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Why is the gene regulation in eukaryotic cells needs multiple level of control than in prokaryotic cells?
That "eukaryotic cells are more complex" and "compartmentalized" are used to justify the need of more level of control of gene expression. I get the basic idea but can't convince myself why complexity or compartmentalization leads to more complex control (i.e. multiple levels) of gene regulation!
In control theory, we often use multiple level of control to minimize the variance (there are few other benefits as well from design perspective); probably that is what eukaryotic cell would also do. Moreover, simple combinatorics suggest that two level of control with $n_1$ and $n_2$ molecules involved at each level respectively would give me $n_1n_2$ possibilities of output which is higher than $n_1 + n_2$ distinct output I might get if I were to use these molecules with 1 level of control/regulation.
I was wondering if such simple reasoning are correct and can be used in the context of evolution? Are there other reasons as well?

There are additional levels of regulation in eukaryotes such as alternate splicing, miRNAs, long distance chromosomal interactions (enhancers/silencers), epigenetic regulation etc. Please add details as your question seems both a bit unclear and broad.

@WYSIWYG I rephrased the question to make is less broad. I may still be unclear since I am poor in Biological vocabulary/terms.

Some gene expressions need to response quickly by stimuli. In this case, cells may degrade mRNAs or proteins rather than inhibit gene promoters. Even if cells need proteins in some small areas of cells, cells could not turn down the promoter activity of the gene. Instead cells control translocation or degrade mis-localized  proteins. Space and time are also important. Multiple ways of regulations make cellular activities possible.

You don't want all genes expressed at all timepoints. Some need a tight control, while other shall react quick upon stimuli. This is only possible with a complex regulation.

I think you need to consider the overall amount of information that is needed to implement a proper control system in living organisms.
In prokaryotic cells, in most of the cases, you will find that one gene code for one enzyme, so if a simple organisms need 500 enzymes to stay alive you can expect 500 genes that code for that enzymes.
A more complex organism may need 100 times more enzymes to stay alive and so theoretically 100 times more genes. Now, evolution wise, to have a linear increase of DNA vs complexity is not a good option for very complex organisms. To keep everything compartmentalised in one single membrane is also not a good idea if you need to run millions of chemical reactions using thousands of enzymes that can cross react and need different optimal conditions to work properly, so multi-compartimentalization is a must.
Linked with it arises the problem of sending the right enzyme in the right place and this has been solved by adding tags, transporter enzymes, etc... in the pot... So, lots of more information is needed to make everything run smoothly.
It turned out that an efficient way to code for all that enzymes, tags, promoters and other regulators without increment the size of the DNA too much is by multi level control of the expression of a gene i.e. the same gene can be used to produce different enzymes (splicing etc...). The tradeoff to pay to have a more compact genome is to increase the complexity of its control system.
Lastly, consider that differently from normal electronic controllers, the biological one do affect each other. A biological controller system may produce an output molecule that interact with the system under control but also with other reactions going on all over... that is another burden that require an increase of complexity in the control system to make it work.


text:
Can these "Promega Wizard genomic DNA Purification kit" be used for samples not stated directly?
I am not sure if this is a duplicate of my previous question, it is somewhat related, so sorry if I misunderstood.
The question is, can i use the above kit for samples like hair, fingernails, etc?
Here are the guides:
https://www.promega.com/~/media/files/resources/protcards/wizard%20genomic%20dna%20purification%20kit%20quick%20protocol.pdf
and the extended guide:
https://www.promega.com/~/media/files/resources/protocols/technical%20manuals/0/wizard%20genomic%20dna%20purification%20kit%20protocol.pdf
It says that for the animal tissue:
Animal Tissue (Mouse Liver and Brain), so I figure it wont apply given that these cells might have higher percentage of DNA that hair(roots/shaft) could have, or fingernails.

You may want to look for forensic kits. These are specially adapted for the needs you habe. But make sure that you have a seat when you read the price quotes, these kits are really expensive. It may be worth to contact a sales representative and tell them that you do a research project and are not a professional analysis lab. Sometimes you can get a good discount then.

If you have a question about a kit, I strongly suggest contacting the manufacturer instead of just asking random people on the internet.

In addition, the kit clearly says "DNA". "Genomic RNA" makes little to no sense in a biological context.

@MarchHo       sorry it was a typo, i fixed it

It is difficult to isolate good quality genomic DNA from fingernails. PCR for specific genes is much easier. What do you want to do ultimately?

The column size should be appropriate. And you have to solubilize enough for DNA to come out. But why don't you use kits showing gDNA extraction from nail. http://www.epibio.com/docs/default-source/forum-archive/forum-14-1---pcr-analysis-of-fingernail-dna-using-quickextract-dna-extraction-solution.pdf?sfvrsn=4 And this information may be useful. http://link.springer.com/article/10.1007/s12033-010-9273-6/fulltext.html

@WYSIWYG         I was going to PCR for specific genes, the CODIS standard 13 loci for the human genome, using extracted DNA from hair or fingernails, thanks for the reply.

@RoSiv You don't need to extract DNA to do PCR. You can simply use a small part of the sample. Like you do in colony PCR.

@WYSIWYG          so are you telling me I could just break down the hair/fingernail and then perform PCR on that solution? if so would you have some type of protocol for that?

@RoSiv See this article. And for hair you should use the hair root (that is where you will find viable cells)

source: Stack Exchange

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

sort: votes


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How do Mockingbirds find each other during mating season?
Since mockingbirds imitate songs of other birds, how do they find each other during mating season? How can they tell it's a mockingbird singing, instead of other birds? Is there something in their imitations that still identifies them as a Mockingbird?

Wildlife biologist Daniel Edelstein implies as much here: he says that there are in fact variations in tone and context that distinguish mockingbirds from other birds they imitate. (He was writing about the possibility of mockingbirds attracting the birds they are imitating, which doesn't happen. I can't find much about what specifically attracts female mockingbirds, except for the variety he alludes to.)

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


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Vegetable Cellulose
I'm a pharmacy student working on my thesis. I just want to ask the probable sources of vegetable cellulose found in vegetable capsule? Note: I'm referring to the capsule itself not for its possible content. Thanks.

There are "vegetarian" capsules?? I didn't know about this..

Vegetarian capsules are made of hydroxypropylmethylcellulose (also called hypromellose). The cellulose from which this material is prepared is usually from tree fiber, commonly from pine or poplar species (as noted here).


text:
How can octopus walk if muscles can only contract?
From this video it is evident, that octopus can make tentacles push:
https://youtu.be/zaE-LwDowcU
How is it possible, if it is said, that muscles can only contract?
What types of muscles can distract?

Octopuses have "functionally antagonistic longitudinal and transverse muscle fibers" that "not  only  create  the  movements  but  also
supply the skeletal support".  It's basically the same as your tongue.

Can these fibres push?

One can probably extend @Armory's comment to make an answer explaining how those muscles can explain tongue and octopus movement.

Kier and Smith wrote a paper on how tongues tentacles and trunks worked. It explains in detail exactly how their legs (and our tongues) elongate, shorten and move about without any bones for support. It's called muscular-hydrostat.
Movement of the limb actually depends on which muscle is being contracted. If it's contracting the muscles longitudinally it will make the limb short and wide, while if it contracts laterally it will cause the limb to extend and be short and thin.
If you watch the video carefully you can actually see the changes in thickness of the limbs as the lateral muscles release and the longitudinal muscles contract so the octopus can move its leg forward.
If you want to see it work in person, go into the bathroom and move your tongue around and watch in the mirror. It uses the same mechanics to move your food around your mouth, lick your teeth, help you get that bit of food that is stuck up against your gum, and who can forget rolling the tongue into a cylinder or making tongue clovers.

@SolarLunix I believe Chris suggested you edit your existing answer to include the source, rather than add it as a comment. Might also be helpful if you could add more details to your answer. If I'm reading this right, figure 5 suggests that the muscles around the tentacle contract, squeezing the tentacle into a smaller diameter. Since volume must be constant, the tentacle gets longer. Once the tentacle grabs something, the longitudinal muscles contract and pull the octopus forward, allowing it to walk.

Sorry I'm quite new to this site @user137, and as for what you read, that was my understanding as well.

@SolarLunix That's fine, just make the edits and you'll be ok.

Shame for me: forgot about myself tongue :)))

@Dims lol we all forget sometimes :D


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What is effectiveness of methyl-alcohol as sporicide?
Methyl-alcohol is the weakest alcohol in terms of bactericidal properties. However, I have read that it also works as sporicide.
What is the effectiveness of methyl-alcohol in killing the spores of fungi and bacteria compared to other substances and what is the best dilution?

Are you specifically looking out for fungal spores, or do bacterial spores work too?

I would say that a little bit of information about also the bacterial spore is not useless... Question edited! @MarchHo

From page 233 of this book: Bacillus anthracis spores resist methanol completely at concentrations of 0.004% to 95% but are killed by ethanol in 48h at concentrations of 42% to 100%. Methanol can be oxidized to formaldehyde (which is a disinfectant) but this reaction cannot be performed without certain catalysts.

Methanol (methyl alcohol) tends to lack sporicidal activity on its own. However, fresh mixtures of methanol and hypochlorite, with at least 15% methanol, are known to have low sporicidal activity.
With an increasing methanol concentration, right up to about 50% methanol, the sporicidal activity can be increased. The preparation, however, isn't overly stable and the sporicidal activity will start to decrease after 8 hours. It is thus recommended, should a methanol + hypchlorite mix be used to counteract spores, to only use a freshly prepared solution of 50% methanol and a sufficient amount of (sodium) hypochlorite that provides 2000 parts per million available chlorine in distilled water and allow for a contact time of at least 15 minutes.
Sources:

Russell 1990 - Bacterial Spores and Chemical Sporicidal Agents
Kelsey JC, Mackinnon IH, Maurer IM Sporicidal activity of hospital
    disinfectants Journal of Clinical Pathology 1974;27:632-638.


