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Hayflick limit and hair or nails
I am not a bio major but I have heard about Telomerese shortening in each cell division which leads aging and cellular death. I also read that Hayflick limit is about the number of divisions a cell can make before it dies.
So my question is, how is it possible for us to have constantly dividing cells such as in our hair or nails. They are also cells right? They constantly divide almost our entire life, so how come they do not die out of Hayflick limit?
Or is it like, when a cell divides for the first time, it loses one unit of Telomere but the second cell also have the same number of Telomeres as the first one? I mean if Hayflick limit is 50 for the first cell, is there like 49 and 49 for both cells after division? And when do they decide to divide, is the first cell waits its child to reach Hayflick limit before it divides again? Is this just too complicated to explain in layman terms or are we just not sure yet?
Please do not go hard on me if I have conceptual mistakes, I am just really curious about this.

IIRC, hair follicles/nail beds don't create hair by cell division, but instead by producing the keratin directly.

And Adult Stem Cells replenish the tissue and have Telomerase turned on to extend the telomeres to overcome the 3' replication problem which causes telomeres to shorten. The net effect is that Adult Stem Cells do not lose telomere length.

Let's do some math.
Also, let's ignore your examples, and use a clearer one - instead of fingernails, let's look at the cells that line the intestine.  Intestinal epithelial cells are shed and replaced constantly and very rapidly, roughly every 5 days.  So that means about 50-70 cell generations per year.
Each time the cell replicates, it loses a little bit off the end of its telomeres.  How much does it lose?
We know that for lymphocytes, adults lose roughly 30 base pairs of telomeres per year.  Lymphocytes don't replicate as fast as the colonic mucosa, though.  The estimate for these rapidly-dividing cells is about 44 bp/year. We can say 50 for a round number.
That doesn't tell us much unless we know what we're starting and stopping with.  Humans start life with about 10,000 bp of telomeres.  At least in cultured cells, once telomeres reach 1000-2000 bp, cells become senescent and stop, or greatly reduce, their growth rate.
So we start at around 10,000, we can lose up to 9000, and we lose around 50 per year. That means that the intestinal epithelium, which have about the most rapidly-dividing cells in the body, are good for about 180 years of life, assuming that the loss remains constant.
(I don't know if loss does remain constant in these cells, but in lymphocytes, the loss of telomeres accelerates in elderly people, from about 30 to about 60 bp/year in people over 60. However, it's likely that reflects increased lymphocyte turnover in older people, not something intrinsic to the age per se.)
So bottom line, we're good for it.
More generally, keep in mind that the popular media have seized on telomeres as a simple answer for everything related to aging.  Obviously, that's not reality.  Telomeres certainly reflect aging; in some cases, perhaps many cases, they may be one influence on aging; but in most cases, telomere shortening is probably only a minor aging factor, and many other causes are more important.

Is there a clean explanation for why telomere length decreases roughly linearly with time (or with number of cell divisions) rather than exponentially? Or is this mostly an empirical observation?

The end-replication problem means that there is a loss of a constant number of telomere bases, not a fraction of the length.  Hence, linear loss

I'm sorry, but your answer is wrong. The cells that are lost are replaced by adult intestinal stem cells http://www.nature.com/nrm/journal/v15/n1/fig_tab/nrm3721_F1.html Adult stem cells keep telomerase active so that telomeres are extended with each replication.

I admire your confidence in not even reading the references I helpfully linked for you before your attempted correction.
While embryonic stem cells have active telomerase, adult stem cells (which is what we're talking about here) do not have enough to maintain telomerase length.


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What does `knee atlas` means in an IEEE's paper?
I am referring an IEEE's paper for my project which has a term called knee atlas, I am not getting the exact meaning of this term, does they mean it a processed image or something else? I am working in matlab and here is the paragraph of IEEE's paper:

Six atlases were derived from 3-D DESS WE series from six subjectswith visually normal knee images ... The series for three of these atlases were selected from the public release OAI image dataset 0.D.1 and three were from the baseline pilot study. Trained human observers created the knee MRI atlases using manual segmentation.

Could you link the article or provide a full reference? An excerpt out-of-context is difficult to interpret. For example, we might need to know what OAI means.

The knee atlas is an MRI generated with the intent of identifying anatomical features, much like this.

source: Stack Exchange

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

sort: votes


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How would substances that have anti bacterial characteristics interact with yeast?
This question has its origins at home brewers where the question was asked how would substances with anti bacterial qualities interact with yeast a fungus?
No one at home brewers was really sure so I thought I would ask here.
LINK

Welcome to Bio. That would depend on the type or class of substance. Can you narrow the question down?

Substances that exhibit antimicrobial activity do so because the microbe itself is susceptible to the mechanism of action. For example, some bacteria crosslink their peptidoglycan cell wall with a transpeptidase (aka penicillin-binding proteins), and penicillin antibiotics block this step. Other bacteria don't do this, and so if you use penicillin there will be no effect.
Likewise, some antimicrobial methods have very broad efficacy against everything, like drugs that inhibit ribosomes, or at the extreme end, bleach. Being said, ginger as in the homebrew link is shown to have a broad action on microbes as denoted in the following article. The question now is does ginger affect yeast?
Google search "gingerol antifungal" (gingerol is apparently one of the potent effector molecules in ginger) and you get a host of results detailing it's efficacy on C. albicans. This doesn't necessarily mean it has the same efficacy on S. cerevisiae, but it does mean that, and this is just a number out of the literature, but a 10% ginger solution may have deleterious effect on fungal growth.
Outside that, I can't really find anything on the actual antimicrobial mechanism of action for ginger, either, so it's difficult to say other than for some reason, they inhibit microbes. They did show that 6-gingerol induces ROS production in tumor cells, which results in DNA damage, but I'll continue to look for an explanation.
What remains, now, is too broad. The ways that antimicrobials interact with different microorganisms is a lot to consider and I can only be about as broad as I've written above without going into a novel worth of text. Hopefully this was helpful!
You can check out this Sigma page on antibacterial modes of action to get an idea of the ways different antibiotics are made to affect microbes.

Remember, the reason we make antibiotics is so that they will work in eukaryotic people.  So antibiotics usually target proteins or processes in bacteria that eukaryotes do not have, or where the eukaryotic version of that target is different enough that the antibiotic doesn't react.  So most yeast will be unaffected by most antibiotics.

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What stimulates a nociceptor?
For instance, when pressure is applied to the skin, what determines how much pressure results in nociceptor stimulation. And when a sharp object pierces the skin, why is pain, rather than simply touch, perceived? Also, what causes nociceptors to sometimes be stimulated when there is no painful stimulus present, such as during a migraine when the skin feels painful to touch and in chronic pain?
Thank you in advance :)

All of these are affected by specific characteristics of the nociceptors.

Nociceptors are only sensitive to high pressure. The low pressure stimulus would only stimulate mechanoresceptors which would not cause a perception of pain. Receptors like $TRPA1$ sense mechanical stimulus of a higher degree. $P2X/P2Y$ sense ATP which is released due to mechanical tissue injury, as mediated by high pressure or a sharp object injury. Further more, several cells die as a result of nociceptive mechanical stimuli releasing mediators the receptors to which also act as nociceptors.
Exaggerated response to a noxious stimuli is called Hyperalgesia. A sensation of pain in response to a normal stimulus is called Allodynia. Both of these are mediated by specific sensitizing receptors on the nerve endings sensitive to Bradykinin, %HT, Serotonin, Substance P etc. All these are commonly found in conditions where these two are observed, as in the case of burning on touching following sunburns, or increased pain adjacent to an inflammatory foci.

Source:- Ganong's Review of Medical Physiology


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Why are vegetables either red or yellow?
Have you ever wondered why these two colors occur so often? Take these:
onion
waltnut
potato
carrot/parsley
and even cabbage which can be green or red.
Why these two pigments? Or is it just one pigment and it's just its concentration that makes the difference?
Thanks for any explanations!

As many plants do, many of vegetable do photosynthesis. For photosynthesis, chlorophylls, which are green, and carotenes, which are yellow to red, play important roles. When chlorophylls get less, you might see yellow to red color due to carotene. When chlorophylls are degraded, they get light brown. In some vegitable, such as tomatoes, lycopene, which is an intermediate of carotene synthesis, is accumulated.
https://en.wikipedia.org/wiki/Lycopene
Another popular pigment is anthocyanin, the color of which is red to purple. Various functions of anthocyanin are suggested from sun-shade, to an antioxidant, to attracting birds in fruits.
https://en.wikipedia.org/wiki/Anthocyanin

A lot of fruit and veg are green when unripe and become brightly coloured when they are ready to eat (obviously not true for all, but most fruit/veg does).
This is probably deliberate as a mechanism to signal to birds and animals that it is ready to eat, so that they can disperse the seeds inside.
Red and Yellow are bright colours not usually seen on plants except of fruit/veg, and flowers (which are brightly coloured to attract bees and whatnot), so it makes sense these could be used as signals.
http://www.rosincerate.com/2015/07/colour-changing-fruits-and-veggies.html


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Why aren't gene drives extremely common?
The ability for gene drives to sidestep the Mendelian mechanism and rapidly spread through populations (even if the gene is slightly fitness reducing) is extremely powerful. Why aren't normal populations riddled with parasitic gene drives?  What mechanism keeps naturally occurring gene drives suppressed to (apparently) very low levels?

You are going to need to provide references to back up the claim in your first sentence. If you mean this, it is because you need to edit the genome of the organism in order to accomplish the task.

Yes, by "gene drives" I mean "gene drives".  As described by Wikipedia.  To introduce new artificial gene drives you need to edit the genome of organisms.  But gene drives also occur naturally. (Mentioned here, for example.) The question is, why don't these dominate? Edits made artificially by experimenters can also occur naturally.  (Or if they can't, why?)

