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

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

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

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

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

and antibiotics as:

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

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

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

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

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

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

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

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

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

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

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

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


text:
Differences between comatosed states and brain death
What are the neurological, physical, etc. differences between someone who is in a coma (one that is not medically-induced) and someone who is colloquially deemed "brain dead" (being physically kept alive by machines)? Is there a certain minimal brain activity that is present in a comatosed state that is not present in brain death?
I found a decent definition here which defines the difference as:

Brain death: Irreversible cessation of all functions of the entire brain, including the brain stem. A person who is brain dead is dead, with no chance of revival
Coma: A state of profound unresponsiveness as a result of severe illness or brain injury

I can find other similar, vague definitions in a few other places.
I am wondering what is different about the neuronal structures or electrical activity between brain death and coma. Is there simply no (zero) neural/electrical activity with brain death, whereas there is with coma? What would be physiologically different with brain death that would prohibit such neuro-electrical activity?

Why the DVs? The question is on topic, is not a dupe and shows preliminary research. I had asked this on MedicalSciences.SE and they told me to ask it here instead.

I suspect the issue is that you haven't shown any research or attempt at answering your own question. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Additionally, the answer is kind of obvious - the difference between someone who is comatose and one who is brain dead is that the comatose person still has brain activity, while the brain-dead person does not. You need to specify what else, if anything, you want to know beyond that.

Thanks @MattDMo (+1) - please see my edits. Online definitions (like the one provided) are all vague and seem to target edifying the laymen.  I am wondering from a physiological perspective: what would cause brain death to the point where there is no neuro-electrical activity possible or observed across the brain? But, that does not inhibit such activity in an individual who is only comatosed?

I'd recommend reading a review paper on disorders of consciousness, which cover the spectrum of minimally conscious states, vegetative states, and coma. Brain death is outside the context of disorders of consciousness, but is often discussed for comparison. Nico Schiff is one expert in the area; I've attached a reference to a review he coauthored at the bottom and I'll draw mostly from that review in this answer.
Schiff and Fins write, with some bolded emphasis by me:

At present, brain death is diagnosed if clinical evidence of the complete loss of brainstem function is present at the bedside and the patient demonstrates a failure of ventilatory drive in the setting of documented hypercapnia (significant elevation of blood partial pressure of carbon dioxide over a chosen threshold) — the ‘apnea test’. Fulfillment of these criteria should invariably associate with an ‘empty skull’: no sign of any metabolic activity or blood flow measured by positron emission tomography, a ground truth linking the biological model to the clinical assessments

The first two statements are most relevant clinically; PET is not commonly used except in research and rare cases of uncertainty. Biologically, brain death is when the brain is...dead. There is no recoverable neural function. The signs are a lack of any brainstem reflexes, including lack of respiratory drive. Additionally, other potential causes of these symptoms (such as pharmacological causes) must be ruled out.

Coma is a state of unconsciousness, but some brain functions are preserved. Again from Schiff and Fins:

Both comatose and vegetative state patients are unresponsive to environmental stimuli, although reflex movements may be present; in neither condition are goal-directed behaviors initiated. Comatose patients lack state variations and typically remain in a closed-eyes state that is unchanging even when presented with the most vigorous stimulation.

Comatose patients do not meet the criteria for brain death described above, but do have a complete inability to respond to stimuli and do not make purposeful movements besides reflexes. Schiff and Fins (and others) compare this state to deep anesthesia. Though your question posits that there should be some distinction between medically-induced and one that is not, there is really no functional difference. The possibility of recovery is tricky to assess, but generally patients who spend a long time in coma have a worse prognosis than those that do.
The clinical approach is different. A brain dead patient is dead. Nothing can be done to recover function; potential for organ donation can be considered, but there is nothing medically to do for the individual. For a comatose patient, it's more complex, and decisions need to be made regarding the level of medical support to provide given expected prognosis in both probability and extent of recovery.

In brain death, the neurons are dead. The lack of electrical activity is not because they are in some quiescent state, it's because they are dead. With coma, it's less clear except that there are signs that some neural function remains. Coma is really a clinical state, not a biological one. It's not always possible to determine the level of irreversible damage in a comatose patient, nor the extent of possible recovery.

Schiff, N. D., & Fins, J. J. (2016). Brain death and disorders of consciousness. Current biology, 26(13), R572-R576.

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Is there is difference between "homozygosity" and "homozygosis"?
Are these just two terms for the same phenomenon, i.e., the state of being homozygous? Merriam-Webster says so, but I know dictionaries sometimes miss the nuance of scientific terms. If they are indeed synonyms, it seems homozygosity has won out, according to Ngrams

The question is currently receiving close votes because it looks like a homework question. You should try to show your attempt at answering your question if you want to avoid having your question closed.

Ha, fair enough. I am not student. I am a hamster breeder with a keen interest in genetics. I had this question because I only saw the term "homozygosis" in publications from several decades ago. I edited the question as suggested.

I edited my question to show my attempt at an answer. Can it be returned to open status?

I made the changes that were requested. Why was this question closed?

Homozygosis and homozygosity are NOT synonymous. The two terms refer to the same concept though.
Homozygote
An indivdidual or a cell is said to be homozygote for a particular gene (or any DNA sequence) when identical alleles of the gene are present on both homologous chromosomes. (Wikipedia > Zygosity).
Homozygosis
Homozygosis is the state of being homozygote (Wright 1933) for a particular gene (or any DNA sequence). According to freedictionary.com, homozygosis may also refer to the process of formation of a homozygote. I have never encountered this sense in the literature though. As you found out by yourself, Homozygosis is a term that is rarely used in the literature (in comparison to homozygote and homozygosity)

Expected Homozygosity
Expected Homozygosity is the probability of two randomly sampled alleles (in a population and at a given locus) to be identical by descent.
Expected homozygosity and Expected heterozygosity
As shown in Nei 1973, the mathematical expression of expected homozygosity $Ho$ is
$$Ho = \sum_{a=1}^{n} x_a^2$$
where $n$ is the number of alleles and $x_a$ is the frequency of the allele $a$.
It is more common to use the concept of expected heterozygosity $He$ (a.k.a. gene diversity) rather than the one of expected homozygosity $Ho$. By definition, $He=1-Ho$, that is
$$He =1- \sum_{a=1}^{n} x_a^2$$
In the special case of a bi-allelic locus, and replacing the two allele frequencies $x=1$ and $x=2$ by $p$ and $q=1-p$, the above formulations becomes
$$Ho = p^2 + q^2$$
$$He = 1 - (p^2 + q^2) = 2pq$$
Hardy-Weinberg equilibrium
Under the Hardy-Weinberg assumptions, the observed frequency of heterozygote (a.k.a. observed heterozygosity) is equal to the expected heterozygosity and observed frequency of homozygotes (a.k.a. observed homozygosity) is equal to the expected homozygosity.

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text:
Potential evapotranspiration constant for trees in the area of London
I am trying to find the ET0 (Potential evapotranspiration) under the climate conditions of London (UK) and Coimbra (Portugal) for each month. From what I understand these data is available in the FAO's website but I was struggling to find it.

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Is there a more updated version of the book "Genome?"
I read the book Genome by Matt Ridley for my AP biology course. I found it fascinating, although it seems another book must have been written on the topic since 1999. Anything you can recommend?

How much science have you had sense AP bio?  It would effect my a recommendation.  More details are always nice for a question like this, so that an answer doesn't seem primarily opinion based.

Not much. I took it last school year, so I finished it last May. What I liked about Genome is that it didn't require a ton of understanding of genetics and explained many things without using advanced science jargon. That being said, I myself could probably take on something a bit more challenging with the help of Wikipedia and my science teacher.

What is AP biology?

@WYSIWYG Advanced Placement Biology. High school Biology course equivalent to a first semester college Bio course. The syllabus is defined by CollageBoard.


text:
Is there an entry-level circadian model of serotonin, ghrelin, dopamine and the sense of well being?
I've long been interested in circadian rhythms and recently came across a variety of articles that appear to indicate that the following neurotransmitters, transferases and hormones are connected. There are mentions of some circadian rhythmicity and maintaining homeostasis for these compounds(Are serotonin levels in humans affected by light?):

Serotonin
Dopamine
Melatonin
HIOMT, NAT
Ghrelin
Leptin

Additionally, their expression is related to Suprachiasmatic Nucleus and light exposure.
I'm interested if there's a good article or a talk that discusses the homeostatic system that those compounds are a part of. I'm particularly interested in their effect on the feeling of well being.
It seems to me that all these compounds are in some way related to moving and feeding. However, I cannot wrap my mind around multiple separate articles that describe how, and am looking for a single paper that may shed light on the connection between these compounds.