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Proline Iminopeptidase v Proline Aminopeptidase
We're an undergraduate independent research team and we are having trouble purchasing commercial proline iminopeptidase as it is unavailable on Sigma Aldrich and very expensive on other websites. We need to test that this peptidase will cut a series of tripeptides we are synthesizing in e coli.
Could we purchase proline aminopeptidase instead of proline iminopeptidase; will the peptidase function the same way?
This paper says that they are the same, but this paper says that they are different. Does anyone have any experience with this commercial peptidase?

Chemically, proline does not contain an imino group. http://goldbook.iupac.org/I02959.html More on topic, you can send an email to the manufacturer of the aminopeptidase and ask if it cuts the tripeptides.

The peptidase cuts the tripeptides after the proline in that sequence. The purpose of purchasing this peptidase is to compare our experimental results (the results of the cleavage) to the results of the commercial peptidase cleavage. We work in synthetic biology so both the tripeptides and the peptidase will be in a single plasmid.

There are two related enzymes that cleave an N-terminal residue. Enzyme 3.4.11.9 cleaves any residue from a peptide when the next residue is proline. Enzyme 3.4.11.5 cleaves an N-terminal proline from a peptide. Unfortunately, it appears that both are sometimes referred to as proline aminopeptidase. However, only 3.4.11.5 is referred to as proline iminopeptidase.
The vendor should certainly specify which enzyme they are offering.


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CRISPR-Cas Systems
In the context of the bacterial systems (not the gene editing tool), I was wondering what happens to the foreign DNA after the Cas proteins have created a new spacer.
It is really not clear to me, most of the documentation I have found focuses on the subsequent steps (expression and interference) and do not discuss the fate of said foreign DNA. For example, see this image from wikipedia https://en.wikipedia.org/wiki/CRISPR#/media/File:Crispr.png

It's not really clear to me what you mean.  Do you mean what happens to the foreign DNA or what happens to the spacer?  The former is cleaved to form a spacer, the latter is inserted into the genome.

Ok thanks, how do you know that it is cleaved? Are there endonuclease activities in the proteins that deal with the foreign DNA? I was under the impression that the spacer was created by copy of the protospacer of interest.

@AlterSid Cas is that endonuclease. Please read about CRISPR-Cas and ask specific questions if you have any. Wikipedia is good enough.

Try this paper http://www.ncbi.nlm.nih.gov/pubmed/20056882 it makes a nice overview of the all process and if you want to go deeper check the references, they cover all the passages involved in the CRISPR mediated immunity.

Do CRISPR systems attack the entire DNA of the virus or certain specific DNAs (dictated by the spacers)?


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How do nuclear membranes form during Telophase of Mitosis/Meiosis?
During Telophase, homologous chromosome pairs reach the poles of the cell with the help of microtubules. From there, nuclear membranes form around each new set of chromosomes.
My confusion originates from a single question: How did these nuclear membranes form around the chromosomes?

I think that is a great question, but as far as I know not a great deal is known about the process. The nuclear membrane, as depicted in textbooks, is contiguous with the endoplasmic reticulum. So when the nuclear envelope breaks down it would seem like the membrane components join a pool of structures poised to reform. In the first published experiments using nuclear extracts from the eggs of X. laevis, just adding purified DNA from bacteriophage lambda could enucleate membrane formation.

According to this book, during disassembly of the nuclear envelope, the nuclear membranes are broken down into vesicles. The nuclear membranes reform at the end of mitosis as the vesicles bind to the surface of chromosomes and fuse with each other to form a double membrane around the chromosomes (how this happens is not clear, except that integral membrane proteins and lamins may be involved, but physical contact is supposedly the first step).


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Non-cumbersome respiration sensor for sleep study?
I'm working on a project where I collect ECG signal from multiple volunteers, derive ECG derived respiration(EDR) from the timestamped ECG signal and calculate the cross correlation between EDR and Respiration signals collected from NeuLog device which is treated as reference respiration signal. The problem is that the NeuLog moniter, although widely in use for monitoring respiration, is very cumbersome and uncomfortable for the volunteers to wear and restricts breathing. Is there any alternative respiration monitering devices which doesn't have to be strapped around the chest and less cumbersome to wear?
The following are the other requirements.

Respiration signal should be time stamped(to synchronize with ECG signal).
Minimum Sampling rate of atleast 5sps.
Should collect data offline for atleast 10 hours in single charge of the battery.

I found this device which seems to be more comfortable than NeuLog but it is not clear whether it measures only respiration rate or can also log Respiration signals along with timestamps.
If anyone knows any alternative products meeting the above requirements, please do share the details.


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Do I need to serially dilute E. coli cultures for optical density measures?
I am expected to track cell growth by measuring the incubating culture's cell concentration every 30 minutes or so. So my questions are: Why do I need to do serial dilution (assuming that I do)? Why can't I just fill up a cuvette with the cuvette's volume's worth of incubating culture and measure that against the blank every 30 minutes? And if I do need to dilute, how far should I dilute (1:100, 1:1000, etc)? This is for a culture filled with E. coli.

One is not normally required to serially dilute E. coli cultures for spectrophotometric measurements, at least in the experiments where the OD value is important.
For most protein expression work, the consensus is to start the induction at OD 0.6, and for most chemically competent cells, the optimal OD ranges from 0.3 to 0.8 depending on the competency protocol. At no point in time do you need to perform dilutions, as they are all within the linear range of cell count:OD ratio.
The only time you need to dilute the culture is when you want to find the OD of a very concentrated culture (for example after 24 hours of vigorously shaken incubation).

Reading the optical density of a log phase microbial culture at a fixed wavelength approximates the Beer-Lambert law where A = ecl. This relationship is not linear as the Absorbance approaches 1.0 so at higher cell densities you will eventually underestimate the cell density of the culture. Likewise the law is not accurate below an Absorbance below ~ 0.05, so a 10-fold dilution should be fine.  Eventually the culture's growth will slow down.

You should dilute (not necessarily serially dilute) if:

You are exceeding the concentration range detectable by the machine
Scattering starts overwhelming absorption (at high cell densities scattering will overwhelm absorbance). In such cases you can use a turbidimeter.

As such there is no issue of the law not holding true at certain limits of absorbance.
So a general thumb rule for dilution of cells is that the suspension should not look very turbid (You should be able to see your thumb from the other side of the test tube ;-) ).

It depends on your purpose, but you could seed cells into multiwell plate and let microplate reader monitor the growth. Some microplate readers can incubate cells at a temperature you set, shake the plate, and monitor OD.


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How to prove that pork meat has parasites
I suspect that the pork sold at a certain shop is infected with the parasite pork tapeworm (Taenia solium).
Is there a way I can prove this without special equipment? Would it work to leave the raw meat in the fridge (at 4 degrees Celcius, or higher?) for a week or so and the worms will come out of their eggs and grow big enough for the eye?

Short answer
T. solium infection can be identified in pork meat by visual inspection.
Background
The stage of the life cycle of the tape worm T. solium in pigs is characterized by cysticerci, which is the larval stage consisting of a protoscolex (head) of the tapeworm. Humans are the definitive host, which means they are the species in which the parasite completes its life cycle, reaches adulthood and is able to produce eggs.
The larvae are observable in pork meat, and cysticercosis is generally identified during slaughter when cysts can be seen in muscle or organs (Fig. 1).

Fig. 1. T. solium cysticerci. (A): as seen in infected pork. (B): excised into a Petri dish. The white dot in each cyst corresponds to the scolex. Source: Garcia et al. (2011)
It is not until these cysticerci are ingested by humans that the tape worm starts to develop fully into a meters-long tape worm, as it enters the next and final stage of its life cycle (Fig. 2).

Fig. 2. Taenia life cycle. Source: CDC
Hence, leaving the meat in the fridge will not induce growth, as a human is needed to induce outgrowth of the protoscolex into the mature tape worm.

Reference
Garcia et al., Lancet (2011): 362 (9383): 547–56


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Would it be possible to regulate proper phosphorylation so the UPR wouldn't initiate a reactionary cell death in important cells?
In studying the correlation of folded versus unfolded proteins and their impact on neuro-degeneration, it looks like improper phosphorylation in the chaperones (at least, in part) causes the mis-folding of proteins? If so, would it be possible to regulate proper phosphorylation so the UPR wouldn't initiate a reactionary cell death in important cells?

I think it is lot more complicated. Because amyloid and prion develop intercellular space, while chaperones are expressing inside of cells.

Please define UPR.

UPR: Unfolded Protein Response.


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Why is triclosan not considered an antibiotic?
Triclosan is a chemical often referred to as a "biocide" instead of an "antibiotic". However, its mode of action seems to suggest that it is an antibiotic.

Triclosan binds to bacterial enoyl-acyl carrier protein reductase
  (ENR) enzyme, which is encoded by the gene FabI. This binding
  increases the enzyme's affinity for nicotinamide adenine dinucleotide
  (NAD+). This results in the formation of a stable, ternary complex of
  ENR-NAD+-triclosan, which is unable to participate in fatty acid
  synthesis.

This is nearly identical to the action of many other antibiotics, such as penicillins (inhibits cell wall synthesis enzymes), quinolones (inhibit DNA gyrase) or sulfonamides (inhibit folate synthesis).
In fact, this paper describes the mechanism of resistance to triclosan and notes that it is identical to many antibiotics. Why then, is triclosan not classified as an antibiotic and is still prophylatically used in so many places (such as hospitals)?

"Antibiotics" mean a versatile group of compound released from a microbe (term commonly include bacteria and fungus, sometimes other-group of microbes such as algae etc), that kills some-other specific group of microbes. So to call a compd as antibiotic, it have to be 1. synthesized by living microbes, 2. Acting on certain-other specific-groups of microbes.

I agree with @Chris that this is mostly a matter of definitions -
Greenfacts defines biocides as:

According to the Biocides Directive (98/8/EC), biocidal products are those that are intended to destroy, render harmless, prevent the action of, or otherwise exert a controlling effect on any harmful organism by chemical or biological means. Examples include disinfectants, preservatives, antiseptics, pesticides, herbicides, fungicides and insecticides.

and antibiotics as:

Antibiotics are widely used as medication against disease-causing bacteria. However, bacteria can acquire resistance to particular antibiotics through mutation or gene transfer.