From what they are describing, this is double-stranded break repair. You need a break to occur in the locus of the gene for it to happen. And as only about 1.5% of the human genome is protein coding, random breaks are more than likely not occurring in genetically important regions. For it to happen non-randomly you need an endonuclease to make a break in the chromosome. There are a few examples or genes where this occurs naturally, but more often times you see it as a viral mechanism to integrate into the host chromosome. It is estimated that upwards of 8% of the human genome is viral DNA.

And to be passed on, all of these changes need to occur in germ line (sex) cells. If they occur in somatic (body) cells, then either they will be killed by the immune system if they are deleterious, or they will just sit there until the organism dies and they are lost.

OK, but double-stranded breaks occur naturally, and you only need a handful (or even one) gene drive created through chance to take over a population.

Not without endonuclease activity. There is meiotic recombination that could easily delete the driver in the next generation, assuming that the gamete that had the mutation fertilized/was fertilized to form an embryo. Also if a gene is not under selection, especially when it comes to duplications, they rather quickly become pseudogenes through genetic drift. If the random driver confers a significant survival or reproductive advantage, then natural selection will select for it, otherwise it has far less of a chance of being maintained than the wild-type gene, as it is just a numbers game.

Are you saying breaks don't occur spontaneously without endonuclease?

Are you referring to the same thing as meiotic drive?

Spontaneous ds breaks occur and are repaired, but there are billions of possible locations that they can occur in higher Eukaryotes, so the odds of those breaks occurring in a productive way in the germ line without an endonuclease to specifically localize the break are slim. Also, there are other DNA repair mechanisms that do not go through Homologous recombination, such as non-homologous end joining, or even apoptosis (cell death) due to chromatin damage, that too reduces the probability even more. The key to the technology for synthetic drivers is specific breaks and providing template DNA.

Ok, you have started to sketch an answer, but its still not at all clear that those suppressive effects are nearly sufficient. Analogously, there are many ways that cells repair DNA and protect against cancer, and if you just listed those mechanisms and said "therefore it's highly unlikely cancer will ever develop", you'd be wrong. In the case of cancer, one can argue that the suppressive mechanisms will drive the rate to be low enough to allow procreation, but for gene drives there is no such argument (unless you go with group selection).

Compare: "The only way you can have a de novo mutation in the species is through a spontaneous event in the germline, and the chance that this would lead to anything useful is slim. Furthermore, there are lots of DNA repair mechanisms the cell uses which reduces the probability even more. Therefore, usefu de novol mutations cannot appear in a species."

I have a feeling that the OP is confusing naturally occurring so-called selfish, or parasitic genetic elements and the CRISPR/Cas9-based gene drives that have been making news as potential tools to eradicate disease vectors like the aedes mosquito. My answer is working from that assumption.
The big difference between naturally occurring "parasitic" genetic elements (including bacterial CRISPR elements and things like transposons) and the gene drives that are being tested as vector control revolves around what we put inside the latter class of gene drive.
The OP hit on this difference in his question, when he mentioned the decrease in fitness caused by engineered drives. In the naturally occurring drive-like elements, there is rarely ever a decrease in fitness in the organism and when it does occur, it is unlikely to be passed on to future generations.
Transposons, for instance, are largely active in somatic cells, whose DNA is not passed on to descendants. Semi-randomly occurring genetic changes are sometimes passed on, but this is relatively rare and evolution favors those that are either neutral or that increase fitness. A brief search doesn't turn up, and I can't think of, any cases of naturally occurring deleterious genetic alterations caused by something like a transposon having been found to remain in a population long enough to be studied.
Engineered gene drives, on the other hand, particularly in the cases of those meant to combat mosquitos, are purposefully designed to reduce the fitness of their target host.
The last question, of what keeps naturally occurring drives at low levels, requires either a rather vague, or a very long answer. I'll go with vague and provide some links to longer ones. Briefly, our genomes have evolved a lot of ways to maintain genomic integrity, in the forms of proteins responsible for proof-reading DNA, repairing breaks, and destroying any "free" pieces of DNA found outside of a chromosome. We've also evolved a lot of mechanisms to maintain genomic integrity through small non-coding RNAs.
Here are some good papers (without paywall) on the subject:

How p53 restrains mobile genetic elements
Proteins that function to restrain mobile genetic elements in rice
Good review of transposons in general
Finally, how people are engineering gene drives to combat malaria

Hope that helps!

Thanks very much for your answer.  In my defense, I don't think I confused anything so much as I just didn't state my question in the standard terminology.  This obviously is not my field, so thank you for filling in the gaps of my knowledge and answering the clearer version of my question.  Your paragraphs 2-5 point out that most naturally occurring parasitic gene elements have neutral, rather than negative, effects on fitness.  This is useful to know and much appreciated, but of course it just makes my question more pointed.

Paragraph 6 sounds to be essentially the sketch of an answer described by AMR in the comments on my question.  It may be that there simply isn't a clean, precise answer known.  But, as I pointed out there, an analog of this sort of argument exists for cancerous mutations, yet cancerous mutations are common.  And it does not explain the essential mechanisms by which lab-engineered gene drives can avoid these natural protections which are apparently so effective against natural parasitic genetic elements.

@JessRiedel - sorry for the radio silence. With respect to your original question, I wouldn't think of cancerous mutations as a 'gene drive'. Most cancers only occur after child-bearing age, so doesn't have much of an effect on an organism's fitness. That holds for both hereditary and acquired mutations, the latter requiring a long time to develop. Exceptions, like childhood leukemias, are interesting but quite rare.

Regarding lab-engineered gene drives, I doubt that they avoid cellular defenses, although it would be hard to measure that. Essentially, they overcome defense mechanisms by being targeted to a specific site and by carrying active payloads. That is, when they integrate, they do so in a functionally important location and deliver genetic code that has a measurable effect. This does not hold for many transposable elements. Although sometimes an endogenous TE gets lucky: http://www.the-scientist.com/?articles.view/articleNo/32298/title/Jumping-Genes-a-Cause-of-Cancer-/

To be clear, I am not considering cancerous mutations to be gene drives.  I was drawing an analogy between (a) the explanation suggested here for the rarity of naturally occurring gene drive with (b) an argument that cancerous mutations should not arise.  We know that (b) does not actually rule out cancer, so it would seem that, without further detail, (a) does not rule out widespread natural gene drives.


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Locomotion of Hydra: Why Somersaulting is better than Loop locomotion when moving to a larger distance?
In my text I read about different types of locomotion of Hydra where I learnt that generally Hydra moves by somersaulting and it is faster than 'Loop locomotion' which Hydra uses for moving to a large distance. At the end of the chapter the question is "Why somersaulting is better for going to a larger distance?" I cannot find a good answer to it.

Is not saving time a good enough argument?

generally Hydra moves by somersaulting and it is faster than 'Loop locomotion' which Hydra uses for moving to a large distance. by 'Which' I mean 'loop locomotion' so in fact, when Hydra goes to a larger distance it chooses the slower process


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At what point during an action potential are the sodium potassium pumps working?
I'm trying to understand how all of the potentials during an action potential are created. My question specifically is about the sodium potassium pumps, however I would also be grateful if someone could verify if I have grasped the concepts correctly.
From what I understand, the resting membrane potential is at around $-60\rm\,mV$, close to the equilibrium potential for potassium (from the Nernst equation) because the permeability of potassium is much greater than that of sodium, even though the permeability is low.
However, the resting potential is not as negative as the equilibrium potential for potassium because of some permeability of sodium and the permeability of potassium is very low so the tiny permeability of sodium has some impact in preventing the potential reaching the equilibrium potential of potassium.
When the threshold potential of $-50\rm\,mV$ is reached, the voltage gated $\ce{Na+}$ ion channels open, and sodium ions enter the cell, causing depolarisation. The potential rises to about $+40\rm\,mV$, which is close to the equilibrium potential for sodium (because the permeability for sodium is much greater than for potassium). However, it doesn't quite reach the equilibrium potential for sodium because of some potassium ions leaving the cell.
When the $+40\rm\,mV$ threshold is reached, sodium channels close and potassium channels open. Because of the now much higher permeability of potassium ions compared with when the membrane is at its resting potential, the potential becomes much closer to the equilibrium potential for potassium, which I think is about $-90\rm\,mV$, and therefore the cell hyperpolarises. Then the potassium channels close.
Now I'm unsure as to how the resting membrane potential is reached from the hyper polarised state, and I also do not see where the action of the sodium potassium pumps comes into this.

The Sodium-Potassium Pumps are always at work. One can think of them as a continuous process that maintains the equilibrium potential for the individual ions. They always are grabbing internal sodium and exchanging it with external potassium at the cost of ATP.
However a neuron's rest state (in your example -60 mV) is a combination of the equilibrium of the Sodium, Potassium, Chlorine, and other ions. Thus when the membrane hyperpolarizes beyond the rest potential, it is actually the leak potential that brings the membrane potential back up, not the Sodium-Potassium pump.
Leak potentials arise from ions (usually chorine) that pass through the membrane via channels that are always open. Furthermore, sodium channels reactivate and a small amount open to  sodium to enter. (Recall as a population there is usually a small amount of sodium channels open at rest. Another contributing factor is as the potassium channels close the other to factors dominate and slowly bring the membrane back to rest state. Remember that rest is defined as the balance of currents, there will always be small amounts of currents flowing. So even though the neuron is rest small amounts of sodium leak in and less potassium out. The sodium potassium pump maintains the equilbrium potential that allows these currents to flow.
The Sodium-Potassium pump is a slower process, so it usually can be ignored over a single spike. But If there is a high frequency spike train then the small amount of sodium that enters the cell and potassium that exits the cell can add up and effect the equilibrium potentials of the individual Ions. This of course changes the firing properties of the neuron.