Most hormones have some circadian/ultradian/infradian component. These questions are somehow related to what you're asking: http://biology.stackexchange.com/questions/2732/do-men-have-significant-hormonal-cycles http://biology.stackexchange.com/questions/1982/what-can-the-timing-of-human-urination-tell-about-the-humans-physical-condition/ http://biology.stackexchange.com/questions/3590/how-are-long-time-periods-measured-in-biological-systems/


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Do hormones make men think of sex?
I remember hearing a saying that goes like "men think of sex every 7 minutes (or seconds?)". I take this saying to mean that men have sex related thoughts more often than women.
I'm interested if these thoughts are related to hormone expression within the male body. particularly, I'm interested in the very few seconds before a sexual thought emerges - one moment a man is thinking about daily stuff, next moment his thinking has sexual content. What is responsible for this shift in thinking?
I've read that oxytocin is responsible for men feeling romantic attachment to a partner, but is there a hormone that initiates sexual thoughts or fantasy? For example, would a burst of testosterone increase the likelihood of a man thinking of sex?

Interestingly it does seem as if this is at least in part the case.
Testosterone levels are tied to sexual impulses, but also risky behavior and aggression.  Its responsible for sexual drive in women as well.  Low testosterone can cause depression and loss of the ability to make decisions.
You'll note that the work cited is done on criminals, patients and rats.  Remember that is not medically or scientifically ethical to change the androgen levels of a functioning human being.  Testosterone supplements might increase the chances of prostate cancer.
While its not scientific, there's a fascinating set of interviews about how testosterone affects human thinking at this transcript of American life, Act 2 :

After testosterone, there was no narrative. There was no language
  whatsoever. It was just, I would see a woman who was attractive or not
  attractive. She might have an attractive quality, nice ankles or
  something, and the rest of her would be fairly unappealing to me.
But that was enough to basically just flood my mind with aggressive,
  pornographic images, just one after another. It was like being in a
  pornographic movie house in my mind. And I couldn't turn it off. I
  could not turn it off. Everything I looked at, everything I touched,
  turned to sex.

thanks for putting in the quote @AlexStone!  Well done!  This is all anecdotal, but a lot of men seem to find it a reasonable reaction to a flood of testosterone in their brain.

"Low testosterone can cause depression and ability to make decisions" ?? Does low testosterone give the ability to make decisions, or is this a typo?

its not a typo.  the hormone doesn't do anything though.  For humans it is interpreted by our brains and other tissue to all these effects.  It could easily not mean these things if the selection pressure of human evolution had been different.  I have no doubt that some individuals have very low testosterone and do not have these problems, but its a common problem in testosterone inhibition therapy for instance.

Yes, I understand that. In that case I believe there is a grammatical error in that sentence, as it doesn't really make sense.


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Why do grapes not pea shrink when placed in strong sugar solution?
I tried an experiment. First, I placed grapes in pure water(hypotonic solution). The grapes burst because of endosmosis. Then, I placed new set of grapes in strong sugar solution(fully saturated) but they did not shrink. And then when I placed it in strong salt solution(fully saturated), they did shrink a little. Why does this occur?
How is this possible?

What is a strong sugar solution? Grapes contain ~15-20% of sugar.

According to Wikipedia fully saturated sucrose solution should be 2000g/L, way above the 15-20% sugar content of grapes. Interestingly the versions of this experiment that I can find online all use salt for a hypertonic solution. Of course this could be just because it is cheaper than sugar.

Why are we so sure that osmosis can happen in both directions in grapes?

@rwst - The grapes are probably dead, so any trans-membrane pumps would most likely be inactive. That leaves pores and other entry points for water to equilibrate. There's also evidence in the experiments above; because of the membrane potential maintained by ion concentrations (fewer in the cytosol) the saturated salt solution would cause water to leave the grapes and also cause the smaller ions to enter the grapes to dissipate the membrane potential. Sugar isn't small, though, and requires active transport (to the best of my memory).

Well, without the details of your experiment to cross-check with the sugar and H2O content of your average grape, I'd say the saturated solution probably approximated the natural molarity of sugar in the grape. At least to the point it didn't make any advese effects noticeably on your time scale.
That seems the most apparent solution to me. I suppose it's also possible (though I don't know the mechanics behind it) that hypertonic solution might have acted as a preservative - similar to jam. It's not just water which will attempt to reach an equilibrium, but all compounds that can pass through the membrane - perhaps sucrose/fructose/glucose can do so, maintaining the structural integrity of the grape.
Both are guesses until you reveal more information, though.

please see the question now .... I have added some more information and then help me!

It is important to note that osmotic pressure is a colligative property, which means that it does not depend on the identity of the solutes, but simply their concentration. This also means that in considering the grape, we have to estimate the concentration of all solutes, not just the one you used to make the (possibly) hypertonic solution.
I'll assume the sugar used was sucrose, which is the common table sugar. I guess I should also mention that I'll assume the salt was NaCl, which is the common table salt.
Wikipedia says that the solubility of sucrose is 2000 g/L. As the molar mass is 342.3 g/mol, the concentration is approximately 5.8 M.
NaCl on the other hand, has a solubility of 359 g/L. At 58.44 g/mol, the concentration is approximately 6.1 M. However, the Na+ and the Cl- dissociate in water, so the concentration is effectively double when counting solutes. That gives 12.2 M, which is much higher than a sugar solution. This accounts for why grapes would shrivel in a salt solution more than in a sugar solution.
As to why the grapes did not shrink in a sugar solution - I don't think it is unreasonable for a grape to have total solute concentration in the range of 5.8 M. Estimates of the sugar concentration in a grape are given in % w/w. Clearly grapes are denser than water (you can test this by putting a grape in water and seeing it sink). Therefore if you were to calculate in % w/v, you would find it to be more concentrated than a the same % w/w solution in water. Moreover, according to this site grapes have a significant amount of glucose and fructose. These are monosaccharides, as opposed to sucrose which is a disaccharide. This means for the same mass of "sugars" there are more individual sugar molecules, resulting in more osmotic pressure.
In sum, I think the sugar solution is probably isotonic, not hypertonic.

i tried this experiment but failed.
The reason for our failure in this experiment might be as follows:
 1. The grape coating might be immpermeable.
 2. It may happen that the solution might not be hypertonic but isotonic(equal concen. of solutes in both)
 3. The salt solution might be less dilute than the sugar one.
i am just a student but giving my point of veiw....

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What is the biological basis of "energy" that extraverted humans draw from social engagements and introverts expend?
This question is related to this question about introverts becoming exhausted after extended social events on cognitive sciences stack exchange.
As I read more on the topic of human extraversion-introversion, I keep seeing the mention of "energy" which extraverts draw from social engagements and introverts expend in such engagements.

When energy is drained, the state can be called "exhaustion", depletion, being drained
When enough energy is accumulated, the state can be called "elation", being energized

The idea makes sense, and I see many diverse writers use it, but nobody defines what this energy is in a biological sense.
What is the biological mechanism behind "energy" spent/gained in social interactions - what is it in brain terms? I'm looking for an answer like: Dopamine in X part of the brain? Mirror neuron activation? Amygdala overreacting?
I found a quote from this article on introversion, although it does not seem to have any sources listed

Research has shown that the mind of an introvert works differently
  than the mind of an extrovert. Introverts have more pronounced
  activity in the parts of the brain that deal with long term memory,
  planning, complex thinking and organizing. Our introverted mind is
  always turning and running and because of this, we need very little
  outside stimulation. The extrovert's brain has more pronounced
  activity in the areas associated with sensing and processing
  information from the outside. That's why extroverts seek outside
  stimulation

What are the scientific names of the brain regions described in the quote above?

You are probably asking this question 50 years too soon. If we don't know how sleep works then I doubt we know how psychic energy works.

A completely anecdotal observation: extraverted people are more physically active in social situations and use more gestures/movement. They would be moving more than introverted people (who are more likely to just sit and listen), thus extraverts may benefit from improved blood circulation, thus sustaining higher levels of engagement for longer. An introvert who's engaged in an interesting conversation moves/gestures just as much as an ordinary extravert, and thus feels less fatigue from social situations.

Another observation: Both extraverts and introverts would be fatigued by an extended "sit here and listen to me talk" kind of meeting that runs for 2 hours.


text:
Who were "Dawson and Wilson" (mentioned as authors of an embryonic postmortem examination method)?
A sentence from a Russian text I'm translating:

Following the drug administration period, the pregnant animals were euthanized in order to examine the embryos using the method developed by Dawson and Wilson.

That made me curious. Who were they? Google fails to bring up both these surnames at once in response to queries like "Dawson Wilson embryo necropsy" etc. Maybe one of them developed an embryo examination technique, and the other perfected it?

So this isn't a citation? Those surnames are not followed by a year, like Dawson and Wilson, 1972?

@LinuxBlanket - no, there is no reference, no footnote. There's another mention of Dawson several pages down the document - a mention of "embryos stained using the technique developed by Dawson".

I updated my answer. I couldn't find any specific reference to some article by Wilson, but I think I found out which Wilson is it.

This article (A Note on the Staining of the Skeleton of Cleared Specimens with Alizarin Red S) looks to be the one by Dawson.
Update: I think the Wilson your text is referring to is James G. Wilson, an important researcher on terathology. I can't find any reference to a single article, though.


text:
Meaning of the word "targeted" in a description of chromatin immunoprecipitation
From a research paper:

The ChIP assay demonstrated that CIC physically binds to the promoter region of FOLR1, PCFT and RFC1.
Compared with IgG control antibody, CIC antibody enriched 4.1-fold more targeted FOLR1 promoter DNA, 13.8-fold more targeted PCFT promoter DNA and 4.2-fold more targeted RFC1 promoter DNA (figure 3B).