So the key difference is that antibiotics act more specific and may induce resistance. Antiseptics such as alcohol stay active, even after repeated use, because they act broadly. Now that triclosan is argued to have a specific molecular target, it may have to be re-defined from a general biocide to antibiotic. This means that its widespread use may be alarming, and I quote from your linked article (Schweizer, 2001):

[Triclosan is used in a] multitude of health care and consumer products [and has] germicidal properties [and has] flooded the market in recent years in response to the public's fear of communicable bacteria.

Reference
- Schweizer, FEMS Microbiol Lett (2001); 202(1): 1-7

Your second quote specifically mentions "used as medication", and I'd say this is the real distinction, not the specificity or resistance-inducing effect.

@VonBeche - you mean that an antibiotic is always a medicine and biocides are not? I'm unsure about that.

I'd say this is consistent with the list of antibiotics on wikipedia https://en.wikipedia.org/wiki/List_of_antibiotics, those are all for oral / intravenous use. The list of common antiseptics: https://en.wikipedia.org/wiki/Antiseptic#Some_common_antiseptics, consists of stuff that you would definitely NOT want to take orally / intravenously.

Triclosan binds to bacterial enoyl-acyl carrier protein reductase
  (ENR) enzyme, which is encoded by the gene FabI. This binding
  increases the enzyme's affinity for nicotinamide adenine dinucleotide
  (NAD+). This results in the formation of a stable, ternary complex of
  ENR-NAD+-triclosan, which is unable to participate in fatty acid
  synthesis.

If you notice, you would see that this mechanism is attributed to low concentrations of triclosan when it acts as a bacteriostatic. Disinfectants, IMO cause direct chemical damage to cell (denaturation of proteins/destruction of the membrane etc) unlike antibiotics which inhibit some vital metabolic processes. Triclosan is generally used in the form of a disinfectant (at high concentrations). Even though its enzyme inhibitory properties have been studied, it is not systemically administered in the form of an antibacterial drug.
The terms antibiotics and bactericidal were coined when mechanisms were not really known. Even then, antibiotic is traditionally known as a substance that is produced by one organism (a fungus in case of penicillin) to prevent the growth of the other.
I would like to differ from Christiaan's opinion that antibiotics are substances against which resistance can be developed. It is possible to acquire resistance towards a conventional, broad spectrum, direct damage agent. For instance there are bacteria that can survive heat/UV/γ-rays (which are physical disinfectants). Microbes can also develop resistance to chemical agents and though I cannot cite an example at the moment, I can think about how the cell can achieve it. One way is to develop a stronger cell wall.
Also note that alcohol is not considered a disinfectant at concentrations < 70%. At much lower concentrations alcohol can actually serve as an energy source.
So I think this is the tacitly accepted definition:
Disinfectants are usually synthetic chemicals that inflict direct damage whereas antibiotics are primarily natural chemicals that inhibit some vital metabolic process.
The term bactericidal or biocidal denotes the consequence rather than the nature of the mechanism. Antibiotics can be bactericidal too. Many herbicides are inhibitors of chloroplastidial metabolism.

Nice addition +1. I think the question is quite prone to discussion, and an interesting one too!

I think this is mostly a semantic differentiation, when you look up definitions for antibiotics you can find very narrow which only include the classic and modern antibiotics, while others include almost everything which has an bacteriocidal (or also anti-fungal) effect, regardless of the mechanism.
The Wikipedia article on antibiotics contains the following paragraph, which I find pretty good as a definition:

Sometimes the term antibiotic is used to refer to any substance used
  against microbes, synonymous to antimicrobial. Some sources
  distinguish between antibacterial and antibiotic; antibacterials used
  in soaps and cleaners etc., but not as medicine. This article treats
  the terms as synonymous and according to the most widespread
  definition of antibiotics being a substance used against bacteria.


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Why do epithelial cells arrest in response to serum?
Primary epithelial cells, for example human mammary epithelium, fail to proliferate (arrest) in serum-containing medium. Therefore, a common growth medium for epithelium contains pituitary extract instead of serum (Hammond et al, 1984). This may be related to the fact that epithelium is normally not in contact with serum in the body.
On the other hand, many epithelium-like cell lines grow well in serum, and most tumor-derived cell lines are cultured this way. But it can be difficult to establish such lines from epithelial cancers: often, only fibroblasts grow out of tumor explants in serum-containing medium, while the (epithelial) cancer cells do not. In contrast to epithelium, fibroblasts increase their proliferation when exposed to serum, and this process is well studied (Iyer et al, 1999).

Why does epithelium arrest in response to serum? Are any mechanisms known? Is there any study of epithelium gene expression response to serum? Why is the behavior of epithelium so different from that of fibroblasts --- is there a physiological explanation, perhaps related to wound healing?
Is this true for all types of (human) epithelium?
Should we consider epithelial-like cells growing in serum to be adapted / selected? Have such cell lines then lost some part of the epithelial phenotype? Is this a serious artefact?

Any pointers to literature would be appreciated!

TGF-beta would be a good candidate. To cite:
"TGF-β inhibits G1/S progression in a variety of eukaryotic cell types. Among these, untransformed epithelial cells are particularly sensitive to the growth inhibition by TGF-β."
http://genesdev.cshlp.org/content/14/24/3093.full
Fetal bovine serum (FBS) contains a high level of latent TGF-β. Human serum as well has high level of TGF-beta (20-50ng/ml)
It is also possible that growth arrest is part of the induction of terminal differentiation by serum factor(s) such as TGFb.
"Type beta transforming growth factor is the primary differentiation-inducing serum factor for normal human bronchial epithelial cells."
http://www.ncbi.nlm.nih.gov/pubmed/2871553
Edit: got more reputation, so now I can post more than two links. Here is a review on TGFb signalling: http://genesdev.cshlp.org/content/14/6/627.full
Also a link to serum levels of TGFb:
http://www.ncbi.nlm.nih.gov/pubmed/16845225

Thanks, this is useful! Will continue to look in this direction.

I don't think that there is a one-size-fits-all answer to this question. There are different types of arrest and there might be different triggers depending on the epithelial cell type.
Even in the cited Hammond et al paper, note that the effect of serum is not an immediate arrest. Human mammary epithelial cells (HMEC) could already go through 3 to 4 passages in serum (at 1:10 splits), according to the Introduction to the paper; the improvement with the serum-free medium was to allow 10-20 passages. And even in that paper, near the end of the Results you will see a difference between HMEC and human keratinocytes in terms of response to calcium; calcium makes keratinocytes differentiate and lose proliferative capacity, while HMEC do best at high calcium.
Recent work has developed ways that can allow many types of epithelial cells (both normal and tumor cells) to proliferate indefinitely in culture, in the presence of 5% serum. Inhibition of the Rho-associated kinase ROCK is critical, as is the production of some yet-undefined factor by feeder fibroblasts. So even if some component of serum tends to lead to differentiation or senescence and growth arrest, that effect can be avoided.
Note, however, that the authors of this newer work do call the cells treated this way "reprogrammed," recognizing that they are not the same as the original epithelial cells in some important ways. What that "reprogramming" entails is under active investigation, and your concerns about selection, adaptation, and potential artifacts of culture are very important. But even if this is considered an artifact, understanding the mechanisms at work should produce some important advances in understanding epithelial biology.


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Why is Electrical Cardioversion contraindicated in AF and Digitalis Poisoning?
I am thinking why electrical cardioversion is contraindicated in atrial fibrillation with digitalis toxicity/poisoning.
Cardiac digitalis is also called digoxin and cardiac glycoside.
It is antiarrhythmic agent against supraventricular arrhythmias.
It is contraindicated in Atrial Fibrillation with digitalis toxicity.
The Pubmed's article about the topic is a stub without describing its Pharmacology.
Digitalis toxicity is a complication of digitalis therapy, here used for atrial fibrillation.
This may be due to kidney failure when the medication accumulates in the body.
Its treatment is activated charcoal and gastric lavage.
However, assume that these methods do not help in treatment or that we in acute digitalis toxicity.
I think the reason why we cannot recently do electrical cardioversion in digitalis poisoning is the high probability of repolarizing incidences so the likelihood to stimulate heart at the right moment is very small.
This is because digitalis poisoning is associated with cardiac disturbances: ventricular tachycardia, ventricular fibrillation, SA block and AV block.
Without knowing more precisely about the complication, I think the electrical cardioversion has high risk of failure.
Why is electrical cardioversion contraindicated in Digitalis Poisoning of AF treatment?

The mechanism of action of digitalis-like preparations based on inhibition of myocardial NA+/K+-ATPase as well as of cardiac conducting tissue. The inhibition of latter (conducting) is 2.5 greater than those of former (myocardial). This is why the main feature of digitalis intoxication are arrhythmias due to ectopic electric impulses and spontaneous depolarization (there is overloading of conducting system by Calcium as well as excess amounts of Noradrenaline released from sympathetic endings).
These metabolic changes in a case of digitalis intoxication could lead to irreversible ventricular arrhythmias after cardioversion - there are sporadic reports about this phenomenon. Based on these reports, it was thought that the use of digitalis during electrical cardioversion would provoke ventricular arrhythmias in patient even with clinically desirable concentration of digitalis.
In a study in patients with therapeutic nontoxic digitalis levels determined that these patients may safely undergo electrical cardioversion without reducing or withholding the dose of digitalis. Thus, the cardioversion is not contraindicated in a patient without signs of digitalis toxicity.
Although, the exact mechanism of the ventricular arrhythmias after cardioversion is not well understood, it is clear that mentioned above changes in electrolytes concentrations with electrical stimulation lead to premature beats overtaking restored sinoatrial pace. The rate of ventricular arrhythmias is in direct correlation with the level of the energy used for the cardioversion (this is why there is "pre-cardioversion" with low-energy pulses). Until these metabolic changes are not corrected, the resulting ventricular arrhythmias can be irreversible. This is why, digitalis intoxication is relative contraindication to electric cardioversion of atrial fibrillation/flatter.
Excerpt from the article mentioned:

Excellent sentence The rate of ventricular arrhythmias is in direct correlation with the level of the energy used for the cardioversion (this is why there is "pre-cardioversion" with low-energy pulses). I would like to get more understanding about the nature and characteristics of this energy. What is the energy form? Ellipsoid pulses? Which other energy pulses are provided along the main energy signal? Any more studies about this?