I am having trouble finding non academic sources for my last claim, I shall come back and add more sources later once I find them.

thank you for your reply! I'm just slightly confused as you said that it is the membranes leakiness  that restores the equilibrium potential, however from what I understand there is only significant movement of potassium ions when the ion channels are 'closed', in which case the positive potassium ions would be leaving the cell and it would become more hyper polarised? Please correct me where I have misunderstood!

@21joanna12 The wrong idea that you have that is blocking you is that at rest there are only potassium channels open. That isn't the case. There are a small amount of sodium channels and a decent number of chloride channels, too, and putting them all together gives rise to a resting membrane potential of around -65mV. It would be great if there were some kind of equation that took all this into account. Hey, there is! http://paynesnotebook.net/Research/Neurotools/GHKEquation/

"Thus when the membrane hyperpolarizes beyond the rest potential, it is actually the leak potential that brings the membrane potential back up, not the Sodium-Potassium pump." - hey xelo747 do you have a reference to this statement?

@bonCodigo Here is a link that describe everything in great detail. https://www.khanacademy.org/science/biology/human-biology/neuron-nervous-system/a/the-membrane-potential

Very good question. Most of your arguments, to the best of my knowledge are accurate. As to answer your questions, I'll provide a basic model of understanding. (Disclaimer:- I'm sorry if the explanation seems overly-messed up and confusing)
At any moment, the potential difference across the cell membrane has to be such that it makes all fluxes balanced. Let us assume there is a cell with nothing but potassium and non-diffusible negative porteins. Since potassium is the only ion that can have a flux, the only balanced position will be the one with zero flux, because any net ionic movement will cause a change of potential and hence will not be the balanced state. Zero flux will be reached when the concentration ratio of potassium outside and inside is such that the potential difference is equal to potassium's Nernst potential.
To complicate it, let's add sodium. Now the balanced state should have zero net flux. But this does not mean that the fluxes of both the ions is zero. They can be equal and opposite. Let us assume that the permeability of the membrane is equal for both. Then, the balanced potential would be equidistant from the Nernst potential of both the ions. This is because, permeability, in an abstract way, is a measure of the resistance. Flux is the potential difference (between the Nernst potential, where the flux would be zero, and the membrane potential) divided by the resistance (like a simple current), which would be equal only if this difference is same, which is, for a membrane potential midway between their Nernst potentials. Hence, the ion which has a higher permeability, will have a lesser resistance, and would hence require the potential difference to be low, so that the ratio of $PD$ and $R$ be equal to the other ion with a large $PD$ and a high $R$ (low permeability). This $PD$, is not the membrane potential but the difference between this potential and the Nernst potential.
Now, for your first question

...resting membrane potential is reached from the hyper polarised state....

This is simple to understand because the opening of the potassium channels which caused the potential drop to $-90$ has now been reset and the permeabilities have been reset to the original resting values. Since the balanced state depends on the permebilities only, the balanced state of this is the RMP ($-60$), which the cell will achieve. Since $-90$ is unbalanced, the slightly unbalanced flux will cause a drift of the potential towards $-60$ and when it reaches it, the fluxes will match and hence won't deviate any further. The drift is because more of one ion is moving than the other, causing a net movement of charges across the membrane.

.... action of the sodium potassium pumps comes into this....

This is easy to understand but tough to compute. Since the sodium potassium pump is unbalanced, (it puts out 3 sodiums and takes in 2 potassiums), it contributes a net flux always. Hence, the remaining channels, instead of having exactly equal sodium potassium fluxes, will have to have a slight potassium excess to offset the minor flux contributed by the pump. As a result, the effect can be computed in two ways.

We find the net flux contribution of the pump. Now we know by what amount should the potassium flux be greater than the sodium in the remainign channels which follow the PD/R formula and hence we can caluclate the PD such that the fluxes have a certain difference (equal to the flux contributed by the pump)
We perform experiments and directly find a net amount of potential "correction" which has to be added to the potential calculated by matching fluxes because of the pump, which will remarkably stay constant. This method is easier and the value of the correction can be obtained from literature online.

Hope this helped. Feel free to ask for clarifications. If you want net links or references, ask. :)


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What is the instructional language of DNA?

DNA carries most of the genetic instructions used in the development, functioning and reproduction of all known living organisms and many viruses (Wikipedia).

Is it already know how ATCG's sequences create theses instructions? Or equivalently, what is the instructional language of DNA? My interest in this question is to know if we already understand how ATCG's sequences can create, for example, human epidermis with an excess of a determined mineral or change cell's shape for more fundamental geometrical ones (triangles, rectangles, diamonds, etc.).
Please, forgive me for this foolish question: I'm not a biologist.

I think the general dogma is that DNA is transcribed to RNA which is translated to Proteins. Proteins have various functions such as the assistance in creating and destroying cells, providing structure, sending signals to the body, and so on. The DNA is the ATCG's.

This is more difficult than it looks. Developmental/Systems/Structural/Etc. Biology are rapidly evolving fields with a lot left unanswered. The answer to that question is probably extremely interdisciplinary and complex.

There are multiple questions stacked on one question. Each one separate look OK.  Consider splitting them up.

This language is called the genetic code. But before talking about this specific code, it is important to talk about how the code is read. Please note that the below answer is a simplification of the reality.
Mechanism by which the code is read
To make things easier (reality is a little more complicated), DNA is "formatted" into RNA which is then "formatted" into proteins. When "formatting" occurs, we do not lose the previous format but we only copied the information into a new format. The formatting from DNA to RNA is called transcription and the formatting from RNA to proteins is called translation.
Proteins are the active units that affect cell activities. The activity of the proteins is a function of their sequence. As a consequence the language/code we must understand is the relationship between DNA and proteins.
Numeral systems of DNA
DNA, as you said, is written in quaternary (=numeric system at base 4). The four letters are called A, T, C and G which stands for Adenine, Thymine, Cytosine and Guanine (4 nucleotides).
Numeral systems of proteins
Proteins, on the other hand, are coded in a system at base 21 (21 amino acids).
Redundancy
Because $4^2=16<21$, we need to use (at least) 3 letters in DNA to code for 1 amino acid. Because $4^3=64>21$, we necessarily have several codes of 3 nucleotides that match to the same amino acid. We talk about redundancy. In computer science, a byte is a series of 8 bits. In biology, a codon is a series of 3 nucleotides.
Code
Below is the code:

, where Phe, Leu, Ser, etc... are an abbreviation for specific amino acids. Phe for example is the phenylallanine.
As you can see in the above table, most of the redundancy is caused by changes in the third letter of the codon. More information on why it is the case on this post.
There are 4 special codons.

AUG: Is the start codon. It is an indication of where translation should start.
UAG, UAA and UGA are stop codons. They are an indication of where translation should stop.

Possible confusions
Central Dogma of Molecular Biology
The unidirectional relationship between DNA, RNA and proteins has been called Central Dogma of Molecular Biology. Of course, there is no place for dogma in science and the term is very improperly used. Interestingly enough, the Central Dogma of Molecular Biology is partially wrong because this relationship between DNA, RNA and proteins is not necessarily unidirectional. The reverse transcriptase is an enzyme that reformats DNA from RNA.
Genetic code
If you google "genetic code", most hits will display the letter U instead of the letter T. The reason is that the code is often presented for the relationship between RNA and DNA and the only difference in the code between RNA and DNA is that T (Thymine) is replaced by U (Uracile).
mRNA vs RNA
Not all RNA are meant to be translated into proteins. Only mRNA (m stands for "messenger") are. For example, the process of translation is itself catalyzed by RNA (called rRNA, where "r" stands for "ribosomial")
Note also that DNA is first transcribed into pre-mRNA which is then modified into mRNA before being translated.
Is all of DNA transcribed?
No. In eukaryotes (which include pretty much all the living things you may think of to the exception of bacteria and viruses), most of the DNA is not transcribed. The rest is used for regulatory purposes or might not be used at all. The regions (called locus/loci) of the DNA that is being transcribed are called genes

Nice answer! +1. You might want to add little bit about developmental biology, French flag model etc to touch OP's question about cell shape and geometry.

Not to mention epigenetics

The genetic code is a hash table, not a language.

@David Sure.... A dictionary is a hash table too. Note that I used the term language in the informal sense and mainly because OP used this same term.

Too many poor questions receive poor answers imho because the respondents do not challenge the false assumptions in the questions. A dictionary is not enough to define a language; it needs a grammar too.

The functions of DNA and proteins are determined by their shape, and while their shape is mostly determined by their sequence, there is no computational way to design proteins from scratch to do whatever we want.  The modeling is just too complex.

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What effect does a bat's echolocation have on other bats?

Bat echolocation is a perceptual system where ultrasonic sounds are emitted specifically to produce echoes. By comparing the outgoing pulse with the returning echoes, the brain and auditory nervous system can produce detailed images of the bat's surroundings. This allows bats to detect, localize, and even classify their prey in complete darkness. – Echolocation, Wikipedia

Furthermore, we read that:

[ . . . ] these bats contract their middle ear muscles when emitting a call, so they can avoid deafening themselves.

So far, so good. But this gives rise to two questions I've been challenging with. (And unfortunately I seem not to be able to find the correct search terms and I don't get relevant results)
Imagine two bats close together, flying in a distance of, say, 1 meter from each other. As we know, both echolocate in order to perceive the whereabouts of their surroundings. Bat #1 emits ultrasonic waves, but contracts its middle ear muscles so it won't get hurt. I imagine these two bats are close enough to each other for the waves to be harmful to bat #2's hearing as well.
Hence, two problems arise

Either the waves aren't harmful to the other one (I'd love some calculations on this, or hints on how to do some myself) or something's happening to bat #2 that doesn't let the ultrasonic waves damage its hearing. Certainly bat #2 isn't supposed to know when #1 will emit those waves, so what is happening?
Won't the waves bat #1 has emitted affect the waves bat #2 will emit? So, won't this affect bat #2's perception? We've seen many bats flying together in real life with [maybe seemingly] no trouble visualizing the surroundings, so this mustn't be the case, but why?