As far as I understand, the authors used chromatin immunoprecipitation to look whether and to what extent the CIC gene influences the promoters of folate-related genes (FOLR1, PCFT, and RFC1). And well enough, they discovered that the antibody to CIC precipitates more "promoter sequences" compared with the control antibody (IgG).
What does the word "targeted" mean here? If I remove this word, the meaning seems unaffected to me. In my Russian translation, I just omitted this word, because it does not seem to bear any additional meaning, but I'm not sure.
Can one simply omit "targeted" or does it have a meaning?

Looking at the article, I think they could leave out the word "targeted".
I think they used it because what is being enriched is not a promoter DNA, but the section of promoter DNA bound to the protein and antibody.
I suppose they could use  "...enriched 4.1-fold more FOLR1 Promoter DNA-CIC protein complex,..."
It is a little awkward or clumsy because the protein targets the DNA, and the antibody targets the protein.
So it is not always very obvious what the word "targeted" is referring to.
But without "targeted" I think the meaning is still clear enough.

I think you're right. By definition, any sequence amplified in ChIP is "targeted" by the antibody, because that's the assay. Seems strange they put it in there...


text:
meaning of "initial gene constructions" vs. "under the control of plant promoters" in an article on GM plants
From "Risks from GMOs due to Horizontal Gene Transfer", by Paul Keese:

Antibiotic resistance genes have been introduced to GM plants either as part of the bacterial cloning vectors used for the initial gene constructions or under the control of plant promoters to select for successfully modified cells. The concern is that the presence of antibiotic resistance genes in GM plants could provide a reservoir for the appearance of new drug resistant bacteria through HGT from plants to pathogenic bacteria.

I'm afraid I don't understand the "either ... or" contrast here. As I understand, antibiotic resistance genes are routinely introduced into GM plants with the sole goal: to check what cells have underwent transformation (got the neccessary foreign genes in their genome) and what have not.
I would be grateful to learn what are "initial gene constructions" here, and how does the method using "the control of plant promoters" differ from the first method. Is the purpose of introducing antibiotic resistance genes similar in both cases - to check what cells have underwent transformation? Sorry if the questions are too stupid. Please direct me to relevant Wikipedia pages or articles.

I think the distinction here is: When you want to introduce a new gene, then you either design a plasmid de novo and transfer it into the cell, or you insert the gene into the genome. But in the latter case you have to put it into a region that is controlled by a promoter (hence under the control of a plant promoter). I am not sure on the  initial gene constructions part, though.

I think initial gene constructions is referring to the construction of the actual vectors i.e. you build the antibiotic resistance marker into the vector. In the latter case they simply edited a resistance marker into a region controlled by a promoter. Pretty straightforward in my opinion.

@Kendall - Did they simply edit the marker into a plant? Before shooting with bio guns? But why use bio guns and vectors at all, if you can simply edit a gene precisely "under the control of a plant promoter" by some other means?

So basically, most plasmids that you buy have an antibiotic resistance marker, I think it's relatively standard, because you want to know which bacteria were transformed, right? Ergo, the initial cloning vectors being used. These markers are under control of a plasmid promoter like T7, for example, not a plant promoter (unless you contsructed it de novo to do this). But your plasmid is going to have a cloning site where you can make a cut, insert more DNA, and ligate it back together.
At least pursuant to the patent by Monsanto here, my assumption is that if you're looking to modify plants, your insert for the cloning site is probably a plant promoter, followed by a structural gene, and then a UTR sequence. I think what the authors are saying is that some groups put an antibiotic resistance gene into the insert as the structural part, and when you use something like an A. tumefaciens system to integrate that vector into the plant genome, you end up with an antibiotic structural gene under the control of a plant promoter. You should keep in mind that the whole plasmid gets integrated, but not all of it is transcribed by the plant, only that within the transcribed region controlled by a promoter the plant can utilize!!*
*I'll add, what they're worrying about in the linked OP article, is that whether or not the plant is actively producing antibiotic proteins, that the sequence for the antibiotic resistance has been introduced at any point in the plant's genome carries the risk that some bacteria will randomly obtain it through horizontal gene transfer.


text:
Can we call a sorbent-filled pipette tip "microcolumn"?
I came across the use of the word "microcolumn" in a Russian text. This word was used to describe a ZipTip® C18 Pipette Tip. It took me some time and some e-mailing to the author to realize that the pipette tip was the "microcolumn".
Is it okay to use the word "microcolumn" when describing such a pipette tip in English? Would the English reader understand?

The samples were applied to the MALDI plate using the dried-droplet method.
  To apply the samples, we used ZipTip C18 (microcolumns for desalting and concentration of proteins and peptides). We washed the microcolumn with 80% acetonitrile, then with 0.1% TFA in water. We next performed the binding of the sample by aspirating and dispensing it through the media multiple times (10 cycles), then washed it with 0.1% TFA in water. We eluted the sample using a 20 mg/ml solution of the matrix (2,5-dihydroxybenzoic acid) in 50% acetonitrile with 2 mM sodium acetate.


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How much does a typical biologist know about signal processing, machine learning, and (theoretical) computer science?
How much does a typical biologist know about signal processing, machine learning, and (theoretical) computer science?
Coming from a neuroscience background where knowing about algorithms and computer science is a must, it seems to me that in biology there is much less cross disciplinary work. Though, yes, there are bioinformatics (but you only do sequence alignment and clustering?).
Anyway, given a typical PhD student in biology, how much does he/she need to know about programming, signal processing, etc?

I think this question could improve if you added the reason why you're asking this (depending on which it may or may not have an actual answer). As it is, you're just requesting comments and the StackExchange Q&A format isn't really useful for that. Feel free to take this to chat of course: http://chat.stackexchange.com/

I don't know what a "typical" biologist is, but I'd guess they don't know much about computers, because the population in general is computer illiterate. In my department, we do have a lab that does a lot of computational work on proteins. And of course bioinformatics relies on computers.
I can see where programming would come in handy for an ecologist, and maybe hardware and electronics too. Lets say you want to track animals in the woods. Traditionally, you'd give them a radio collar, then you'd have to triangulate their position in the woods, and at the end of the day all you'd have is location data. You could use something like a Raspberry Pi or Arduino to create a device that has GPS, a camera, and cell phone antenna, which could record much more information about the animal's location and activity and send it back you without as much effort.
In our modern computerized age, knowing some programming is always a plus, no matter what field you're in. Finding ways to apply that skill aren't always easy. I know both Java and C++, but I've really only written a few programs that I've used in research, 1 to calculate number of possible peptides given a size and some amino acids that won't change, and one to calculate how much DNA to use in ligation reactions.

First I want to say that studying the dynamic of enzymatic reactions, studying the movement of the arm, studying the structure of the DNA, Using mathematical modeling (and individual-based simulation) in population genetics, studying the turnover of soil nutrients, and others, ... require cross-disciplinary. Cross.disciplinary knowledge in biology is not restricted to the intersection between computer science and Biology.

Then I guess/hope that if I give you an overview of my knowledge in computer science and how I acquired it, it may help you (in addition to other answers) to estimate the level in computer science of an average biologist.
From my Bachelor and Master
During my Bachelor and Master degrees I have learned about statistics (and statistics applied to genetic data) and learned to program in R for data analysis purposes. I have been involved in a project during my Master where I had to use Approximate Bayesian Computation.
Self-learning
I have learned by myself the basis of theoretical computer science (NP-hard, genetic algorithm, running time function (the Big O notation), …) but I still know very little. I also learned Python (and a bit of Java) and Object-oriented programming. I also learned HTML and CSS in order to construct my website. All I know about information theory and signal processing comes from a bunch of Khan academy lectures on the subject that I watched.

I agree that a "typical" biologist (if such thing really exists) is generally not skilled in CS nor, very scaringly, in statistics.
My experience is that most biologists think of these things as burdens that do not really interest them and only get to do some basic statistics (most biologists would sort of know what a t-test or an ANOVA is, although they most probably won't master the statistical theory behind it) before writing a paper, so that they can put the little stars on their graphs.
However, if you go into fields like neuroscience (which I count as biology, I am not sure why you seem to imply it is not) then you start meeting people who know quite a bit of CS. Generally you either have these hybrid mathematician/statistician/programmer/math-y guy/biologist or you have biologists working together with more CS people.
In my last lab, for instance, we used to have a physicist and a programmer to help out with biological data analysis.
Furthermore, if you're into imaging, then there may be a lot of programming needed  for 3D reconstruction, image segmentation, particle tracking, etc. etc. Although there is some fairly impressive off-the-shelf software out there for the most common tasks, as soon as you want something a bit more specific you're better off programming it yourself, or finding a collaboration with some computer scientists.
I would say that as a biologist it is important to understand these things, but not necessarily to be able to actually perform them, as you can rely on CS specialists/bioinformaticians to do that for you. However, it is very important for the biologist to understand what the bioinformatician does, and vice versa, as communication is obviously of great importance in these situations.