@Masi It is clear that the more energy was used for cardioversion, the more its influence on the conducting system and myocardium. Since, the metabolic changes did not allow "actual" ventricular cardioversion, the higher-enegly impulses would have greater arrhythmic effect.


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

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

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

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

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

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

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

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

@SanjuktaGhosh I have added some information about scavengers.

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

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


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Are there eukaryotes with fully working mitochondria but without mitochondrial genes?
Are there eukaryotic organisms with fully working mitochondria that do not have genes in the mitochondria?  By fully working, I mean ones which can carry out oxidative phosphorylation, unlike reduced mitochondria like organelles such as mitosomes in Giardia lamblia.
Is it possible to transfer all mitochondrial genes to the nuclear DNA and still have fully-functioning mitochondria?

No there aren't any organisms with fully functional mitochondria which (the latter) do not retain the minigenome.
On whether it is theoretically possible to transfer all the mitochondrial genes to the nucleus:
Perhaps it is possible and mitochondria may work just like lysosomes and ER, but I think that the responses will be greatly delayed. At present there are no mathematical models that can provide a better understanding of that possibility. Nonetheless, some studies have shown that chloroplasts and mitochondria also have redox dependent gene regulation by which the expression of some components of the ETC is regulated by the redox state of the quinone. This helps in optimization of the ETC; if all genes were in the nucleus then this would not be possible. This pheonomenon is, however, better studied in chloroplasts. See this review.


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Value of mathematical models in biology
Sorry if this is too much of a soft question or if it is too broad for this site.
As a person who has much more experience with math than biology, I've always been really interested in the mathematical side of biology. As I study math in biology, however, I am left with the question of "how is this actually useful?"
What kind of unique insight can mathematical models give us about biological systems that we couldn't just find experimentally?

Experiments are challenging. Thus all sciences model experimental results, often mathematically, so that future study can be simplified.

This is actually broad. There are a lot of applications of mathematical models in biology and there have been many books written on this topic.  See this related meta post

I also think this is too broad and unspecific. Mathematical biology is a huge topic with many different types of applications. However, these two questions might be useful to you: What physics knowledge can be applied to biology of organisms and ecosystems? and When are population dynamics models useful?.

This question is broad.
There are plenty of uses of mathematical modelling in biology.
Wikipedia
You may want to read the wikipedia article: Mathematical and Theoretical Biology.
Books
There are tons of books on theoretical biology. I am personally working in the field of population genetics, a field where much of the theory has been expressed mathematically. Here are book recommendations for this particular field.
On Biology.SE
We have a tag for mathematical-models (you used it in your post). You may want to see what kind of posts are tagged for mathematical-models.
To repeat @fileunderwater's comment, What physics knowledge can be applied to biology of organisms and ecosystems and When are population dynamics models useful? are examples of posts you may want to read.
What prevents predator overpopulation? will give you an example of an easy and classical mathematical model to describe population dynamics of predators and preys.

Personal historical/philosophical note: At some point physicists have started to describe the laws of nature with mathematical expressions and at that time many physicists didn't quite like the idea that physics could be described by math. Biology has gone through the same phase but much later. Early mathematical biologists developed the modern science of statistics (Francis Galton, Karl Pearson, Ronald Fisher). Biologists used existing mathematical tools such as diffusion processes (Kimura). Note that part of the work in the field of diffusion equations have been done by physicist (Einstein solved the 2D equations for diffusion processes). Note also that the dynamic of diffusion processes called brownian motion have been named after a biologist. Today, biology produces massive amount of data that require good computational skills to treat. The time when biologists had only to know how to recognize species is over, now there are few biologists left that aren't able to code in at least one programming language.

Models are often used to calculate the probability of certain biological outcomes. Such predictions are great help for prioritization of further studies or making other decisions.
Example: EPA uses an array of in vitro assays for fast and cheap analysis of thousands of potentially toxic environmental compounds (ToxCast and Tox21 projects).
Next, they use the obtained data to build mathematical models to prioritize chemicals for further more expensive and slow animal studies or to decide on administrative actions to restrict usage of high priority (most dangerous) chemicals. Their prioritization models integrate toxicity data and complex exposure models (including manufacturing and usage logistics, possibility of accidental exposure etc).


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Will tagging a protease with HlyA for secretion inactivate the protease?
We are looking to secrete the protease proline iminopeptidase by attaching the secretion signal HlyA to the protease in a gene circuit. Since the natural HlyA secretion sequence in Escherichia coli isn't cleaved from the protein, it will remain attached to the protease in the extracellular matrix.
Will the protease still function and cleave the peptide chain at the n-terminal proline residue with the HlyA signal still attached?

Unless someone has actually done this specific fusion and reported on the activity, this question won't have an answer. I can't find anything about proline aminopeptidase fusions, but enzyme-HlyA fusions have been done that retained activity similar to the wild-type protein (examples: cutinase, β-lactamase). Your fusion might work fine or folding might be disrupted after secretion (either by the tag itself or by the absence of chaperones, if required). In other words, you need to try it yourself.
Bacillus subtilis is commonly used for secretory protein production and may present another/better option.


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Are there constraints on where intron/exon boundaries occur with respect to the triplet codons of the reading frame?
I did a quick search (here and elsewhere) and couldn't find anything on this subject.
If all introns in a given primary transcript were spliced out in the same way, then this wouldn't matter.  But lots of eukaryotic transcripts have alternate splicing patterns so that one version of the mRNA will contain coding regions that are absent in other alternate forms.
The problem relates to maintaining an open reading frame, avoiding a frame shift and the attendant (and unpredictable) consequences. If a splice donor site occurs within the 3-base codon, it might require that the two (or more) alternate acceptor sites would be in the same relative position in a related codon.
The simplest solution to this problem in my view is to make sure that all splice donor and acceptor sites would be at a codon/word boundary.
Is there any evidence that this is true?

As pointed out by others this is not true. I just verified this for humans (annotations from gencode21).
Methodology:

Obtained the start points of the CDS for all genes
For each exon of each gene, calculated the distance between the CDS start and exon end
Obtained the remainder after dividing this value  by 3 (modulo)

Commands:

Command-1:
    awk 'BEGIN{FS="\t|;";OFS="\t"} $3=="CDS"{print $4,$9}' gencode.v21.annotation.gtf > cdsstart.txt

Command-2:
    awk 'BEGIN{FS="\t|;";OFS="\t"} NR==FNR{a[$2]=$1;next} ($3=="exon" && $9 in a){if($4>a[$9]) q[($5-a[$9])%3]++} END{for(i in q) print i,q[i]}' cdsstart.txt gencode.v21.annotation.gtf

Result:

position | # cases
_______________________
   -2    | 101191
   -1    | 100954
    0    | 99499

As you can see the exons do not necessarily terminate at the third position of the codon.

Here is exon size data of some random gene (human ROR-gamma).
Link: http://www.ncbi.nlm.nih.gov/nuccore/NM_005060.3
It gets cut at all three possible positions of codon:
exon 2  30
exon 3  86
exon 4  142
exon 5  513
exon 6  122
exon 7  133
exon 8  108
exon 9  111
exon 10 110
Alernatively spliced isoform B of this gene gets different first exon. At the junction codon ACA (isoform A) gets replaced with codon TCA (isoform B).

I don't have time to find examples right now but no, it's not true. You often get cases like this (lower case letters represent the intron):
ACCTGTaccttgcaacttgcatAGCTGAC

Which would be spliced to:
ACCTCTGAC

Note that the second codon consists of one nucleotide from exon1 and two from exon2. I'll try and update this with real world examples, but I can assure you it is possible and I have seen it quite often.

As Alex M shows, many lengths of exons are 3n+1 or +2. It seems cells do not care about in-frame.
In some cases, exon insertion by alternative splicing shift the frame and produce a short version of gene product or introduce premature stop codon (PTC). When PCT is recognized in cells, the spliced transcript is quickly degraded. This is called nonsense mediated decay (NMD).
Splicing machinery does not care about frame of CDS, and this makes various gene regulations possible.
http://genesdev.cshlp.org/content/24/21/2343.full
This review shows an example of NMD by alternative splicing. See the description about caspase-2.


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From a computer science perspective, how is DNA compared for various purposes?
I am very interested in privacy preserving technolgies, such as Microsoft PINQ and would like to see if this is applicable to DNA comparison.

Given that I don't have a background in biology, I would appreciate it if someone could tell me how DNA is represented in a computer (in computer science terms), and how DNA is compared in a binary format (or logical equivalent).

The privacy preserving technology I'm using allows the patient to have granular control over what DNA data they share, and how it's used. The receiving agency (medical research, FBI, fertility clinics) will receive cryptographic proof of a DNA result, without exposing all DNA values.
I suspect that each of the following use-cases focus on a certain subset of data, and if the same information was presented to all of them, it would be a breach of privacy:

Combined DNA Index System, or CODIS
State DNA index system (SDIS)
National DNA Index System (NDIS)
FBI's 13-Loci
Other government's DNA matching requirements for inclusion/exclusion
Disease susceptibility via single nucleotide polymorphism (SNP), and related heredity
Paternity tests
Evolutionary patterns

Furthermore, based on my independent research, I understand that there are many ways to determine the DNA of a given sample.  What I don't understand is if every test has the same output? (e.g. are all chromosomes are returned, vs only 23? (or less))
The value-add I am trying to provide the patient privacy, while fulfilling all legal, moral, and ethical disclosures of data requested of them.  The recipient will have assurance the data is authentic, despite the inherent double blinding of the field data.
The cryptography allows for

Redacting (or black out) certain values
Anonymously compare a numerical value, (greater than, less than, equal to) without disclosing that value.
Prove, or verifiably disprove, that a value is not in a certain list of arbitrary values.
The agency to know which DNA testing firm generated the results
The DNA testing firm to not know who the patient is, especially in cases of partial disclosure of DNA data.

