those being palpable and close to skin, this might be a reason to compare it to "a crab under the skin".


text:
Does an increased reproduction/mortality rate provide an evolutionary advantage?
If a species has a high mortality/birth rate, then it is able to adapt to changing environments more quickly than species that live for a long time.
Without a high mortality rate, food and other natural resources are hogged by previous generations and the gene pool is polluted when less evolved, older animals reproduce.
Because of this, wouldn't it make sense to conclude that a high mortality/birth rate is better for a species as a whole?
This advantage could snowball out of control, because faster evolution would lead to superior reproduction methods which would lead to faster evolution etc...
If this is true, then why are mice not more successful and adapted to their environment?

House mice were chosen because of their high birth and mortality rates.
Birth rate:
"Approximately 6 mice can multiply into more than 60 mice in 3 months."
http://www.crittercatchersinc.com/critters/Mice/Mousereproduction.html
Lifespan: 1 year
http://themysteriousworld.com/top-10-shortest-living-animals-in-the-world/
One of the reasons these traits may be more harmful than helpful is that predators benefit from a population increase. I managed to find this article in my research:
http://www.ncbi.nlm.nih.gov/pubmed/12675374
Feel free to include this source in your answer if I have interpreted it correctly. The reason I am posting this question answerless is because I am not sure enough about the conclusions I have drawn to answer it on my own and (mostly this) because I am very interested to see what other disadvantages this evolutionary strategy would have.

The first part of the question is interesting.

Does an increased reproduction/mortality rate provide an evolutionary advantage?

The concept of evolutionary advantage for a species needs to be used with much cautious as different definition of evolutionary advantage may exist. You should typically have a look at game theory beforehand to understand the issue of definition.
A species that have shorter generation time tend to respond faster to new selection pressure (even more so in species that have short generation time and also have high population size).

why has humanity not been enslaved by mouse¹ overlords with superior intelligence and adaptations to suit the environment perfectly?

You seem to be viewing intelligence and/or species competitive ability as end goal of natural selection which suggests important misunderstanding of how evolution works.

One of the reasons these traits may be more harmful than helpful is that predators benefit from a population increase

You might want to have a look at the post What prevents predator overpopulation?

"You seem to be viewing intelligence and/or species competitive ability as end goal of natural selection which suggests important misunderstanding of how evolution works."                                                                                It was a joke, but since it is detracting from the quality of the question I will remove it. Sorry about that.

1) Reproduction is metabolically costly, so a high reproduction rate, such as that seen in fishes that lay thousands of eggs at a pop, is generally a strategy to compensate for a high mortality rate. On the other hand, bacteria, that can in some cases double every 20 minutes, have the advantage of rapidly evolving resistance to antimicrobial agents.
2) Primates and elephants are examples of successful species that have a very low birth rate. The biological investment here is in nurturing and protecting offspring for many years to reduce mortality and to transfer cultural knowledge to the next generation to improve reproductive success and community success. In the case of humans, long lifespan, even beyond reproductive age, is an advantage because the older generations can help care for children while the parents work, and they support the community through leadership and by imparting to younger generations a lifetime of cultural knowledge. Unfortunately, the very success of humans may lead to its ultimate downfall, due to overpopulation and environmental degradation.
3) Mice are successful because they eat our crumbs and our crops, and take refuge in our shelters. So, in a sense they have enslaved us: we work for them without pay or benefits.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3353347/
https://frontiersinzoology.biomedcentral.com/articles/10.1186/s12983-014-0054-0
http://www.cell.com/trends/ecology-evolution/fulltext/S0169-5347(15)00104-4
https://en.wikipedia.org/wiki/Grandmother_hypothesis
https://en.wikipedia.org/wiki/House_mouse

Please add some citations in your answer, lest it is likely to be downvoted and removed.


text:
Is it safe to feed an adult fire salamander with slime maggots?
As a reminder, maggots feed of a flesh, while fire salamander consumes his prey alive, without killing it.
Can it happen that the maggot will start eating the salamander from the inside?

I'm voting to close this question because it is off-topic for Biology, and instead should be posted at [pets.se].

Maggots typically eat dead/rotting flesh, not live. Maggot therapy is used in clinical settings in the US and around the world for debridement of necrotic wounds.

@MATTDMo reluctantly I can see your point. I feel it could be edited into a more general question about ingesting live larvae that would be on-topic for Biology though - OP, would you have any objection to that?

@arboviral no objections, since i've got my answer.

Although I am afraid I don't know much about fire salamanders specifically, it is certainly possible for ingested fly larvae (or larvae hatching from ingested eggs) to survive ingestion and subsequently cause intestinal damage. Parasitic infestation by fly larvae that grow inside the host while feeding on its tissue is called myiasis. Enteric myiasis (also called gastric, rectal, or intestinal myiasis to indicate the affected part of the digestive system) occurs occasionally in humans following the ingestion of cheese infested with cheese fly maggots. Casu marzu, a traditionally produced Sardinian cheese, is supposed to have live cheese fly maggots in it, and cases of bloody diarrhoea following its consumption are known. If they're dead the cheese is considered unsafe to eat (although personally I'd correct that to 'more unsafe').


text:
Why is the protein ubiquitin so ubiquitous?
Ubiquitin is a protein tag that is attached to proteins in order to mark them for destruction/proteolysis by the cell. This system is sometimes used for clearing out harmful viral proteins that infect the cell, but is used in concert with the 26S proteasome to degrade proteins in many cells throughout the body. I just want to know why is ubiquitin so ubiquitous?

First, plus points for the pun.
Second, I suppose natural selection is at play. Those cells which don't have proteases like ubiquitin would die, and the ones with the enzyme would survive.
(Just my opinion. I don't have any source, I'm sorry)

when I was in graduate school I worked with a faculty member - https://profiles.psu.edu/profiles/display/112215 - who had done a lot of work in the basic biochemistry of the ubiquitin-proteasome pathway. He had been in the field when it was still very young/early and knew many of the early players in that field of research. He always said that the protein was named "ubiquitin" because in nearly every tissue or cell they looked they found it being expressed - they figured it must be important if it was expressed in nearly every tissue they looked in... turns out they were correct

What do you mean by "why"? It is used by all cells and that's why it is ubiquitous. Just like why actin is ubiquitous.

@MalharKhushu ubiquitin is not a protease, or any other kind of enzyme. It is a small marker protein that is covalently attached to other proteins (and itself) by ubiquitin ligases to perform a number of signaling functions, including targeting their substrates to the proteasome for degradation.

@MattDMo thanks for the heads up, I'll edit my comment

@MalharKhushu Of course natural selection is at play. Isn't it everywhere? ;-)


text:
What legal possibilities exist to get access to articles behind paywalls?
Many publications, be it in high-profile journals, proceedings, book chapters or any other medium, cannot be accessed without subscription alongside substantial costs, even though most of the published work has been financed publicly. I was asking myself if there are options to get legal access to these publications and if so, what these options are.
As a concrete example I would like to give the following. I am
searching for the following article that has been published as a book chapter in Molecular Biology that is behind a paywall:
Protocol
DNA Repair Protocols
Volume 314 of the series Methods in Molecular Biology™ pp 183-199
Quantitative PCR-Based Measurement of Nuclear and Mitochondrial DNA Damage and Repair in Mammalian Cells
Janine H. Santos, Joel N. Meyer, Bhaskar S. Mandavilli, Bennett Van Houten

What possibilities are there to get access to this?

You have all the information ready to easily find it. Is a paywall the problem? If so, probably nobody will infringe copyright (be it ethically valid or not) here and you should try to get access by your/an institution/library or contact one of the authors to see if they are willing to share their work.

This is not really a question.

I edited the question for making it interesting for many biologists. It, of course, is not a question about biology per se but is still relevant to many, if not all, biology researchers. In a way it is about techniques that biologists have to deal with in their research life.