Without addressing the "typical biologist" aspect of your answer, I have some computer science background but mostly programming and little "theoretical."  In my initial Ph.D. program in the late '80s and early '90s, I took several programming classes in Pascal and C.  I wrote a fairly involved dBase program for a systematic research fish collection.  I haven't messed with these for a number of years but I've retained enough knowledge to write programs in R and dabble in Python. I've used these for various professional reasons, from research to teaching. I teach very basic R in my biogeography class so my students even get some exposure. I'm teaching myself Postgresql as time permits. I use LaTeX regularly, which isn't always programming but its draws from a similar mindset. Plus, I can read the LaTeX code when I want to learn how something works.
I have a colleague in my department who is very fluent in SAS programming but I don't know what other programming skills he might have. Yet another colleague took lots of computer science courses during his Ph.D. program. And yet another colleague, now departed to the administrative dark side, was very proficient in Perl and probably a few other scripting languages.  On the other hand, many of my colleagues use word processing and spreadsheet programs and that's about it.
Scientists are no different from other people. They go where their natural interests take them. For some of us "typical" biologists, that includes computers.

As much as they need to know, but rarely more.
I would say that the 'typical' biology undergrad is not so much of a tech freak and thus has not so much knowledge about programming and computer science in general. One might speculate that young people that feel attracted to these things tend to study math or physics rather than biology. Machine learning just isn't such a fundamental part of basic biology as it is to other scientific disciplines. This is by no means a as there are lots of other things to learn and understand before you can even apply computer-based solutions to biological problems. Many biologists will hardly need any programming skills ever.
However, as a PhD student you will need programming skills at least to some degree, let it be some R to do statistical analyses or some Python to automate workflows. And of course you will find really skilled programmers among biologists as well. As an ecologist, the first thing that comes to my mind are complex ecological models mostly written in C++.
To summarize, the pressure to be familiar with concepts of CS increases with the academical degree, and so does the proportion of proficient biologists.


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How much are phase-contrast and dark-field microscopy used in biological research?
How much are phase-contrast and dark-field microscopy used in biological research today? It seems these were invented a long time ago, so I am thinking would it be a good idea to learn these techniques. (I will start an undergraduate program in biology next spring.. but I am still mostly interest how much the researchers use these technologies: if little, I should use my time better)

both are primarily used in cell culture work such as cell assessment and imaging. I have posted an answer to a similar question here (http://biology.stackexchange.com/questions/5470/what-to-look-for-when-buying-a-light-microscope/17313#17313)

I use phase contrast very often, as it is only a matter of switching a lens group from bright field. Instead of spending hours with staining, or, worse, immunostaining, I get the big picture (cell diameter) in a few seconds. I can even go back to the same cells next day. Switching to dark-field is also a matter of turning a dial or pushing a switch.
If you already use brightfield, there is not much to learn about them in terms of actually useful physics, or sample preparation. The things you could learn - say, that colors are altered in darkfield - will rarely be needed in practice. These methods are the sort of things you don't really need to know in depth unless your experiments require them. Even then, practice and elbow grease would be more helpful than advanced optics. Remember that in most cases, the scientific hypothesis is more important than the tools you can use to solve it.

If you're planning on doing any kind of cell biology work (and if you're going into biology, it is almost certain you will at some point), learning how to use a microscope is a must. You will use a scope frequently when growing cells to analyze their morphology, count them, look for signs of contamination, visualize differentiation, etc. Microscopes are also used when performing immunofluorescence and immunohistochemistry staining protocols.
So, even though the instruments and some of the techniques have been around for quite a while, they are still very relevant today.


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19th century Latin species description
While reading a 19th century text of new species description, I'm confused by some Latin phrases.
The case here is:

Corp. long. 8 poll., caud. 9 poll.

I guess 'corp.' and 'long.' are abbreviations of some Latin terms, and the whole meaning of the combination of these two words is probably "body length". But I still can't figure out what "caud." and "poll." (the number seems like is in inch though) are stand for.
The species described is a rodent species. Full text could be found here (p.185).

"Caud." refers to the tail (lat: cauda) and, judging from the description, "poll." seems to be another word for inch. So the translation should be something like:
Body length: 8 inches, tail length: 9 inches.

The pollex was a Roman length measurement, approximately equivalent to an inch. The pollex was also known as the uncia, which is where the word "inch" comes from. There were 12 unciae in a pes ...

Thanks for the further explanation. Sorry don't have enough rep to upvote.


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What kind of spider is this? (Central Texas)
This is in Austin, TX, USA. Photos taken at night on a phone with a flash, so colors may not be entirely accurate.

I found this spider hiding inside my motorcycle cover, which I'd thrown in a pile on my front porch for a few days.
It wasn't aggressive nor skittish, although it did scuttle away at a relatively slow pace as soon as I tried to move it using a large envelope. I would estimate its diameter (legs included) at about 1-1/2 to 2 inches (38mm - 51mm).
I was very cautious around it since I thought it might be a brown recluse, but I know there are a number of Central Texas spiders that bear a resemblance. I couldn't make out the "violin" on its back but I also didn't get close enough to make sure.

Maybe a Southern House Spider? It appears very similar to the brown recluse although without the violin you were unable to find on the thorax.
https://en.wikipedia.org/wiki/Southern_house_spider

Photo from Spider ID

Not sure why the downvotes - I think you're likely correct! (I'll leave this open for contributions but then accept your answer if there's not a better guess soon.) The picture in the Wikipedia article doesn't strongly resemble my photo; but, that species has strong sexual dimorphism. Of the other photos I googled, I found a few that look spot-on. Maybe the Wikipedia photo shows a male and this was a female, or vice-versa. This photo, for example, looks like the exact same spider (note eye position, abdomen size & texture, leg gradation, etc.): https://www.pinterest.com/pin/391109548883253068/

@Bungle & JEJS: I can't speak for the downvoter, but answers are more likely to get a positive response if they explain why an identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion, which is inappropriate for this site. ——— You may also wish to consult the [help] pages for additional advice on [Answer] effectively on this site.

I agree with K. hibernalis. The answer should probably be modified from "Maybe a..." to "This is a..."


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Are harmful gases abiotic or biotic factors in our environment?
As we all know, harmful gases play a negative role in our society and our environment. Are these gases playing as abiotic or biotic factors in our lives?

About what gases do you think?

The harmful ones such as Carbon dioxide and Carbon monoxide. @Chris

Isn't definition of biotic a living thing? gasses are not living (i.e. abiotic) harmful or non-harmful, or am I missing something? (http://en.wikipedia.org/wiki/Biotic_component). If so, could you clarify the question? If you mean whether bionics can use harmful gasses, then it depends on the species. e.g. plants can use CO2 but mammals can't.

I'm voting to close this question as off-topic because it is about the English language rather than Biology.

Bez is correct, biotic and abiotic refer to the nature of the agent performing the stress.

biotic = living thing (lion that is actively engaging in catching you as food)
abiotic = non-animated (far from optimal temperature)

Now the example "shade" is trickier; because it depends on the perspective you choose.
There's always a context. Does the element creating the shade matter in your context?
If so, and this element happens to be animated/living:  stress = biotic (though you should reference at some point that the object at hand is animated).
If it doesn't matter what object generates the stress since you are only interested in the effect of the shade on a system: shade = abiotic
Pipeline: Analyze the context, choose and communicate your choice of perspective/angle and then remember what biotic and abiotic literally mean.
Coming back to "harmful gases": What is your context meaning harmful for whom? Specify that first. Carbon Dioxide is an example of something that may be deleterious at a specific concentration for one system and at the same time beneficial for another.
Does it matter how these gases were produced? CO2 may be a product of an animated system's metabolism and thus may be called abiotic. It may also be a product of oxidation of a multitude of carbohydrates.
I don't know of an example where Carbon Monoxide is produced by living things.
You could of course circumvent this discussion by analyzing what harmful effect the gases have on your system of interest. For example: they generate respiratory stress on humans, and then you use the effect of the gases on the system to characterize them.


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Determining and Differentiating specific ATPases

In respects to this certain ATPase transporter. What do i look for in respects to determining what specific kind it is out of:

F-ATPases
V-ATPases
A-ATPases
P-ATPases
E-ATPases

Im assuming that analyzation of the gradients dealt with will guide me to the answer. With that logic, i can assume that this is an F-ATPase since i know this membrane protein can synthesize ATP using a H+ gradient, and work in the reverse to create a H+ gradient using the energy gained from the hydrolysis of ATP.( I see 2H+ cations being expelled) Is this a correct method in differentiating ATPases ?

Can you please rephrase your question, as I don't understand it? You want to know if you identified the ATPase in the image as the F0-ATPase? Or do you want to know what is different between the different subtypes?

Sorry for the confusion. My question is, am I going about determining what sort of ATPase this is in the correct way? I determined that this photo depicts a F-ATPase by analyzing the 2H+ cations going through it. And is this an F-ATPase at all? You seem to be "the guy" in molec bio, I appreciate it.