Your response will help me contribute what I believe to be the moral, ethical, and socially responsible way to handling PII and DNA data.  (yes it will be open source)

DNA sequences are typically stored in FASTA format. There are indeed many methods to sequence DNA, on which depends the data that is returned (ie the output) and the analysis required. You're not going to sequence all 46 chromosomes in a single experiment. Analysis of CODIS markers, for example, only requires amplification of specific short tandem repeats (STRs) and does not even require sequencing.

DNA sequences are usually compared using BLAST (https://en.wikipedia.org/wiki/BLAST), which breaks sequences into short words which can be searched efficiently. However, that does require having entire sequences around somewhere, which might be a privacy violation.

From a computer science perspective, there's nothing at all special about DNA. It's stored as a simple ASCII text file consisting of repetitions of 4-15 different letters.
DNA, the molecule, is a long chain of nearly identical smaller molecules (nucleotides) joined together. The nucleotides differ only in which of four possible bases (A,C,T/U or G) they have attached. Therefore, when representing a DNA sequence, we only need to represent the bases.
There are also the so-called "ambiguity codes" which represent different possibilities:
IUPAC Code   Meaning
  A            A
  C            C
  G            G
  T/U          T
  M            A or C
  R            A or G
  W            A or T
  S            C or G
  Y            C or T
  K            G or T
  V            A or C or G
  H            A or C or T
  D            A or G or T
  B            C or G or T
  N            G or A or T or C

The vast majority of sequences, however, won't use the ambiguity codes and will only have A,C,T,G and the occasional N.
The most common DNA sequence format is FASTA, which consists of one or more sequences each of which has a header (lines beginning with a >) and 60-character long sequences. This, for example, is an excerpt of human chromosome 17:
>chr17
AAGCTTCTCACCCTGTTCCTGCATAGATAATTGCATGACAATTGCCTTGT
CCCTGCTGAATGTGCTCTGGGGTCTCTGGGGTCTCACCCACGACCAACTC
CCTGGGCCTGGCACCAGGGAGCTTAACAAACATCTGTCCAGCGAATACCT
GCATCCCTAGAAGTGAAGCCACCGCCCAAAGACACGCCCATGTCCAGCTT
AACCTGCATCCCTAGAAGTGAAGGCACCGCCCAAAGACACGCCCATGTCC
AGCTTATTCTGCCCAGTTCCTCTCCAGAAAGGCTGCATGGTTGACACACA
GTGcctgcgacaaagctgaatgctatcatttaaaaactccttgctggttt
gagaggcagaaaatgatatctcatagttgctttactttgcatattttAAA
ATTGTGACTTTCATGGCATAAATAATACTGGTTTATTACAGAAGCACTAG
AAAATGCATGTGGACAAAAGTTGGGATTAGGAGagagaaatgaagacata

So, in conclusion, there's nothing special about DNA. If you're writing software that compares DNA sequences, you are writing software that compares ASCII text. You can hash it, salt it and anything else you might want to do.
The only thing you should be aware of is that minor variations are very rarely meaningful. The level of identity you will need will depend on the precise biological question being asked but as a general rule, a single nucleotide difference is as likely to be a sequencing error as a real difference. You will need to collaborate with biologists in order to set up the right threshold for whatever your project is looking at.

Thanks this is a great primer! Do you know why some letters are lowercase? Also do you know where I can find sample data for any of the above listed purposes (paternity, disease testing, other examples...)?

@LamonteCristo lower case can mean various things depending on the source of the sequence. It is often used to indicate i) low quality data, cases where sequencing errors are likely or ii) masked sequences, repetitive elements and the like. You probably don't need to worry about it. As for sample data, no, sorry. I've never worked with that sort of thing. Sample sequences in general are trivial to fins (have a look at the NCBI nucleotide database.


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Measuring body size in flies/insects

"Mesothorax length (the distance from the tip of the scutellum to the
  most anterior part of the mesothorax)"

From Bergland et al 2008.
Would that be this distance (green line)?

If not, how would you describe that distance?

I think you are correct, but I'm not an expert in Diptera/Drosophila morphology. Since the prothorax (pronotum) and metathorax are greatly reduced in flies, you mostly see the mesonotum in dorsal view, and this includes the scutellum. Personally, I think it would have been more accurate of them to label this structure mesonotum, or at least dorsal mesothorax length, since mesothorax could just as well imply a ventral view (mesosternum).
More information can be found at this webpage: Flies - Morphology and anatomy: Thorax, which state that:

The mesonotum occupies most of dorsal view of the thorax. In order anteroposterior we can identify four parts, called as follow (McAlpine, 1981): prescutum, scutum, scutellum, and postnotum. The scutum is the most large, condition considered apomorphic for the entire order of Diptera.

Also see this picture of the mesonotum from diptera.net


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Differing number of "things" in mammals
I'm not a biology expert, but I have often wondered about the following facts of life:
All mammals have precisely 5 fingers on each of our 4 extremities. Granted, some may not be seen, but the bone structure of 5 fingers is there in all mammals, from whales to bats to humans. This, I guess, tells me that changing the number of finger bones is, genetically speaking, fairly difficult (as it never happened during the evolution of mammals.
On the other hand, pigs have 12 nipples, dogs have 6, and humans have 2. Pigs have 44 teeth, dogs have 42, and humans (the lucky ones) have 32. This, I guess, means that it is easy to change the number of teeth in a species, as this happened often during the evolution of mammals.
My question is this: What is the reason behind this discrepancy? Why is it that much easier to change one thing and not the other? And a subquestion: why do we still have 32 teeth when the 4 wisdom teeth cause nothing but trouble? Wouldn't having only 28 teeth be an evolutionary advantage?

The number of fingers is not really same for all mammals: See this picture. It shows limb bones of some even-toed ungulates. And whales have totally lost the hindlimb. So your presupposition is not correct.

The genes, and the complexity of the genetic networks, underlying each trait are not necessarily the same.


text:
What is a genetic marker?
In DNA sequencing and analysis, what is a genetic marker? I've heard that microsatellites are genetic markers? Those are repetitive strands of bases such as GCAGCAGCAGCA etc. Why are they markers and what defines a genetic marker?
There are many different KINDS of genetic markers as defined by wikipedia, RFLP, SNP and many more. But when you click these, you get a technique not a sequence. So I'm confused as to whether markers are techniques to find DNA sequences or if they are literally DNA sequences?
If they are literally DNA sequences, are they sequences that everyone has?
Example of RFLP:

In molecular biology, restriction fragment length polymorphism, or
  RFLP (commonly pronounced “rif-lip”), is a technique that exploits
  variations in homologous DNA sequences.

Is there something missing from Wikipedia that's confusing you?  https://en.wikipedia.org/wiki/Genetic_marker and the links on that page seem quite sufficient to me.

@WYSIWYG the OP is trying :) I asked that they break their question into smaller ones and they've done so. Paze, WYSIWIG has a point though, what is it you don't understand about markers? The first line of the WP article seems clear enough: "A genetic marker is a gene or DNA sequence with a known location on a chromosome that can be used to identify individuals or species." What more do you need?

I made some edits to my question. Hopefully it is clearer now.

Can look ask, lf you had a genetic marker say DYS392=11 and someone else had DYS392=12 because there is only one point difference between the markers will they be related to say race or ancestry ?

Genetic markers are sequences of DNA that tend to co-occur with some biological property, in a population.
Examples
E.g. Imagine you have 200 individuals in a population. 100 individuals have some sequence GGGCCCGGGCCC at some locus (position on the genome), and those 100 individuals have blue eyes. The remaining 100 individuals have AAATTTAAATTT, at the same locus and happen to have other eye colors (green, brown, etc). Then GGGCCCGGGCCC is a marker for the biological property that is "blue eyes".
Other biological properties with associated markers can include the following: (i) predisposition to having a certain disease, e.g. Alzeimers, (ii) high intelligence, (iii) and even the presence of another gene, that is you can have markers for the biological property that is "presence of gene X".
Markers of genes vs. the genes themselves
One often finds that markers for certain biological properties are the genes themselves. But this is not obvious unless one sequences the entire genomes of several individuals of a population, and doing so is expensive. It is cheaper to rely on screening for markers.
One marker to many properties, many markers to one property
You do not always have to have one marker per biological property, there may be several markers scattered across the genome that are all associated with some biological property. You can also have a marker associated with several biological properties.

As hello_there_andy (and also the Wikipedia page) has indicated, genetic markers are DNA sequences that can be used to distinguish individuals (can also be tissues, cells, etc.).
Linkage of a phenotype with genetic markers is used to identify regions of the genome that are likely causative for that phenotype, as hello_there_andy says, but there is nothing inherent to how a marker is chosen that says it has to be linked to any phenotype. Markers are typically chosen for an analysis because they are easy to measure and track, individuals differ at the locus (so you know that if your phenotype of interest segregates perfectly with the marker, it's unlikely to be chance), and they cover the genome (or the region of the genome you already know is linked) appropriately, among other things.

You put it concisely, but please be careful of using jargon like "Linkage", I will reward you upon replacing jargon with concrete analogies or clear definitions

@hello_there_andy I added a link to the Wikipedia page for linkage analysis. As genetic linkage is the topic of entire lectures in undergraduate genetics, I don't think I can summarize it in a few sentences, but that should be a starting point for the OP if he/she has further questions.