Maybe somewhere in this search? https://scholar.google.com/scholar?hl=en&q=bat+group+dynamics+and+echolocation&btnG=&as_sdt=1%2C33&as_sdtp=

Maybe they can tune the frequency of their hearing to the frequency of emission, as per this paper? http://www.pnas.org/content/107/15/7048.short

Just came across this. Very interesting 1st question!! I had wondered this many years ago and never looked more into it.

Bat echolocation is an incredible and complex process. Bats can emit two kinds of ultrasonic signals. One is a short pulse (less than 5 ms long) that sweeps a wide range of frequencies (100 Hz to 25 kHz) and is referred to as a FM sweep, or a broadband signal. The second kind in a constant frequency (CF) and is much longer in duration (5-30 ms) and held at a specific frequency. In addition to the fundamental frequency there are first and second harmonics. This important for depth perception, pursuit of prey, and location of other bats!
Specifically, bats measure distance by comparing the time between emitted sound pulses and its returning echo. Rapid FM sweeps are especially well suited for target distance so the bat can adjust easily and locate the target. Bats can determine angle, size, elevation, azimuth, and velocity/movement of object from these time and frequency differences as well. Now, bats calculate their own velocity using the Doppler shift concept of their own echos. Meaning, when their signals comes back to them, they compare the amplitude of what their ultrasonic sound wave would be if they weren't moving to the received sound and calculate actual velocity off that (it is a very complicated process and I'm trying to simplify it to get to your question).
Ok, now that is the basics of echo location, but back to your question: What happens when there are multiple bats? Well, when you have many ultrasonic waves going at once, it might get confusing about which is your signal. At least that what you would think. Since the bats have such a wide range of frequencies they can vocally create (100 Hz to 25 k Hz), bats usually simply change the range they are vocalizing to prevent wave disruption. If you do get an overlap of waves from bats using the same frequency, you get something similar to Doppler effect where amplitudes are not what expected. Since they are pretty drastic changes (sometimes even canceling out the wave entirely), and a bat can sense if another bat is around them by calculating the size of the objects producing noise, a bat will know this distortion is due to another bat and not the prey. As a result one bat will have to change their frequency range. This has become sort of a dominance game for them as a result. The bats heightens (I think, might be lower) the frequency of their signals until one cannot go any farther. The one with the wider range is considered dominant and rules that frequency range. Neat right! Hope that answered your question!
Sources: http://scitation.aip.org/content/asa/journal/jasa/54/1/10.1121/1.1913559
Behavioral Neurobiology by Thomas Crew copyright 2000 (most of info from this source, great read if interested)

Interesting and accurately explains OP's 2nd question.

Thanks! Be sure to upvote the answer so other people know it is a good explanation :).

@ephackett Have you heard of the proposed Bioacoustics Stack Exchange? It seems like you might be a valuable member of that community. Please consider committing to the page so we can get closer to making it to the Beta stage. Cheers! https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=NDI3NDRkN2RkYmQ2M2Q3YTk5YjhlNjk0ZTFkZmY3MGIwNmM1ZDliNWMxNzMxOGIzOGVlNTMyY2M2NDAzNzY4N76lf0C63DSZ9D1MFeu97ZyTQM5mgMh5iflfL5ArRRe80


text:
If so many different hormones/molecules work by activating adenylyl cyclase, how do they have different effects?
It seems that many hormones and molecules work by activating adenylyl cyclase to convert $\text{ATP}$ to $\text{cAMP}$, such as adrenaline and glucagon. Both of these seem to bind to $\text G$ protein receptors, cause an alpha subunit to dissociate and bind to adenyly cyclase to activate it, and then adenylyl cyclase forms $\text{cAMP}$. If so many molecules work in the same way, how can they have different effects?
My guess is that perhaps they may have different molecules inside which respond differently to elevated levels of $\text{cAMP}$? I presume both cells affected by adrenaline and by glucagon have the protein kinase which, when activated by $\text{cAMP}$, is able to activate glycogen phosphorylase to break down glycogen, as both adrenaline and glucagon increase blood sugar levels. Perhaps liver cells have more of the glycogen phosphorylase enzyme for a greater rate of breakdown of glycogen?
But then when I consider the heart, adrenaline increases heart rate but glucagon does not. If they have the same mechanism of action, how can this discrepancy arise? Could it perhaps be that adrenaline increases heart rate not by acting in the heart cells but in the medulla oblongata to increase the heart rate? But then again I come to the problem of why glucagon does not have the same effect. In this case I could hazard a guess that the glucagon molecule is too large to pass across the blood brain barrier.
But this is just one example of a possible problem in how two different molecules use the same mechanism. Although I cannot find a link now, I think I remember that long term potential ion to for new memories involves activation of adenyl cyclase. If that is so, it doesnt make much sense becaus adrenaline certainly doesn't help in the formation of new memories!
EDIT: I have just also read that insulin works by activating cAMP in hepatocytes/muscle cells, however it also seems that glucagon works by activating cAMP in the same cells! Two directly opposing effects using the same mechanism in the same cells- I'm very confused now!

Slightly different shapes mean that they will bind to slightly different receptors. The receptors will be the first step in a cascade, at it is what happens after. There are a lot of other reasons, like tissue specific chromatin structure can effect the genes that are available for transcription, etc. Your question may be a little too broad to provide a good answer. If you could compare and contrast one example of a hormone induced signaling pathway to another and ask why the specific results of one might be different from the other, then that might allow for a more specific answer.

I think this is a good conceptual question. It does seem perplexing from many cell biology books that a number of dinstinct signals with different meanings all go appear to go through the same "node" --- why don't they get mixed up?

@21joanna12 sounds like you found an error in your textbook because insulin does not increase the amount of cAMP in the cell (it suppresses it) and antagonizes the increase stimulated by glucagon.

@21joanna12 in reference to the question above - adrenaline (i.e. epinephrine) increases heart rate through actions on the pacemaker cells of the heart - there are no glucagon receptors on the pacemaker cells (this is why there is no response to glucagon in those cardiac myocytes).

@Roland A lot of cartoon representations in textbooks happen to be generalized in a way you can look at many possibilities (sometimes even the entire known pathway) in the same image much like this. In reality, we know the response depends largely on the downstream interactions that are actually available, and if we know those, we can produce an image more similar to this one.

@VanceLAlbaugh I approved your edit, but I am not 100% sure that I agree that this is essentially a question about metabolism, so I am not 100% sure that I agree that it should be tagged as such. Technically almost any process that the cell undertakes is metabolism, but I am not sure that we should add it to every question related to cellular function.

@AMR Point taken – if you want to remove the metabolism tag I guess I'm fine with that but I think the other text edits are necessary for grammar clarification, etc. thanks!

@VanceLAlbaugh I am going to raise as a meta question and see what is said. The edit review didn't show any text edits. Are you sure those were not approved in a previous edit of the question?

@AMR yes I think you're right – I think I was thinking of the edits on the answer not the question

@21joanna12 - does that answer below clarify your question? If so, check it as the answer so we can move on... if not, are you still confused?

How can hormones/molecules have different effects if they all work through cAMP? The short answer is that receptor expression on cell types is highly specific, and only if a cell has a particular receptor will it respond to a particular hormone. Thus two different hormones can have different biologic effects because the cells that contain those receptors are highly specific. Overall it is the presence of specific cellular receptors that determines the specificity of hormones and their effects.
A little more in depth of an answer... This is a classic concept from graduate physiology and was a real step forward in our understanding of hormone action in the 1950s/1960s. Earl Sutherland, who received the Nobel Prize in 1971 in Physiology or Medicine for this work, was on the faculty at Case Western Reserve University (and later at Vanderbilt University). Dr. Sutherland was studying the actions of hormones that were involved in glycogen metabolism (i.e. glycogen synthesis and glycogen breakdown). These classic studies identified a substance, now recognized as cyclic AMP (cAMP), whose intracellular concentration was increased in liver cells that were treated with hormones that stimulated glycogen breakdown. Conversely, cAMP was decreased by hormones or other conditions that were associated with glycogen synthesis. Most interestingly, it was identified that different hormones that either increased or decreased glycogen synthesis/breakdown had similar effects on the intracellular concentrations of cAMP (e.g. epinephrine, glucagon). This suggested that somehow cAMP was a common signaling molecule (or "second messenger") that transmitted the extracellular hormonal signal to the inside of the cell to have a biochemical effect (in this case stimulating glycogen breakdown).
In the case of Sutherland's studies, the increased concentration of cAMP stimulated the activity of Protein Kinase A (PKA), and the lack thereof decreased PKA activity and allowed the actions of protein phosphatases to predominate. For example, when glucagon binds its receptor on hepatocytes (liver cells), that receptor is coupled to an intracellular enzyme ($G_S$) that is activated and then can activate an enzyme called adenylyl cyclase, which increases synthesis of cAMP from ATP. The increase in cAMP then binds to PKA and phosphorylates the glycogen synthesis enzymes and breakdown enzymes. When the glycogen synthetic enzymes are phosphorylated by PKA they are inactive and, conversely, when the breakdown enzymes are phosphorylated they are active. Thus, glycogen receptor activation leads to activation of the glycogen breakdown machinery and inhibition of the glycogen synthetic machinery. This makes sense physiologically if you think about it - glycogen acts to increase hepatic glycogen breakdown and increase hepatic release of glucose into the circulation.
In brief, once Sutherland's group demonstrated the importance of cAMP as a second messenger protein within the cell, other groups began realizing that many other hormones led to changes in intracellular cAMP but each had there own effects. The differences in these effects were determined by the cell type that the hormone was acting on and whether or not that receptor was coupled to a particular second messenger system. Thus, you could have any number of receptors on the cell surface that are available to bind extracellular ligands (e.g. hormones, nutrients, drugs). However, each of these different hormones can be "coupled" or linked to different types of intracellular "second messenger" processes to transmit a signal. There are many types of second messengers that help transmit extracellular signals to the inside of the cell.
As you mention in the question, cAMP is a common second messenger system for a variety of different cell types. However, those different cell types have different receptors that are coupled to cAMP. Thus, hormones can have different effects depending on the tissues that express the receptors. For example, the glucagon receptor is expressed on hepatocytes which increases $G_S$ activity and thus cAMP, leading to glycogen breakdown and increased hepatic glucose production. Similarly, the $\beta_2$ adrenergic receptor that binds epinephrine/norepinephrine on smooth muscle is also coupled to $G_S$ which increases cAMP and leads to smooth muscle relaxation. These very different hormones have different biologic effects in different tissues, even though the effects are both driven by cAMP-dependent mechanisms. Briefly stated, it is the receptors that are present on a cell, that determine the response of a particular cell to that hormone.
This is graphically shown in the image below from this medical biochemistry link in adipose tissue - though the same concept is true for liver cells. Glucagon signals through its receptor to increase adenylyl cyclase, cAMP and then PKA activity, while insulin inhibits that activation by increasing the activity of PDE (a phosphodiesterase) that works on breaking down cAMP and subsequently keeping PKA in its inactive form.