First of all, I think you need to research the subunit structures of the various ATPase classes in the list because I am pretty sure that several of them are not as complex as this.
Although this superficially looks like the F-ATPase responsible for synthesising ATP by using the proton gradient generated by the electron chain, there is a clue in that diagram that this may actually be a V-ATPase. The V-ATPases use ATP hydrolysis to move protons from the cytoplasm into the lumen of acidic organelles like lysosomes. The diagram in the question depicts a process like that (ATP is being hydrolysed). Now, you can drive the F ATPase in reverse to achieve this situation, so that isn't definitive.
The labelling of the two compartments is also consistent with the idea that it is a V-ATPase since 'lumen' isn't a word that is usually used in the context of the mitochondrion (it would normally be 'matrix').
So I would suggest that you find out if the subunit labelling is like that used in F-ATPase or V-ATPase (or both). A Google image search will help you to find cartoons of ATPases.
My guess, before doing the suggested research, is that this is a V-ATPAse.

I think that, too. Have a look at the direction in which the ATPase is working, this should give the final clue. It pumps from the cytosol into the lumen.

Yes, but as I said in my answer, you can artificially get F-ATPase to do that, although probably not in the context of cellular compartments.

The F-ATPases are locared in the inner mitochondrial membrane and are not in contact with the cytoplasm if I remember correct.

Thank you for the insight. With further research i've found that this is indeed a V-ATPase.(Learning that the V stands for Vacuole surely helps). Also, V-ATPases hydrolyze, ATP which is clearly seen in the illustration. While F-ATPases only synthesize ATP using a H+ gradient.

http://www.bio.davidson.edu/courses/molbio/molstudents/spring2010/sween/V%20vs.%20F%20ATPases.jpg


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Transmembrane Protein Problem
Problem
A transmembrane protein has 1000 aa. The 5th aa is found on the external side of the cell membrane. It interacts with the aqueous environment outside the cell. Amino acid 90 is inside the membrane bilayer. Aa 100-600 are intracellular, and 200-400 make a tight ball with minimal exposure to the aqueous cytoplasm. Amino acid 979 is found on the extracellular side of the protein where it forms a weak ionic bond with Cl-.
a. Can you draw the protein and mark positions of all mentioned aa in it?
b. What are the properties of these amino acids?
￼￼￼￼￼

I dont necessarily want/need the exact answers to these questions, rather i would like some guidance in what principles i would need to understand and conceptualize to attack this problem. Thanks all !

Please read our homework policy. For questions like these, we want to see some effort from you in trying to answer your question(s), and then we can clarify/correct you from there.

@MattDMo Please do note, that he is NOT requesting answers. He needs help figuring out where and how to start :)

Thank you L.B If there is anything more i need to add by all means please let me know. I would just like more knowledgable members to help me on the core "philosophy" to this.

@Macedon93 It would be great if you could share some of your thoughts about this. It is easier to help people when you know where they got stuck.

Ok, I see that this problem is a test to my knowledge of membrane proteins, atleast that is what i am assuming at this point. I can assume that question A.) is referring to the protein connexin, which traverses through lipid bilayers. However not completely sure. What really stumps me is the jargon in the question, such as "1000 aa", and "Aa 100-600".

Not completely sure as to what they signify.

I would start by drawing 2 horizontal lines. The space above the top line is the external side, the space below the bottom line is the cytoplasmic side, and the space in between is the membrane bilayer itself. Now fill in what you're told, placing dots and lines and circles to represent the structures were given in the right spaces. Then connect the dots.

@Macedon93 those are the amino acid residues. 1000aa is 1000 residues long, aa 100-600 means amino acids 100-600.

What is a weak ionic bond?

All ionic bonds are considered relatively weak in comparison to other bonds. Ionic bonds are forces of attraction between ions of opposite charge

Ionic bonds and covalent bonds are stronger than hydrogen bonds which are stronger than weak bonds like van der Waals. The term 'weak' isn't usually used in connection with ionic bonds in my experience, which is why I was puzzled.

I made a quick sketch on the basis of the information you gave (this is not to scale):

Aminoacid 5 (aa5) of the protein is on the outside, aa90 is inside the membrane. What we don't know here where the transmembrane part starts (directly with aa6 or later) and how it is organised (I indicated this as a transmembrane helix, but this can of course be different). Then we know that the border between the transmembrane part and the cytosolic part is somewhere between aa90 and aa100, that aa100 to aa200 seems to be some connecting part. The aa200 to aa400 is a globular domain which shields hydrophobic amino acids from the cytosol, so this part has to contain a high percentage of hydrophobic amino acids.
The part from 400 to 600 is again cytosolic but with no further information about the structure. After aa600 starts a second transmembrane part of the protein, but here we don't know how long it is. The maximum possibility would be until aa977, since we know the aa978 is outside of the membrane.

Thank you for your help. I followed your lead and my professor told me this is what she wanted to see, and with the help of shigeta, I now know how to illustrate this problem. However, what exactly tells you where aa5, aa90, aa200 etc are located ? What information are you basing its locations off of ? Or are you simply drawing a transmembrane protein, and labeling its respective amino acid sequences based off of common knowledge

@Macedon93 No, I am going along the text you provided. As I said, this is a quick sketch, for a more detailed figure you need to have more information (for example where the transmembrane sections begin exactly and so on). I knew that aa5 is outside and aa90 in the membrane. I also knew for example the aa200-400 is globular.

Duh, so stupid i realize these were stated in the question. Thanks again !

Membrane proteins are usually drawn as topological digrams with two parallel horizontal lines representing the membrane.  lines as 'extracellular' and below the lines as 'intracellular' for instance, but that is not what is being asked for here.
Its not clear to me that the number of transmembrane spans are fully described, nor are the boundaries of the transmembane spans.  I think what is being asked for could be a domain diagram of the amino acid chain.
Draw a line on graph paper representing the peptide and use a scale to label each point described. For regions draw a box around the peptide line to describe a domain, and label it.
I think its hard to talk about amino acid properties other than hydrophilic/hydrophobic.  hope this helps?

I think there's enough information given here to map out the protein. It probably starts on the external side, moves inside the cell, has a large cytoplasmic domain, then moves back out. The position and descriptions of the AAs also tell us something about their properties, even if it's subtle, such as "forms a tight ball with minimal surface exposure". The chloride ion interaction should also tell you something about charge.

Possibly, but if you had the full amino acid sequence, you would normally use a transmembrane domain algorithm.  There could be three helices.  Such mps are known.  The problem is a pretty limited set of facts and it doesn't seem like you need to jump to any conclusions imho.

Thank you for the insight. Illustrating this has become much more logical. Still have a decent way to go !


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Bacterial Cell Problem
A microbiologist has discovered what she thinks are two new types of algae. The first cell
(Organism 1) appears cubic and is approximately 1.5 μm long, 1.5 μm wide and 1.5 μm deep.
The second (Organism 2) is rectangular and 2 μm wide by 5 μm long by 2μm deep.
a.  What is the surface area/volume ratio of each organism?
b.  Which organism will find it more difficult to interact with surrounding environment (receive nutrients, excrete metabolites etc.)?
c.  How will this organism cope with the reduced capacity to interact with environment?

In respects to question A.

V of Rectangular organism= (V = L x W x D)
Surface Area= (L x W)
Im assuming these simple rules still apply to organisms concerning minuscule measurements.

Im assuming for question B., that the molecule with the smaller dimensions will have the most difficult time interacting with its environment, due to the fact that it has a smaller perimeter with less channels & ports.
I am completely lost for problem C.

Any insight Would be awesome. Thanks all !

The surface area of a rectangular prism is not length times width. Questions B and C are related to the ratio you calculate in A.

Woops. I mean A=2(wl+hl+hw)*

B. Higher surface to volume ratio allows better interface with environment.
C. To increase surface area the cell can form processes such as microvilli.


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Alkaline Phosphatase
What is the predominant purpose of Alkaline Phosphatase in skeletal muscle fibers and liver cells. I know that it is a hydrolase enzyme that speeds up the degredation of proteins, lipids, starch and other biomolecules. But what does it does it specifically do in muscle and liver cells. And why is it in higher concentration in the liver ? Is it because of the livers purpose as an organ (cleanse and detoxification) ? Therefore pino/or endocytosis occur in higher rates ? I appreciate anyone with any intelligent insight.

http://pharmascope.org/ijrps/downloads/Volume%204/Issue%203/08-10265.pdf

It has a very wide role and there are multiple types of alkaline phosphatases...


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Mode of Enzymatic Inhibition via R-Allele

The photo above shows the effects of the R allele of the pea shape gene on the synthesis of an enzyme that converts unbranched starch into branched starch. The r allele of this gene determines an inactive form of the enzyme, leading to a buildup of linear, unbranched starch that ultimately causes seed wrinkling. My question is, How does the r allele specifically prohibit the activity of the enzyme?

Does the DNA/Gene sequence simply code for proteins that create an enzyme which cannot bind to its respective substrate ?
Is the substrate in the above illustration the unbranched starch itself ?

