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Does DNA have the equivalent of IF-statements, WHILE loops, or function calls? How about GOTO?
Does DNA have anything like IF-statements, GOTO-jumps, or WHILE loops?
In software development, these constructs have the following functions:

IF-statements: An IF statement executes the code in a subsequent code block if some specific condition is met.
WHILE-loops: The code in a subsequent code block is executes as many times as specified, or as long as a specific condition is met.
Function calls: The code temporarily bypasses the subsequent code block, executing instead some other code block. After execution of the other code block the code returns (sometimes with some value) and continues the execution of the subsequent block.
GOTO-statements: The code bypasses the subsequent code block, jumping instead directly to some other block.

Are constructs similar to these present in DNA? If yes, how are they implemented and what are they called?

while(telomeres>0){DNA.replicate;cell.divide;telomeres-=1;sleep(x);}

A function call is just a fancy GOTO statement.

To me, GOTO only makes sense for sequential code execution, and this is not the case for DNA (lots of transcription is happening all the time in parallel).

@fileunderwater Serial execution happens during signalling cascades

@MichaelKjörling A fuction call necessitates that there be a separate environment for the function. It can take arguments as inputs and returns some output. GOTO on the other hand is the part of the main program and just controls the flow of instructions. While the information flow in biological system can be controlled, it is almost impossible to provide a separate environment necessary for true functions.

@WYSIWYG yes, but isn't this more a case of positive feedback (or activation/inhibition) similar to IF-statements, and not GOTO, as in executing-bypassing-executing. Just my perception, but I don't know enought about the specifics of DNA transcription to really say. Maybe shows how hard it can be to draw clear programming-DNA analogs though.

@fileunderwater There are programming alternatives to GOTO. In most languages it is deprecated. So the action of GOTO can be performed by other statements. So you are right. Moreover, GOTO requires labels; even though a promoter for a certain TF can be thought of as a label, it is more of a logical condition to be fulfilled. So more important than actual statements is the underlying logic.

I think with DNA we are closer to bits and bytes themselves or maybe machine code than to a programming language.

@WYSIWYG True, although most control flow statements translate to a machine instruction similar to GOTO, such as a jump or conditional jump.

@skymninge Even at the level of bits and bytes, the hardware itself acts as a kind of Turing machine.

It's crucial to understand that your computer does not have loops and function calls. It does have comparisons and jumps.

DNA is not a program in the sense you're thinking. I suppose it could be considered a declarative program with the proper interpreter, though?

I am pretty sure DNA is more like generic data than a fully fledged executable program. Its the datafile that the bio-program uses

I think DNA is more like a HTML page: it's just a declaration of what elements could be visible on a page, (although display:none is perfectly allowed in DNA); these elements can include protein Javascript. Here and there a rudimentary form of PHP is present (see @WYSIWYG's answer).

This is a probably relevant article that I think nobody mentioned yet.

@WYSIWYG I would argue that nuclear receptor activation can represent a function call. They hang out in the cytosol until activated by binding of their ligand, and then trans-locate to the nucleus to perform their function.

To learn genetics and molecular-biology this-way; could anyone refer me some books, or at least which area of study I have to look for?

Related nature paper: Large-scale design of robust genetic circuits with multiple inputs and outputs for mammalian cells.

This has aged well. There are numerous regulatory mechanisms and feedback loops of which our knowledge is still being developed. In fact we could probably learn new coding tricks by looking at how DNA can control gene expression.

Biological examples similar to programming statements:

IF : Transcriptional activator; when present a gene will be transcribed. In general there is no termination of events unless the signal is gone; the program ends only with the death of the cell. So the IF statement is always a part of a loop.
WHILE : Transcriptional repressor; gene will be transcribed until repressor is not present.
There are no equivalents of function calls. All events happen is the
same space and there is always a likelihood of interference. One can
argue that organelles can act as a compartment that may have a
function like properties but they are highly complex and are
not just some kind of input-output devices.
GOTO is always dependent on a condition. This can happen in case of certain network connections such as feedforward loops and branched pathways. For example if there is a signalling pathway like this:  A → B → C and there is another connection D → C then if somehow D is activated it will directly affect C, making A and B dispensable.

Logic gates have been constructed using synthetic biological circuits. See this review for more information.

Note
Molecular biological processes cannot be directly compared to a computer code. It is the underlying logic that is important and not the statement construct itself and these examples should not be taken as absolute analogies. It is also to be noted that DNA is just a set of instructions and not really a fully functional entity (it is functional to some extent). However, even being just a code it is comparable to a HLL code that has to be compiled to execute its functions. See this post too.
It is also important to note that the cell, like many other physical systems, is analog in nature. Therefore, in most situations there is no 0/1 (binary) value of variables. Consider gene expression. If a transcriptional activator is present, the gene will be transcribed. However, if you keep increasing the concentration of the activator, the expression of that gene will increase until it reaches a saturation point. So there is no digital logic here. Having said that, I would add that switching behaviour is possible in biological systems (including gene expression) and is also used in many cases. Certain kinds of regulatory network structures can give rise to such dynamics. Co-operativity with or without positive feedback is one of the mechanisms that can implement switching behaviour. For more details read about ultrasensitivity. Also check out "Can molecular genetics make a boolean variable from a continuous variable?"

I would classify intron splicing as a kind of GOTO, since it essentially skips the ribosome "pointer" to a different value.

Very nice! Where would alternate reading frames fit in?

@MarchHo Yes that can also be considered an example. Lots of analogies can be drawn. Spinal reflexes can be an example of BREAK

@CRags I guess alternate reading frames can be an example of SWITCH-CASE. It all depends. The logic gating is of more relevance here than program statements. After all these statements are based on logical tests.

While your examples are clever I feel the analogy used here (DNA against computer code) is so very poor as to be misleading.

@JackAidley It is true that molecular biology cannot be directly compared to a computer code. I intended this answer for someone who is curious if a cell can perform computations like a computer program. I already mentioned that it is the underlying logic that is important and not the statement construct itself and these examples should not be taken as absolute analogies. I'll add this in the answer to avoid confusion.

And @JackAidley I nowhere mentioned that DNA is performing all the functions. A TF is a protein. Complex though it may be, the property of the system may be predictable based on the DNA code.

I really think compartmentalizations as accomplished by cellular membranes could be compared to functions. This is an impressive answer @WYSIWYG

WYSIWYG, it's good that you did not mention that DNA is performing all the functions you describe, but you should really consider explicitly mentioning in your answer that DNA doesn't and can't perform them; the fact that computer code describes such control structures really is a pretty fundamental aspect of Turing-completeness, and it's very important in the context of this question to note that DNA does not share that feature.

@KyleStrand IMO neither DNA does the function nor does the HLL code. Both of them just provide instructions; DNA is much more cryptic. Just because a Turing Machine has not been developed using the DNA code doesn't mean that it is theoretically impossible. This is just my opinion. There are several differences between DNA and computer code. The objective of this answer was just to point out some rudimentary similarities. I have added your suggestion though.

@WYSIWYG Thank you. I guess what I meant about "performing all the functions" is more that HLLs (and LLLs) prescribe the actual process for executing them--where jumps occur, etc.--even if they do not actually perform that process themselves. DNA, as far as we know, does not (although admittedly it could do a lot more of this sort of thing than we realize). I guess by analogy, if DNA is like a blueprint, code is somewhat like a blueprint combined with work instructions for the people actually building the thing described by the blueprint.

"organelles" seems to be like interrupt handler, or maybe events.
I think an events based language may be better comparison for logic comprehensions.

To produce computation, all you need is just a conditional jump (i.e. if X goto P). All other control statements are just for convenience and can be simulated by conditional jump. A computational system that only have a conditional jump for for control is Turing Complete.

@lesto organelles are like subprograms that interact continuously with the main program. They have their own environment and some level of autonomy, but are dependent on the cell.

@LieRyan Agreed. All you basically need are logic gates.

There are some hypotheses regarding chromatin microenvironments that would be analagous to namespaces in programming.

"Biological examples" — But the question specifies DNA, so clearly this answer is wrong. Shows you shouldn't allow some people to vote.

@David I agree that this question is not great (and the answer too) but unfortunately the most well-posed (and researched) questions are often not so popular. Anyway, what do you disagree about "biological examples"? I meant analogous situations in biological systems, by that term. Note that OP is comparing DNA with a computer program. Since DNA encodes all biological information, DNA is the program. Most of my examples are related to transcriptional regulation i.e. direct operations of/on DNA. So the answer, although not great, isn't wrong.

Sorry. Didn't notice it was you. Don't want to get into a flame war. Just that the question seems to me a typical computer scientist's false analogy between the explicit information in code and in that in DNA, which provoked my recent answer to an old question. The information in DNA is not explicit and I doubt whether you could ever hope to understand the effects of the expression of proteins from reading the DNA alone.

I would say that chromosomal regulation is a kind of function call (DNA is 3D) DNA is activated in one part of the chromosome. Then downstream at some point this effects the opening of the chromosomal region for transcription downstream the initial DNA activation (methylation of chromosomal regions). This is kind of a stupid question honestly. We are no where close to being able to model synthetically a whole system either in vitro or in silico. Way too many moving pieces that we don't yet even have interaction models with entire important fields like biophysics not even sharing in importance.

DNA is not analogous to computer code which renders your search for similar constructs in it meaningless. To give a couple of simple examples why this is:

Computer code has a sequential order of execution; DNA acts in
parallel and out of sequence, it is not "executed".
Computer code has a strict and consistent meaning so the line if x==4 : x=7 always does the same thing; coding DNA
translates to amino acids and it's the complex chemical interactions
between these acids which give proteins their function thus no piece
of coding DNA can be understood outside of its protein.

