If alcohol is a depressant, why does it makes certain people more hyperactive? Alcohol is by traditional definition a depressant from what I have been taught, ergo it shows down CNS responses.

However, why does alcohol then make some people act out and be more energetic than when they don't drink?

These types of reactions in pharmacology in general are called paradoxical effects.

The main effect of alcohol on the CNS is the potentiation of GABA receptors. GABA receptors are (mostly) inhibitory receptors in the CNS, so potentiation of GABA receptors mostly decreases brain activity by increasing inhibition.

However, you can distinguish between neural inhibition and behavioral inhibition. Some brain regions, like the prefrontal cortex, seem to primarily have inhibitory effects on behavior. That is, usually prefrontal cortex is active when suppressing actions. If you were to suppress the prefrontal cortex, you would get the opposite effect on behavior. When there is "inhibition of inhibition" the term often used is "disinhibition."

It isn't yet clear why exactly alcohol leads to behavioral disinhibition at lower doses, but this is one possible mechanism. In general, U-shaped dose-response curves are quite common in neuroscience, so alcohol isn't all that unusual in that sense.


Could a strong magnet field repel the body before damaging it? Could a magnetic field be strong enough to damage the body or erase the brain?

Blood is slightly diamagnetic, so if the field was strong enough, could it repel a body evenly?

Could a diamagnetic material go through electrolysis with water then ingested to give the body more diamagnetic properties?

While mammalian blood is characterized by diamagnetism (as demonstrated here), as far as I know, the human body as a whole is more or less electrically neutral—that is, with all of its summed components the negative and positive charges balance each other out or there are extremely insignificant differences.

If you want to get strict though, it's theoretically possible to use a super strong magnet to repel or attract someone's entire body to a meaningful degree as long as it's not electrically neutral at a given point in time. But even in the video linked above, the guy is using a super strong magnet to observe its repulsive effects on blood and the blood is just barely moving away; definitely not forceful enough to where someone wouldn't be able to resist moving with just their body weight alone.

So to answer your question: can someone be repulsed or attracted by a magnet practically? No. Can someone be repulsed or attracted by a magnet theoretically? Yes.


Role of ATP and AMP in functioning of Phosphofructokinase I know that when ATP is more then it inhibits PFK and hence regulate the number of ATP. But how does PFK reactivates itself? Is it due to removal of ATP from allosteric site that just reconfigures the enzyme back to normal functional state, or does binding of AMP (after ATP removal) does that?

To clear the meaning,

PFK+ATP= (inactive PFK+ATP)

So is it (1) or (2)?

(1) (inactive PFK+ATP) => (Active PFK)+ATP

(2) (inactive PFK+ATP) => (Inactive PFK)+ATP removed => (Inactive PFK)+ attached AMP => (Active PFK) + removed AMP

This is clearly explained on the Wikipedia page for glycolysis under the heading Phosphofrucokinase. AMP is an allosteric activator of the enzyme and ATP competes for binding at the same site but is not an activator.

You should think of the interaction between the two regulators in terms of reversible binding of both: since they compete for binding at the same site the proportion of the enzyme with bound AMP will go down if [ATP] goes up, for example.

Neither of your proposed schemes is   correct: the enzyme is more active with AMP bound and less active with ATP bound. The idea that AMP binds, activates, then wanders off is wrong.


Pipetting: do human experimenters need liquid class information? I've been working on a protocol standardization project where, among other things, we want protocols to be able to be run equivalently by both humans and robots.
Something that I've noticed in doing so is that there's a radically different amount of information typically assumed needed by a human vs. a robot when it comes to pipetting.
With a robot, it is generally recommended to understand the nature of the liquid thoroughly, specify the liquid class (which includes information on viscosity, volatility, polarity, etc), and do quite a bit of quality control to make sure than when you want to pipette 100 µL you actually get 100 µL. A typical example is shown on this page by Hamilton.
With a human experimenter, however, the protocol pretty much always just says "pipette 100 µL" and assumes that the human can figure out all of the potential issues that we have to be so careful for with robots.
Is this actually a safe assumption, or just something that we don't typically check during protocol development for humans? Is it really intuitively obvious for nearly all liquids, or should our protocols be providing more guidance for humans as well?