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Gemini usage of --sample-filter
I am using gemini to query databases made from vcf files, which contain data from multiple samples. However, I need to query data only from one sample, (for which I currently use grep to filter the results and > it into a txt file).
I tried experimenting with the --sample-filter option in gemini, the documentation I found however says only:

gemini query --sample-filter "phenotype=2" -q "YOUR_QUERY"

db_info says the table samples contains name, but when I try doing

gemini query --sample-filter "name='S2'" -q "YOUR_QUERY"

I'll get error, that I have an syntax error in my query. I tried putting there "sample_name=='S2'" even tried other criteria, like sample_id, but couldn't get this work.
So please, do you know how should I get this work, or have any other advice?
Thank you very much.

I've found a possible workaround to my problem, I filter the vcf input file before loading it into the db by vcfkeepsamples from vcflib.
But I still don't know if the --sample-filter in gemini works, so if you have any ideas, it would be helpful.


text:
Is a nucleus more dense than the rest of the cell?
On the one hand, it seems like there's a higher density of 'stuff' in a nucleus, so it should be more dense. On the other hand, if it was more dense, I'd imagine that nuclei would 'settle' to the bottom of a cell, which would be rather surprising.
Update:
http://www.eng.umd.edu/~nsw/ench485/lab10.htm reports nucleic density of 1.4 g/cm3.
https://books.google.com/books?id=t4ZQRWvr510C&pg=PA85&lpg=PA85&dq=cytoplasm%20density%20g%2Fcm3&source=bl&ots=rEkcu0HzZE&sig=Bs4MVad_pbS7vWY2pRv6ALWf-bc&hl=en&sa=X&ved=0ahUKEwj2rLXVnLbJAhVSlogKHUjAAS8Q6AEIMTAD#v=onepage&q=cytoplasm%20density%20g%2Fcm3&f=false
reports a density of 1.03 - 1.1 g/cm3 for cytoplasm, so less dense.
do nuclei sink then? or is ICF too viscous / there too much disturbance through movement for nucleus to sink?

When you search images of cells by electron microscopy(EM), some nuclei are denser than cytosol, but others are not. You could also find partial dense area in nuclei. EM is telling how crowd with atoms the areas are. https://www.google.com/search?q=electron+microscope+cells&safe=off&client=safari&rls=en&biw=1318&bih=542&tbm=isch&tbo=u&source=univ&sa=X&ved=0ahUKEwjhrZe_h7XJAhWMOiYKHY4QCMEQsAQIHA#imgrc=_

When you hang up your shirt does it fall to the bottom of your closet?
The nucleus is a dense fibrillar network of DNA, RNA, and proteins, yes, but the subject you should take a look at is the cytoskeleton of the cell. It will will answer all your unanswered questions on the intracellular network that stabilizes, supports, and aligns the organelles within the cell.

If the shirt isn't hung up correctly. :D That makes sense, thanks for the explanation and amusing analogy.


text:
Is there a difference between visual sensation and imagination in the brain?
How substantial is the difference between the neural signal associated with seeing an image and the imagination of that image? Surely, it can not entirely copy the pathway from the sensory organs to the emotional centers, but approximately how large is the common pathway for both processes?
Is there some principal difference in the neural pathway of these two processes, or is the imagined image just more of a slurred version of the visual image?

Interesting question, but typos and grammar mistakes in the text severly hinder comprehension. Could you restate your question more simply?

@Nicolas Thanks for your edit. I included the additional question (second paragraph) just to let the reader know that I'm interested in the topic even if the signal would be exactly the same, but in different centres of the brain. But the simpliest (most measurable) version would be, I think: "If I'm imagining stressful situation, does my Amygdala relies stress (hormones)?

Assuming, like most humans, you have a sense of consciousness, then you should be able to distinguish that there is a difference between sensory perception and imagination. Where you may run into problems, and many people do would be when trying to discern memories of actual events versus imagined circumstances. There has been a good amount of research into how false memories can be implanted into a persons brain and that their brain will then embellish on it and fill in the details. See the work of Dr. Elizabeth Loftus

@AMR I wasn't claiming it's the same, then my question would make no sense. My question is how does this difference look like in brain. I think making up fakememories it's something different. This effect has nothing to do with how the brain recieves (and stores) information which comes, I think, the fake memory is being built up continuously as brain makes connections in order to make it sense as is goodly explained in question: http://biology.stackexchange.com/questions/775/how-and-where-in-the-human-brain-are-memories-stored

In a nutshell: Are you asking on the commonalities between sensation and imaginations of sensation, in terms of neural circuitries?

@Christiaan Yes. But this way interpreted it sounds maybe like something subjective, which is not. By the "commonolaty" I mean the shared neural pathway or shared system in different brain center.

I have re-edited the question in the hopes of getting those downvoters to reconsider. It is a great question, albeit, admittedly, vaguely formulated, especially taking your comments into account. Nonetheless, I hope your bounty and some of my edits draw in your deserved answers. If my edits have defied their purpose, feel free to roll back.

Short answer
Visual perception and visual imagery draw on much of the same neural machinery.
Background
I have interpreted your question as: What are the common neural circuitries between visual sensation and the imagination of sensation?
In neuroimaging, mental imagery of visual images is a big deal. For example, there is a large body of literature on cross-modal activation of visual areas in the brain in blind people. It is known that visual deprivation results in neural plasticity and the recruitment of visual areas in the brain for other sensory systems. For example, blind Braille readers show activation of the primary visual cortex when reading Braille (reviewed in Stronks et al., 2015). However, interpretation of these findings is difficult in late-blind individuals, because they have experienced visual input earlier in life. Hence, while Braille reading they can be mentally reproducing the visual representation of the Braille cells using visual neural circuitry.
Indeed, it has been shown with fMRI that visual imagery and visual perception draw on most of the same neural machinery (Ganis et al., 2004). However, the spatial overlap of the activated regions is neither complete nor uniform. The overlap in this study was more pronounced in frontal and parietal regions than in temporal and occipital regions, indicating that cognitive control processes function comparably in both imagery and perception, but not identically.
Various studies reveal different results, however. In another imaging study, 'just' two-thirds of brain regions overlapped in visual sensation and imagery (Kosslyn et al., 1997). Indeed, the experimental task used may have important effects on study outcomes.
Most notably in this regard is that approximately half of the studies done have found activation of the primary visual cortex during imagery (Kosslyn et al., 1999). This is interesting, because the primary visual cortex is generally thought to be an early, low-level area in the visual system that depends on thalamic input that relays information from the optic nerve to the brain. I.e., it is generally believed to depend on sensory stimulation. Generally, only the higher-level associative visual areas are associated with higher cognitive processes.
References
- Ganis et al., Cognitive Brain Res (2004); 20: 226–41
- Kosslyn et al., Neuriomage (1997); 6; 320–34
- Kosslyn et al., Science (1999); 284; 167–70
- Stronks et al. Brain Res (2015); 1624: 140–52

I read some articles on the thalamus, can't currently remember which ones though, that suggested that there is overlaps, but when you are imagining something the thalamus blocks the signals from entering the perceptual system. This is still speculative though, as current the resolution of current measurement methods leaves a lot to be desired.
In some mental disorders the signal isn't blocked by the thalamus (if this is what happens) and is instead experienced as an hallucination, there is also some evidence that this also happens in a less intrusive way in some people we perhaps wouldn't not call mentally ill.
Nikola Tesla for example suffered from what we would call hallucinations, but was able to learn to control it to some extent so he could use them as a tool for helping him making machines. I think the following section of his biography is quite interesting.

There was another and still more important reason for my late
  awakening. In my boyhood I suffered from a peculiar affliction due to
  the appearance of images, often accompanied by strong flashes of
  light, which marred the sight of real objects and interfered with my
  thought and action. They were pictures of things and scenes which I
  had really seen, never of those I imagined. When a word was spoken to
  me the image of the object it designated would present itself vividly
  to my vision and sometimes I was quite unable to distinguish whether
  what I saw was tangible or not. This caused me great discomfort and
  anxiety. None of the students of psychology or physiology whom I have
  consulted could ever explain satisfactorily these phenomena. They seem
  to have been unique although I was probably predisposed as I know that
  my brother experienced a similar trouble. The theory I have formulated
  is that the images were the result of a reflex action from the brain
  on the retina under great excitation. They certainly were not
  hallucinations such as are produced in diseased and anguished minds,
  for in other respects I was normal and composed. To give an idea of my
  distress, suppose that I had witnessed a funeral or some such
  nerve-racking spectacle. Then, inevitably, in the stillness of night,
  a vivid picture of the scene would thrust itself before my eyes and
  persist despite all my efforts to banish it. Sometimes it would even
  remain fixed in space though I pushed my hand through it. If my
  explanation is correct, it should be able to project on a screen the
  image of any object one conceives and make it visible. Such an advance
  would revolutionize all human relations. I am convinced that this
  wonder can and will be accomplished in time to come; I may add that I
  have devoted much thought to the solution of the problem.