There are several ways you can try to get legal access to publications that are not open access.
First, and most simple, subscribe to the medium or pay for the single publication. This is usually very expensive, so you might want to look for other ways.
Second, you can try to get access by your/an institution by logging in over your institutes network. They might have access to publications from that medium. If not, ask your institution if they can get that access (some libraries offer this based on requests).
Third, go to a public library or a university library and see if they have access to the medium. If so, you can register to the library and then have access as a library member. There might be fees involved but these should be substantially lower than paying for the article directly.
Fourth, you contact one of the authors to see if they are willing to share their work, either as copyright holders or in form of drafts/pre-prints (in that case you should write to the corresponding author, the last author or the first author, maybe include all these three to your email as cc).
This leads to fifth, look at pre-rint servers like the bioRxiv, maybe you are lucky and the publication has been put there by the authors.
Sixth, closely related to four and five, look for the authors on scientific networks like Research Gate. Many scientists share their public articles there or allow requests for sharing their work.
In your special case example you are lucky ... You can find the first author (Janine H. Santos) on Research Gate and she has the article downloadable. If your are not a member you can register without fee and just download the article.


text:
Does class switching occur both in B cells and Plasma cells?
I understand that the cell class switches to change the type of immunoglobulin it is producing. The B-cell produces the membrane bound B-cell receptor (BCR) while the plasma cell produces the the secreted form of Ig, the antibody. Now, the isotypes are different in their constant regions and I'm assuming switching only matters if it is an antibody. (differences in avidity, permeability, antibody receptors, etc.)
How would a B-cell receptor (membrane bound Ig) even benefit from class switching? Does class switching even happen in activated B-cells? Or is it a process limited to plasma cells? I read up that BCR also has the 5 isotypes.
What are the specific chronological milestones at which class switching happens in plasma cells and B-cells (if it does)?

This question is pretty broad. What kind of research have you done on your own to try and answer it? Any decent immunology textbook should have a fairly detailed section on class switching. Since plasma cells are B cells, your question title is rather silly. Some cells only have the membrane-bound BCR, regardless of isotype, while others secrete soluble Ig. While they do, through, they still express a membrane-bound BCR.

@MattDMo I've found the answer to the question and it happens pretty significant. I'll frame it up and post it in a while.

@MattDMo Here is the answer. B-cells and Plasma cells aren't one and the same. I agree the question is broad, but your rant is silly and nowhere close to constructive criticism.

Short Answer : B-cells class switch to become Plasma cells in the germinal centre of the lymph node.
Long Answer :
There are two important concepts addressed in the question. One is the Immunoglobulin structure - isotype and membrane/soluble type. And the other is the germinal centre B-cell paradigm. Understanding both the concepts are a prerequisite to understand the answer to the issue.
First of all, immunoglobulin synthesized by the lymphocyte can either be membrane bound (known as the B-cell receptor (BCR)) or soluble antibody. After gene rearrangements, the B-cell (still immature) begins to produce membrane bound IgM/IgD. This continues even in the mature B-cell. The membrane bound Ig or mIg has an extra sequence (refer image) on the carboxyl end adding a few hydrophobic amino acid sequences so that it gets anchored well in the hydrophobic part of the membrane. Also at the end is a series of hydrophilic residues involved in downstream cell signalling.

Class switching is process that leads to a change in the isotype of Ig that the cell is producing. Class switching involves excision of DNA which implies that the cell can not revert back to producing the Ig once it used to. The sequence of the gene segments on the heavy chain gene hence becomes important.
When there is a first time exposure to an antigen, the mature B-cells follow a classical paradigm to T-cell dependant antigens, which is shown in this picture below.
Class switching occurs in B cells that are participating in a germinal center reaction, after the naive B-cell has been activated by antigen and a cognate T cell. There also is germinal centre independant class switching that we ignore here.
After a B cell has undergone somatic hypermutation and class switching of its immunoglobulin gene, it may or may not be positively selected to differentiate into a plasmablast. Plasmablasts proliferate rapidly before terminal differentiation to plasma cells, which secrete affinity matured, class-switched antibody. So in other words, class switch recombination is largely restricted to activated, germinal center B cells. These B-cells class switch, as one of many processes to produce soluble antibody producing plasma cells.
Plasma cells and B-cells aren't just one and the same. B-cells undergo a series of processes to form the plasma cells which are also different in morphology.

As already has been mentioned, it should be remembered that class switching involves excision of the intervening DNA between the rearranged VDJ exon and the constant exons being switched to, meaning that they are deleted from the allele. Thus, a B cell that has class switched from IgM to, say, IgG would delete the IgM and IgD heavy chain exons on that allele, and would be restricted to IgG (or IgE and IgA, which lie downstream).
But then, if the B cells bearing IgM had already class switched (to their possible downstream counterparts), how can the primary immune response be IgM dominant? How could IgM antibodies come from class switched plasma cells?
This is because, this whole germinal centre spectacle takes time to happen and in the meanwhile, there are extrafollicular mechanisms of antibody production in place in extrafollicular foci in the spleen or in the medullary cords of lymph nodes. Since antibodies that are develpoed in a germinal centre dependant manner (IgG) are from somatically hypermutated cells, they have more affinity to the antigen than IgM produced by germinal centre independant plasmablasts.

BCR generally has only two types, mIgM and mIgD. If there is a class switch, they turn to soluble antibodies (IgG/IgA/IgD).
Secretory antibody here refers to soluble antibody that is exocytosed from the WBCs, not the IgA that is found in bodily secretions.
Reference, Picture credits :

Nature reviews immunology, Germinal centres: role in B-cell
  physiology and malignancy
Kuby Immunology. 6th Edition
Immonological reviews, Extrafollicular antibody responses

There was a factual error that, plasmablasts from the figure above secreted IgM antibodies. Actually, these IgM are produced by plasmablasts only but not in a GC dependant fashion. This happens as an extrafollicular response in extrafollicular foci in the spleen or in the medullary cords of lymph nodes.


text:
Is it possible to have a random un-mutation of genes?
According to this article:

Gene mutations can be classified in two major ways:

Hereditary mutations are inherited from a parent and are present throughout a person’s life in virtually every cell in the body. ...

Acquired (or somatic) mutations occur at some time during a person’s life and are present only in certain cells, not in every cell in the body. These changes can be caused by environmental factors such as ultraviolet radiation from the sun, or can occur if a mistake is made as DNA copies itself during cell division. Acquired mutations in somatic cells (cells other than sperm and egg cells) cannot be passed on to the next generation.

The "random mutations in genes" appear to be called Somatic mutations. For the context of this question, these are the mutations I am asking about (not the hereditary mutations).
My question: Is it possible for there to be a random un-mutation of genes? Some sort of reverse-somatic mutation. If so, have there been any clinically proven instances of it?
After-thought: Or is it all a Somatic mutation, aka you can experience a mutation that makes you more susceptible to a particular disease, then another mutation that makes you less susceptible to the same disease... so not necessarily a reverse mutation, but a 'forward' mutation that negates the original ill effect of the first mutation.

Of course a mutation can revert back to its old state via random mutagenesis (un-mutation as you call it). Nobody has kept a track of it I guess but it is not such an uncommon thing. But think of its probability; it would be low (just a simple calculation). You may also want to look at PAM matrices.

A large part of the body of your question seems relatively unrelated to the main question which is a little confusing. I will focus on the question

Is it possible for there to be a random un-mutation of genes?

Yes, these are usually called reversed mutation. It is quite common though that a second mutation at a distinct locus may reverse the phenotypic effect of a first mutation. This is called a compensatory mutation.


text:
Is every evolutionary change an improvement?
In evolution, an species mutates and evolves over large genetic time spans. But every big change (say, swimming to walking, or walking to flying) is made up of countless micro-changes over the course of many many years and many many generations.
My question, does each "micro-change" have to be an improvement over the prior iteration? Or can evolution initiate micro-changes, knowing the current generation won't see the final result for an arbitrary number of years?

Related: http://biology.stackexchange.com/questions/13680/why-specifically-does-each-generation-on-average-improve-upon-the-design-of?rq=1

@arboviral Actually, that answer is enough to answer my question. I'm content calling this a duplicate question and closing it. Thanks for the link!