Biological systems do have some pathways that operate in a similar way to computers, but you should be looking for these at the protein level not the DNA level and, even then, you need to be extremely careful that your analogy does not impair your understanding of what is really happening.

When you say DNA needs proteins to execute its functions then computer programs also need compilers to execute their code. It is ultimately the machine language that tells the computer what to do.

I'm not saying that DNA needs proteins to execute its functions; I'm saying DNA is fundamentally unlike computer code.

OK, but there exist massively parallel programming languages Where every line is executed at the same time and can be out of sequence.
And just because lines are context sensitives does not make it not a programming language, it just makes it far more complex.
That said, the way I understood DNA it was more data than program.

Even in parallel programming languages, each statement in executed sequentially. It's just that there are multiple "threads" of execution going at the same time. DNA is neither data nor program. The analogy is totally inaccurate.

I think DNA is data and program at the same time. Its regulators of expression act as logic clauses, so the analogy is at least curious.

"Computer code has a sequential order of execution" - Joule would like a word.

@JackAidley - "each statement is executed sequentially.". This is untrue, both at the language level (Joule for instance) and at the processor level (the CPU of the machine I'm typing this on can have several hundred instructions in flight at the same time in varying stages of execution).

It sounds like you could probably implement the world's worst Verilog backend with DNA :-)

Computer code is essentially 1-dimensional, because it is "read in" sequentially. DNA is literally 3-dimensional and many, many non-coding constructs take advantage of that. This is a good review, for example: https://www.annualreviews.org/doi/abs/10.1146/annurev-biodatasci-122120-110102

There are certainly some comparisons that could be made between the way genes are expressed from DNA and logic functions, but they aren't great.
But synthetic Biology is really a blossoming new field that is attempting to integrate logic functions into biology, see e.g. Siuti et al (2013).
The above paper is a brilliant example of a group using bacteria to store information and assembling into biological circuits that can then be used to process logic functions. So its being done but not exactly in the way that you propose.

Just to add to previous answers, but transcriptional interference (see e.g. Shearwin et al., 2005) can be seen as a form of IF-statement (or WHILE) in the sense that:
if(x transcribed){not y transcribed}

The interference does not have to be binary though, and more common are graded responses. Transcriptional interference can also take place at the RNA stage (see e.g. Xue et al, 2014), using antisense RNA and often providing a negative feedback loop, but the interference is then removed from the DNA, and does not represent a direct IF-statement analog at the DNA stage.
To me, GOTO mainly makes sense for sequential code execution, and this is not the case for DNA (lots of transcription is happening all the time in parallel). More generally, the parallel "execution" of DNA along with the continuous interactions and feedback loops between DNA, transcripts and proteins (among other things) also means that cellular processes are far less clear-cut and traceable than computer code, which means that computer code is a very poor metaphor for cellular processes and the functioning of DNA.

I think the intrinsic parallelism is a key point.  Biological 'processing' is really more analog than digital, as even discrete neuron firing is an encoding of analog processes in the neuron.  The processes of a cell are much better approximated as a horrendously (gloriously?) complex set of overlapping, cross-wired analog feedback loops.  Gene expression makes up part of this, though it is intimately tied into many other cellular processes.

@DanBryant Great description and agreed - I have tried to clarify this point further.

As WYSIWYG said there is no equivalent for function calls, as there will always be some interference. However one could argue that some modular pathways (eg. apoptosis signalling) can be seen as a "code block" where a certain input will (almost) certainly lead to a certain effect. The analogy with function calls is that, in describing many different mechanisms, it makes for shorter and more efficient "code" to consider everything between eg. caspase activation and cytochrome leakage as one block. Also, marking a protein with ubiquitin can maybe be seen as a function call for degradation.
If you are interested in the building blocks for programming with biology, check out the biobricks.org program, which aims to define modular parts (bricks) which can be sensors, logic functions, effectors,...

There is interference in function calls too: they're called global variables, system configuration, hardware support, etc.

Regarding function calls:

There are no equivalents of function calls. All events happen is the same space and there is always a likelihood of interference. One can argue that organelles can act as a compartment that may have a function like properties but they are highly complex and are not just some kind of input-output devices.

and

As WYSIWYG said there is no equivalent for function calls, as there will always be some interference.

I think that nuclear receptors are great examples of function calls. They hang out in the cytosol allowing normal programming to function in a normative fashion. Upon activation with their ligand, they translocate to the nucleus to activate subroutines of gene repression/activation and subsequent downstream processes.
In this fashion one could even argue that most initial ligand interactions that kick off cellular signaling are function calls.

In addition to the excellent WYSIWYG answer, there are some programming-like constructs at the lower level:

FUNCTION CALL - replacing a single sub-unit inside a complex protein, assembled from multiple sub-units, each encoded by separate genes. This can also be seen as COMPOSITION, another programming concept.
IF - alternative splicing, a piece of DNA (exon) may be included or not included into transcript that encodes the final protein.

I rolled back the edit that put back tics around portions of this answer that are not code. Here, FUNCTION CALL, COMPOSITION, and IF are not code, they are programming concepts


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Optical density machine name
What is the name of the machine used to measure optical density? We used it in a lab but I can't remember what they called it.

densitometer? turbidometer? spectrometer? spectrophotometer? There are many such devices and some details on the type of experiment may help here.

Hmm I think it was the spectrometer. That sounds right. We where measuring the growth of cell cultures.

I'd bet the farm that it's a spectrophotometer.

Optical Density is synonymous with absorbance which is based on the principle of absorption of light. The machine that is used to measure absorbance is called a spectrophotometer. Spectrometer does not indicate that light absorbance is being measured. A spectrometer can measure any spectrum; for e.g. Mass Spectrometer measures the spectrum of molecular mass (to be precice mass per charge).
Cell density can be also measured by the level of light scattering; turbidimeters or nephelometers are used for these kind of measurements.
PS: You should pay more attention in your class :P

Also called a spec, for short.

When you use a spectrophotometer to measure culture density you are actually measuring turbidity/light scattering, not absorbance.

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Sensitivity of eyes to flashing lights
My eyes are very sensitive to flashing lights - for example I'm always the first person to notice that a fluorescent tube is about to fail because I see it flickering when other people can't.
When I'm driving at night, I perceive LED rear lights on cars as being a series of unconnected dots when I scan my eyes quickly across the scene. Evidently, many, if not all, LEDs are actually flashing at a high rate which most people don't perceive.
It almost seems as though I have a higher "refresh rate" than most people. How unusual am I? What is the physiology of it?
EDIT: I suppose what I find most fascinating is that at times when I see a trail of flashes, the spacing between them is remarkably consistent. This implies to me that there is an incredibly accurate timing mechanism somewhere in my visual system that is taking "snapshots" with clockwork regularity - probably between 50 and 100 samples per second. I'd like an insight into this "clock" and why mine seems to be faster than anyone I've ever met.
This similar to what I perceive:

two related Qs and maybe partial answers: http://biology.stackexchange.com/questions/7445/perception-of-artificial-light-flickering?rq=1 and http://biology.stackexchange.com/questions/9277/are-human-eyes-equally-sensitive-to-ac-and-dc-lamps

@fileunderwater Thanks for that - I couldn't find anything when I searched the archive, hence the question. I know about the peripheral vision thing and rod density. I can verify that the fluorescent tube thing is much more sensitive at the periphery of my vision - which makes it even more annoying! It's much more difficult to say with the rear-light scenario, I mainly notice it when I sweep my eyes rapidly so I guess the periphery is playing a greater part in vision at that time than during normal, focussed driving.

4 clarifications would come in handy to answer this question. (a) You speak of LED lights being unconnected dots. Often these are in fact unconnected dots? Is this so extraordinary?; (b) Comment (a) seems to address spatial resolution, whereas the rest of the question seems to address temporal resolution. Are you saying both spatial and temporal resolution are extraordinary? (c) the edit: what trail of flashes? A trail is spatially defined while sampling rates are temporal characteristics (d) where do you live? The mains in the US is 50 Hz, which is not unusual for folks to perceive.

@Chris Stronks I've added an image to explain what I mean a little better. I'm not talking about the individual LEDs in the light cluster - the entire group of LEDs must flash in unison because I see the multiple images like the photo. So as you can see, the movement across my vision (in time) captures the rear light as images separated in space. I'm in the UK - our mains is 50Hz too - but I've never met anyone who can see the flashing of a fluorescent tube the same as me. In what way do you think people are able to perceive 50Hz?

The site where I got the image has a few people who can also perceive these light trails. The suggestion there is that these rear-lights actually flash with a frequency of 200Hz!

seeing trails of dots means you are NOT perceiving individual flashes - otherwise you would see a single moving and flashing dot. but you may be still able to detect something IS flashing, this is probably handled by a different part of our brain visual circuitry.

Interesting point @szulat. Arguably my visual system is failing 100 times per second. It's really the accuracy and regularity of the timing that interests me. It's not something I associate with biological systems at all, hence the question - but maybe biologists see nothing strange in this at all...?

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What network motifs or other mechanisms can make the expression of a gene invariable to the environment?
Next to double positive feedback loops and chromatin modification, which other mechanisms can make a gene susceptible to a certain environment in one cell-type but not in another?