A genetic marker is, by empirical definition, something that you can unequivocally place on a genetic map.  A genetic marker may be an allele of a known gene that confers either a dominant, or a recessive phenotype. Alternatively, a genetic marker could be either a restriction fragment length polymorphism--whose segregation can be detected by either a Southern blot or a PCR experiment, or a single nucleotide polymorphism--whose segregation could be detected by a PCR experiment, or by DNA sequencing.
If two genetic markers segregate independently after a genetic cross the we say that they are unlinked--by which we mean they map to separate chromosomes. If two genetic markers do not segregate independently after a genetic cross (i.e., a mating) then we say they are linked--by which we mean the map to the same chromosome.
Knowing nothing about chromosomes, or DNA, it is still possible, given enough genetic markers, to construct a genetic map for an organism. All of the markers that map as if they are linked to each other are said to form a "linkage group".  When there are enough genetic markers to identify all of the linkage groups then the number of different linkage groups will equal the number of chromosomes (this assumes one crossover per chromosome during meiosis).
It is important to remember that chromosomes can only be seen with a microscope, cytologically, typically after fixation, and staining, whereas linkage groups, and genetic maps, do not require, or rely on, chromosomes. A genetic map, made up of different genetic markers, is an abstraction.  In some cases a genetic marker can actually be placed on the physical map of a chromosome--for example, in a species with a sequenced genome--this allows us to coordinate the genetic map with the physical map (for that locus).


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Background correction when reading ELISA with TMB substrate
I'm doing some ELISA development, and I'd like some justification/best practices for background correction. I'm using a horseradish-peroxidase (HRP) detection system along with a TMB substrate and an acid-based stop solution, which is quite common. When TMB is cleaved by HRP, it produces a blue (maximum absorbance (Amax) of 650 nm) product. The addition of the acid not only stops the reaction for endpoint detection, but it amplifies the signal two- to three-fold, and turns the solution yellow, so that it should be read at its Amax of 450 nm. The acid itself supposedly has an Amax of 540 nm, which is why you should use that wavelength for background correction, subtracting it from the A450. Other sources claim the A540 reading is supposed to correct for "optical imperfections" in the plate.
Using either of these explanations, one would assume that the A540 would be relatively uniform across the plate, independent of the A450 of the same well. However, in my experience, that is not the case at all. My blanks and negative controls are averaging about 0.041 absorbance units (AU) at 540 nm, with an average A450 of about 0.065. However, an A450 of 0.9 gives an A540 of 0.051, 1.4 gives 0.6, 2.0 gives 0.73, and 3.5 gives about 0.14. The absorbance spectrum (Fig. 2) of the substrate appears to be quite minimal at 540 nm, so why am I seeing this dose-dependent increase as the A450 increases?
More practically, how should I do background correction? Currently, I'm subtracting each individual well's A540 from its A450. Should I continue this practice, or should I determine an average plate background at 540 nm using my blanks and negative controls, and subtract that value from each individual A450?

Using different wavelength for reference give some advantages. You can measure a baseline of each well. All well might not have the same baseline because each well might not be the exactly same as others. In addition, you could make scratches on it, you might touch the bottom, or you get some dirt from your bench. And this can be corrected by A540 in your case. So, variations at a lower range are not much concerned. Sometimes, even if you choose a wavelength where the absorbance seems not to change after reaction, there might be a small change. This is not concerned ether, because both absorbances are concentration dependent unless states in solution do not change (froming complexes or something like that).
But still, you get high background from samples showing 1.4 or more at A450. I do not have experiences for this substrate, but you might want to think several possibility:
1)You might get bubbles on the top of your solution in the wells,
2)You might not get accurate values because OD is too high,
3)The solution might get precipitates
4)This may be a very less possibility, but some secondary reaction occurs.
For 2), 3), and 4). You might want to check linearity by drawing a standard curve, and avoid to use the range deviating from the liner relation.
PS
I should've mention that you would check the specification of your plate reader. OD=3 could be way to high to measure it. Because light intensity decreases to one thousandth though 1 cm light path at OD=3. It is very hard to measure such weak lights exactly. Probably many specifications of plate readers say you could measure ODs up to around 2, but some people think it is ideal to measure ODs up to around 1.


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What's a segmented copy number profile
I am studying copy-number variation. I am reading

C. H. Mermel, S. E. Schumacher, B. Hill, M. L. Meyerson, R. Beroukhim, and G. Getz, “GISTIC2.0 facilitates sensitive and confident localization of the targets of focal somatic copy-number alteration in human cancers,” Genome Biol., vol. 12, no. 4, p. R41, 2011.

Here, it is written that

Segmented copy number profiles represent the summed outcome of all the SCNAs [somatic copy number alterations] that occurred during cancer development. Accurate modeling of the background rate of copy-number alteration requires analysis of the individual SCNAs. However, because SCNAs may overlap, it is impossible to directly infer the underlying events from the final segmented copy-number profile alone.

It is not clear to me how a segmented copy number profile represents the summed outcome of all the SCNAs. Is it because different alterations can be present in the same sample, or can alter the copy-number in different moments, or both?
And, do they overlap spatially, temporally, or both?

Yes, one sample can contain different alterations. For each patient there is typically one tumour specimen that is removed. That specimen may be divided up into several samples (e.g. one for DNA sequencing, one for RNA sequencing, one for methylation microarray, and one for copy-number variation microarray), however each sample contains thousands of individual cells and two adjacent cells may have different CNVs (depending on their clonal ancestry, etc.). In other words, a tumour is a heterogeneous collection of cells. For some tumour types there can even be healthy cells mixed in.

Hi, can you please put it in an answer, if it's an answer.. and with references.. so I can accept it.

There you go. Done!

Yes, one sample can contain different alterations. For each patient there is typically one tumour specimen that is removed. That specimen may be divided up into several samples (e.g. one for DNA sequencing, one for RNA sequencing, one for methylation microarray, and one for copy-number variation microarray), however each sample contains thousands of individual cells and two adjacent cells may have different CNVs (depending on their clonal ancestry, etc.). In other words, a tumour is a heterogeneous collection of cells. For some tumour types there can even be healthy cells mixed in.
The term in the literature is clonal evolution, there is a nice image in this article: Tumor Heterogeneity

To directly respond to the quote presented,

Segmented copy number profiles represent the summed outcome of all the SCNAs [somatic copy number alterations] that occurred during cancer development.

As a tumor progresses, genomic instability can often increase.  That is, more and more SCNAs occur.  Because of this, one SCNA can overlap another.

For example, look at the tumor progression of the chromosome above.  Let's say you have a loss on this chromosome (Event 1 the MATERNAL chromosome).  This loss can occur by many mechanisms which I won't go into.  The tumor proliferates, splitting many times, and mutations are accumulating.  These mutations can cause more events to occur, and perhaps on this same chromosome arm, the distal part of the remaining copy is duplicated (Event 2 the PATERNAL chromosome).
In the copy number profile, it will look as though you had a loss on just an interstitial part of the chromosome.  But looking closely at the data, you can see that you've lost heterozygosity on the distal portion of the chromosome as well (we now have two copies of the PATERNAL chromosome, and 0 copies of the MATERNAL).  This is a simplified example, and many events can occur along the same chromosome arm.  If the paternal chromosome holds a mutation, this can mean a selective advantage for the tumor or resistance to drug therapies.
Therefore, the CN profile represents a snapshot in time of what the copy number state was at that moment, with no explicit information on how that copy number state was obtained.


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How can electric fields inhibit tumor growth?
In MIT's Technology review it is explained that electric fields can cause dividing cancer cells to explode, while these fields have no significant impact on non-dividing tissues. The original research was done by Palti et al.
What is the mechanism behind this? It does not seem to be related to thermal effects.
Edit: The treatment in question seems controversial. A clinical trial showed improvement but it is not rock-solid data.

Could you link to the trial paper?

@RoryM http://www.ncbi.nlm.nih.gov/m/pubmed/15126372/

http://en.m.wikipedia.org/wiki/Alternating_electric_field_therapy

I am deeply suspicious of this. It's not theoretically impossible but if it worked the way it is supposed to work patients should experience hair loss.   It's been shown to be not worse than chemo for treating recurrent glioblastoma, but that's a far cry from a real benefit.

I edited your question somewhat in terms of style. Please feel free to roll back.

@Resonating: Even if it is only as good as chemo that would still be great news since it can adjunct on top of chemo with negligible side-effects.

In a PNAS paper by Palti's group (2007) they explain the hypothesis behind the technique:
They reason alternating currents of 100 kHz to 1 MHz specifically affects dividing cells and thereby targets cancer cells. Note that this is the same basic idea as chemotherapy and radiotherapy, which also target dividing cells mostly. The mechanism of action of alternating electric fields on dividing cells is though to be the result of a specific effect on the  bridge separating the daughter (cancer) cells during cell division (Fig. 1). They think it interferes with spindle tubulin orientation and induces electrophoretic effects (Kirson et al., 2007), resulting in a pile-up of cytoplasmatic organelles at the cleavage furrow. This is thought to interfere with cytokinesis, and to lead to cell destruction** (Kirson et al., 2004).
Note it is the frequency that differentiates between the various effects of current stimuli. At very low frequencies (1 KHz) electric fields stimulate excitable tissues through membrane depolarization. At higher frequencies this excitatory effect is lost. At very high frequencies (>1 MHz) tissue heating results (e.g., microwave ovens).  Hence, alternating electric fields of intermediate frequencies (10 kHz to 1 MHz) were considered not to have any meaningful thermal effects (Kirson et al., 2004).

Fig. 1. Palti's electric field hypothesis. Source: Kirson et al. (2007)
References
- Kirson et al., Cancer Res (2004); 64: 3288-95
- Kirson et al., PNAS (2007); 104(24): 10152–57

This is just a hypothesis, there are unanswered questions such as why does it have little/no side effects like hair loss that normal anti-mitotics do.

@KevinKostlan correct, it's a hypothesis. The reason why there is no hair loss is that the electrical field was applied locally via electrodes, so there were no systemic side effects reported.

@AliceD The missing hair loss is kind of strange. We expect an effect on the deeper lying brain but see no effect on the hair bulbs which are located directly in the skin? I don't believe this.