Delighted to help! I'd also suggest taking a look through https://en.wikipedia.org/wiki/Genetic_drift, and bearing in mind that 'improvement' depends on the environmental context, which changes constantly.


text:
What is heteroduplex?
I fail to understand the what exactly is heteroduplex due to unavailability of a suitable diagram. According to wikipidea:

A heteroduplex is a double-stranded (duplex) molecule of nucleic acid originated through the genetic recombination of single complementary strands derived from different sources, such as from different homologous chromosomes or even from different organisms.

Should the following highlighted structure be called heteroduplex?

Heteroduplex is also frequently used for duplex formed of strands of different kinds of nucleic acid. For example RNA-DNA heteroduplex. As a matter of fact, that's the only reference of heteroduplex that I am aware of.

In 'An Introduction to Genetic Analysis. 7th edition' the DNA structures formed from crossing over between homologous chromosomes have been called heteroduplex through out the text.

Perhaps, but as I said, I was not aware of this usage.

What you've circled is not a heteroduplex. A better name for it would be "crossover" or "junction". Instead, the two duplexes at the bottom of your diagram are what should be labeled heteroduplexes. Your diagram shows one process by which you could generate heteroduplexes starting from homoduplexes.
Here's a better picture from the NCI Dictionary of Genetics Terms that more clearly shows the difference between homo- and heteroduplexes:

The two strands in a heteroduplex still have to have a high degree of sequence identity or they won't be able to form into a duplex in the first place. However, because they come from different sources there's likely to be many short subsequences in which one or more base pair is mismatched, causing a deformation as shown.

So it is a ds DNA molecule in which the two strands are not fully complementary and derived from two different sources?

Yes, with one edit: it is possible for two strands from different sources to be fully complementary. In general it's just extremely unlikely, although exactly how unlikely depends on your sources and your strand length.

What you have shown above should be (and often) called a mismatch instead of a heteroduplex. I have never come across any recent literature that refers to the above kind of arrangement as a heteroduplex. Most modern studies use heteroduplex to mean a duplex formed of different kind of nucleic acids (RNA-DNA, DNA-PNA etc)

@WYSIWYG It's both! (a mismatch and a heteroduplex, I mean) The fact that there's a mismatch is less important than the fact that the two strands come from different sources (which is something we're assuming for the sake of the diagram). Though I too was unaware of the more expansive definition before I started writing this answer, NCI seems to back Wikipedia up on this.

I also was not aware of the definition given in this answer but for the sake of congruence it absolutely makes sense or even has to be that way as two strands of different origin are pairing.

Okay. However, heteroduplex is a term that is technically applicable to a molecule (as it is a molecular property) and not really the genetics behind it. How would the DNA, "know" what is its source? For example, a newly replicated DNA has one of the strands that is brand new while the other is old. Would you call that a heteroduplex too? There is a flaw in this definition.

The Wikipedia entry is (as often) clearly nonsense. Howevear there is no reason why the two strands of a hetero-duplex should not be identical. It may occur in practice, it may be useful for drawing a diagram, but I maintain it is definitely not part of the definition of the word. As it stands, therefore, I suggest your accepted answer is incorrect. You might consider whether you should modify it to make it clear that it is the origin of the strands that makes them hetero, not a lack of perfect complementarity.


text:
How do drugs enter synapses?
Many psychopharmaceutical drugs change synapse chemistry or directly agonize neuroreceptors in the brain. For example, cabergoline is a D2 agonist.
How do these compounds enter the physical synapses? Are they simply lipid soluble and diffuse throughout all cells?

The answer is that cabergoline does not need to enter a cell in order to function.
Cabergoline (as well as most (possibly all?) other drugs that target synapses) interact with proteins on the surfaces of the synapses. For example, the D2 receptor that you mention is a dopamine receptor which in its active form is expressed on the surface of neurons near the synaptic cleft.


text:
Can you knockout a gene specifically in the dorsal root ganglion in adult mammals?
Since the dorsal root ganglion is so small, would that be easier than the entire body?

Welcome to BiologySE - do you know how to make a whole body gene knockout? Or perhaps a tissue specific knockout? Those might be better questions to ask because then you'll understand why the size of a particular tissue or organ that matters, but rather the gene expression of a particular organ. There are a number of review articles on gene knockout techniques, I would recommend you read one of those and then post a more specific question that would be more helpful.

what is the exact problem you want to solve?

It requires two genetic constructs to create a conditional KO organism. One parent with a transgene that expresses a DNA recombinase (such as Cre) after the promoter of a gene that is ONLY expressed in your tissue of interest. The other parent contains a modified gene of interest to be removed in the presence of said DNA recombinase but is fully functional otherwise.
Therefore, the ability to target a Knockout to a specific tissue is dependent on identifying a gene that is only expressed in the tissue of interest.
It is actually easier to create a whole animal KO, but because gene products can have different functions temporally in development and in different tissues, a whole animal KO may be lethal, whereas removing it in a specific tissue may not be and allows study of the effects of said removal.
Thus, if your gene of interest were lethal when removed from whole organism, AND you know of a gene that is only expressed in the DRG, you would have incentive to see if a CKO animal could be made.
A brief search on Cre Lox technology will bring up 1000's of images and articles.
Here is one and a nice illustration:

@Hamham just a note on this technique... this technique works well but you can control the timing of the knockout... that is, if you want to make some mice and then induce the expression of the Cre enzyme in the adult animal (if you have an inducible-Cre system) you can do that; however, if the Cre is expressed in embryos during development then the gene will be missing from birth and may have a different phenotype compared to if the gene knockout is induced in an adult animal.

@VanceLAlbaugh Can the "if you want to make some mice" part be switched to "if you catch some wild mice"? Aka, Unlike the picture above, I can just use any mouse without transgenic parents and induce the gene knockout in it...? Thanks!

@Hamham No, this wouldn't be successful with wild mice - you have to use laboratory mouse strains for which DNA sequence information is known. As indicated above, the idea is to breed one strain of mouse that has loxP sites flanking the gene of interest to another strain that expresses a tissue/cell-specific Cre recombinase enzyme. There are other technologies to do knockout (like CRISPR https://en.wikipedia.org/wiki/CRISPR ); but again, this is to begin breeding mice, not to knockout a gene in an adult mouse


text:
Tree ID request
We have a small tree (more like a shrub) in our village in North Eastern Anatolia, and it is known for its local name which is not Turkish. Even worse, I don't know which language it is, but most likely there are Armenian, Georgian, maybe Russian influences in the regions' language. So I cannot find it in literature.
It is spelled as "syr-sun-syllic". Its fruit has a name too, that is pronounced like "lyllic". It gives red and round fruits in autumn, which are edible.
Here are some photos.

It is said to be "lonicera iberica" by http://nhm.co.uk, which has edible fruits.

In addition, it gives fruits in autumn.

could you describe the flowers and the fruit? the way the leaves grow reminds me of honeysuckle (Lonicera).

What's the local name?

It is spelled as "syr-sun-syllic". Its fruit has a name too, that is pronounced like "lyllic". Our villages have more words that are not Turkish. Even the villages called with their non turkish old names by the peasents. I think probable languages affected us are armenian, georgian, maybe russian etc.

Nope it is probably not a honeysuckle.

It has a layered trunk and one can easily tear them off by hand.

The leaves are indeed similar to lonicera (honeysuckle). How do the flowers and fruit look? What color, size and shape do they have? Do they grow solitary or in groups? Any info might help (and a picture would be fantastic).

Its fruits are small red rounds and are eatable.

Interesting. Red and round rules out Eucalyptus, that does have opposite-leaves and a peeling bark. Honeysuckle has red and round fruits but afaik they are not edible.

It is said to be lonicera iberica by nhm.co.uk, which has edible fruits.

@AhmedBilâl You should post this as an answer. Posting answers to your own questions (if you find them) is encouraged in the StackExchange network. Then your questions is also removed from the unanswered queue.