This phenomenon of being insensitive to certain fluctuations is called robustness. The fluctuations can be of two kinds for an input-output device such as a gene that is activated by a signal:

Fluctuations in the signal
Fluctuations in the intrinsic parameters

Signal fluctuations can be temporal but parameter fluctuations are not (parameters are supposed to be time invariant). Parameter fluctuation can exist in a genotypic space or a population of cells because of variation.
Some motifs are robust to signal perturbations whereas some are robust to parameter fluctuations.
Negative feedbacks and incoherent feed-forward can confer robustness by correcting the output fluctuations because of fluctuations in the input.
When an all or none sort of (binary: one state need not be smaller in magnitude than the other) behaviour is important, then positive feedbacks confer robustness to such systems because of their property of bistability.
I cannot recall any particular motif that is robust to parameters. There are certain cases though (I am still working on that!! :P).
In any case environment can be thought of as an input.  For your question "what mechanisms can make a gene susceptible to a certain environment in one cell-type but not in another":
There can be a heterogeneous population of cells which can arise because of bistability or even otherwise, due to stochastic effects. If the gene that is in one of the two states (expression levels) in these two sub-population of cells, and this gene is responsible for the expression control (the controller gene in feedback), then one sub-population will be sensitive to the environment while the other will not be.
For more information on biological robustness read this review.


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What is our skin made up of?
Again, it is a basic question. What is our skin made up of? is it made up of many cells arranged in a systematic way or is it just like any layer say of a book?? what is the difference? where is the living and dead thing coming into picture? is it the fact that skin can self-heal makes it living and in turn made up of cells??

The human skin is indeed made off a number of different layers, the three most important are epidermis, dermis and hypodermis (also called subcutaneous fat), see the figure (from here) for details:

All three layers can be subcategorized further, I'll only give a few details here. More can be found for example in the Wikipedia article on skin.
Epidermis: Top layer of our skin, is covered with the stratum corneum, which consists of several layers of dead cells, which protect the layers below. New cells of the epidermis are made at the border between dermis and epidermis and travel upwards (actually the top layers are worn off). The epidermis is the place where the pigmentation takes place due to melanocytes embedded in the keratinocytes of the epidermis.
Dermis: The next layer is the dermis where a lot of important functions on the skin happen. Sweat and oil are produced in the dermis. The feeling of the skin is also mediated in the dermis where the ends of the nerves are embedded. The hair roots of the hairs of the skin are also located here as well as the blood capillaries which supply the skin.
Hypodermis or Subcutaneous fat: The last layer is the hypodermis. It attaches the dermis to the underlaying muscles and bones and houses bigger blood vessels and nerves which go up into the dermis. The fat layer is also important for controlling the body temperature and storing fat reserves.


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How does the value of K determine number of local optima in NK model?
BACKGROUND
The NK model of fitness landscape considers N states which can interact with K other states. For example N is the total number of genes in a haploid genome and K is the number of other genes that each gene may interact with.
In this article Kaufman says:

The fully connected NK model yields a completely random fitness
  landscape. For K = N - 1, the fitness contribution of each site
  depends on all of the other sites in the sequence and therefore
  altering any site from one to the other value, 0-1, alters the fitness
  contribution of each site to a new random value. Thus the fitness of
  any 1-mutant neighboring sequence is completely random with respect to
  the initial sequence. The landscape is fully random. As was shown in
  Kauffman & Levin (1987), Weinberger (1988), and Macken & Pereison
  (1989), such random landscapes have very many local optima, on
  average, 2N/(N +1).

I did not read the references mentioned in the text but I read the related section in Kaufman's book: Origins of Order: Self-Organization and Selection in Evolution.
In the book he says that the fitness of a genotype can be ordered and given ranks; the probability that a genotype is fitter than its neighbours (local optima) is same as its probability of ranking higher than its N neighbours. So this probability:
$$P_m=\frac{1}{N+1}$$
and if each gene can have only two states lets say on or off then the expected number of optima with respect to one-mutants (i.e. the difference between a gene and its neighbour is just one mutation) would be:
$$M_1=\frac{2^N}{N+1}$$
What I don't understand is the role of K in this expression. This reason should be valid for any number of K (See the quote above). Even in the book this explanation is given in the case where K is maximum i.e. N-1. I can understand that K can affect the ruggedness of the landscape but can anyone explain how K affects the number of optima? (or are they just two separate statements written together, which is confusing me)

Let's take the opposite extreme, $K=0$, so that each site has an independent effect on fitness. Without loss of generality, we can say that at each locus $n$, the $1$ allele confers an advantage $s_n$ over the $0$ allele. Then there is just one local optimum, the global optimum, at $\vec{1}$, so $M_1=1$ (and $P_m=2^{-N}$).
The key difference is that in the $K=0$ case each fitness comparison of a focal genotype with a neighbor is independent of the rest: the fact that mutating the first gene decreases fitness, for instance, doesn't make it any more likely that mutating the second gene will decrease fitness. For any $K$, it is necessarily true that the focal genotype has a probability $1/(N+1)$ of being fitter than all of a set of $N$ other randomly chosen genotypes, but we're interested in comparing it to its neighbors, which are not a random selection, and are only equivalent to a random selection when $K=N-1$.

Thanks Daniel. Sorry I for the late response. Was out of town and didn't check. So except for the N=0 case, it is not straightforward to predict the number of optima from the value of K or is it monotonously increasing?

No need to apologize! I think that it's monotonously increasing, but I'm not sure if it's been proved in general. There are a couple of papers by Vlada Limic in Ann. Prob. (2003 with Rick Durrett, 2004 with Robin Pemantle) that look at related questions.


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What is the maximal insert length for PCR based homologous recombination in S. cerevisae
I would like to insert a 6 kbp construct, which I have on a plasmid into the genome of S. cerevisiae. This plasmid was originally constructed to integrate at the HIS locus via homologous recombination after transformation with the plasmid. The problem is that the strain I would like to use is HIS-Δ0, so the complete HIS-ORF has been deleted so that the plasmid will not insert via homologous recombination.
My question is now whether I can still insert my construct into the genome via PCR based homologous recombination, by amplifying the region of interest on the plasmid with primers which have a homology to the genomic sequence where I would like to insert my construct. I am afraid that 6 kbp are too much to transform yeast cells efficiently. Does anyone have experience with such long inserts?
thanks for your help,
Jannis

Are you having trouble with the amplification or the transformation?

No, I have not even tried yet. I am just worried that the homologous recombination will not work with such a long insert and I wanted to know if other people have done similar tranformations before.


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Telomere and its effect on aging
The cloned sheep, Dolly, was said to have died very soon because the cells used to create it were taken from an adult sheep with an aged telomere. Why doesn't this happen with humans? Why aren't we born with 25 years less lifespan?

Our telomeres shorten as well with every division, except for stem cells (which have an active telomerase). The maximum number of divisions is called Hayflick limit.

Broadly speaking there are two classes of cell in an organism:

Somatic cells

These are by far the most numerous in your body, and are the differentiated cells including everything from retinal cells to liver cells to neurons.

Stem cells and germ cells

Stem cells reside in tissues and replenish the somatic cells as they are damaged or removed, or as the organ grows,
Germ cells - in particular oocytes in women's ovaries - are pools of immature eggs that are generated when a women is still a foetus in her own mothers womb!

The difference between these two types that relates to your question is that somatic cells have a limited replicative lifespan - a limit to the number of times they can divide - because their telomeres (caps to the ends of chromosomes) erode during cell division, whereas stem cells are able express the enzyme telomerase which extends the telomeres and allows cells limitless replicative potential (excluding other factors). Replenishing telomeres is a major step in cancer progression [1].
Embryonic cells have 'complete' telomeres when they are fertilised and begin to proliferate into a new organism. Interestingly the telomere length of the germ cells is not at all related to fertility [2], suggesting to me that telomerase is expressed for a while post-fertilisation, so the length prior to fertilisation is not important.
Dolly was produced by a process called Somatic Cell Nuclear Transferase, where the nucleus from a somatic cell from an adult organism is transplated into an embryo with its nucleus removed [3]. A study found that she had consistently shorter telomeres corresponding to the fact that the original donor was 6-years old already [4]

You might also be interested in my answers to these questions

Are human bodies programmed to die?
Cell proliferation limit and senescence of embryonic stem cells and fibroblasts
Do trees age on a microscopic level?
Difference In Telomeres Between A Thale Cress Plant And A Methuselah Tree

Shay, 2001, Human Molecular Genetics. Telomerase and cancer. http://hmg.oxfordjournals.org/content/10/7/677.full
Turner, 2013, Mol Hum reprod. Telomere lengths in human pronuclei, oocytes and spermatozoa. http://www.ncbi.nlm.nih.gov/pubmed/23519357
http://learn.genetics.utah.edu/content/cloning/whatiscloning/
Shiels, 1999. Cloning. Analysis of telomere length in Dolly, a sheep derived by nuclear transfer. http://www.ncbi.nlm.nih.gov/pubmed/16218837


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meaning of the "reads" keyword in terms of RNA-seq or next generation sequencing
I'm an undergraduate student at computer science and currently, I'm interested in bioinformatics. Today, I've started to read a paper about clustering and classification of non-coding RNAs can be found here and I've seen a word RNA-seq read. Altough I searched a lot to learn about, I can not find the definition of it, the thingsI found was about performance issues of techniques rather than explanation of the word. So, is there anyone who can simply explain me what is the meaning of this word as well as RNA-seq technique?