Bhattacharyya M, Martin C, Smith A. 1993. The importance of starch biosynthesis in the wrinkled seed shape character of peas studied by Mendel. Plant Mol Bio 22(3):525-531
Abstract:

The wrinkled-seed mutant (rr) of pea (Pisum sativum L.) arose through mutation of the gene encoding starch-branching enzyme isoform I (SBE1) by insertion of a transposon-like element into the coding sequence. Two isoforms of starch-branching enzyme have been documented in the developing pea embryo. The second isoform, SBEII, is expressed towards the later stages of embryo development while SBEI is expressed highly in the early stages. Due to mutation of SBEI the total amount of starch and the proportion of amylopectin, a branched starch polymer, are greatly reduced in the wrinkled (rr) line as compared to that in the wild-type, round (RR) line. Consequently, the level of sucrose in the rr line is nearly two fold that of the RR line. Increased sucrose concentration in the developing embryos of this mutant line causes increased uptake of water and thereby increases the cell size and fresh weight. During seed maturation in these mutant seeds a greater loss of water occurs. As a result, the wrinkled seed phenotype develops. Besides this morphological variation, the mutation also causes changes in the amount of lipid and of one storage protein, legumin. This review article discusses the role of the SBEI enzyme in causing such metabolic changes in the developing embryos with the implication that metabolism can play a central role in plant development.

These authors claim that the mutant protein is not present in peas, so the wrinkled phenotype is not due to an inability of the protein to bind its substrate (amylose and amylopectin - the linear and branched components of starch, respectively) but rather its complete absence. The mutant is due to an 800 bp transposon insertion into the coding sequence of SBE1. If it was expressed, it would be reasonable to expect that it wouldn't be able to bind its substrate. The authors also discuss mutations at other loci that have been shown to be responsible for the wrinkled phenotype, but it is believed that these are relatively newer and would not have been observed by Mendel.


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Dopamine and other neurotransmitter release during music listening
I'm looking for any studies that show a positive curve in respects to music sessions in humans and neurotransmitter release (specifically dopamine, epinephrine, and serotonin.) Any direct links would be great as I attempted googling and cannot find any at all for some reason.

Have a look at this question and answer: http://cogsci.stackexchange.com/questions/5627/is-there-evidence-to-suggest-that-music-can-trigger-release-of-a-particular-kind/15203#15203

It's a lot easier to measure brain electrodes for alpha wave activity, and MRI brain scans while listening to music, so those are more common studies.

Here is an article I found on google scholar. It links an increase in 5-HT a serotonin neurotransmitter when listening to pleasant music.
https://link.springer.com/article/10.1007/s004060070031

Thats pretty funny. 3 years later i randomly look at this question ive posted and you answered within the past hour. Ill take a look. Cheers

Since links die more frequently than you think, please provide a citation in your post as well as a summary in your own words. We want answers to be useful for the long-term. Thanks!


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Jurkat single cell clonal expansion
I'm hoping to do a clonal expansion of Jurkat, expressing my construct which is currently transduced virally. From the FACS data I currently have roughly 30-40% expression in my culture but I need it to be close to 100% as the effect I'm looking for I believe to get diluted by the reduced presence of my molecule of interest in the total culture. I can do cell sorting but usually what happens is that the 5% cell population that do not express the construct eventually take over after a few passages.
I'm planning to do a 96 well plate format single cell seeding and expansion of Jurkats but it has been done before by another member of our lab and the person suggests that single cell Jurkats (unlike CHO cells) do not survive a single cell state although they are suspension cells and do not necessarily require contact to survive although they clump. Hence I'm wondering if anyone has any protocols they could suggest such as contents of the media (e.g. conditioned media) or any other recommendations for Jurkat single cell clonal expansion.
P.S. I am fully aware that there might not be a single right answer to this and the answer requires a degree of experience/opinion on the working method but I would fully appreciate any helpful suggestions/responses.
Many thanks

Is there a chance to use a selection marker like G418 to kill all the cells which do not express your construct?

I will look to see if the vector has this otherwise a fresh co-transduction or a new vector containing antibiotic resistance selection marker containing something like G418 might be required. I think people are unsure as to exactly what backbone the construct is in so that could be tricky and require month of cloning and sub-cloning. Are Jurkats tend to be difficult with clonal expansion?

Jurkats shouldn't be difficult to clonally expand. If you're having problems, get a fresh culture from ATCC. You really also should know what kind of vector you're using - if you don't know what your reagents are, there is no way to independently verify your results. Therefore, they are invalid.


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What are "intrinsic hypothalamic fibers"? (From an article on neuronal mechanisms of sexual desire)
I came across the phrase intrinsic hypothalamic fibers which I cannot understand. What is meant by intrinsic - that these fibers (long myelinated axons?) start in the hypothalamus? Or that they start and end in hypothalamus? Or something else?
The article is "Pathways of Sexual Desire" by James Pfaus (2009).

Figure 8 Brain opioid systems overlaid on opioid binding regions (high density of receptors indicated by red to yellow, lower density in green to blue). Three systems exist: the pro-opiomelanocortin (POMC)-derived opioids such as р-endorphin, which arise from the same population of projection neurons that produce the melanocortins; the interneurons in the cortex, limbic system, hypothalamus, and brain stem, which produce enkephalins and dynorphins; and the intrinsic hypothalamic fibers, which contain endo- morphins. These systems are activated at orgasm in humans, at ejaculation in male rats, and during paced copulation in female rats. They shut down hypothalamic regions associated with sexual arousal and desire, thereby inducing refractoriness. However, opioids are also released in the VTA during phases of sexual arousal and desire and help to disinhibit DA neurons and, thereby increasing DA release in mesolimbic terminals. This is an important mechanism by which experience with sexual rewards sensitizes sexual excitement once the inhibitory effects of refractoriness and satiety wear off. VTA = ventral tegmental area; DA = dopamine; mPOA = medial preoptic area; mPFC = medial prefrontal cortex; NAcc = nucleus accumbens; PIR = piriform cortex; MeA = medial amygdala.

"Intrinsic hypothalamic fibers" are fibers instrinsic to the hypothalamus; so yes, these are fibers either projecting from somewhere in the hypothalamus to somewhere else in the hypothalamus, or locally in the hypothalamus (the hypothalamus itself is a pretty complex structure containing many distinct nuclei). The paper you reference specifically mentions the medial preoptic area, mPOA, as a target:

Infusions of mu opioid receptor agonists to the mPOA inhibit sexual behavior in male rats

and

infusions of a mu antagonist to the mPOA, but not NAcc, block sexually conditioned place preference

"Fibers" does not necessarily refer to myelinated axons, just axons of any sort.


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Do "transcription factor binding site" and "operator" mean the same thing?
Can the terms "transcription factor binding site" and "operator" be used interchangeably in all contexts when referring to a DNA sequence, e.g. regardless of a cell type, whether or not the binding sequence is synthetic or natural etc.? If not, what are the differences?

As you no doubt know, the term operator was coined by Jacob and Monod as part of the formalism they developed to explain the properties of certain mutants in the lac operon in E. coli. In physical terms it is indeed the site of binding of a transcription factor, the lac repressor.
My understanding is that technically it is best to restrict the use of this terminology to bacterial systems in which the idea of an operon is useful. I don't think it would be wise to extend it to cover any site in eukaryotic DNA where a transcription factor is shown to bind.

To add about it: I am working with transcription factors for a few years now, I have never heard of anybody using it in eukaroytes. The sites are simply called transcription factor binding site.


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What is this creature?

Since it has six legs, I believe it's some sort of insect, but I could be wrong.
I spotted it in my Central Texas backyard (Austin area). It was very slow and not at all skittish.
For size reference, it's standing on a 2x4. It was a good 3-5 inches long, not counting antennae.

I don't know anything about Texas insects, but it almost looks like a species of walking stick or other phasmatodea. I don't think I can get any closer than that.

I think you may be right. I looked into it a little more after posting this, and the nearest match I've found is the Two-Striped Walkingstick: http://www.insectidentification.org/insect-description.asp?identification=Two-Striped-Walkingstick. Thanks for your input!

It is the Two-striped walking stick

Walkingsticks, like that in your photo, belong to the insect order Phasmida (also sometimes called Phasmatodea). The species in your photo belongs to the family Pseudophasmatidae. Texas has two species documented for this family. One is Anisomorpha ferruginea, commonly called the dark walkingstick or northern two-striped walkingstick.  The other species is Anisomorpha buprestoides, commonly called Florida stick insect or two-striped walkingstick.
According to W.S. Blatchley's Orthoptera of Northeastern America (1920), pg. 145, A. ferruginea has narrow stripes and is a bit shorter than A. buprestoides, which has broad stripes. Based on the appearance of the stripes in your photo, I'd say you have A. buprestroides.


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Does photosynthesis begin instantly when a plant is exposed to light?
I'm curious to know if the process of photosynthesis has a "ramp-up" time to become useful to a plant, or if it begins instantaneously when the plant is exposed to light after a period of darkness.
For example, if I'm growing a plant indoors using artificial light, does the plant start converting CO2 the very moment I switch on the light, or does it take a certain period of time for the reaction to reach a critical momentum for the plant to be able to produce sugars?
Or, as a thought experiment, if I turned on the light for 10 minutes, would the plant produce roughly the same amount of sugars as if I toggled the light on for 1 minute, then off for 10 minutes, 10 times in a row?