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What is the difference between a spore and a cyst?
Last year I read a course in biology. During that course I learnt that Protozoa like Lamblia intestinalis or Entamoeba hystolitica form cysts in unfavourable conditions.
This year I read a course in microbiology. I learnt that bacteria like Clostridium perfringens or Bacillus anthracis form spores in unfavourable conditions. So far so good. But then I learnt that prokaryotic Borrelia burgdorferi can form a cyst, not a spore.
Firstly, I would highly appreciate any comments that would cast some light on these terms.
Secondly, I would also like to know if the spore inside, say, B.anthracis is the same organism as B.anthracis that produced the spore. Does a spore and the bacteria that produced it have the same DNA sequence? In other words, if I were a sporeforming bacteria, would my spore be myself, my bodypart or my child?

I'd like to draw your attention (if you haven't already seen it) to the comments by Souvik - I've edited my answer a bit, but hopefully someone more knowledgeable will come in.

I am in a biology course right now and am learning a lot from it.
A spore is all the important parts of the cell gathered up and get cased up like a hard-shelled suitcase.This spore can survive and reproduce when the right conditions come up.

The bacterial spores you are referring to are called endospores. The spore is formed during unfavorable conditions, by duplication of the bacterial chromosomes, and consequent envelopment by various membranes and protective coatings (while still within the original cell). The spore is dormant and remains so as the outer cell degrades during harsh conditions, releasing the spore. I guess I'd call the spore a clone of the original?
You may enjoy reading the relevant sections in this book, which go into greater detail.
edit: as Souvik has pointed out, this is only one type of "protective" spore. Actinomycetes also form spores, via differentiation of the cells, and cyanobacteria form akinetes also via differentiation (but this structure is not as durable as endospores).
Information about cyst formation is difficult to find, but in bacteria it appears to develop via changes in cell wall composition.

@ddr3 why are you referring to only a specific sub-group of bacterial spores??....I am a li'l rusty on this section...but as far as I know akinetes & actinomycetes also form spores...which are not endospores....

@souvikbhattacharya ah, I missed that on the page. I think I've conflated two different things - I'll try to edit my answer but I'm not an expert on this topic. Please feel free to edit it as well.

dd3 summed up the 1st part of your q nicely.....now 'bout the second part...bacterial spore-s (not necessarily endospores only...but akinets & spores produced by actinomycets) are produced by simple mitosis...so the genetic make-up stays the same as the parent cell.....so if  you were a spore-forming bacteria, the spore would be essentially you..in scientific jargon...your "clone"...

Well, certain bacteria form endospores to tide over unfavourable circumstances. The bacterial cell withdraws its contents so as to form a spherical-shaped mass. This spherical mass is still covered by the original cell wall of the bacterium. This microscopic rounded  body  covered by the cell wall is called a endospore(endo : inside).It is just like a tortoise tucking its body into its shell. Some other bacteria , to overcome unfavourable conditions develop a hard, protective covering called cyst around themselves. When the conditions become favourable, the cyst ruptures and the bacterium emerges, grows and reproduces. In this case, the bacterium forms a protective covering, while in the former, the cell wall is the protective covering. That, young man, is the difference between a spore and a cyst.

Thank you for your explanation. I am wondering now if in order to form an endospore a bacterial cell has to withdraw all of its contents. Bacillus anthracis has an endospore within itself. This endospore is less than the bacteria surrounding it. What is more, this bacteria is still active while having an endospore within.

A spore is the reproductive part having a protective covering as a spore for its germination has to face harsh environmental conditions such as air currents whereas cyst is the group of cells which come together to protect themselves from harsh conditions. Cyst has nothing to do with the reproduction of the cell.

Welcome to Bio. A reference would be appreciated to allow for background reading.


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Do humans have skin cells that trigger oxytocin release in the brain?
I was reading an article by Montgomery on the therapeutic effect of pets (Boston Globe, January 12, 2015), and I found this quote:

All animals appear to have cells directly under the skin that activate oxytocin in the brain. So gentle touch — from grooming your
  horse’s coat to making love with your spouse — is a powerful trigger.
  But so is simply thinking about someone you love, whether it’s a
  person or a pet. And in fact, a small study published this fall at
  Massachusetts General Hospital found that MRI scans of women’s brains
  lit up in the same areas when shown pictures of their pets as when
  shown pictures of their children.

Do humans have oxytocin triggering skin cells or formations under the skin? If so, are there higher concentrations of these cells in certain areas of the body? In the human erogenous zones, like neck, lips, etc?

Short answer
Oxytocin release has been associated with the cutaneous low-threshold (CT) afferent fibers in hairy skin.
Background
Oxytocin is released from the paraventricular nucleus in the brain in response to low intensity stimulation of the skin, such as touch, stroking and warm temperatures.
In a recent review Uvnäs-Moberg et al. (2015) report that the specific sensory nerve type mediating oxytocin release in the brain is unknown. Although myelinated somatosensory fibers mediating the discriminative sense of touch may be involved, a more likely candidate mediating affective touch are the unmyelinated low-threshold mechanosensory nerves, called C low-threshold mechanoreceptors (CLTMs) in animals or C-tactile afferents (CTs) in humans. Their terminal morphology (i.e., the skin receptor they connect to) is currently unknown. The fibers have been characterized mainly through  electrophysiological and electron microscopy research (McGlone at al., 2014).
The association of CT fibers with affective touch stems mainly from the finding that their activation patterns with various stroking velocities correlates with subjective pleasantness ratings. Specifically, the relationship between brush-stroking velocity and firing rate was distinctly different between CT and myelinated afferents. CTs showed an inverted U-shaped relationship,
whereas mean firing rates increased monotonically with brushing velocity in all myelinated afferents (McGlone at al., 2014).
However, CT fibers have only been identified in hairy skin in mammals, and the fibers mediating affective touch through glabrous skin (including the fingertips, palms and lips) are unknown (McGlone at al., 2014).
References
- McGlone et al., Neuron (2014); 82: 737-55
- Uvnäs-Moberg et al., Front Neurosci (2015); 5(1529): 1-16

to clarify - are hairs involved in triggering those fibers? For example, would a person who undergone laser hair removal feel the same as a hairy person?

@AlexStone:  Their terminal morphology (i.e., the skin receptor they connect to) is currently unknown This includes the hair follicle receptors.


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Are Humans Considered Keystone species?
Do humans have a huge impact on the ecosystem ? is it possible for other animals to live without us ?

Welcome to Biology! Homework questions are welcomed, but it should be accompanied by some evidence of research effort before it will be considered.

@Remi.b - Someone has undermined my authority with a brilliant answer :)

I am voting to close as homework question.
I felt like I would give you a few hints though.

is it possible for other animals to live without us?

Life on earth have existed for almost 4 billions years. Animals have existed for about 600 millions years. Modern human (AMHS) have existed for 0.2 million years.

Do humans have a huge impact on the ecosystem?

Here are just a few pictures taken by airplane of agricultural lands

and a koala searching its home after a rapid man-made deforestation

I like the aerial pics but they don't show animals :)

ha ha I inverted the OP questions though. I fixed it. The pictures were there to adresse the question of whether human affect their ecosystem (not talking about animals specifically). But I added a picture of Koala just for you @AliceD

oh no, not a remi-alone-in-the-world koala.... That is so sad.... I nearly not +1'd because of this painful addition

I call BS. The photo has clearly been cropped to hide the vast koala paradise of eucalyptus and...and...what else do koalas like? anything? ...just above the frame.

@Corvus yes maybe. This (and other similar) picture went kinda viral in the past weeks. If it was to be true that the koala was living at this exact location before, then it was probably not too far away during the deforestation and therefore, there must be some green stuff not too far outside the frame of the picture anyway.

@Remi.b, I'm just kidding of course. The koala picture is a nice touch in this great answer!


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Can someone identify this plant?

Can someone identify this plant? It was growing under my 2 year old's climbing wall / play house thing. I live in West Virginia, USA and it's currently June 3rd (if that helps from a climate standpoint).
I know there are some potentially dangerous invasive plants like the giant hogweed. I hope someone here can help me identify this and give me any tips on what to do about it if it is in fact hogweed.

My guess, some kind of wild lettuce.

Looks similar to spiny leaved sow thistle, but I'm no expert on plants.

Your question is fine but I would request that you clearly explain your geographical location instead of using the US state codes. We have users from all over the globe and not everyone would be aware of these codes. Also, it is good to describe the climate and other geological details especially if the place you are referring to is not likely to be known by many (in any case, it is generally a good practice and your post becomes more useful to others).

As @dd3 stated, it's a spiny (or prickly) sow thistle. It's an annual common in most of the US.
The leaf itself does not have a stem, and if you break the central stalk, it should be hollow and there should be a milky exudate. The plant spreads by fluffy seeds produced from a small dandelion-like flower.
If you pick it while young, it won't hurt (as much); if you prevent it from flowering, it should not spread, although unsprouted seeds can sprout still for a few years (it can come in on the wind as well.)

Prickly Sowthistle


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What is the name of this flower? The photo was taken in the Okanagan Valley, British Columbia
This little flower was growing on dry ranchland in Kelowna, it flowered in April:

Looks a lot like Claytonia lanceolata

Yes it is.rundown


text:
Primer heterodimer problem
I design my primers in Primer3PLUS and analyze them in Oligoanalyzer3.1, A big problem that I have this is that I got very nice output in NCBI-Primer BLAST for their specificity but a very negative ΔG for self or hetrodimer even under -7 or-13. is it possible use them for PCR by adding DMSO or Formamide? what other way may be helpful?

Is it possible for you to provide the primer sequences. Sometimes it may not really matter because the primer dimer may not be extended by the polymerase. What is the Tm of primer-template and primer-primer pairs. You may not need DMSO at all.


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Flower identification (England, late May)
I took this photo near Stratford upon Avon by the side of a road. Can anyone identify this flower?

Do you have a closeup of the petals?

@dd3 Unfortunately not, sorry.

MY guess would be Centranthus ruber coccineus, also known as red valerian. See this picture (from here):

Could be pink allium, considering the thickness of the stem?