In RNA sequencing, the RNA is fragmented, DNA is synthesized complementary to the RNA fragments, which is  followed by a complementary strand synthesis. Fragmentation can be done after the cDNA synthesis too.
This DNA is then amplified to form a cluster that is sequenced. Most Next-Gen sequencing approaches sequence a short segment of the DNA (it has improved with experimental and technical optimization).
A read refers to the sequence of a cluster that is obtained after the end of the sequencing process which is ultimately the sequence of a section of a unique fragment. If an RNA is expressed in high copies then there will be more reads coming from it; reads can be redundant as well.

Courtesy


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What's the maximum pressure inside a bombardier beetle?
This question got me wondering about the pressure inside a bombardier beetle.
Lots of articles mention pressure, but don't specify the amount of it:

One study records the velocity of the spray to be within a range of 325 to a stunning 1950 cm/s.
  [...]
  Once the muscles around the reservoir squeeze the first amount of
  reactants through the valve into the reaction chamber, the resulting
  explosion causes the pressure to rise rapidly in the reaction chamber,
  forcing shut the one-way valve. The products of the reaction then exit
  the chamber with a pop and a puff, and the pressure inside the
  reaction chamber lowers again, falling below the pressure of the
  collection reservoir, which is still being squeezed by the reservoir
  muscles.

Calculating from the spray characteristics is beyond me.

According to this study, model data shows a maximum pressure of 110 kPa, that's 16 psi and only 1.086 atm:

The three-phase process involved in the beetles explosive secretory
  discharge (ESD) process. The inlet size is shown as a proportion of
  the inlet radius. During the first phase of refill and heating (blue),
  only the inlet valve is open. During the second phase (red), the
  chamber is closed. Finally, the third phase (marked by an arrow) is
  the exhaust phase, when only the outlet valve is open. This phase is
  significantly shorter than the first two phases. This cycle then
  repeats with phase 1 starting at approximately 5.1 and again at 7.8
  ms.


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

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

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

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

Shotgun sequencing uses Sanger sequencing protocol.

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

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

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

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

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

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

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

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

can you add a reference?


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Layman definition of genetic polymorphism?
I am reading an article about Genetic Polymorphism and there are lines in the article about genetic polymophism that I don't quite understand like.

In this area, there are six different chemotypes that are the expression of a genetically controlled polymorphism in T.vulgaris(24).

Can someone explain genetic polymorphism and morphic distribution in layman terms.
Thanks

Can you link the article.

Read the wiki article on polymorphism (genetic section) and then ask if you don't understand something specific http://en.m.wikipedia.org/wiki/Polymorphism_%28biology%29

Polymorphic sites
Consider the following sequence of DNA
ATTTGC
Now consider that in a population of 5 haploid individuals (in reality populations are larger of course) you have the 5 following sequences

ATTTGC
ATTTGC
ATCTGT
ATTTGC
ATCTGC

Looking at those sequences you can identify two sites (site 3 and site 6) for which the nucleotides vary throughout the population. For example, at site 3, 3 individuals have a T while 2 individuals have a C. Sites 3 and site 6 are said to be polymorphic sites (a.k.a. segregating sites).
Statistics of genetic variance related to polymorphic sites
Note that there are all sorts of ways to describe the genetic diversity in this population. You could calculate the total number of segregating sites or the average number of pairwise difference between any two sequence. Or the average expected (and not observed) heterozygosity (which is sometime refer to as genetic diversity). One could calculate the frequency distribution of the number of individuals carrying a given variant (called the site-frequency spectrum).
Other polymorphism
Note that I emphasized on polymorphic sites for the moment but there are a whole bunch of different reasons that two genomes may differ. Two sequences may differ in their length as well (insertions and deletions of nucleotides). Genomes may differ in the number of copy of a given sequence (copy number variation). Genomes may differ in the number of copy of very very long sequences or in the order of those sequences (synteny). Genomes may differ in their number of chromosomes or in their ploidy level.
About the citation

In this area,there are six different chemotypes that are the expression of a genetically controlled polymorphism inT.vulgaris(24)

It is hard to say anything without the link to the article.
There are six different chemotypes (found in the population). Not all individuals have all chemotypes (eventually each individual has one or two chemotypes). Having one or another chemotype depend on your DNA sequence.
Assuming that the difference is due to polymorphic sites (which is impossible to say for sure without reading the paper), there is therefore one (or several) polymorphic sites that explain the variance in chemotypes in the population.

Did you mean nucleotide instead of amino acid?

Google NINJA!!! http://www.pnas.org/content/110/8/2893.full


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Cellular Respiration/Fermentation Problem Leading to Lack of Energy
A young animal has never had much energy. He is brought to a veterinarian for help and is sent to the animal hospital for some tests. There they discover his mitochondria can use only fatty acids and amino acids for respiration, and his cells produce more lactate than normal. Of the following, which is the best explanation of his condition?
A) His mitochondria lack the transport protein that moves pyruvate across the outer mitochondrial membrane.
B) His cells cannot move NADH from glycolysis into the mitochondria.
C) His cells contain something that inhibits oxygen use in his mitochondria.
D) His cells lack the enzyme in glycolysis that forms pyruvate.
E) His cells have a defective electron transport chain, so glucose goes to lactate instead of to acetyl CoA.
Answer:  A
A) So, from this assumption, pyruvate would build up in the cytosol of cell. However, I do not see why lactate would be formed. Lactate forms when there is a lack of NAD+. In this case, there is no problem with NAD+. All NADH will be recycled into NAD+ by the Electron Transport Chain in the mitochondria.
B) I do not know what will happen in this case. Too many contradicting factors. Can anyone explain?
C) This is clearly not correct. If there were no O2,then there would only be lactic acid fermentation; the protein and fatty acids would not be used.
D) If lactate is formed, pyruvate must have been formed.
E) The electron transport chain needs to work. See C). Same explanation.
So, I am debating between A and B. Can anyone explain why the textbook says A?
EDIT :
If anyone could give me a step-by-step approach to solving this problem, I would really appreciate it. This is supposed to be a challenge problem not representative of test questions, but I still want to fully get it.

Short answer
(A) is a possible answer and is indeed cause for fatigue, as pyruvate is needed for the Krebs cycle to run. The krebs cycle is an essential step in the generation of ATP in aerobic organisms. (B) is incorrect because NADH is never transported into the mitochondria in any organism (it is a nonsense answer).
Background
NADH is not transported into mitochondria. Instead, its electrons are transported into mitochondria, and I quote from Berg et al. (2002):

NADH cannot simply pass into mitochondria for oxidation by the respiratory chain, because the inner mitochondrial membrane is impermeable to NADH and NAD+. The solution is that electrons from NADH, rather than NADH itself, are carried across the mitochondrial membrane. One of several means of introducing electrons from NADH into the electron transport chain is the glycerol 3-phosphate shuttle (Figure 18.37).

Electrons from NADH can enter the mitochondrial electron transport chain by being used to reduce dihydroxyacetone phosphate to glycerol 3-phosphate. Glycerol 3-phosphate is reoxidized by electron transfer to an FAD prosthetic group in a membrane-bound glycerol 3-phosphate dehydrogenase. Subsequent electron transfer to Q to form QH2 allows these electrons to enter the electron-transport chain.

Hence, (B) is incorrect.
EDIT: Now why would lactate be formed in (A)? Pyruvate builds up in the cell, as it cannot be transported into the mitochondria. Since lactate dehydrogenase has pyruvate as a substrate, the equilibrium of this reaction will be pushed to the right and lactate will be formed:

Source: wikipedia page on lactate dehydrogenase
The lack of glucose oxidation takes away the main power supply of aerobic organisms, causing fatigue. Lactate buildup may also induce fatigue.
Reference
Berg et al. Biochemistry 2002, Freeman, New York

why would A be a cause of fatigue? Lactate is not formed.

Let us also assume that B was referring to the electrons of NADH rather than NADH in itself just so that I can be sure I understand the biology behind this.

(B) is simply not true, as the claim is false - healthy dogs also can't move NADH across the mitochondrial membrane. It is simply a nonsense answer. I have added an explanation of why lactate is formed.

Lactate as such can cause fatigue, @ChrisStronks. Accumulation of lactate will cause acidosis which then will cause fatigue.

Very nice answer


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Why mutations in genes involved in general processes like DNA repair increase the risk of developing specific types of cancer?
For example, mutation in MHS2, which encodes a protein involved in the repair of mismatches that occur during DNA replication, dramatically increases the risk of developing colon cancer.
(There are many other examples, like the RB gene which encodes a tumor supressor protein and is correlated to retinoblastoma, thus its name)
My question is: how a gene like MHS2 which participates in a general mechanism of DNA repair increases the risk of a specific type of cancer? Why doesn't it increase the risk of developing cancer in other tissues as well?

I can't fault @WYSIWYG for mentioning the cited Vogelstein article in providing an answer. You point to what seems like a great explanation for why certain cancers arise in some tissues but not others. However, for those who look closely this paper has some serious errors in its derivation of the model, and for good reason it has come under strong fire in the last couple of months.
See this for a really important rebuttal:
http://ameyer.me/science/2015/01/02/vogel.html
Unfortunately, the paper provides an elegantly specious explanation for, in part, the longstanding paradox of why cancers more readily arise in some tissues like the intestines and from seemingly identical mechanisms, but do not seem to arise in other tissues. My favorite example, though @El Cid you do list some good ones, are inactivating BRCA1 mutations which normally play a role in repairing double stranded DNA breaks. And yet even when mutated in the germline this only seems to increase cancer risk in the breast, and really only in one gender (females).
So the answer is still quite certainly that the field does not understand this paradox, and the cited Vogelstein paper was a total tragedy of a publication. There have been a number of officially submitted critiques of the paper and the Vogelstein lab has been trying to defend it as best they can. This is however a great example of how big name labs can seem to get anything published in Cell/Nature/Science.
Another thing to consider and @El Cid points to a good example, is the pRb mutations (in a very central tumor suppressor pathway for all cells) cause retinoblastoma and not for instance intestinal or blood cancers very readily, and the retina is not a rapidly dividing tissue. So the Vogelstein paper cannot explain this.