This is a really interesting question! It gets to the heart of how photosynthesis works.
First, note that whether or not the plant will immediately start producing glucose depends on a variety of factors (what type of plant, what type of light). For example, many succulents undergo CAM photosynthesis (Crassulacean Acid Metabolism) in which light capture and CO2 fixation are temporally separated (the former during daylight hours and the latter at night). Additionally, artificial light comes with different wavelength compositions (ratio of red to far-red light  can differ) and photosynthesis rates will change accordingly read more here.
But I haven't yet addressed the heart of your question: how long does it take for a plant to start photosynthesizing once it is exposed to light? To think about this, consider what is actually happening when light hits a leaf. Light energy is absorbed by pigments in the chloroplasts, which transfer energy to neighboring pigments until an electron is transferred to a reaction center. From here, "light reactions" of photosynthesis continue and usable chemical energy is obtained. From there, the CBB cycle (sometimes called the Calvin Cycle, Calvin-Benson, or "dark" reaction) continues, which is where the CO2 from your question comes into play, and 6-carbon sugars are produced. It isn't a matter of "ramping up", so much as completing this series of chemical reactions.
So now, it is time to consider your thought experiment. Let's say that you have a bean plant in your kitchen (C3 photosynthesizer), and you conduct your experiment shining a white-light lamp on the plant with the experimental conditions as described. I believe that you would produce roughly the same amount of sugars in each because glucose synthesis occurs on the order of seconds (~30s). If you exposed your bean plant to white light for only 5-second increments, there would not be time to produce the energy needed to complete the CBB cycle.
Aside: the experiments that first elucidated the CBB cycle were conducted by exposing cyanobacteria (a photosynthetic bacteria) to labeled (heavy) carbon, and exposing it to light for a few seconds, and characterizing which compounds were produced from that heavy carbon within that few-second time frame. Read more about that experiment in the previous link. It sounds like Calvin himself wondered the same thing you did!
For further reading on the basics of plant physiology, including photosynthesis, I always recommend the plant bio "bible": Plant Physiology and Development by Taiz L., Zeiger E., 2010. I still consult it often.
Hope this helps. Stay inquisitive!

This is a fantastic answer! Thanks so much for taking the time to write it. Very interesting.


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Are a child's traits truly random?
To me, there are two definitions of "random" in common usage: effectively random, where predicting the outcome is beyond most reasonable effort (e.g., drawing a card from a deck); and truly random, where predicting the outcome is beyond known science (e.g., radioactive decay/QM).
With this (possibly flawed) perspective, I'm very interested in sources of true randomness. I started thinking about how parents never know exactly what their child is going to look like. Is this because there are aspects of reproduction that are fundamentally unpredictable (true randomness) or because we lack the sophistication/motivation to predict it (effective randomness)?

Its unclear what process you are referring to, are you talking about recombination? If so then like all chemistry it is just effectively random and in a way not even be that since position on the chromosome has an effect.

You true randomness definition is partially wrong! Something does not need to be fundamentally random to be beyond known science.
Also, it is unclear what process you are referring to when talking about a child's trait. I would assume you are thinking about crossover but then, summarizing crossover positions by "child's trait" shows that you misunderstand a number of things!
To my knowledge, outside of quantum physics, in no field of knowledge has it been shown that true randomness has any measurable effect. So, no what chromosome an individual inherits is only random in the sense that it would be necessary to know exactly the position of every molecule in the cell to know where the crossover will happen.


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Why Hasn't my Cactus Grown Deadly Spines?
I recently purchased a small cactus plant from my local store for about $5.
I've been giving the cactus lots of sunlight and a good watering every week.
I've noticed that since I bought it, the other cactii at the store have sprouted long and deadly looking spikes of at least 2 inches in length. My cactus has extra little clones growing out of it but its spikes are stunted and disappointing.
Why won't my cactus grow spikes?
My cactus is of this variety:
http://www.friendsschoolplantsale.com/sites/default/files/images/colors/a-flat-cactus2-ns.jpg?1364265449

Cross posted and answered on [gardening.se]: http://gardening.stackexchange.com/questions/13989/why-hasnt-my-cactus-grown-deadly-spines

This question has been cross-posted to "Gardening & Landscape" and answered there. The answer can be found here: http://gardening.stackexchange.com/questions/13989/why-hasnt-my-cactus-grown-deadly-spines


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Is it possible for a human to wake up in a wrong way?
There's an old folk saying that goes like "He got out of bed on a wrong foot" - to indicate that the person's day is going poorly because of the way that person woke up.
Is it is possible for a human to disrupt the awakening process, causing negative cognitive side effects for the rest of the day? If so, how long does it take to restore normal cognition?
There's this related question that I asked - if different parts of a human brain can be asleep independently of each other? This question is a variation on that one, and specifically deals with the process of awakening or activating brain regions in the morning.
I'm aware of the concept of "Sleep inertia". However, it does not seem to be the phenomenon in question, as sleep inertia is frequently mentioned in the context of napping. (where napping over a certain time leads to sleep inertia). Additionally, sleep inertia has been described in terms of decline of motor activity, and not as cognitive side effects lasting for a whole day.
From personal experience, it seems that I'm doing best if I get out of bed immediately following a natural awakening, even if it is rather early, as opposed to snoozing for another 30-40 minutes.

I want so badly a response to that...

I think the "sleep inertia" you refer to is the reason - if you are woken by your alarm during a particular cycle of sleep this would have an effect lasting all day [haven't looked this up - anecdotal]. This would then be referred to as having woken up on the wrong side of the bed (which is just a saying not a literal reason why you are having an off day).
Could be due to all sorts of reasons though, including nutrition, recent physical activity, stress, alcohol/drug consumption... etc!

I'd say anytime a human hasn't slept enough, of course how much is enough sleep depends on the individual.

Isn't sleep paralysis another kind of disrupted sleep phenomenon?

I did a quick search and found some research in this area. Sleep inertia is the technical term for feeling groggy for a while after waking up.
In a review article by Patricia Tassi, Alain Muzet (Sleep inertia. Sleep Medicine Reviews. Volume 4, Issue 4, August 2000, Pages 341–353), they define sleep inertia as

Sleep inertia is a transitional state of lowered arousal occurring immediately after awakening from sleep and producing a temporary decrement in subsequent performance.

and also says,

Depending on the studies, it [sleep inertia] can last from 1 min to 4 h. However, in the absence of major sleep deprivation, the duration of sleep inertia rarely exceeds 30 min.

Same article reviews several studies (first report in 1964) on sleep inertia relating to sleep stages:

Abrupt awakening during a slow wave sleep (SWS) episode produces more sleep inertia than awakening in stage 1 or 2, REM sleep being intermediate.

So yes, sleep stage seems to correlate with "waking up in the wrong way" as @CactusWoman suggested.

Good find, I especially appreciate the up to 4 hour timing information. This may also interact with caffeine, which is frequently consumed in the morning. Apparently caffine half-life is about 5.7 hours (http://www.caffeineinformer.com/the-half-life-of-caffeine)

Sleep occurs in stages. There are three stages of non-REM sleep followed by REM sleep. Natural waking occurs during the REM stage. If your alarm goes off while you are in the middle of deep sleep, you are going to feel different from if you had woken up naturally. That's why there's a market for alarm clocks designed to wake you up during light sleep.

do you have references for this "feel different" claim?


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How does a plant grow before photosynthesis is possible?
During photosynthesis, a plant translates CO2, water and light into O2. I assume the carbon C is further used for the growing process. I wonder how the plant grows before the time where photosynthesis is possible, i.e. before there are even leaves, in which photosynthesis occurs.

To what extent does the plant grow from the seed/the minerals in the ground?
How much carbon are relevant for which parts of the plant and at what times of the evolution of the plant?

I don't know if there are only these life periods of the plant, i.e. if there are other major biochemist-of-growing changes, than in the comparison before and after the plant got leaves. So are there other relevant aspects to this? If there are leaves present, is the rigid structure of the plant only coming from the CO2 in the air and not from the ground anymore?
The answer will probably depend on the plant. So here is another formulation of the question:

What are typical characteristics of different plants in this regard? I.e., how do common species of plants manage their C consumption before (and after) the development of leaves?

Photosynthesis fixes carbon dioxide into organic molecules - the water is broken up during the process and the oxygen from it released and light also doesn't really belong in the equation.  I think the important bits you are looking for are about carbon fixation specifically but I didn't want to edit your original meaning out - could you clarify? =)

@RoryM: Okay, done.