Allium is an onion; they're monocots (would have blade-like leaves from base, not stem.)


text:
How are behaviors genetically coded in animals?
I am curious as to how complex behavior is passed down genetically? For example, how is the building of a web genetically coded in a spider? And how is the complex behavior of constricting prey coded into a boa? As these critters do not get raised by their parents, and hence cannot learn to copy these behaviors, it has to be genetically imprinted. How?

Some will probably be genetic, yes, but many will be learned. Just like you learned from your parents and will teach your children. What makes you think that any learned behaviors are passed down genetically? They might be, perhaps through some form of epigenetic modification, but it's unlikely to be very common.

user1894167 - I edited your post as it contained inconsistencies as rightly pointed out by @terdon. If, however, this edited version no longer reflects your original question, please feel more than free to roll back. However, in that case additional edits are recommended, as your original question was confusing.

There can be whole books written on this topic and we wont still have answered this question. How instincts are genetically coded is still under research. For some there is an answer. Therefore I ask you to narrow down to a specific case.

@WYSIWYG - I must say I find this question highly intriguing. How could it be narrowed down? Perhaps focus on a single well-investigated species with a known, reproducible complex behavior such as a web-weaving spider? If I wasn't rep farming I would be bountying this question heavily.

@AliceD primitive instincts like fear can be explained based on epinephrine signaling. But web-spinning and all are much more complex and you very well know that we don't know the answer to these complex instincts and these are actively being researched upon. This is one of those unanswerable questions :P

thanks for the edit Alice. I think you phrased it better.

WYSYWIG could you point me towards the examples where there is an answer. I can only access free links, Or even just to links on active research not solved questions.

I will focus my answer on the evolution of orb web spiders (Fig. 1), because arachnids, like insects, are relatively non-complex creatures with an obvious systematic behavior (the weaving of highly symmetric, repeating structures). Hence I reasoned this would be a good approach of investigating the answer to this question.
The orb-weavers (Orbiculariae, an informal name for the taxon containing the superfamilies Deinopoidea and Araneoidea) are among the most diverse lineages of spiders (Hormiga & Griswold, 2014).

Fig. 1. Orb web. Source: Encyclopedia Britannica
Bond et al. (2014) report that according to various estimations the date of the origin of the orb web was somewhere around the Lower Jurassic 201 million years ago and 52 million years ago, and the authors support the view of a monophyletic origin of the orb web.
Despite this excellent opportunity to elucidate the (monophyletic) genetic underpinnings of the evolution, and hence the passing down of orb weaving, are largely unknown. Not only is the evolution of orb weaving unknown, even the evolution of the intricate physical properties of the silk are largely unknown. For example, how the sticky glue araneoid orb web evolved is a mystery. This complex multicharacter trait is hypothesized as a key innovation to explain the increase in diversity of araneoidea. For example, araneoid orbs contain viscous adhesives and they have low UV-reflectance and are hence less visible to insects. There exists one proposed evolutionary pathway from the dry, cribellate orb web of deinopoids to the sticky glue orb web of araneoids, but that's about it (Hormiga & Griswold, 2014).
In all, physical properties of silks contained in webs are hardly explained in evolutionary terms, let alone the behavioral profiles necessary to make a web out of it.
References
- Bond et al., Curr Biol (2014); 24(15): 1765–71
- Hormiga & Griswold, Annu Rev Entomol (2014); 59:487–512

I think http://www.thenakedscientists.com/forum/index.php?topic=26203.0 is claiming to answer the part of the question re spiders.

@user1894167 - that link describes arachnid behavior

well the first post does seem to be claiming a genetic explanation that leads to structured web building in spiders. I'm not saying I believe it since it doesnt cite any sources but just thought I would post an alternative explanation.


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Dynamic mutation and huntington's
I read that Huntington's is a disorder caused by dynamic mutations in the DNA, which means that a triplet sequence of DNA changes from generation to generation. Say we have the sequence ATGATGATGATG. The child of this person with have ATTATGATGATG and the grandchild will have ATTATTATGATG etc.
This means that Huntington's will be worse (debut earlier) the longer the generation lasts.
My questions are: Is my understanding of dynamic mutation correct? Is there no MINIMUM age where Huntington's will debut? In other words, if a generation is very long and has Huntington's, can a baby have symptoms at birth?

In triplet repeat diseases it's a probabilistic addition of more repeats. 30 repeats goes to 32, or maybe to 30, or maybe less. The longer the repeat section, the more likely it is to gain or lose repeats due to duplication errors. You're not guaranteed to get just one each generation. There is likely to be a minimum age of onset where more severely affected individuals do not develop normally or die before developing chorea.

At the moment, the youngest diagnosed Huntington's case was 2 years of age. This paper appears to discuss not only this boy's onset, but also the diagnosis of symptoms in the early-onset disease.
Here they research a link between age-of-onset and the length at which the repeats are.
The thing is that these repeats won't just constantly get longer. There is "slippage" during replication which causes the repeats to get longer, but it also causes the repeats to get shorter. It's possible that mom's bad chromosome may have been inherited but because of the slippage, it no longer produces Huntington's symptoms.
This image doesn't show actual mechanics of it happening, but it shows how the repeats can be added and subtracted.

As it turns out Kayser et. al decided to look at chimps and humans to discover which of two proposed mechanisms are more likely. Their findings suggest the slippage is closest to the "heterozygote instability model".
The model suggests:

heterozygous loci might have a higher mutation rate due to mismatch repair events that occur during synapsis

To answer your question in short:
It appears that the "minimum age" so far is 2, however, that does not mean that it hasn't occurred earlier. Huntington's is characterised by a change in motor skills, and if the change occurs before birth it might not be noticed. In theory, it is possible that Huntington's symptoms can start pre-birth.


text:
Write the haplotypes of the family
I'm doing old exam assignments to prepare for my finals on Monday and I've stumbled on one assignment that I'm not sure how to tackle.
A family with 2 children is examined for cataracts using PCR with 4 markers, A, B, C and D. The results are seperated on a gel and the genotypes are as follow:

Where Far = father, Mor = mother, Barn = child.
Notice that there was an error with the analysis so child 2's alleles are undetermined.
The question states: Draw a pedigree with each of their haplotypes. What is the most likely haplotype of child 2?
I don't understand exactly what it's asking. I'm not sure what a HAPLOtype is. I know what a genotype is and that is what the answer seems to indicate.
The answer for the father is: 4 3, 1 2, 11 5, 7 4. Now the only difference between these numbers and the given numbers are the re-arrangement of 5 and 11 in marker C?

The first paragraph of the Wikipedia article should help - it's the combination of alleles inherited from one parent i.e. on the same chromosome. It derives from haploid genotype.

I still don't understand the assignment. What do the numbers mean exactly? Are they related to this picture and if so what does each number represent in terms of letters on the picture?
http://i.imgur.com/0yiiBrP.png

all you need to solve the problem is to know they indicate different marker alleles. The alleles could be due to a variable number of repeats at the loci (see microsatellites and variable number tandem repeats on Wikipedia for examples if you are interested), but that information is not necessary to solve the problem. On your picture, the markers could be any of the alleles.

Why do they occasionally switch between the numbers when writing the haplotypes?
In the diagram the father has:
3,4
1,2
5,11
4,7
But the answer for the haplotype is
4,3
1,2
11,5
7,4
Why is the 11 and 5 re-arranged when telling his haplotype? This is pretty much the only thing left that confuses me.

I think that is supposed to mean 4, 1, 11, and 7 are on one of his chromosomes, but I've not seen it written that way before (or I don't remember it). I am not sure how you can figure out the parental haplotypes in this case, either. You can figure out which alleles are inherited by each child from each parent (the child haplotypes), but I don't think this would give you the parent haplotypes, unless you are assuming meiotic recombination does not occur. (eta: I haven't worked out the problem yet)

Definition of Haplotype
The concept of haplotype has the default to be subject to several definiton that differs mostly by their complexity to be understood and by their specificity but different definitions also sometimes differ slightly in their meaning.
In simple terms the concept is pretty easy. A haplotype is a porte-manteau word of haploid genotype and it refers to half the genotype.
What the question is asking
The question is asking is Here is half of the genotype of the child, what do you expect the other half to be?. Note however, that for the last two markers, the first haplotype is not indicated so they are just asking for the genotypes here which makes the question slightly poorly phrased IMO.
The answer key
The answer concern the father, which is silly as the question is about the child. So the answer you stated definitely does not answer the question.
The answer
We have to look marker per marker to answer the question and then consider them all together to reconstruct the haplotype. In absence of information on the subject, we are going to assume that the markers are completely independent (unlinked, eventually on different chromosomes). We will also assume no mutation (probably negligible anyway) and we assume no crazy kind of inheritance such as some selfish elements. You will note also that information about the first child tells nothing about the second child.
Marker A
The first allele inherited necessarily comes from the mother and therefore, the second allele must comes from the father. As a consequence the second allele is either 3 or 4 with equal probability.
Marker B
The first allele inherited necessarily comes from the father and therefore, the second allele must comes from the mother. As a consequence the second allele is either 1 or 4 with equal probability.
Marker C
The four possible genotype are [5,7], [5,11], [11,7] or [11,11], that all occur with equal probability. This means that for Marker C, at one haplotype, the probability of being 5 or 7 is $\frac{1}{4}$ and the probability of being 11 is $\frac{1}{2}$.
Marker D
The four possible genotype are [4,7], [4,8], [7,7] or [7,8], that all occur with equal probability. This means that for Marker D, at one haplotype, the probability of being 4 or 8 is $\frac{1}{4}$ and the probability of being 7 is $\frac{1}{2}$.
Whole Haplotype
From the above, you can compute all possible haplotypes and calculate the most likely to occur. However, there are some ties. The most likely genotypes are (3,1,11,7), (3,4,11,7), (4,1,11,7) and (4,4,11,7) that could occur with probability $\left(\frac{1}{2}\right)^4 = \frac{1}{16}$.