Retinoblastoma happens in early childhood. This is a carryover of actively dividing cells during embryonic development. pRb is involved on other cancers too.

From here.... In addition to bladder cancer, somatic mutations in the RB1 gene are associated with many other types of cancer. For example, changes in the RB1 gene have been reported in some cases of lung cancer, breast cancer, a bone cancer known as osteosarcoma, and an aggressive form of skin cancer called melanoma. Somatic RB1 mutations have also been identified in some leukemias, which are cancers of blood-forming cells. Somatic RB1 mutations in cancer cells inactivate pRB so it can no longer regulate cell division effectively.

Yes, both good points. First you are right, pRb is going to be found other cancers but why it cannot sometimes be found in every Cancer is the paradox. And about retinoblastoma occurring during early age you hit on the most widely cited criticism of the aging-Cancer theory. However, it does overlook an important difference, and that is germline versus somatic mutation. The reason we often associate retinoblastoma with childhood disease is because when they carry a germline mutation, every cell in the tissue carries this, therefore they do not need a high division rate to drive oncogenesis.

With germline mutations it is no probably more a question of overall somatic fitness. Every cell carries an oncogenes mutation, and is therefore at a functional disadvantage thereby more likely to allow for the expansion of a newly acquired secondary mutation.

Yes it is perhaps not understood why germline pRb mutation is manifested (first?) in Retinoblastoma why can't it cause some other cancer. I am not really sure if pRb's connection with retinoblastoma is anecdotal or whether it predominantly is manifested in this cancer.

Definitely not just anecdotal, we should never use anecdotes as support. http://cancer.sanger.ac.uk/cosmic/browse/tissue#in=t&sn=eye&ss=all&hn=retinoblastoma (not sure how to post a link in comments) but as you can see here pRb may not be essential to drive this Cancer, as we see in every Cancer I Can think of. But this still does not answer the original question of why certain central mutations like this are preferentially found in only a handful of cancers.

I should look at the rebuttals. The points raised in the linked one are not very strong; for e.g. plotting on log-log axis. I'll read the actual paper more carefully. Regarding "anecdotal": I meant, though most cases of disease is because of pRb mutation, the converse may not be true. That is what I was saying

Okay yeah that makes more sense. And yeah you can look around there are a few that have already been officially submitted to Nature and I think they might have been in press already? I'm not entirely sure because I read them as drafts.

I think it would make sense that I don't delete my answer until the paper is retracted. It is controversial but not yet proven wrong. At least the OP will have an idea of the entire picture.

Yeah don't ask me I'm very new to this site if I were in charge of the site I would see keep all relevant answers. Even if yours turns out to be incorrect I think it is always good to have contrarian view. It gets people to think.

You should have a look at this interesting article published earlier this year in Science.
There are two mechanisms by which cells can accumulate mutations in DNA:

Replication errors
External physicochemical agents such as UV, carcinogens etc

In the abovementioned paper, the authors classify cancers into two types:

That arise predominantly because of environmental agents (D-type)
That arise predominantly because of replicative errors (R-type)

Moreover in the same article, the authors point out that the lifetime risk of a cancer is positively correlated with the number of stem cell divisions in the associated tissue. FAP colorectal carcinoma features highest with respect to, number of stem cell divisions and consequently lifetime risk.
Since these cells divide more, they are likely to accumulate more mutations and a defective DNA repair process will worsen the situation. I cannot find a great amount of study on MHS2 gene and its connection with different types of cancers but in general, the above explanation would be applicable to most genes that are involved in DNA repair.

NOTE: As mentioned in the other answer, the abovementioned paper has received some criticism from the scientific community for making far-fetched claims which apparently fits so beautifully with the theory that it seems quite correct. The article however is not retracted. Therefore, it is important to not completely believe in this hypothesis but at the same time keep it in mind considering it as a possibility that needs further verification.


text:
Examples of extant animals in a submature morphologically unstable evolutionary state?
I'm fascinated by evolutionary theory and the predictive aspect of it-the notion of an animal entering a strongly divergent state of evolution whereby it is evolving into a new form yet remains suboptimal, and is therefore undergoing rapid morphological change, and the idea that this allows us to project onto possible new variants of life.
To give a past example, the praying mantis is believed to have split from the cockroach around 250M years ago. During this period the mantis developed its upright stance, large range of vision and pronounced raptorial claws, and has seemingly stabilised into this optimal new form over the past 50M+ years.
The interesting thing is that this change could actually have been predicted by analysis of the animals evolutionary history, niche and further available advantageous adaptive forms.
Can someone give a good example of a current animal in this volatile state that we could make accurate projections for?
And please, no trivial answers like "everything is constantly in a state of evolution", I already know that and thats not I'm referring to.

Can you document the praying mantis example?

Theories based on a the discovery of a cockroach with nascent mantid features-Raphidiomimula burmitica. Though its really just an example...

Though I know a fair bit about evolutionary biology, I have no idea what you are talking about in the title when you write "submature morphologically unstable evolutionary state". Where does this language come from? It doesn't sound like anything I've ever read in the literature. Nor do I find it plausible that "The interesting thing is that this change could actually have been predicted by analysis of the animals evolutionary history, niche and further available advantageous adaptive forms." Which scientists argue this, in what papers?

I mean essentially an organism in a volatile state of evolution. The opposite of say, a shark or crocodile that has remained morphologically and behaviourally similar for millions of years.

Another example I can give you is that of early cetaceans as they colonised water. When assuming a fully aquatic future existence it would be easy to imagine hairless creatures with narrow streamlined jaws, and flippers, though these optimal forms would not be realised for many millions of years. That is a an example of a "submature" morphology. I'm interested in contemporary animals that we could make similar predictors for to some degree of probability.

Not sure exactly what you're looking for, but maybe the Giant Panda is of interest to you. The Giant Panda is an herbivore, but it has evolved from a meat-eating animal (the most recent common ancestor of Pandas and the other bears). It made the switch from omnivore to herbivore just ~2 MYA. According to wikipedia, pandas still have the digestive system of a carnivore. They can still eat meat and do not actually get much protein/energy from bamboo. Thus, you could consider them to be in a state of evolving from an omnivore into a more efficient herbivore


text:
Stable transfection
I need to achieve stable transfection of a pCI-Neo plasmid into the genome of a mouse embryo. The most common way to achieve stable transfection is through positive selection, however positive selection would not work with embryos. How can I ensure stable transfection of this plasmid in a mouse embryo without damaging the embryo? Would this plasmid integrate itself when the cell divided? I plan to use effectene as the transfection agent.
Thank you.

I'm not familiar with that specific plasmid, but if you need integration, I think you need some sort of transposon or to take advantage of homologous recombination.

You can use lentiviral transfection.

don't people use ES cells in culture first and transplant positive cells into blastocyst? and in ES cells, since it is culture, you can rely on very low efficient homologous recombination, but still select your cells by Neo resistance

Thank you all very much for your suggestions, I am looking into integrating my gene into a lentivirus (I can't believe I didn't think of that). I'm very glad I came here for suggestions. =) Thanks again.


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What sort of assay could be used to identify mutants with mutator phenotype?
By mutator phenotype, I mean being more prone to mutations, for example due to mutations in genes involved in DNA repair.
I was thinking about exposing the cells to agents that damage DNA (uv light, for example). Compared to normal cells, mutators would be less likely to survive, because they lack the ability to repair damages in the genetic material. To a certain extent, that's the principle of radiotherapy (cancer cells are more suscetible towards radiation).
Are there other options? Moreover, is it possible to select the mutators (instead of killing them)?

What is proner? Do you mean "more prone"? What is "danificate" ?

Most of your question is answered in this previous post of yours.

There are a number of ways to screen for mutator genes. One straightforward approach in bacteria is to take an antibiotic sensitive non-mutator strain, grow it up, and expose to different antibiotics. Cells that survive in the presence of multiple antibiotics have acquired multiple de novo resistance mutations and thus are highly enriched for mutator alleles. Here is one example: Wiegand et al (2008) AAC.


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How to safely sterilize urea-containing growth medium?
I'm using urea-containing growth medium for experiments with bacteria (1-2 l/day). After the experiment, the growth medium has to be sterilized and disposed. I did this so far by autoclaving, but our technician complained about the ammonia smell that develops (urea breaks down when heated, releasing ammonia).
I'm pretty sure the amount released into the air is not dangerous (I've emptied the autoclave several times), especially if you don't purposefully breathe in the first gust of air that comes out after opening, but I think it's useful to look into alternatives. Also I'm not sure if the autoclave might get damaged on the long run.
Does anyone have experience with this? Do you see a way to sterilize larger amounts of growth medium reliably without heating?

You can use chemical methods to sterilize the media - I have used cleaners which develop chlorine dioxide for this purpose. This is smelly as well as you will always smell some of the chlorine dioxide when emptying the vessels.

Is the bacteria potentially pathogenic? What bacteria is it basically?

It's Sporosarcina pasteurii, not pathogenic and not a GMO. I just wrote an email to our safety officer to inquire if sterilizing is absolutely necessary, but I guess I will have to. Also, I might use GMOs in future, and then it's a must.