It is said to be lonicera iberica by nhm.co.uk, which has edible fruits.

It would be nice if you could expand this answer and add a picture of the plant. Additionally it is always good to not give just a one-line answer but one, that stands on its own and explains stuff.


text:
Link between hypoglycemic events in Type 1 diabetics and clinical anxiety?
I recognize that the scientific community is aware that the chemical stress pathway is mediated by glucocorticoids. The pathway response initializes as a result of some sort of stress (potentially chemical, such as low glucose) and the hypothalamus secretes corticotropin-releasing hormone which binds to targets on the pituitary gland. This causes the release of adrenocorticotropin-releasing hormone, which binds to targets on the adrenal cortex and promotes the production of cortisol.
In the event of hypoglycemic stress, cortisol concentrations rise everywhere in the body as a result of this stress signaling. For Type 1 diabetics specifically, hypoglycemia is a common side-effect of treatment.
I also recognize that the anxiety response is largely mediated by amygdalae activity, and the amygdalae are known to have receptors for cortisol (they are the ‘fear’ center, after all). From my research, the morphology of dendrites in this brain structure as well as other centers for mood/emotion are shifted into less functional patterns as a consequence of chronic exposure to glucocorticoids such as cortisol (Krugers 2010). Additionally, glucocorticoids cause serotoninergic receptors to become less sensitive to activation (van Riel 2003).
So my questions are:
if hypofunctioning of serotonergic receptors in the Raphe Nucleus leads to excess firing of hippocampal and amygdalae neurons, which is believed to be one of the primary mechanism through which anxiety manifests itself, why hasn't chronically high levels of cortisol, as a result of hypoglycemia, been implicated more in anxiety disorders in Type 1 diabetics? Is there a link to clinical depression from here?
SSRIs are consistently used to treat anxiety in the short term, but for diabetics, the crux of the issue seems to be the chronic exposure to high levels of cortisol. Has anyone studied or seen this in their practices/research?
Sources:
Krugers 2010
http://www.ncbi.nlm.nih.gov/pubmed/20820185
van Riel 2003
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059694/


text:
Can pathogens enter the bloodstream if the epidermis has been scraped off?
Assume that the epidermis has been scraped off by a fall (not just scratched). Also assume that the dermis is completely untouched. Does this allow pathogens to enter the body more easily, or does the dermis still provide adequate protection?

Our epidermis is the first line defence against natural infections; it is also a part of the innate immune system. This is due to

it contains a layer of dead cells that separates the living cells of the deeper layers of epidermis and dermis from the environment.
This part of the epidermis is avascular and so pathogens can not easily enter into the bloodstream through it.
It contains natural bacterial flora (like in our gut) that kills a large number of pathogenic microorganisms with their toxins.
secretion of sebaceous gland contains some antimicrobial substances.

There are lots of other protective features of epidermis.
Dermis is richly supplied by blood vessels. So even if all the layers of dermis remain intact its high vascular nature will act as an open entrance of microorganisms. By definition abrasion involves only the epidermis or some parts of the dermis but still we need to take tetanus vaccine after getting an injury contaminated with soil. In diseases like Stevens-Johnson Syndrome (where epidermis separates from dermis) or in burn patients the skin is covered with antibiotics and dressings. The patient is also given high dose of antibiotics to fight those bacteria that still entered into the bloodstream.

Nice answer, I gather that bacteria would enter more easily, what about viruses?

This answer is a reply to the question asked in the comment of my answer given on 13th July 2016. The comment was, " Nice answer, I gather that bacteria would enter more easily, what about viruses?"
In my answer on 13th July 2016, I used the term "microorganisms" - this includes both bacteria and viruses. So the answer provided there can also be applied to viruses.
To specifically discuss on the susceptibility of the host towards viral infections after damage to the epidermis (dermis is intact) the following may prove to be helpful.
Viruses has evolutionarily developed specific surface molecules that either act as a ligand or a receptor being capable of interacting with the host surface-molecules. Example - Influenza virus contains Haemagglutinin that bind to Sialic acid  containing oligosaccharides found in almost every cell. Common entry route of a virus is usually determined by the surface molecules it possesses. Most common entry routes are respiratory system, gastrointestinal system, urogenital system and inoculation by bite of insects(via insect probosis). Viral infections after skin-damage are rather uncommon.
Intact skin is an effective barrier against viral infections. Dead cell layer of epidermis prevent viral growth. Viruses are non living particles outside leaving cells; so when they come in contact with the dead cellular layer of epidermis they behave in the same way as they were in outside environment. The requirement of blood or lymph supply for replication and spread of viruses meets when epidermis is removed. But in that case there occurs an inflammatory reaction causing accumulation of immune cells and antibodies. These antibodies neutralize the viral surface molecules, thus preventing viral attachment and entry into cells ( even in presence of living cells). Immune cells secret chemicals that disintegrate viral particles.
Most common mechanism of entry into the skin, for a viral pathogens are,
1. direct inoculation
2. systemic infection and
3.local spread from an internal focus

Direct inoculation is our topic. It uses two mechanisms -
(i) replication in endothelial cells and then spread into the bloodstream. Entry into endothelial cells are different for enveloped and non-enveloped viruses; enveloped virus fuses with the cell membrane, while non-enveloped viruses enter by endocytosis or receptor-mediated processes. Examples include warts, milker's nodules, primary herpes simplex etc.
(ii) Vectors may introduce the pathogen directly into the bloodstream
Systemic infections- Skin is infected during high viremia. Dermis is affected first followed by epidermis. Example- chicken pox.
Local spread from an internal focus-  Example, recurrent herpes simplex virul infection from dorsal nerve roots to specific skin dermatomes.

For further infomations you may read
1. Fitzpatrik's dermatology in general medicine, 8th edition,
2. Kuby Immunology, 7th edition.

The dermis provides some protection, and if it is removed the danger of deep tissue infection becomes extremely high. However, the epidermis provides an additional and important layer of antimicrobial protection. That is why first and second degree burns, opened blisters, and scrapes should be kept clean and isolated from the environment with bandages, and why antimicrobial ointments are often prescribed in such cases. The epidermis is an important waterproof barrier to environmental hazards, such as germs and dehydration, and its dryness is a natural inhibitor of microbial growth.    https://www.ncbi.nlm.nih.gov/pubmed/17621950  Also: http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0625.2008.00786.x/abstract

Welcome to Biology.SE! You've given some nice details, but additional references would be much more appreciated.

A couple of references added. Thanks for the suggestions.

And here's  your reward: +1! ;)

-1. This is incorrect. The epidermis provides protection, not the dermis (There are fatal diseases in people who have nothing more than occasional epidermal of parts of the epidermis. Your two references do not support your claim, but they do underline the importance of the epidermis.

I am in complete agreement with you that the epidermis provides essential protection, and that was my point and that is supported by the references. However, in areas where the epidermis is damaged or scraped off, the skin will heal completely. But when injury extends through the dermis,  such as with a third degree burn, the risk of infection, mortality, scarring, need for debridement, amputation, etc. goes up dramatically.

Mr. Gold, you are incorrect. A third degree burn forms an eschar, which is not associated with increased risk compared to second-degree burns. Skin healing has nothing to do with susceptibility to infection.

You may be a very good nurse, but you are wrong in this instance. "Because of the high risk of infection and septicemia from third-degree burns, these wounds must be carefully and scrupulously tended". http://www.consultantlive.com/articles/infection-secondary-third-degree-burn  I could get a lot more references if you like. How much time have you spent in burn units?

Sir, I am not a nurse, but a doctor, for over 40 years now. I have not spent any time in a burn unit, but as an Emergency Medicine specialist, I have a lot of experience with dermal injuries of all kinds. You? Of course there is a risk of infection with third degree burns, but it doesn't mean you're correct in your answer that the dermis stripped of the epidermis is still protective from invasion by bacteria.