The rest of his autobiography has more details

What did you read? Statements without proper referencing, let alone memory recollections alone, are not advisable.

Some articles on the thalamus. I don't remember which ones though, but from a quick search I found one that at least partly deals with the topic http://www.biomedcentral.com/content/pdf/1742-4682-7-10.pdf

You might want to edit your answer accordingly, as you take a very interesting approach in your answer.


text:
What type of tree is this?
I photographed this group of trees a couple of years ago at the northern tip of Prudence Island in Narragansett Bay. Any idea what species these are?

Do you have any better pictures (i.e., close-ups of leaves or bark)? Also, what would you estimate their height to be? Any interesting characteristics to note? Did you see any seeds or flowers?

@theforestecologist These are the best photos I have, I'm afraid.  Height maybe 15-20 feet.  I was hoping someone could identify at least down to the family based on the location and overall growth form.

I'll try to give it a closer look then. Orient me real quick - are those flowers or young leaves  at the end of the branches? Is oppositely arranged, which should reduce our options

@theforestecologist Those are young leaves.  The photos were taken in May 2014.

Although it can't be said definitively because of the picture quality, these are actually very likely maple trees. It's possible that they are either Red Maple (Acer rubrum) or sycamore maple (Acer pseudoplatanus) trees in spring leafout.

Source
Evidence:

The branches have an opposite arrangement. Very few tree are opposite (see MADHORSE)
The Rhode Island Wild Plant Society claims that red maple is abundant on the northern part of the island.
The Virginia Cooperative Extension provides an incomplete but detailed list of trees that can tolerate salt spray.

Two maples, Acer psudoplatanus and Acer campestre, (which are tolerant of salt spray) are both present as an exotic plant in that region of the country (see BONAP range map 1 and 2)
The Prudence Island flora mentions that A. pseudoplatanus is a common escaped cultivar on the island.

I'm leaning toward Red maple because of the red leaves appearing -- this is more typical of A. rubrum compared to the often more yellowish spring leaves of A. pseudoplatanus.

Note: The salt spray and windy environment will cause these trees (and most vegetation along a coastline) to develop "strange" (often gnarly) tree shapes.

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


text:
genetic complementation problem
I've attached the picture of the problem.
SO, based on the information I managed to assemble two large cistrons. (if the combination of two mutants yield (-) mutations are on the same chromosome)
A)so my cistrons are:
1)(1,4,5,6,7,9)
2)(2,3,4,7,8,10)
Note: somehow 4 and 7 is present in both cistrons
B) they ask us what mutation could cause two different cistrons have the same mutants
I was thinking maybe an insertion? i just dont get how it's even possible since if they have the same mutants doesnt it mean they overlap and thus are on the same chromosome??
I would appreciate if you could explain me what type mutation could cause it and check if I did the complementation correctly

bacteriophage T4 has a single chromosome (approx. 200 kb in length). The chromosomes are terminally redundant,  so the genetic map is circular, even though the physical map is linear (as I recall).
A mutation in E. coli (or its viruses) that affects two adjacent protein-coding genes is said to be 'polar'. This indicates that the two genes in question form part of an operon. A strong loss-of-function mutation in the promoter for the operon will typically affect the expression of all the genes in the operon. In your example there are two cistrons, or genes, in the rII locus of T4.

It is possible that the data for this question are taken directly from the published literature. I suggest you search PubMed for papers by Seymour Benzer, from the 1950s.

Sorry Perry, I just don't understand what you mean. So you're saying this problem can't be solved or the mutation on operon is the cause?

I was trying to say that these two cistrons form an operon in the phage genome, and that by knocking out the promoter for that operon you would reduce the expression from each cistron. Another way to say this is that there are two genes bedside each other on the chromosome. The upstream gene has a promoter and the downstream gene does not have its own promoter. The downstream gene uses the upstream gene's promoter. this means that the mRNA from that promoter will be polycistronic and contain 2 open reading frames. Breaking one promoter kills the expression of 2 genes.

So how can this mutation be called then? 1 promoter per 2 cistrons? I've never encountered anything like this in my class before

On second thought, the answer they probably want is that 4 and 7 are deletions, or deficiencies, that remove some part of both genes. That is going to be a simpler explanation than the operon with two cistrons.


text:
How does the brain recall information?
In computers, finding a single word is realized through serial attempts across all available connections to find a specified target.
How does the brain solve this? How does the whole process, from the command to recall some memory to actually "play" its algorithm look like?
By "recall" I mean literally, attempting to bring back an image, a word, a melody or any remembrance from memory.

"In computer, for finding a single word there has to be a movable part that tries all the connections to get what you're finding." - there are literally no moving parts in modern computers with solid state drives and fanless processing units. Moving things (e.g. magnetic hard drives) have nothing to do with computer's ability to find information. It's all about file system abstraction and hierarchy.

@EliKorvigo aha...IT teacher told me...anyway, I still can't imagine the mechanism neither for the brain and computer

This is a great quesion! There is lot of work still being done on this. Unfortunately I don't think I know enough about CS or computer engineering to make analogies, so I'll give a quick crash course and some examples instead and hope you find it helpful. Long story short though is that we are just now making really exciting headway into how memory might actually be stored and recalled and its usually a very dynamic, active, and possibly even stochastic process, not really like a search algorithm in a computer at all.
The brain works differently than a computer in that it encodes all of its information in frequency of signal firing and the patterns of firing between circuits with varying stregnths of connections based on experiences. Frequency is dependent on the neuron itself and patterns of firing between circuits are dependent on where the neurons project to, and how strongly they interact with the next neuron. At this very basic level memory is stored and recalled by placing proteins in the membranes of neurons that are strongly activated to make them easier activated in the future. These are sort of the first steps toward memory. This is called long term potentiation and just means that this neuron is primed to fire more readily and stronger in response to similar input in the future.
To build on this,  there is a classic example of this occuring and causing sensitization ( an exaggerated response to the same stimulus) in conditioning experiments in the sea slug Aplysia. Aplysia has a reflex where it will withdraw its gills slightly if you touch its siphon. You can pair a shock to the tail (unconditioned stimulus) which elicits a large withdrawal of the gills, with a conditioned stimulus (touching its syphon to elicit the withdrawal reflex) to get the sea slug to associate the two. The end result is that the sea slug will learn/"remember" to withdraw its gills fully in the presence of the syphon touch. No learning cannot happen without recall of some sort, and in this example the slug was associating and learning from two "circuits" to produce a different behavior.
In something a little more complex than a slug, memory and recall still functions much the same way, its just the circuits that are interacting are entire brain regions. Most people view the hippocampus as acting sort of like a relay center and boot loader for different memories by taking external input and sorting them to the right parts of the brain. A good example of this would be the difference between dorsal and ventral streams of information in the brain. For a really basic breakdown of this phenomenon there are two areas of your brain that I will focus on - the parietal lobe and the temporal lobe. The parietal lobe is known to be involved in spatial processing, and the temporal lobes are known to be involved in semantic and auditory processing. When information enters the brain (eyes, ears, nose etc.) it will be processed by sensory structures, sent to the thalamus and hippocampus to be "relayed" to the right areas of the brain. Relayed in this case is going to be dictated by whatever connections and how strong they are in the brain. In this case from proteins expressed in the cellular membrane that make some neurons in the hippocampus more responsive than others, so they are more likely to fire. Then, it depends on where they are projecting to that determines where they information is sent.
It just so happens the brain is arranged in such a way that neurons projecting dorsally, or to the parietal lobe I mentioned, will tell you "where" the stimulus is, and those projecting ventral to the temporal lobes will tell you "what" it is. This is achieved because these lobes are highly interconnected to even more regions in the brain and send their processed "where" and "what" info as input to other regions. These regions will all fire a certain way in response to this information and that pattern of firing can be considered a recollection or memory. Sorry that this is dense and so crash course-y but I hope it is helpful in clarifying how the brain recalls some information. Of course this is  a developing field and we are learning more about how it functions every day. These are just some classic examples.

The ventral and dorsal streams in the visual system are the what and where streams in visual processing from the bottom up (optic-nerve - thalamus - V1 - etc). OP asks for recall of visual images, i.e. top-down. This is not an answer to the question.

@Christiaan, he answered the question. I think you are getting confused by his reference to the processing of sensory information. What he is saying is that the signals produced by sensory structures trigger a chain reaction (i.e. action potential) that is transmitted from one neuron to the next in a very specific network of neuronal connections to store an equally specific memory associated with whatever sensory signal was sent. Correct me if I misunderstood you drtran, and +1 for a well put and accurate answer.

@ CDB I did mean that sensory input will trigger memory recall by activating specific networks. I should have gone further and said that there can be other types of input into these networks to elicit memory recall other than external stimulus. For example, top down processing from the cortex can be considered an external stimulus to the hippocampus if the hippocampus is your reference frame. I just thought external stimuli would be easier to explain.

@Christiaan, splendid, thank you! I suspected that it was merely a misunderstanding. I'm glad that I could clear it up.