Bacilli can form spores; I am not sure if this one can. Sometimes I use concentrated acid (H₂SO₄) to disinfect stuff, especially flasks that are long unwashed (with media still in it; they contain a variety of organisms). You can neutralize the acid after the treatment. It is a little dangerous though. Common disinfectants should work for you.

Autoclaving is the best way for sterilization. If your growth medium is large, how much chemical disinfectant do you think you would need to bring up to its working concentration?
Add some acid to your waste medium (so that it's only weakly acidic), not as disinfectant, but to suppress ammonia formation. Urea will still break down during autoclave, but ammonium ion (pKa~9) will generally stay in solution.

You should check with your institutions guidelines as different facilities have different regulations but generally it is acceptable to:
In a fume hood and in a ventilated (unsealed) container:
1.add liquid bleach to a final concentration of 20% (add 1 part bleach to 3 parts culture)
2.Let sit overnight
3.Dispose down drain with copious amounts of water


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Why don't vaccines cause bacterial resistance?
Since bacteria can evolve to overcome antibiotic use, why wouldn't they be able to evolve to overcome antibody or cell-mediated immunity?
(One possible explanation: antibiotics have only one target while vaccines elicit antibodies against multiple targets and multiple T-cell epitopes. Even more targets arise when comparing sub-unit vs inactivated vaccines, where the number of targets are extremely higher using inactivated vaccines, containing whole bacterial cell.)

why wouldn't be able to evolve to overcome antibody or cell-mediated immunity?...They can; Vaccines are not 100% effective. In some cases they are quite efficient.

In vaccine development today you try to choose evolutionary conserved targets for the vaccine to prevent this.

Thanks @WYSIWYG, it would be great if someone could give some reasons.

Actually most of the nowadays vaccines activate B-cells and not T-cells. Ofc. there can be resistance to vaccines, e.g. by influenza. Bacterias have more complex surface than viruses, that's why they cannot change their surface as fast as it would be necessary to overcome vaccines.

One major difference is that vaccine acts in human host while antibiotics act on pathogen. Antibiotics target a specific pathway in the pathogen while vaccines sensitize humans to all the antigens present in it.

Unfortunately, we do see examples of bacteria and viruses evolving vaccine resistance. For instance, vaccine resistant strains of polio and pertussis have recently been identified.
Yet these seem like the exception rather than the rule. One thing that makes it harder for pathogens to evolve resistance is that vaccines usually generate antibodies to multiple antigens, all of which the pathogen would have to alter.
Another reason vaccines tend not to drive vaccine resistance is that the diseases for which we vaccinate are typically those that are not antigenically variable. (Haemophilus influenza is a notable exception; there we use a conjugate vaccine). This may have something to do with how we view vaccine efficacy. For example, we don't say that the influenza virus evolves vaccine resistance--yet we need a new vaccination each year due to antigenic shift.
If you are interested in learning more, Angela McLean has a nice article looking into this question.

There is another reason why Hib is a conjugate vaccine: The polysaccherid from the capsule alone only triggers a relatively weak immune response. The antigen which is used for the coupled vaccine (often tetanus toxoid) makes the answer much stronger.

Influenza vaccines are renewed annually because the viruses change continuously and thus become resistant to most antibodies people develop, vaccine-induced or not. HI virus (AIDS) also changes so often that vaccines are extremely ineffective against it.

@Archimedix: Exactly -- yet we don't say that influenza viruses evolve vaccine (or acquired immunity) resistance. We just talk about antigenic shift. So it's not so much that immune resistance doesn't evolve, it's that we call it something else. You make an important point: HIV is good example of a virus where this evolution occurs within a single host during the duration of an infection.

Also it is noteworthy that the general idea behind vaccines is to "train" your own immune system to the pathogens. Since we are all different a little bit we produce a little bit different antibodies therefore the pathogens do not have a general counter-strategy or selective pressure compared to antibiotics.

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


text:
How long can Cholera bacteria survive in a dead host?
How long can cholera bacterium survive inside a dead host? Can they remain dormant in such conditions?
BACKGROUND
On a hill not far from where I live, there was a hospital operating since 16th until 19th century, for cholera patients, and a cemetery for those, who didn't make it. It was closed in 1st half of 19th century and until 20th century not even ruins of the hospital remained; the gravestones got lost under a layer of soil.
Currently, the area is being built over. Large amounts of soil are being excavated for foundations and basements of new houses. Rainwater falling on the piles of excavated soil floats down through driveways, backyards and gardens of houses down the hill, including my own.
Should I worry?

What is the climate of the region that you are talking about? Is the soil generally moist?

Moderate climate, central-eastern Europe, the soil is common clay loam (I may be wrong on this); the hill top area made persistent groundwater non-issue, but the weather is rather on rainy side and the soil is poorly transpiring water and retains it, remaining moist most of the time.

Do you, or your community, readily use ground water for drinking, cooking, or cleaning of food preparation sites?  I'm inclined to think the "Should I worry" part of the question is off topic for medical advise, but the general cholera question is a good one.

@AtlLED: We have gardens with fruits and vegetables. Our pets run free in the gardens. Sometimes we wear sandals, exposing any tiny injuries on feet to the moisture in the grass. I can easily imagine children picking up food that fell on moist ground and eating it, disregarding hygiene. Also, during rain we inhale droplets of water aroused from the ground by rainfall.

None of what you mentioned is likely to have a infectious dose of v. cholerae.  It's more a problem of directly using the water in your day to day life.

This is relevant again now that James Polk might be dug up.

No, I don't think so.
Mostly estuaries (brackish water) and marine biofilms on submerged surfaces are a reservoir for Vibrio cholerae. Vibrio cholerae is isolated from rivers, creeks, washes, irrigation ditches, hulls of ships, etc. (Indeed, cholera spread rapidly throughout the world after the 1817 epidemic, largely due to the inadvertent transport of contaminated bilge water, mainly from British ships.)

Transmission is by the fecal–oral route. Infections are particularly common after ingesting contaminated water or food. Cases are occasionally seen in people who have eaten raw or undercooked shellfish, particularly oysters, from contaminated waters. V. cholerae is excreted in the feces and vomitus. Viable organisms can be found in feces for up to 50 days, on glass for up to a month, on coins for a week, in soil or dust for up to 16 days and on fingertips for 1 to 2 hours. Bacteria survive well in water and may remain viable in shellfish, algae or plankton in coastal regions.

In 1855, a wave of cholera hit London. Thousands became ill and died before John Snow identified the Broad Street water pump as the single point source of that outbreak. Today, patrons of the John Snow Pub (built on the site) can enjoy local ale, and more importantly, a glass of crystal clear, pathogen-free water.

V. cholerae [is] an autochthonous aquatic bacterium rather than a human pathogen that is a transient resident of the aquatic environment. V. cholerae has over 200 serogroups, with O1 and O139 being the causative agents of cholera, due to their carriage of the genes encoding cholera toxin (CT) and the toxin co-regulated pilus. ...[A]ssociations with the human host is only one small aspect of the V. cholerae life cycle and is not necessary for environmental persistence. ...[T]his bacterium is a cosmopolitan aquatic species that is capable of causing illness in humans.

Vibrio cholerae attachment is mediated by pili, which promote surface attachment and subsequent biofilm formation. It is rather difficult to believe that an aquatic biofilm was preserved on the hill for all those years, even in a dormant stage.

...they could transform into a unique dormant stage that was able to survive for months in the sediment of the estuary. ...These exciting new data enabled investigators to now integrate information regarding the seasonal nature of events surrounding an outbreak in populations living near estuaries.

I have found nowhere that the dormant stage can occur outside of water.
Environmental reservoirs and mechanisms of persistence of Vibrio cholerae
Medical Ecology Main Page
Cholera
 Something goofy going on with these, sorry.


text:
In which of the following diseases structure of haemoglobin produced is normal but their amount reduced?
The options provided are-

Chronic blood loss
Sickle cell anaemia
Haemolytic anaemia
Thallasaemia
Transfusion reactions
               -

*Q-15: pg-785; **Review of Medical Physiology - William F. Ganong;    International 22nd Edition***
Here, the answer provided is (4), i.e Thallasaemia...
My point is that, Thallasaemia is essentially a genetic defect resulting in mutation of either alpha or beta or both the chains, thus rendering the structure of haemoglobin fragile....the disease as far as I know don't cause any reduction in blood volume...
According to me option (1) i.e chronic blood loss is more feasible as in case of diseases resulting from nematodes like Hookworm (Ancylostoma duodenale)....
So, where am I wrong???

It's a misleading question, and I agree that Thallasemia is the wrong answer.

1, 5 and sometimes 3 too (based on what is causing hemolysis) can be correct @anongoodnurse

You are correct, Thalassemia is the wrong answer.
In Thalassemia and Sickle Cell Anemia, the structure of Hemoglobin is altered.

Chronic Blood Loss: Here the hemoglobin and packed cell values will be low, however there is no alteration in structure of either RBC or Hemoglobin
Hemolytic Anemia: This is a host of conditions which can cause hemolytic anemia. Some mechanisms where Hemoglobin structure remain normal would be:

The structure of RBC membrane is altered, this will make RBCs less maleable and cause early destruction - Example: Spherocytosis
G6PD Deficieny - In this the deficiency of G6PD will decrease the ability of Red Blood Cells to handle oxidative stress and when subjected to sudden oxidative stress, hemolysis will occur. Here the structure of both RBC membrane and Hemoglobin are normal.