I don't know why you're challenging my answer when I am agreeing with you. My answer stated that the epidermis is an "important layer of antimicrobial protection." Please let's leave it at that. I did spend a month in a burn unit. Full thickness injuries are a whole different horror altogether, and we don't need to discuss that here.


text:
Does increased calorie intake cause increase in libido in humans?
I'm interested in the effect of increased calorie intake on sex hormones and chosen mating strategy in humans.
I'm aware that humans have a dual mating strategy - somewhere between pair bond and casual mating. There are a number of physical measures to indicate this - such as sexual dismorphism between male and female, sperm counts and tested size, as well as age of puberty of females.
I've recently listened to a podcast that suggested that long term increased calorie intake causes differences between two mating strategies in case of apes. An example given was that gibbon ape filled their ecological niche and has no predators. Their population size is controlled by food supply. This makes food scarce and gibbons are more monogamous with more paternal investment (to teach offspring to forage)
At the same time another kind of savanna dwelling ape has natural predators limiting population and thus having more food supply. This ape has more offspring and less paternal investment and more promiscuity. It is as if they are more sexually active.
I'm interested if there is any truth to this and if this is also applicable to humans. Does increased calorie intake long term increases libido, while caloric restrictions reduce it?

The podcast sounds interesting. Could you supply the source?

@James I believe this is the podcast in question:  https://www.youtube.com/watch?v=D9isrAUsQjA


text:
How is a synapse held in place?
Here is a question I've never asked myself until now: All textbooks show synapses with a decently large synaptic cleft between the axon terminal and the dendrite. How is this connection held in place mechanically? How is the axon terminal attached to the dendrite?

The textbooks represent the synapses that way for didactic reasons. But, in fact, there are several protein complexes that keep the membranes (pre and post synaptic) attached. The most famous are the puncta adherentia junctions.
In these structures, several different proteins, like nectins and cadherins, promove cellular adhesion:

(source of the image: http://cshperspectives.cshlp.org/content/1/4/a003079)
These molecules are important not only for cellular adhesion, but for synaptic plasticity as well.
Source: Adherens Junctions: from Molecular Mechanisms to Tissue Development and Disease


text:
Are fish averse to extreme heat?
Terrestrial animals face two common sources of heat extreme enough to pose a danger to them: Sunlight and fire.
It therefore stands to reason that they would evolve systems for sensing heat and behavior making them averse to extreme levels of heat, and most terrestrial animals have indeed done so.
Fish, on the other hand, live in an environment where neither of the above heat sources have a profound impact, and the one source of high temperatures underwater (geothermal activity, such as underwater volcanoes) does not exist within the habitat of many species of fish.
In summary, there does not appear to be any pressure for fish to evolve or retain an aversion to heat like terrestrial animals have.
Are fish averse to extreme heat?

Welcome to BiologySE, you should add some references to the background knowledge that you nicely put in your question. That way people that are unfamiliar with heat response can get a deeper look into the topic, too. And, generally speaking, people on BiologySE will frequently ask for evidence to claims made in answers and questions.

Temperature affect pretty much all metabolic pathways. There are incentive in fishes as well to control their internal temperature.
Control of Body temperature can be categorize along two axes, one concerning the source of heat and the other the magnitude of temperature variation. Please have a look at this post to understand the terms endo-, exo-, poikilo-, homeo- terms.
Below is a figure to give a general overview of the diversity of species in terms of temperature regulation.

As you can see fishes are found in different parts of the figure.
So, yes there is incentive in fishes to control their internal temperature and to avoid extreme heat as well as extreme cold.

This is true. Some species of salmon adjust their depth in the water column to regulate their body temperature as a means to control metabolic processes including digestion to improve efficiency between twilight feeding times. While many have a wider temperature tolerance range than mammals, a preferred temperature range exists for fish.


text:
Why does female's age of puberty inform on mating system?
Reading from Does increased calorie intake cause increase in libido in humans?, @AlexStone says:

I'm aware that humans have a dual mating strategy - somewhere between pair bond and casual mating. There are a number of physical measures to indicate this - such as sexual dimorphism between male and female, sperm counts and tested size, as well as age of puberty of females.

How does the age of puberty of females can inform us on the mating strategy?
Why does the observed age of puberty of females suggests a "dual mating strategy"?


text:
Does tRNA contain parts with double-helix structure?
I read in some place that tRNA has a part which is double-stranded. I wanted to know if that part is similar to DNA (double-helix).
(And I know that tRNA won't contain Thymine)

You need to do some research before asking questions on SE Biology. You can easily find information about tRNA on the internet, e.g. Wikipedia.

It is right that RNA has small areas of complementary base pairing. You asked whether these parts are double helical.
DNA has various types of double-helical conformations. Most popular among them is the B-form, A-form and Z-form. The Watson Crick model is similar to the B-form of DNA. It is right-handed double-helical structure. A-form and Z-form are different from this, e.g,. Z-form has left handed rotation and the number of base-pairs in each helical turn is 12; whereas in B-form it is 11. So, there isn't a single structure of DNA that you can specify by saying the term double helical.
t-RNA has multiple segments that are double stranded, separated by loops (called hairpin loops) and bulges.  These molecules have a complex structure (are not symmetrical like the Watson-Crick model). This confirmation helps in its function. As a general rule, when two complementary base sequences (that may be DNA or RNA) come in close proximity, they tend to pair.
Nascent RNA molecule (single stranded) try to assume a right handed helical conformation, but note that it is very different from double-helix. When two strands of RNA, perfectly complementary to each other come in close vicinity they pair into a right handed double helix(A-form); however these molecules are very uncommon in nature.
Other examples of double strand formation in m-RNA are terminal signal of the transcription process in E. coli.
For further knowledge you may read

Biochemistry by Stryer
Lehninger principles of Biochemistry.


text:
Is the amount of the soil reduced when plants grow?
According to the principle of mass conservation I think the amount of the soil should be reduced when plants grow. But this reduction is not typically observed. For example, some trees (big trees) grow so fast that if the soil was reducing due to the growing trees, it seems like no soil should be left around them (i.e. the soil surface had to go noticeably down). But it didn't occur. So, which matters are reduced by growing plants?

You could even say that the sun has to lose 1.5 million tons of rest mass per second to allow life on Earth, in the first place... and it's been doing that (with some variation) for over 4 billion years...

Have you ever used a fertilizer in your garden? That's more or less what is lost from the ground. Of course, in nature, even that is replenished over time - e.g. through decomposition of dead plants (and animals), erosion (calcium carbonate/oxides washing into the soil), nitrogen-fixing bacteria... And don't forget that naturally, these are distributed or even dissolved in the soil (and water), so even when they're gone, the soil level doesn't necessarily drop noticeably. If you ever tried compacting soil, you know how sparse it can be - which in turn helps absorb rain and prevent erosion.

Since soil includes the organic matter component composed of decaying plant/animal material (for the purposes of simplified discussion we'll only consider the non-living organic matter as soil), and since plant roots die back at certain times of the year or under certain conditions (adding organic matter to the soil), it could be argued that the amount of soil actually increases as plants grow.

@ThatIdiot Really? So wonderful! I never expected increasing the soil. Thank you very much for teaching!

@lucas My comment oversimplifies things. While the plants are shedding roots and adding organic matter (OM), the soil food web of fungi, bacteria, nematodes, etc. continually "consume" this OM and respire the carbon dioxide back into the atmosphere. If these processes are in balance, OM content tends to remain stable in the soil. However if it becomes unbalanced (from changes on soil moisture or nitrogen inputs among other things), the OM content change as well. BUT the question was limited to the effect of plant growth, and plants do add OM to the soil.

The vast majority of the mass of a plant is carbon-based which is obtained directly from the air via photosynthesis. So trees are, in a loose sense, solidified air!
And most of the mass that comes from the ground is water which, of course, is constantly being replaced when it rains (or by Charlie with her watering can).

I suspect that oxygen actually constitutes the majority of plant mass (as it does for the mass in animals. Many carbohydrates like glucose actually have about numerical parity of C and O, and plants contain significant amounts of water). So, water and air mix to build up trees.

@Chieron I suspect you're right. What I meant by 'carbon' was 'carbon-based' - updated.