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Why don't the genetic similarities between ‘unrelated’ individuals of the same and different species outweigh the differences?
Ever since starting to learn about the concept of inclusive fitness during my BSc, I've been bugged by this questions: if inclusive fitness can account for many ‘altruistic’ behaviors, why don't the genetic similarities between ‘unrelated’ individuals of the same and different species outweigh the differences? In other words: when we consider (from a gene-centric perspective) that individuals are temporary vehicles for selfish genes, and if we also consider that the fitness effect of different genes should not be measured in the reproductive success of just single individual, should we not expect to see that genes that promote more broad-scale altrustic behaviour since we share most of our genetic heritage with other individuals?
I understand that my confusion arises from the fact that I fail to sufficiently distinguish between behavioral genes that influence altruism and whose distribution in the population is differentially influenced by different game strategies and genes that have no direct influence on this type of behaviour and are thus not under the same type of selection pressure. However, I cannot seem to manage to produce a clear-cut argument from this distinction.
I'm asking because, when I find myself in the position of having to explain inclusive fitness, I feel a bit awkward when I know in the back of my head that I would not be able to answer this basic question if it comes up.

Relatedness measures a specific type of genetic similarity. In particular, it measures the genetic similarity relative to the rest of the population. When $r>0$, the recipient carries the actor's genes at a higher frequency than the population. When $r=0$ it doesn't mean that the actor and the recipient do not share genes; it only says that the recipient carries the genes of the actor at the same frequency as the population.

I've upvoted your answer, but haven't yet sufficiently thought it through to be able to say whether or not it clears up my confusion.

Saying that we are talking about relative relatedness yield to the question relative to what?. If I am not mistaken, altruism through kin selection does not need population structure to evolve, relative relatedness can only be define relative to other (isolated) lineages. I think I am confused as the OP is.

@Remi.b Assuming that relatedness is modeled as a regression coefficient of the genetic values of the recipient and the actor, doesn't it follow that relatedness has to be relative to the mean genetic value of the population? Hope we are not talking pass each other.

Yes, I think so... Though this implies that 1) population structure is necessary for kin selection to evolve and 2) it brings the question of whether you consider a population that is differentiate enough to have partial reproductive isolation as being included or not in the regression. This is where I get confused.

@Remi.b Right, I think I understand your question. As to 2, my impression is that the boundary of the population is determined by all and only the individuals affected by the behavior in question. The population doesn't have to be partially reproductively isolated (e.g., migration can happen). Or would like to say that the populations in, say, the infinite island model are partially reproductively isolated?

partial reproductive isolation is generally defined in terms of the fitness of their offspring and not on their probability of mating together due to isolation by distance. Am I right that in absence of any population structure (in a panmictic population where a focal individual has equal probability of meeting any other individual) altruism cannot evolve through kin selection if relatedness is defined as a correlation between the genetic values of the actor and recipients? And if yes, then is it really true that altruism through kin selection can only evolve in structured population?

@Remi.b I would say "yes": altruism requires population structure for it to evolve (according to kin selection theory). I didn't know that "partial reproductive isolation" is typically defined in terms of fitness -- instead of mating. My bad...

mmhh... ok. Without population structure, there is no selection for altruism through kin selection. Ok... I guess I can accept that. I feel like there are debates o this question in the literature but am not sure. +1 thanks for the clarification. and...hum I got it wrong to say that reproductive isolation is in terms of fitness and not habitat isolation. So...definitely MY BAD $\ddot \smile$.


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Alternatives to His-tags
What are the alternatives to using a histidine-tag in detecting protein-protein interactions? Why would they be more beneficial than his-tags?

Histidine tags on proteins do not inherently enable the detection of protein-protein interactions. Histidine tags allow one to attempt to purify your protein of choice using affinity chromatography on resins that have been substituted with chelated Ni++ (as I recall). There are two potential advantages to using this approach. 1st, you may be able to elute any bound proteins using a buffer containing histidine (i.e., non-denaturing conditions). 2nd, If your protein is insoluble you can solubilize it with urea and/or SDS, and the protein will still bind the affinity matrix.

This depends on the technology you're using for the interaction detection.  Surface Plasmon Resonance and Isothermal Titration Calorimetry (and others) don't require tagged proteins of any kind.  Though it doesn't hurt either one.
If you're looking purely at chromotography, any tag that will stably capture. I commonly see GST, FLAG, and MBP in order of occurrence.

The His tag is part of a group of small peptides known as epitope tags. They vary in length from 5 or 6 amino acids up to 10-15. Some common ones include HA, FLAG, Myc, and V5. Once common element they share is that the sequences are quite immunogenic, so it is relatively straightforward to raise antibodies to them. They are also soluble, so they don't affect the tagged protein's structure much. This is not always the case in practice, though.
These tags are mainly used in studying protein-protein interactions by antibody-based detection methods - affinity chromatography, Western blot, co-immunoprecipitation, immunofluorescence, etc. They are extraordinarily useful for cases where the tagged protein does not have a good antibody available, or you are doing multiple parallel experiments with many tagged proteins and you don't want to optimize the conditions for each protein-specific antibody individually.
There are various reasons for using another epitope tag over a 6X or 10X His tag, the most common being the His tag is interfering with the proteins structure, function, or binding characteristics somehow. This can sometimes be solved by moving the tag from the amino- to the carboxy-terminus of the protein, if possible, but choosing a different tag is a common strategy. Another purely practical reason to use a different tag is that one protein in your experimental system may already be His tagged, so you need something different. Finally, the conditions of your experiment may be such that a His tag cannot be used, such as harsh elution conditions requiring the denaturing of the protein.


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Toll Like Receptors Vs Toll Receptors
What are the major differences between them, apart from one being in humans and other in Drosophilla?

In Drosophila, Toll receptors are used during embryonic development as well as innate immunity. See The Drosophila Toll Signaling Pathway by Valance, et. al.
Toll-like Receptors are pattern recognition receptors found in organisms other than Drosophila that recognize common motifs found on pathogens.
Toll receptors were first discovered in Drosophila and orthologous receptors were then found in many other organisms, not only Human. Both will transduce signaling and will lead to transcription of genes.


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Santa Fe xeric indigenous tree
The hills around Santa Fe are covered in a particular xeric tree which is quite small and looks like some kind of juniper which I have been unable to identify:

What is this species?

Do you have any close-up photos?

I eventually figured it out. It is the one-seed juniper, Juniperus monosperma.


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Unable to identify a muscle of the anterior thorax
I was watching an YouTube Anatomy Video which goes over the major muscles of the anterior superficial thorax. There is a structure present throughout the video which goes unmentioned, and I can't seem to identify.

It is shown as a pair of structures, each running from the manubrium to the xiphisternal junction along the lateral margin of the anterior sternum, perhaps with a second head attaching to the costal cartilage.
I'm probably missing something obvious, but for the life of me I can't think of what that could be.

This appears to be the sternalis muscle. The reason it is not mentioned may because it is not present in all individuals, and is therefore relatively poorly characterised.
The image is from An Atlas of anatomy by regions by John Charles Boileau Grant.

Another image of the muscle can be found in Pocket Atlas of Human Anatomy by Thieme:


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Experimental Analysis: What are possible reasons for this increase in N₂O production?
My professor wanted us to each conduct an experiment for class on something we thought would interesting. My experiment was very simple, but I'm not sure how to interpret my results. (Please note that this is not for homework – I'm just genuinely confused and trying to understand the data.)
Basic method:
Take soil samples, add varying concentrations of Roundup and water equalling a total of 50ml, seal in airtight jars, incubate for 7 days, run through a Gas Chromatograph, and record the rates of production for CO2, CH4, and N2O. Overall, there was the Control and then three treatments, for a total 8 jars because each had a duplicate:

Control (Roundup: 0, H2O: 50ml),
T1 (Roundup: 10ml, H2O: 40ml),
T2 (Roundup: 25ml, H2O: 25ml),
T3 (Roundup: 50ml, H2O: 0).

I expected the Control to have the highest levels of production, followed with a decrease in production for T1, followed by T2, and then T3, with T3 being the lowest because all microbial activity was inhibited by the massive dose of Roundup.
However, the results were a bit surprising.
In general:

The Control rates were the highest, as expected.
T1 showed a decrease in production, as expected
T2, again, showed a decrease in production, as expected.
And then T3 showed a significant increase in production.

Here are some graphs to illustrate this in more detail:

This is a new field of science for me, so forgive me if I'm missing something obvious, but my natural intuition is certainly not helping me out on this one. What are some possible causes for this increase – in particular for the N2O/denitrification? Or at the minimum, are there any particular resources I can take a look at to better understand why this happened?

Edit
This is my brain on paper, so forgive me again for any ridiculous things I say. But, could it have something to do with the denitrification process such that more gas is given off as N2O because the microbes responsible for processing the N2O into N2 have died. So in the previous Treatments 1 and 2, the N2O was lower because the N2O was being converted into N2 (but we never recorded the N2), but in the final treatment, no conversion occurred, so the N2O appears to go up, even through the microbes are functioning even less.
Thoughts?

What was your process in collecting the soil samples? Prepackaged in any way, dug up by hand?

Dug up by hand, with gloves, placed in plastic bags temporarily for transportation, and then right into the jars. All were collected at the same time/day.

So, you have what could possibly be an outlier that's just due to that soil sample. It's a pain, but basically you would take more samples, have more replicates and data points, and you might see that the particular outlier point is just an artifact. The actual explanation why did that sample do that? would require a deeper investigation!

I am not a biologist so I have no idea. This said, the graphs do no show any error (actually incertainty) bars, which are needed to do any kind of interpretation.

This may have no correlation to your project but many insecticides, bacteriocides, and herbicides need a "solvent" or "transfer medium" such as water to be effective. Even when using ethanol in the laboratory against a variety of bacteria 100% ethanol becomes almost ineffective.
I would take a look at running round-up again by itself versus 95% roundup 5% water, and 90% roundup and 10% water and I am sure you may seem some results that will aid your experiment.
Good Luck!


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What could make a person get ill from not eating often enough?
Say a person needs to eat every 3 hours, or s\he gets physically ill with fatigue and cold sweating, and this is the case every day.
What could cause this?