Transfusion reaction (I am talking about only hemolytic transfusion reaction, there are other transfusion reactions too): Here the problem is the host reaction to transfused Red Cells. The host was initially severly anemic (Therefore low Hb) for which transfusion was done, now the host immunity is reacting against transfused RBCs which have normal Hemoglobin, resulting in reduced RBC counts and Hemoglobin. So this too can be taken as a correct answer as the end-result will be severe normochromic normocytic anemia.

Well-formulated answer+1


text:
What will happen if a scorpion pierces itself?
If a scorpion pierces itself, will it die or immune to its poison? If it produces the venom its blood should be immune to itself poison.

Not necessarily. If the venom is produced and stored in an isolated venom sac or other container, the rest of the scorpion might not be exposed, and wouldn't need to be immune. Not familiar enough with scorpion physiology to really know, but I do know that a common component of scorpion venom is phospholipase, an enzyme that can disrupt membranes. These enzymes are usually produced in an inactive form that must be activated by removing part of the enzyme. Other venom components may be stored in inactive forms as well.

Cross-posted on Skeptics.

I am sorry. I have deleted it on Skeptics.

If scorpions evolve by fighting each other, perhaps there is a kind of 'arms race' where the anti-venom of one scorpion is stronger than the other's sting, it will survive it...but if the sting of one is stronger than the others antivenom, it will win the fight , kill or stun it? Is this how scorpons have become more toxic over time?
https://www.youtube.com/watch?v=zB5xiog7jk8

Scorpions are immune to their own venom (reference) as has been said in some studies as well (reference) But some other studies and eye witness accounts have referred to the contrary.

in an experiment a scorpion, Bulteus australis, was killed by an
  injection of the same venom as its own (reference).

So, it should be safe to say that there is a very low chance for a scorpion to be affected by its own venom. It is said that

Mutations in the scorpion’s own membrane protein genes make the
  arachnid immune to its own venom (reference).

A scorpion could die quickly if venom is injected into its brain (nerve ganglion). Larger species inject a higher amount of venom to overcome the smaller ones and should have specific neurotoxins if smaller scorpions are their prey to disable them (reference).

Didn't know this one was answered +1. I tried, and failed :-) Haven't seen you around for a while!

@AliceD Busy with some paper writing and PhD applications.. hard to get into a decent funded PhD project these days so the effort continues.. :)


text:
How to predict the top microRNAs that bind to 3`UTR of a specific gene
I would like to know whether someone could tell me
1) some of the online programs that will predict the top microRNAs that bind to 3`UTR of a specific gene (for eg-GAPDH).
I am relatively new to the field.
thanks

You'll find TargetScan quite useful. You can pick from a number of species and simply enter a gene name. It will then get the 3' UTR, show its conservation across species (binding sites in a conserved area are more likely to be active), find miRNAs that can bind to the 3'UTR, and then split those up by whether they bind to highly or poorly conserved regions. It also categorizes the hits according to various properties, like proximity to the open reading frame, in case you want to perform any sort of filtering by that.
Edit: BTW, you may want to take the target miRNAs and look at their expression in your tissue of interest. That's a good way to further narrow down their relevance.


text:
Why can bacteria resist topical antibiotics, but not compounds like Benzoyl Peroxide?
I excerpt from p 2 of 4, but p 4 of 4 reviews the entire article by Debra Jaliman, MD on Apr 17 2014.

Usually, topical antibiotics aren't recommended alone as an acne treatment, as they can increase the risk for antibiotic resistance in skin bacteria. However, using benzoyl peroxide with a topical antibiotic may reduce the chances of developing antibiotic resistance.
[Source:] Substances that kill acne bacteria by inflammation, such as benzoyl peroxide, oil of cloves, and chlorhexidine gluconate. Bacteria don’t develop resistance to these treatments, but they don’t kill as many bacteria, either.

If topical antibiotics can cause antibiotic resistance, why can't compounds like benzyl peroxide? I ask in general about other bactericide, not just benzyl peroxide.

Antibiotics ARE compounds, and they kill or inhibit the growth of bacteria by specific mechanisms. Each class of antibiotics has specific mechanism of actions. Given enough exposure to these antibiotics compounds, bacteria can develop specific molecular mechanism to nullify their effect, and hence antibiotics resistance. Antibiotics resistance will eventually develop with enough exposure to drive the organism's evolution . Whereas there are combination therapy, there are multi-drug resistance; whereas there are wonder drug, there are super bug.
General disinfectant compounds such as benzoyl peroxide or sodium dodecyl sulfate (in soap and detergent) have no specific molecular target that would differentiate host and intruders and hence can harm bacteria as much as the host cells. They are safe to use only because you have skin to prevent their intake. Since there is no molecular target to mutate to develop resistance, the resistance to general disinfectant will simply take a very long time.
That is to say, who could ensure bacteria cannot develop resistance to benzoyl peroxide? Resistance to phenyl derivative has long been reported [1], and bacterial catalase can easily break down the damaging effect of peroxide.
[1] Heinz Berger and Orville Wyss. J of Bacteriology (1953) vol. 65 p.103

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


text:
What worms devour the body?
I was reading this site which broached comedones, an esoteric word to me; so I thought to look up its etymology which I find exceptionally singular and peculiar (I would have never guessed that the word originated from to eat up !) :

Etmyonline: "blackhead," etc., 1866, from Latin comedo "glutton," from comedere "to eat up" (see comestible). A name formerly given to worms that devour the body; transferred in medical use to secretions that resemble them.

Footnote: ODO also offers an etymology.

How the body is degraded depends entirely on the manner of body preparation and burial.

And the "worms" most likely to eat a corpse are probably maggots.

Maggots that typically feed on the carrion can be from different flies species, the most common in Europe are from the family of Calliphoridae and Sarcophagidae.

A maggot typically feeds on carrion. A maggot is the larva of a fly and usually  particular to the larvae of Brachyceran flies, such as houseflies, cheese flies, and blowflies.

Interestingly decomposition from maggots has a lot of use in forensic science as the presence or development of maggots on a corpse can be useful to a forensic entomologists to determine the approximate time of death. Depending on the species and the conditions, maggots may be observed on a body within 24 hours. The eggs are laid on the body and when the eggs hatch, the maggots move towards their preferred conditions and begin to feed. Insects are usually useful  25–80 hours post mortem and is contingent on temp humidity and oxygen availability. After 80 hours, this method becomes less reliable.


text:
Are the irises an exact match in a human's set of eyes?
Are the irises an exact match in a human's set of eyes? Assuming the eyes are healthy with 20/20 vision.

Short answer
No. Not two irises are alike, including the irises of identical twins and even the two irises of one and the same person. This uniqueness of the human iris is used in iris scans. The variety of the iris is caused by its complex structure and coloring pattern.

Source: Jean-François Mainguet
Background
The iris is explained on Biometric Technology's website, and I quote:

The iris [...] is a thin, circular structure in the eye, responsible for controlling the diameter [...] of the pupil [...]. “Eye color” is the color of the iris, which can be green, blue, or brown. In some cases it can be hazel (a combination of light brown, green and gold), grey, violet, or even pink. In response to the amount of light entering the eye, muscles attached to the iris expand or contract the aperture at the center of the iris, known as the pupil.

A striking example of the dissimilarity of the iris in one person are people with heterochromia. Heterochromia can result in both eyes having a different color. Examples are given in the figure below: On the left is Demi Moore (if you look closely her right eye is hazel, while her left eye is green). On the right-hand side a more striking example is shown (taken from the Kliproject):

Heterochromia iridium (differing iris colors) and heterochromia iridis (a variety of color within a single iris) are relatively rare in humans and result from increased or decreased pigmentation of the iris. Most cases are the result of an alteration in the expression of the EYCL3 gene (which codes for brown/blue eye color) and EYCL1 (which codes for green/blue eye color), among other genes within the cells of the entire iris or even a particular section. Other potential causes include trauma around the time of birth or later in life, congenital pigmented nevi or even medications such as those used in the treatment of glaucoma.
Fun fact
David Bowie's eyes are in fact of the same color - his pupils are of a different size:

Reference
Scientific American (November issue, 2001).


text:
Are any biology research journals free to publish in?
The research journals Ive published in require significant financial cost to publish. On top of that many require a membership to the society the journal is associated with, in addition to publication fees. I was wondering if anyone is familiar with any journals (reputable hopefully) that do not require fees like this to publish a research article?

I'm not sure if this is on-topic here. Perhaps Academia SE would be a better fit.

Many biology journals are free to publish in. As a rule of thumb:

Most journals from for-profit publishers such as Elsevier, Wiley, etc. charge nothing to the author (but of course bill the libraries handsomely).
Many but by no means all society journals charge page charges even if they are not open access.
Most but not all open access journals charge substantial publication fees. You could try this website to search for open access journals that do not charge publication fees.


text:
Why do people with Down syndrome get fewer cancers?
I'm coming across some conflicting information regarding the correlation between cancer incidents and trisomy 21. I read a report from nature that discusses how Downs are only a tenth as likely to develop cancers, but at the same time are 20x more likely to develop certain B cell malignancies.
One of the more prominent findings show that a regulator of angiogenesis, DSRC1 plays a significant role.
What I'm trying to find out is what gene(s) on 21 contribute to the associated risk for lymphoma?
And does there exist a good list of those genes on 21 that suppress or enhance tumor genesis.

Do the sources you're reading consider the fact that life expectancy is reduced to ~55 in those with downs (http://www.nads.org/pages_new/facts.html), and cancer is generally a late life disease (http://www.cancerresearchuk.org/cancer-info/cancerstats/incidence/age/#Cancer) ? Just a thought..