@DanielSank I am waiting. Maybe, other users want to answer the question. If I mark it as accepted now,  they may discourage.

The soil is the source of a small quantity of vital elements like magnesium (component of the chlorophyll), phosphorus (DNA), sulphur (some proteins) and more. As the plant grows, these are removed from the soil, so its mass shrinks.

DNA (all amino acids) also need fixed nitrogen, which comes through soil and groundwater.

@Whit3rd: Amino acids make up proteins, not DNA. DNA is built from a skeleton of sugars and phosphate, with (nitrogen-containing) nucleobases attached.

Thank you because of your attention! @Martín-Blas Pérez Pinilla

I've extended / formed your answer a little bit to improve its chance to survive the review process of the site. I hope there is nothing added which you hadn't.

As said in other answers, CO2 is pulled from the air, and H2O is constantly resupplied. Then there is Nitrogen, which is either taken from the ground, or from the air, depending on the plant.
Leaving meat eating plants aside, all the other stuff has to come from the soil, but how much is it? This is actually pretty easy to estimate yourself:
Just burn the tree/plant, and all the water will evaporate and all the carbon will be burned, and all that is left are the minerals that that plant pulled from the soil.
So if you ever had a nice campfire burning for quite a while, you get a pretty good idea that while being a fraction of the trees mass/volume, it is still quite some material.

"Just burn the tree/plant, and all the water will evaporate and all the carbon will be burned, and all that is left are the minerals that that plant pulled from the soil." Which plant is this that provides a complete combustion? Might be useful for alternate fuels here soon.

@jwillis0720: not sure what you are after, but I constantly burn my garden waste to ashes, and I am pretty sure only traces of carbon and water are left in the ashes, which gives a pretty good approximation.

@PlasmaHH Thank you very much because of your attention! Your idea (burning) proves that the amount of soil shouldn't change observable so much.

Actually, unless you're really thorough, lots of the ash from burning e.g. wood is still carbon. You can tell roughly how much by the colour - the blacker the ash, the more carbon is left. If your ash is white, it is indeed mostly the minerals - mostly calcium carbonate/oxide, potash, tiny amounts of phosphates and trace amounts of stuff like iron. Depending on the kind of wood, the ("pure") ash is something around 1% of the dry mass of the wood. Needless to say, wood ash is a great fertilizer :)

@Luaan: Indeed it is, but only from wood you burned/processed yourself. Some people want to use the ash from burning charcoal, with questionable sources of the wood, sometimes containing alertingly high amounts of heavy metals. Regarding the thoroughness of the process: as long as the ash is quite a light gray, it is good enough as a proper estimation, since carbon will be present in only negligable amounts. And usually for a good fire, the ash is that colour, at least for me.

"all that is left are the minerals that that plant pulled from the soil" is also probably not quite right, since nitrogen is also pulled from the soil and at least a fraction of it will go up as nitrogen oxides.

@EmilioPisanty: As mentioned, there are different sources for nitrogen, so it may or not be from the soil, depending on the plant. After all, its just a way to estimate. Also afaik the majority of nitrogen will be gone after burning, but I really never did any research or experimentation on that. There will also be things like sulfur that is taken from the soil and burned away, but again, its a suggestion for an estimate for the minerals taken from the soil, not an accurate measurement.


text:
How to find suitable qRTPCR reference gene for a inflammatory response experiment?
I have tried several housekeeping genes – Hprt, β-actin and GAPDH, to analyze the relative expression of a cytokine for measuring the inflammatory local response in mice ears. However, all these housekeeping genes show significant variation in both within and between different experimental conditions.
I really don't know how to solve this. I take the same amount of RNA (quantified by  nanodrop) to make cDNA so I guess I have the same concentration in all the samples.
Any suggestion of what can happens and how to solve it? Could I use something different to measure the relative quantification? (My cytokine of interest is TNF).

When you say, "[they differ] from each other significantly", do you mean between replicates under the same experimental conditions or between conditions? It wouldn't be useful to normalize to a housekeeping gene expression level if it doesn't change between conditions.

They differ between diferent conditions and also under the same experimental conditions. I have checked the DNA concentration of the samples and they are the same.

You don't say how you're measuring but I'll guess that you're using quantitative PCR. A typical approach to handling housekeeping gene normalization in qPCR experiments is described in
Accurate normalization of real-time quantitative RT-PCR data by geometric averaging of multiple internal control genes.

We outline a robust and innovative strategy to identify the most stably expressed control genes in a given set of tissues, and to determine the minimum number of genes required to calculate a reliable normalization factor. We have evaluated ten housekeeping genes from different abundance and functional classes in various human tissues, and demonstrated that the conventional use of a single gene for normalization leads to relatively large errors in a significant proportion of samples tested. The geometric mean of multiple carefully selected housekeeping genes was validated as an accurate normalization factor by analyzing publicly available microarray data.

There is an R package called NormqPCR that implements this approach (publication here).
Briefly, the approach required measuring multiple housekeeping genes and iteratively removing the ones that are most variable, ending up with two genes that are jointly least variable, and making a sort of pseudo-housekeeping gene from them with which to normalize your other genes.
This doesn't magically turn bad data into good data, but it helps clean up some intrinsic problems with housekeeping genes.

House keeping genes are not necessarily constant.
Another way to measure gene expression change is RNA-seq. It normalizes counts against the whole transcriptome instead of against certain housekeeping genes.

If there was no established robust protocol, you could follow Eissa et al. 2017, Scientific Reports. They faced the same problem in another inflammatory model system in mice, and outline a strategy on how to find robust housekeeping genes (and then wrote a publication about this).

Can you include a brief description of the strategy?

I believe to possibly do more harm if compressing the full paper into a paragraph.

It's hard to tell if OP is running an array or qPCR with carefully selected targets. If it were an array I'd suggest the OP take the genes across all samples, calculate %CV and use the lowest CV genes as normalization genes. He'd just have to cut them from the analysis. It's harder to determine what you should use one at a time. Perhaps some RNAseq, microarray or Nanostring data exist in his model, somewhere, he can use to do this.

Why downvote? The above answer is correct. The publication describes a general protocol to deal with the question of OP.

Finding a suitable reference gene is tricky. It depends on your prior knowledge about the system. You may start with the same amount of RNA but errors can accumulate many other steps. That is why you use a reference gene to minimize the effect of those errors accumulated during sample processing. So unless you are very precise, you cannot say that everything was constant and the expression is the source of variation. Once you test a putative reference gene thoroughly you can "believe" that it would not change when you repeat the experiment.
Having said that, I would insist that a much better (and quite easy) method is to use a "spike in". It is a synthetic nucleic acid that you add to your samples. Similar concept can be used for proteins and metabolites too. You can spike in the same amounts of  the synthetic RNA in your different RNA samples. If you keep the volume constant then the concentration of the spike-in would be the same in different samples. So, instead of a housekeeping gene you would now use the spike-in as a reference. Spike-ins have been found reliable for even single cell RNAseq studies (Lun et al., 2017).

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


text:
What is the formula to establish ec50 reproducibility with respect to dose response curves for some drug?
The EC50 is determined by fitting a standard curve to the experimentally obtained control values for each dose response curve using some software that does trial and comparison until satisfactory(nonlinear regression).
In the literature, it is mentioned that experimentally obtained control values for the dose response curves, are EC50 reproducible. To my current understanding meaning that EC50's obtained for different for several dose response curves are actually 'close enough'(in some formal statistical sense) together. Is there some procedure or formula for formally establishing EC50 reproducibility?
Thank you :)

Welcome to Biology SE. What do you mean by "trial and error"? EC50 analysis is usually done by nonlinear regression, typically with some sigmoid function. There are many methods for estimating variances / confidence intervals for parameters in nonlinear regression, so if you can give a bit more details about your specific model and data, that might help. Also, the Statistics SE might be appropriate for your question.