There are quite a few questions and thoughts in there, I'll try to cover them all:
First, to correct your initial word equation: During photosynthesis, a plant translates CO2 and water into O2 and carbon compounds using energy from light (photons).
You are correct to assume the C is further used for the growing process; it is used to make sugars which store energy in their bonds. That energy is then released when required to power other reactions, which is how a plant lives and grows. C is also incorporated into all the organic molecules in the plant.
Plants require several things to live: CO2, light, water and minerals. If any of those things is missing for a sustained period, growth will suffer. Most molecules in a plant require some carbon, which comes originally from CO2, and also an assortment of other elements which come from the mineral nutrients in the soil. So the plant is completely reliant on minerals.
Most plants, before a leaf is established or roots develop, grow using energy and nutrients stored in the endosperm and cotyledons of the seed. I whipped up a rough diagram below. Cotyledons are primitive leaves inside the seed. The endosperm is a starchy tissue used only for storage of nutrients and energy. The radicle is the juvenile root. The embryo is the baby plant.

When the seed germinates the embryo elongates, the endosperm depletes, the testa ruptures, and the cotyledons emerge from the seed. The cotyledons are green, and like leaves can photosynthesise, so as soon as they are in the light the plant is able to make carbon compounds. The radicle elongates at the same time, and becomes the root, so the plant is very quickly able to obtain fresh nutrients from the soil (or whatever it's growing in).
At all stages of a plant's life it is using both energy stored in carbon compounds (from CO2) and nutrients which it took up via its roots. At no point does the plant start to depend solely on the CO2 in the air for its growth.
You are right that the way in which plants acquire energy and nutrients prior to leaves and roots being established varies between plants. Above I outlined the way most plants use. But there are lots of variations. For example, orchids have very tiny seeds, some barely visible to the naked eye, like specks of dust. They have no endosperm or storage tissue, so they have to rely on a symbiotic mycorrhizal fungus to get carbon and nutrients. The fungus grows through the coat of the orchid seed, then provides everything the growing plant needs until it has its own leaves. Then the orchid repays the fungus by providing sugars.
There are lots of other examples, but we could go on all day!

Sweet diagram. :)

Thanks! I always find things easier to explain with pictures.

Simply put. Plant growing from sugar (both energy and material). So if they could store sugar (or even find sugar from anywhere). They could grow even there are no sunlight
And photosynthesis never make plant grow immediately. It just make sugar. And plant store it. Actually many plants grow at night while eating sugar it stored on daytime
Some plant store sugar so much in their root (all root vegetables), so they could survive on dark winter or even all the leaves was eaten. There are one plant even evolve into a parasite without any chlorophyll and live by growing from another plant's root
Another trick plant was used is, it grow by decreasing density, make it bigger with a little more weight compared to the seed. By consume water it spring out larger and ready to catch sunlight. It like you pack your travel bag tightly and it explode when you open it again


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Non-monotonic knock-out effects in prokaryotes
Typically, when performing gene-knockout, the experimenters select one gene to remove/replace-with-junk and then see if the prokaryote can still undergo fission. If it continues to reproduce then the gene is labeled as non-essential; if the organism cannot reproduce then the gene is labeled as essential; and some-times (if the organism can reproduce but only for a certain number of generations) the gene is labeled as quasi-essential.
Typically, if gene X is essential, and you knock-out both gene X and some other gene Y then the organism still dies; this is an example of monotonic behavior. However, this doesn't always have to be the case, it could be that gene X is essential only in the presence of gene Y (for instance if the two proteins produced are in a delicate feedback loop). Is there examples when knocking out gene X makes the organism nonviable, but knocking out gene X and Y maintains viability? In the most extreme case, is there an example where both gene X and Y are essential, but if both are knocked-out then the organism is still viable? I am primarily interested in simple prokaryotes (an answer for Mycoplasma genitalium or Escherichia coli would be best) but more complicated organisms are preferred over no answer.

Here is an example in which the knockout of a non-essential gene in yeast (Saccharomyces cerevisiae) suppresses the lethal effects of a different knockout.

Amy L. Kistler and Christine Guthrie (2001) Deletion of MUD2, the yeast homolog of U2AF65, can bypass the requirement for Sub2, an essential spliceosomal ATPase. Genes & Development 15:42-49

The SUB2 gene encodes a protein which is a component of the TREX complex required for nuclear mRNA export. Deletion of the SUB2 gene is lethal. The MUD2 gene encodes a non-essential protein involved in pre-mRNA splicing.
The authors show that -

"...the essential requirement for the SUB2 ATPase can be bypassed by deletion of the nonessential splicing factor MUD2..."

Detailed information about these (and all other) Saccharomyces cerevisiae genes is freely available at the Saccharomyces Genome Database


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Short-term Lamarckism in asexual single cell organisms
I was reading through the Karr et al. (2012) whole-cell computational model. One of the things they did was to induce single-gene disruptions in their model. They observed several to be fatal, but:

In some cases (Figure 6B, fifth column), the time required for the levels of specific proteins to fall to lethal levels was greater than one generation (Figures 6C and 6D).

As far as I understand this is because when a single-cell divides, daughters get not only get a copy of the mother DNA, but also have their initial levels of proteins and RNA set to those of their mother (or similar, with some statistical fluctuation).
To me this screams of Lamarkism: if an organism during its lifetime came in contact with an environment that caused a greater expression of some protein that in had at birth, its children will also have a higher initial expression of the same protein. In other words, the trait of "level of this protein" seems to be being passed down in a Lamarkian way. Is my understanding correct, or am I missing the point?
If my understanding is correct, then what are some standard methods to account for this short-term Lamarkism in mathematical models of evolution?

Notes

I am primarily interested in mathematical (or other formal) treatments of this. I have a background in mathematics and some work in mathematical modeling for population biology and evolutionary game theory. I have no background in biochemistry or microbiology. I would appreciate answers or references that cater to this awkward background but I am not adverse to plowing through some microbio if it is for something awesome.

Similar partial arguments can be made for non-single-cell and sexual organism by considering hormone expressions of the mother during pregnancy, as in this answer. I am satisfied with an explanation for asexual single-cell organisms, but bonus points if it can also say something about non-single-cell and/or sexual organisms.

Follow up question on modeling the mechanism behind this: Macromolecule levels in daughter cells after fission

The distinction between Lamarckism or not doesn’t make sense for single-cell organisms: the cells acquire features all the time and pass those on to their daughter cells – literally Lamarckism. (Disclaimer: Lamarck of course neither thought of single-cell organisms nor did he imagine a feasible mechanism by which his theory could be made to work.)

Thanks @KonradRudolph, but to clarify from a naive modelers perspective: if I was making a model of the interaction of single-cell organisms learning and evolution then it would be reasonable to have the organism pass on its learned strategy (which would hypothetically be encoded in something like the levels of various proteins) to its offspring?

It does, by necessity: the mother cell splits off into two daughter cells which each “inherit” some of the material from the mother cell. Since there is no “erasing” step going on during mitosis, this means that daughter cells inherit the proteins of the parent. Now, whether this information is sustained across generations is a different question: proteins in particular have a half-life so after some time all this learned “information” is gone unless it’s encoded in the genome or as epigenetic information.

Thanks for the explanation @KonradRudolph, if you have more insights I'd love to hear them on G+. I might ask a separate question about how to best model how the proteins are distributed among the daughter cells.

@KonradRudolph: Looks like you've more or less answered the question; would you mind turning your comments into an actual answer?

This phenomenon is well known and can be observed in several species. In fact, if you look at the time it takes for E. coli to change its transcription program in order to react to the environment (signal->transcription->translation), you will find it can be longer than its ~20 minute doubling time. You can indeed think of it as a form of Lamarckism. However, it is part of a field that has been booming in the last ~10 years, known as epigenetics.
Epigenetics is a field of research that deals with hereditary information that is passed by non-genetic mechanisms, i.e. not in the DNA sequence. This includes several mechanisms including passing of proteins/RNA, chemical modifications of DNA (methylation) and chromatin (histone modification). It turns out that epigenetic effects can be observed in virtually all species (including human) and affected phenotypes can be significant (leading to disease, for example).
This is a very interesting field of research and is very wide, so I would recommend reading a bit. Specifically regarding protein/RNA passing, I believe this is somewhat less deeply studied, perhaps due to the fact that the effect decreases exponentially (due to dilution), can be limited by protein/RNA stability and some measurement difficulties. However, I think I recall mathematical treatment of this in Prof. Uri Alon's book. You can also catch his systems biology course online on youtube, which I think touches on some of this material.

Just to clarify: The most well-known examples of epigenetics are chromatin (DNA/histone) modifications, but there are several other mechanisms that can pass hereditary information, often along several generations. Any such mechanism is considered epigenetic. Passing protein/RNA is one such mechanism and it is certainly being studied by epigenetics researchers.

I would say not, though you might find occasional cases where it is important.
Lamarckism could certainly apply to single celled organisms, but it would still tend to be associated with DNA.  As originally described by Lamarck, the traits cited would be retained through the offspring's lifetime, potentially being passed on to later generations.
Protein half lives vary quite a bit, but usually in bacteria they are about an hour and can change faster than that.  The changes accorded to Lamarckism should at least persistant for most of a lifetime.  If this is Lamarckism then all embryonic stem cells have Larmarckian inheritance... at least for a few hours.
On the other hand... This is Lamarckism in the sense that historically Lamarck was sometimes observing physiological adaptation.  One of his classic examples was how a blacksmith's muscles would become large from working hard.  The Blacksmith's children who also did this work would also become muscular.  That has little to do with inheritance though.