Certainly an important thing to consider. But in many ways people with DS show a progeroid phenotype in that their blood/brain/intestinal systems seem to prematurely age. Other than the cancers mentioned here, they do precociously develop Alzheimer's Disease. Though many doctors like to explain this by the presence of APP on Chr21 rather than a premature aging phenotype.

@GriffinEvo I think that's due primarily to high incidence of cardiac disease in persons with trisomy so maybe a different issue

@The Nightman, what's interesting is data shows critical genes in AD such as ApoE, PS1, APP etc. are also critical in development in some cancers.
http://www.nature.com/nm/journal/v18/n12/full/nm.3033.html
http://www.cancerci.com/content/9/1/15
http://www.ncbi.nlm.nih.gov/pubmed/17332312

This is great I never saw this paper, thanks for bringing it to my attention. And maybe you know a bit more about this than I do, but to me it looks like ApoE is the only protein associated with this metastasis and angiogenesis. How would APP play a role? And also how does that factor into to reduced angiogenesis in DS?

@rhill45 my point was that, if downs sufferers die on average before cancer becomes prevalent, then that could explain the pattern

@GriffinEvo ah is see now. Good point. &I would hope whatever epidemiologist would have restricted the control group down to  include only people under the median survival age of people with downs

This is a great question. Just to make it clear people with DS do have a reduced risk of solid cancers and an increased risk of blood cancers, (B-ALL and AML).
You are correct in picking out DSRC1 because of its angiogenic implications. The current hypothesis centers around people with DS being less capable of driving angiogenesis, and therefore having an internal environment that is less nurturing to metastasized or even developing solid cancers. Current unpublished work I have recently seen shows this very clearly in the eye, where the vasculature in DS is far less branched than in the wild-type population.
Why however they show an increased risk of leukemias is a largely unanswered question, with one exception being AMKL (Acute Megakaryocytic Leukemia). People with DS are at a ~500X increased risk of AMKL over the unafected population, and it appears to be entirely driven by the in-utero introduction of a stop mutation in codon 2 the transcription factor GATA1. This transcription factor is important in driving differentiation of progenitor cells in the bone marrow to become erythrocytes and megakaryocytes. Thus inactivating this transcription factor plays a large role in disrupting normal hematopoiesis such that megakaryocytes are overproduced and become a leukemia.
All that being said, and as you mentioned people with DS have around a 20-50X increased risk of AML and B-ALL. There are certainly some chromosome 21 genes that have been implicated in this like Bach1 (important in DNA repair) Ifngr2 (plays a role in cell death) Usp16 (epigenetic regulator Really important recent Nature Paper) and Runx1 (important in stress response) but the field is entirely unsure why this directly leads to increased risk of leukemias. Many current cancer biologists favor the direct gene-dosage problem that people with DS face in that a some ~120 genes are overexpressed when they shouldn't be, and assume that these gene level cocktail directly leads to this increased risk of leukemogenesis, and this very well may be in part the answer. There is however a great 'contrarian' view, in that hematopoietic stem and progenitor cells will become pro-apoptotic and pro-differentiative when faced with certain stresses like aneuploidy. The effect of this on a global scale would be that many of the stem and progenitor cells in the bone marrow would die or differentiate prematurely. This would then result in teenagers with DS having far fewer blood stem cells then they should, and these cells would then be tasked with pumping out more blood per cell than originally meant for them quite possibly leading to an exhaustive phenotype. In this way the blood systems of people with DS will 'prematurely age', and might thus rapidly increase the risk of cancer.
Make sense?

I know a little soon but I'm gonna take this answer there's some good info and perspective on here.  it's a big area of study and author did a good job of summarizing. Thank you for mentioning additional genes

Glad to hear it. I think this is a really important question, and is an intriguing area of study, especially because the causes of blood cancers in DS may be part of the key to understanding oncogenesis in the unaffected population.


text:
How much pollen is needed to pollinate a flower?
Assuming 100% of the pollen gets delivered to exactly the locations it needs to pollinate a female flower, how much pollen is needed to pollinate a flower? If it's more than one unit of pollen, what, if anything, prevents more than one plant's pollen from pollinating the flower?
If we need an example plant to answer this question, let's assume zucchini. For instance, if you plant a zucchini in the middle of a spaghetti squash and an orange-fleshed squash, is there any likelihood at all that you'll get a single zucchini pollinated by both in one generation (such that the next generation of cross-pollinated zucchini would be both stringy and orange-fleshed instead of just one or the other)?

A single ovule in a fruit is pollinated by a single grain of pollen. So, in theory, a fruit with n seeds can be pollinated by n grains of pollen. In reality, of course, not every pollen grain makes it to the ovules, but if we treat your assumption as true, then a flower can be fully pollinated by as many pollen grains as there are ovules in the flower.
If you plant your zucchini and cross your zucchini flower with pollen from spaghetti squash and orange-fleshed squash, you will end up with a zucchini fruit filled with seeds that are either half spaghetti squash or half orange-fleshed squash. If you planted the seeds from that zucchini, you would end up with some individual plants that have spaghetti-squash traits and some with orange-fleshed squash traits. You would not end up with any plants with both stringy and orange-fleshed fruit.


text:
Why does the protection afforded by some vaccines last longer than for others?
After reading an answer to the question of How Do White Blood Cells Learn? Or Do They?, I came to wonder something. Specifically,

The effect of this is that every new B and T cell that your bone marrow makes will recognize a unique, random protein sequence, and you will have billions of these cells floating around in your blood circulation at any given time. These cells however will only float around in circulation for a short period of time before dying and being replaced by other cells with new random sequence receptors.

Assumption: What I gather from this (and the remainder of the answer) is that basically, a vaccine "teaches" the existing white blood cells in your body; eventually, these cells will  be purged, so you will no longer be immune.
However, many vaccines seem to only be once-in-a-lifetime, or at least require a vaccine only once per decade (or less).
Some examples would be the Varicella vaccine, which can last up to 20 years, the Tetanus vaccine, which recommends a booster every 10 years, and the HPV vaccine, which lasts 5-6 years. Durations also vary with Hepatitis, Influenza, Polio, and numerous other common vaccines.
I would assume that, regardless of what a cell has "learned," it is purged with the same likelihood as any other cell; yet, it seems that some "learned" defenses can be retained longer than others. In essence, my question is: Why do some vaccines take longer to "wear off" than others?
(Note: This question is not a duplicate of Why do I need a flu shot every year, while many other vaccinations last years or even a lifetime?; I understand that some pathogens can mutate, so immune cells are of no use against mutated strains since they were not vaccinated against the mutation.)

http://m.historyofvaccines.org/content/articles/top-20-questions-about-vaccination#5

"It’s not completely understood why the length of acquired immunity varies with different vaccines... Recent research has suggested that the persistence of immunity against a particular disease may depend on the speed with which that disease typically progresses through the body. If a disease progresses very rapidly, the immune system’s memory response may not be able to respond quickly enough to prevent infection—unless they’ve been “reminded” about the disease fairly recently and are already watching for it. Boosters serve as a “reminder” to your immune system." (taken from ref. above)

The first thing I want to make clear is that, the B and T that "will only float around in circulation for a short period of time before dying and being replaced", are not the ones that have already learned to recognise a certain diseases (or vaccine) but rather the naive cells that haven't yet done so. This is also made clear later in the same answer you cited:

As these injected protein sequences circulate through your blood they
  will eventually bump into a B or T cell that has a receptor that
  recognizes them. When this happens, the B or T cell will now start to
  divide and give rise to long lasting memory cells that express the
  exact same receptor and will therefore recognize the exact same
  protein sequence again in the future. These cells will float around in
  your blood for most of your life and make you 'immune' to the
  recognized pathogen.

In order to understand why some vaccines hold for your whole life, while some need a booster every few years we need to look at the life time or recycling of those memory cells, which stay in your body for much longer than the naive immune cells.
Now we come to the actual answer(s) to your question and there multiple  factors that (can) have an influence on this:

Initial strength of the immune response: Every vaccine (and/or disease) evokes an immune response with a different strength. Generally the stronger the first response is, the more memory cells will be created initially (those actually don't have correspond to the same molecular memory either, they might recognise different aspects of the vaccine/disease) and with more cells available it will take longer until none are left
Natural exposure: memory cells start proliferating when they encounter the molecule (protein/virus/bacteria) which they have 'memorised', if there is an acute infection they will do so a lot in order to produce a lot of antibodies against it. However, even a very small amount of virus/bacteria, that wouldn't actually make you sick, will allow induce them to proliferate and preserve their numbers. Therefore memory cells against a more common or prevalent disease should be more stable in your body, than ones against a very rare one.
There very likely more factors that either I or the whole scientific community don't really know about. Cellular systems and the immune system in generally are rather complicated ...

This issue is deep but one answer is bacteria/virus genetic variability. Some organisms have the ability to change their DNA in just a few generations (for example the influenza virus which requires a new vaccine every year). When you take a vaccine for influenza virus you expect that will protect you in a short period of time (winter season) because this virus is a nasty one, i.e it has the ability to present antigen variability due to mutation/constitution of its DNA and antigen is the source of power of vaccine (a vaccine assumes the organism has a antigen that could be a protein or other biomolecule that is relatively fixed between generations and is specific to that organism) so the vaccine loses its effect because the organisms are no longer susceptible which causes immune response to be weak (no longer recognizes the organism as it recognized) and you get sick. If the organism has slow mutation/variability the vaccine will last longer because the antigens are present for a longer period of time but eventually you will need to get another vaccine years later (for example tetanus).

References are appreciated here at Biology.SE. Nice answer, though +1

So the vaccine for tetanus changes over time?

Please see the note below the question.