This could be a symptom of hypogylcemia.
Hypoglycemia causes symptoms such as:

hunger
shakiness
nervousness
sweating
dizziness or light-headedness
sleepiness
confusion
difficulty speaking
anxiety
weakness

Hi and welcome to Bio.SE. This is a very sensible suggestion, but as the tour points out personal medical questions are off-topic. Medical questions that focus on the underlying biology are preferable. As it stands this question should be closed soon because it channels answers into a diagnosis rather than a mechanistic answer.


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Why are plants classified in living things?
@Volunteers Beware that I am none of the biological magnates. Nor a philosopher. This is just a sign of curiosity. And, I want only an intuition that enables me to see the difference.
As far as I know, the growth of the plants and their metabolism is induced by Chemical laws and physical laws (govern matter and energy). Whatever, absorbing sunlight, photosynthesis, pollination etc are persuaded by physical and chemical laws. And, it is not surprising because all matters experience Physical and Chemical laws. The Food going upward in a plant is illustrated by Capillary Action. Pollination is influenced by wind and like that.
In my opinion, the chief thing which differs us from non-living things is the existence of 6 senses. At least, (various) animals have some of these. But as far as I know, plants possess none of that. So, after all, why are they classified in group of Living things? (Or, why plants' behaviour is not classified in Physics and Chemistry in stead of Physiology?)

First of all, plants do have all "feelings" in terms of their ability to response to environment . By your definition bacteria are dead, because they don't have a nervous system, but that is a very metazoa-centric view of life. There are many scientific definitions of life. I prefer a physics-inspired definition: life is a self-organizing self-reproducing system. Plants perfectly comply with this.

Please read the Wikipedia article about life.

Plants can sense IR light and adapt their above-ground growth accordingly. Chemoreceptors underground do the same thing for root growth. A plant is a living thing that senses, responds to the physical stimuli sensed, grows, reproduces and dies. The latter are referred to as the reproductive cycle. Never seen inanimate matter do all these things..

I'm voting to close this question as off-topic because it is philosophy and a mere attractor of philosophical debate.

The definition of life is definitely a question of philosophie. In the past however, we did make the effort to answer these questions by mainly focusing on describing the lineages of interest and not commenting too much on the philosophy part of the question. This question is similar to previous question about why viruses are not alive except that it is a lower level question. I think that it can be answered by listing a few life-sounds-alike properties of plants (as I tried to do).

Short Answer
Yes, plants are alive!
How to define life?
It is up to anyone to define what is living and what is not. In other words, the definition of what is living is arbitrary. Viruses are a common limit case (see the post why-isnt-a-virus-alive?).
What are plants able to do?
Now coming to plants, everyone seem to agree quite well on whether plants are alive or not. I think that you misunderstand what plants really are and that  brought you to eventually consider them as non-living. Here is a short list of things you might want to consider about plants.

Plants have DNA (plants often have very large genomes compared to animals).
Plants reproduce
Plants evolve (wiki > Evolutionary_history_of_plants)
Plants grow
Plants have a rich and complicated physiology and metabolism (wiki > plants_physiology)
Plants interact with other individuals of the same species and different species.
Plants can communicate (chemical cues) with other plants.
Plants are made of cells. Their cells contain a nucleus and a mitochondrion (just like animals). They also have other double-membrane organelles than mitochondria.
Plants are more closely related to animals than they are to bacteria. Animals are more related to fungi than they are to plants. (Explore the tree of life by yourself on tolweb.org)
Some plants also consume organic material (wiki > carnivorous plants)
Plants get diseases such as all kind of infection and cancer (wiki > Lists_of_plant_diseases)
Plants can be parasitic.
Some plants are motile (SE post > are-there-any-motile-plants)
Some plants are symbiontic (including endosymbiontic) and some are parasiti

Sensing
You seem to consider senses as an important distinction between living and non-living things. Note that the 6th sense that we attribute to humans have a pretty bad semantics and one could count more or fewer senses. Anyway, plants have tons of sense. They are able to sense:

chemicals
gravity
light
moisture
infections
temperature
oxygen and carbon dioxide concentrations
parasite infestation
disease
physical disruption
sound
touch

Conclusion
It would actually be quite complicate to find a definition that is not based on phylogeny or structural differences that would allow you to exclude plants but nothing else from the realm of what is considered alive. So, Yes plants are alive!


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How does the immune system recognize pathogens?
There are useful and pathogenic bacteria in our body. How does the immune system differentiate between them?

Pathogens will often have non-peptide antigens, peptide antigens, and pathogen-associated molecular patterns that are recognized by innate and adaptive immunity mechanisms. Useful bacteria are not differentiated, and often sit beyond the grasp of our immune system, or have mechanisms to escape an immune response. When contacted they do, however, produce an immune response and due to their location, this often involves mucosal immunity:

This portion of the immune system varies greatly in response to the systemic immune response because it is constantly stimulated, and in a way trained, by the presence of all microbes, such as gut flora. As a result, it often resolves infection quickly with low severity, and little lasting tissue damage. Keep in mind that self cells have mechanisms which desensitize them to autoreactivity with immunity. Microbes don't share these same mechanisms, but can evade or escape the immune response through their own methods. But by no means are microbes of any sort, for the average immune system, disregarded.
Unfortunately, to respond more specifically would go into textbook chapters of material so to that end I'm going to cut the explanation here, and recommend you do some research of your own.


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Why do nerve cells convert electric signals to chemical signals?
One would assume that a faster response time in the nervous system would be beneficial. However, nerve cells have to convert electrical impulses to chemical signals and cross a synapse. Why didn't nerve cells evolve in such a way as to transmit signals purely electronically, and what was the evolutionary need for the current, more complicated structure of the nerve cell?
I've seen answers on how synapses ALLOW for more complicated structures, but never how the synapse came to be. Is it even possible to have a brain structure without converting between electrical and chemical signals? If not, why not? If so, why synapses?

You are mingling two questions together. I would suggest editing this one to only ask about the difference between electrical and chemical synapses, and then open a new question asking about the evolutionary story of synapses. Be careful not to ask a question that's too similar to this one.

I concur with @James - there's a concoction of evolution (question body) and neurophysiology (title). The answer below is quite apt but receives the dreaded "yes, but that's not what I'm asking". Please follow James' instructions and make the current questions the physiological counterpart, because that received an answer from Ben2209

There are two types of synapses:

Chemical synapse
Electrical synapse

The first one is the one you are asking about.  The second one corresponds to the faster synapse you are imagining. It consists of two neurones connected by a gap junction. Gap junction form a cytoplasmic bridge between the neurones and thereby allow electrical signal to directly go from one neuron to the next through ion diffusion without converting to chemical signal.
The second one implies release of chemicals (neurotransmitter) in the synaptic cleft, the extracellular space between the two neurons. It is indeed slower than the electrical synapse. However, unlike the electrical synapse, it enables a variety of postsynaptic effects. Some neurotransmitter elicit excitatory effects, some elicit inhibitory effects (electrical synapses where the presynaptic side is an axon only allow excitatory effects). Some postsynaptic receptors to neurotransmitter are ionotropic whereas some are metabotropic. The former are neurotransmitter-gated ion channels, which means that they let specific ion cross the postsynaptic plasma membrane when they bind neurotransmitter. The latter trigger intracellular chemical reactions, such as production of cAMP, which is a companent of a signalling pathway and can for example influence the expression level of specific genes.
This more diverse set of postsynaptic response enabled by chemical synapses explains why they dominate our nervous system.
Reference: Purves et al., Neuroscience, 5th ed., 2012 ISBN 978-0-87893-695-3

Thank you for the answer. I understand now why chemical synapses are more useful, but I still wonder how they came to be evolutionarily. How could there have been a jump from the creation of electrical synapses in organisms to chemical synapses (or vice-versa)?

Please consider adding a couple of references to you answer.

why would an electrical synapse only allow for excitatory events? Gap junctions couple cells in a tissue and mediate, e.g. oscillatory behavior, i.e. wave-like spread of activity. I think you lay out an incorrect view of electrical synapses.

+1 for your answer btw, but some additional referencing and adjustment of the function of gap junctions may improve your answer.

@Christiaan: yes you are right the sign of postsynaptic current equals the sign of presynaptic current in case of electrical synapses. When saying they are excitatory I was referring to synapses involving an axon. An action potential is always hyperpolarizing, thus the postsynaptic effect is excitatory.


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Why are there only 6 molecules of water produced in the synthesis of the fatty acid, palmitate?
The equation for biosynthesis is
1 Acetyl-CoA + 7 Malonyl-CoA + 14 NADPH + 14H+ -> Palmitate + 7 CO2 + 14 NADP+ + 8HS-CoA + 6 H2O
I really don't understand how there is only 6 H2O produced... and not 7?
Every cycle, there is the condensation of one molecule of water.
The first turn yields a 4 carbon molecules. Since palmitate is a 16C fatty acid, and two carbons are added each turn, there should be 6 turns remaining, for a total of 7 turn.
All the other numbers seem right. At first I thought my teacher could have made a mistake but everywhere I look on the net, it say 6 H2O.
Someone has an explanation for this?
Thank you :)
Edit: I found the answer in Voet & Voet yesterday. I add it here in case it can help someone else!
At the end of the biosynthesis, the palmitate is bonded with the Acyl-Carrier Protein (ACP) and it takes an hydrolysis to separate it, hence the missing H2O.

instead of using the biochemical names, use the chemical formulas and write out the balanced chemical equation. Ex. palmitic acid is C16H32O2. Etc.

I didn't think it was relevant since it didn't seem to be a matter of balancing formulas.
I found the answer in Voet & Voet, edited the original post to add it.

I found the answer in Voet & Voet yesterday.
At the end of the biosynthesis, the palmitate is bonded with the Acyl-Carrier Protein (ACP) and it takes an hydrolysis to separate it, hence the missing H2O.