Hi Roland, thanks for your reply! Actually from your reply I can phrase better what I meant to ask. Basically a sigmoid is fitted to experimental data using nonlinear regression as you said for each experiment. Now the aim is to  conclude reproducibility of these sigmoids for added experiments(dose response curves). So basically comparing the fit parameters(EC50, slope) and establishing that they follow a concentrated pattern. Some researchers refer in articles to this as 'EC50 reproducibility'. I was wondering whether there are widely used methods of establishing this reproducibility.

And the data itself is confidential btw. But the model used is basically a sigmoid as you mentioned. Thank you for your reply.

If you have multiple EC50 estimates from separate independent measurement series, then it should be easy to see if they are in agreement?  You could do mean +/- std dev of the EC59 values (assuming a normal distribution), but personally I prefer just tabulating/plotting the data.  If the data is tight, is usually obvious.  The situation is more tricky when there is only one measurement series and some variances estimate must be derived from the regression analysis.

The DRC package, in the paper from my answer, includes functions to directly compare parameters such as the slope, from nonlinear regressions.

Thank you for your reply Michael_A. I'm looking at the article.

The different models that can be used to fit the curves do differ.  The linked paper and this website outline the differences; the discussion revolves around an R package called DRC but much of the information is generally applicable. Modelling can also be used to estimate ED50.
The parameters and models that are being used need to be consistent with the biology that is being studied. If it's appropriate, scaling the upper and lower bounds of your data can improve the consistency of ED50 estimates as this removes the requirement for the model to estimate those parameters. Something like this can be used for scaling;
(VALUE - topdrugmean)/(nodrugmean-topdrugmean)

The Akaike Information criterion can be used to measure the goodness-of-fit for different models (see the preceding links).


text:
Scaling down amount of DNA for transfection: what factor to consider?
I am interested in transfecting HEK293 cells with a BAC. One paper suggests using 24 ug of DNA to transfect a 55-cm^2/10 ml culture plate. I am using an assay optimimzed for a 96 well plate so I am interested in scaling down the amount of DNA.
If I consider by volume: I will be going from 10 mL to 100 uL, scaling down by a 1/100, suggesting 0.24 ug of DNA.
If I consider by cell number: I will be going from 10^7 cells to 10^4 cells, scaling down by 1/1000, suggesting 0.024 ug of DNA.
If I consider by cell concentration: I will be going from 10^6 cells/mL to 10^5 cells/mL, scaling down by 1/10, suggesting 2.4 ug of DNA.
What factor should I scale down by? I want to say that it's volume but I don't really know why.
Thank you for any help or suggestions!

Are you using lipofectamine? They provide tables to sort of help streamline the process: 3000 reagent, 2000 reagent.

Hi - No, I'm not using Lipofectamine but I did see the table online. I'm wondering why they decided to use volume instead of cell # or conc which seems much more intuitive to me.

Well if you think about a plate-based transfection, only a certain number of cells will viably fit into a well, and you want them in a replicative state. So you try to get them 90% confluent, which is easier visualized in a 6-24 well format, but for 96-well other groups have worked out the best cell/well in their protocols already. Consensus is at around 50,000 cells per well. So the cells numbers are actually standardized for the plate format. The only question that remains is how much volume of reagents will work with said cell counts!

Wait, I don't think that answers the question. If the cell # is standardized, then amt of DNA transfected should be scaled down according to cell # not volume

If you know how many cells will give you confluence in a 96-well format, you just scale down on the size of the well. So 1:100 or 0.2 ug DNA.


text:
Query individuals with both WGS and RNA-Seq data
Using the SRAdb R package, I am looking to query individuals who possess both WGS and RNA-Seq data on the SRA. So far I believe I have been able to query specific samples with both WGS and RNA-Seq experiments, however a specific sample, provided by the sample_accession, is not exactly what I'm looking for.
For example: I'm interested in finding human data in which one human was used to derive WGS data, and several tissues from that same human were used to derive RNA-Seq data.
Is there any easy way to accomplish this using SQL and/or R?
So far, this is my approach to identify samples that have both WGS and RNA-Seq data, using the local database, SRAmetadb.sqlite:
con <- dbConnect(SQLite(),'SRAmetadb.sqlite')
query <- dbGetQuery(con,
                    paste(
                          "SELECT
                            sample.sample_accession,
                            sample.scientific_name,
                            experiment.experiment_accession,
                            experiment.library_strategy
                          FROM sample
                          JOIN experiment ON
                            sample.sample_accession = experiment.sample_accession
                          WHERE experiment.library_strategy in ('WGS','RNA-Seq')
                          GROUP by sample.sample_accession
                          HAVING COUNT(DISTINCT experiment.library_strategy) = 2"
                        )
                    )

With this approach, I can see query contains 181 human samples that have at least one WGS experiment and one RNA-Seq experiment. That's great, but I feel I must be missing out on data that came from different samples but the same individuals.

Why do you feel so?

A liver sample and a brain sample from the same individual would have different sample_accession values, correct?

And it's remarkable to me that there are only 4 Mus musculus samples that meet this criteria, using the method above


text:
Are a bonsai tree and its normal version the same species?
I would like to know if bonsai type of a tree is a separate species from its normal version. Do they differ by genes, or is it just a matter of different physical care?
Can I grow a bonsai tree from seed of a normal outdoor tree (of course, I understand that not every species will endure being dwarfed)? Can I grow a normal outdoor tree from some seeds labeled "bonsai"?

I'm voting to close this question as off-topic because it should go to Gardening.SE

Yes. For any species that it is possible to grow as a bonsai tree, it is also possible to grow that species as a non-bonsai tree. The process of creating a bonsai tree involves growing a tree in a severely restricted pot with a minimal amount of soil, and trimming both the roots and branches to maintain a desired shape and size. It is the small growing space and regular pruning which keeps bonsai trees small, not the genetics of the tree.
You may wish to check the list of species used in bonsai on Wikipedia to get a sense of which species make good bonsai plants.

What if we grew bonsai trees for many generations, selecting the individuals "most suited" for the bonsai process? I don't know how long it would take, but eventually there should be genetic changes to help the plants adapt to the selection.

Sure, you could. That would be standard artificial selection. But given that bonsai as currently practiced doesn't require such selective breeding, why would you make the effort?


text:
Dopamine receptor count: Role and Measurement
Can the Dopamine (DA) receptor count take a significant drop over the course of life or does it stay constant? I read that low D2 (Dopamine receptor type 2) receptor count does not cause Parkinson's Disease (PD) and has some interesting effects instead, but what abut low D1 (Dopamine receptor type 1) receptor count? What are its effects? All I found is this. Is D1 receptor only related to motor activities?
I found some research papers on how to measure the DA receptor count, but are those tests publicly available and affordable? Is there any indirect way to determine D1 & D2 receptor count?
Disclaimer: This is not a self-help question, and PD is not my focus. I am trying to form a theory that requires easy way to measure DA level plus D1 and D2 receptor count, but sadly I am not part of any university with biology department to go seek advice from.

Welcome to BiologySE! Your question, for me, is a bit unclear. You could help people that are not experts in the field (but may still be willing and capable to help you with your question!) by (i) giving full name of abbreviations before using abbreviations and (ii) providing references (Wikipedia articles are sufficient for basic concepts) to both the major actors in your system (e.g. the receptors) and some claims. If you mention something like 'I found some research papers', people will definitively want to know which, so please provide the reference to these papers.

Sorry for the poor accessibility. I have edited the question. I am not allowed to most more than two links. So here is one link I wanted to post: Effect of low D2 receptor count: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2871784/.


text:
Fabric melting spider juice
I live in the southern rocky mountains of Canada. I was in bed the other night when I saw a small scurrying shadow out of the corner of my eye. The source of the shadow was a small spider (95% sure it was a barn funnel weaver), approx 2cm in diameter. I killed the spider.
Interestingly, what intrigues me is that the place on my bed where I killed the spider the jus of the spider had melted to the sheet (!). How could that happen?

I tried to cut out the extraneous wording from your question - what do you mean by the spider jus had "melted" to the sheet? Can you clarify?

I think what he's saying is he smashed the spider and left it overnight on the sheet and it broke down the sheet fibers or left a hole.

Please look at sheet label and state cotton/linen/other fiber.

Some spiders are known to eat their own silk when breaking down a web and reconstructing it (https://en.wikipedia.org/wiki/Spider_web#:~:text=It%20is%20common%20for%20spiders) or even stealing the web of other spiders and eating it (https://frank.itlab.us/photo_essays/papers/Argyrodes_kleptoparasite_spider.pdf). It may very well be that some types are able to digest various silks or other fibres. I'm not aware of any studies that test whether a spider could digest - say - wool or other natural fibres.
If your sheets were silk or other natural fibres, it's feasible that their digestive juices were strong enough to break down your fibres. Who knows, maybe their digestive juices are even strong enough to break down synthetic fibres (unlikely, but I don't know any study that has looked at that).

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


text:
Adaptation by standing genetic variation and fitness variance
I've read a couple of paper on Fisher's Fundamental Theory of Natural selection that states:
$W(t+1) = W(t) + Var_{W}(t)$
Given a population with some degree of genetic variability, and assuming that no new mutations can appear, eventually the most fit strain will be fixed (discarding the effect of drift). The FFTNS allows to predict, given the mean fitness at any point and the fitness variance, the mean fitness of the population in the next generation.
However, can we predict the variance on fitness for the new population?
Given the possible complexity of the problem, the situation I'm focus have specific conditions, but I would also like to know the general answer. But in my case:

Individuals reproduce asexually
Random mating
Diploids
Expanding population with recurrent bottlenecks (we can approximate to Wrigth-Fisher population with certain effective population size)

More generally, given only the initial mean fitness and variance of the fitness can we predict the trajectory of the mean fitness during adaptation? If not, what do we need more? Number of strains present? Or only the full composition of the population allow for such prediction?
Thanks in advance

Welcome to Biology.SE. Your question is a possible duplicate of How does Natural Selection shape Genetic Variation?. You might also have a look at this post to understand Fisher's Fundamental Theorem of Natural Selection

Thanks for point that out! I will read with more attention, but I still think that it is not clear in that post whether, given only the mean fitness and fitness variance of a population, one could predict the future mean fitness and how. One of my conditions is saying that the G matrix is unknown (population composition is unknown).

The evolution of the G-matrix is exactly what you are interested in if I understand your post correctly. Once you read the other post, you might want to ask your question in reference to this particular post.

Although I understand the point of the G-matrix, what I was looking for was a way to predict mean fitness without direct access to the G-matrix... Given only the measured fitness variance of the population and assuming no new mutation, no recombination, no migration, can we predict future fitness variance (and by the FFTNS the mean fitness) of the population.

Given the measured fitness variance of the population you can construct a G-matrix (if you have sex-specific variance and cross sex covariance estimated, it would be a 2 x 2 matrix) and perform the prediction using the multivariate breeders eq. $\Delta \bar{z} = G \beta$ where $\Delta \bar{z}$ would be the change in fitness, $G$ is a 2 x 2 matrix as above, and $\beta$ is the sex-specific selection coefficient, thus fitness after selection would be $z + \Delta \bar{z}$. Price equation is also likely very useful.

Thanks a lot!! Can you point out a reference for constructing the G-matrix from the variance in fitness alone? By the way, if the species is asexual, then G is a 1*1 matrix right? And how does G changes for every generation?

Asexual would be complicated, not something I've considered before, so I'm not sure how that would affect it off the top of my head. Just a note, you may also want to consider the effects of non-genetic variance in fitness and how that impacts selection (see Hansen and Houle's papers on the concept of evolvability)

Sure! Although I want to start with a simple model, without external complications... It's funny, I had always the felling that asexual populations would be easier to model than sexual!! :)

Given the asexual condition in my question I think that the linked question does not answer it, so can the "This question may already have an answer here:" be removed?


text:
How do you call the species that gives its name to a upper-level clade?
Just a silly question: I don't remember how the species giving its name to an upper-level clade is called.
e.g. the name of family Canidae derives from Canis lupus
You could say it is the "name-giving" species, but I'm certain a specific term exists.

I guess you are looking for the type species.
Although it is defined to be a "name giver" for the genus or subgenus level you could potentially extend this to higher up levels.
EDIT: After looking this up and actually reading the full article myself, yes, at least in zoology you can extend it to higher levels by for example using the type genus.

Hmm... Thank you
I guess "type genus" is closer to what I was looking for, since it concerns supra-generic clades.
Although I recall once using a term of somewhat greek origin, like blahblah-nymic... but I don't recall what it was...
Maybe "hyponymic species"?


text:
Why doesn't Poison Ivy cause a reaction under one's fingernails?
Okay, so I pulled up a bunch of Poison Ivy last week and I got itchy up and down my arms. I scratch and I think that causes the oil to spread causing more misery. However I notice that I don't get a reaction under my nails where I would think the oil might accumulate. Why not? The skin under the nail seems relatively delicate and yet it doesn't react. ?


text:
Assume the gene for freckles is dominant. A woman with freckles has a son that does not. What would have to be the genotype of the mother?
I need help understanding the question I guess. I have read the chapter in my book but still confused.

Welcome to Biology.SE. Please read about how to ask questions and take the tour. This is not a homework forum. If you want an answer, you should show attempts to answer the question yourself, or at least provide some background knowledge on the topic you are asking about. Also provide references and state your questions clearly.

@AlexDeLarge so why did you then give an answer? From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here. Providing answers to crap questions like this just encourages more of them, and shows people we don't really care about or enforce the rules.

@MattDMo: Yes, that would be a never ending dilemma. Actually, i did not say this was a crappy question - I think it would be an appropriate one, if properly stated. Therefore, my comment was meant to be encouraging to improve the question according to the rules. Additionally, I tend to be very indulgent with newcomers - they might not know, they might want to learn. But fact is: they have a question and need help. So I took the 3-5 minutes to answer the question and tried to help T.Seevers out. But, of course, you are right in that this is a bit inconsistent and I will keep that in mind.

@AlexDeLarge like when dealing with children, consistency is key. (No, I'm not implying that all new users are like children.) "Being indulgent" is exactly the wrong attitude to take. Be welcoming, but firmly point them towards the help center and the various meta questions on common topics. If they want to learn, they'll know how. If not, they'll know our reasons. Read the entire help center yourself, especially what's on- and off-topic, how to write good questions, and how to write good answers. Use this for some good comment templates.

@MattDMo: Thanks. As I already said, I will keep it in mind.

The mother needs to have a heterozygous genotype. This means that she carries two different alleles at that gene locus. She needs to carry one allele for freckles (since she has them herself) and one recessive allele that does not.
Her son must have inherited her allele that does not cause freckles, otherwise he would have had freckles himself. Accordingly he is probably homozygous for that gene which means that he has two equal alleles, both not causing freckles. Alternatively, he could also be heterozygous but have two different alleles that both do not cause freckles (and therefore the allele he inherited from his father is different from both alleles his mother carries).

So would that mean the mothers genotype is Ff? And that the father doesn't have the same genotype?

Yes, the mother would be Ff (where f is any allele not causing freckles). No, the father does not need to have the same genotype. He could, but he could also be Ff*, where f* $\ne$ f but both f* and f alleles do not cause freckles.

Since dominant trumps recessive, the mother, who has freckles, must have at least one F allele. However, since the son doesn't have freckles, and he gets one allele from each parent, it follows that the second allele the mother has is a recessive f.
For extra credit, the father could either have ff or Ff, following the same line of reasoning.

This only works for biallelic loci which does not need to be true.

@AlexDeLarge So what's the difference between my answer and yours?

First, I provide references so that T.Seevers can look these things up, second I account for the possibility that the locus is not biallelic and therefore discuss his genotype, as this might give further insight + account for T.Seevers terminology (genotype) and link this to related and useful concepts (zygosity, gene locus, allele) and third, when I started writing your answer was not there, yet. ;)

Fourth: you can edit your question accordingly and I will happily delete my answer. :)