In my experience it is very rare to see a protocol for humans that describes how to pipette a certain liquid, but I don't have as many years pipetting as others do.
In general, it is left to the experimenter to observe the behavior of the liquid and act accordingly. It is quite easy to determine when a liquid is leaking (e.g. ethanol) or when it is very viscous (e.g. glycerol), and determine that a change in technique is required. In this case, I would ask someone else in the lab how to deal with the situation. This is something that robots cannot do.
However, not everyone has expert help available, and although it is fairly obvious when a technique isn't working, often the solution is not intuitive. Additionally, the advice of others in the lab could be unhelpful or even inaccurate. For example, I was told to cut the tip off a pipette in order to pipette Tween-20 more easily, however in reading for this answer have discovered that this is not recommended at all! (See eppendorf FAQ linked below).
Therefore, I would say that, unless the liquid is to be pipetted in the same way as water, it is always useful to provide information for those who are not knowledgeable or do not have easy access to expert practitioners.
For some examples of the sorts of problems that experimenters come up against, and therefore which liquids especially could use instructions in protocols, see this set of FAQs from eppendorf on handling liquids.


Could humans breathe if the average methane content of the atmosphere increased to 1%? Below is a table of atmospheric composition. Could humans breathe if the average methane content of the atmosphere increased to 1%?

  Table 7a-1: Current Average composition of the atmosphere up to an altitude of 25 km.

Gas Name          Chemical Formula    Percent Volume

Nitrogen          N2                  78.08%
Oxygen            O2                  20.95%
*Water            H2O                 0 to 4%
Argon             Ar                  0.93%
*Carbon Dioxide   CO2                 0.0360%
Neon              Ne                  0.0018%
Helium            He                  0.0005%
*Methane          CH4                 0.00017%
Hydrogen          H2                  0.00005%
*Nitrous Oxide    N2O                 0.00003%
*Ozone            O3                  0.000004%

* variable gases

Methane is biologically inert and can only act as an asphyxiant at high concentrations by displacing oxygen. An environmental exposure limit has been set at 5,000 ppm, though 10,000 ppm (1%) had no effect:

It is obvious that an exposure limit that presents an explosion hazard cannot be recommended, even if it is well below a concentration that would produce toxicity; thus, exposure limits should not exceed 5% by volume in air.
Animals exposed to methane at 10,000 ppm showed no toxic [effects]; an uncertainty factor of 2 is suggested to derive an EEL—5,000 ppm. There is no evidence that duration of exposure is important in methane toxicity.

Source: Methane in Emergency and Continuous Exposure Limits for Selected Airborne Contaminants Volume 1 (1984)


genes map to eQTL/pQTL Of the 192 target genes, 79 map to a significant eQTL or pQTL in at
  least one dietary condition.

is the line for a paper "Multilayered Genetic and Omics Dissection of Mitochondrial Activity in a Mouse Reference Population"

As far as I know an eQTL is a SNP (particular genotype) affects gene expression. How can I map then a gene to an eQTL? A gene is a sequence on a reference genome. Genotypes of one specific gene are just variations of the sequence of this specific gene. So, a gene itself cannot be an eQTL, a specific genotype (with a variation) can be, right?

So, how can it be possible that one gene (let say GENE22, location: 10-100) is mapped to eQTL(SNP within GENE22, location: 12) in one dietary condition but is not mapped to eQTL in another dietary condition if we are still speaking about the same gene and the same location of an eQTL? So, I am not quite sure what they mean or what they mapped there.

You take a list of SNPs and a list of gene expression values and you plug it into something like this: http://www.bios.unc.edu/research/genomic_software/Matrix_eQTL/

  So, how can it be possible that one gene (let say GENE22, location: 10-100) is mapped to eQTL(SNP within GENE22, location: 12) in one dietary condition but is not mapped to eQTL in another dietary condition if we are still speaking about the same gene and the same location of an eQTL? So, I am not quite sure what they mean or what they mapped there.

The SNP is associated with expression level changes in that gene for one dietary condition but that same SNP is not associated with expression level changes in another dietary condition. Its possible that the SNP never appears in samples from the other dietary condition.


Using egg whites as DNA destruction test possible? My current theory to test for the destruction of any DNA that may be used as forensic evidence is to use an egg white. I would like to test various myths and methods for destroying DNA evidence and need a sure-fire method of testing whether or not the DNA is destroyed. The reasoning behind the egg white is because when you cook one or expose it to strong acids or bases, it turns white. Indicating the denaturing of the proteins within the whites. Would this work to test for the denaturing of DNA molecules to? Several experiments would be conducted with each method, using egg whites to determine whether or not the DNA would be destroyed. Would egg whites, with great accuracy, determine whether or not the sample can be identified. If not, could you please suggest another alternative?

Cooking DNA will absolutely not destroy it. Few things will actually destroy DNA. Bleach is one of the only common substances that will do it.

To test for DNA quantity you need to perform qPCR. The equipment is $20,000+.


How does having spare receptors change ED50 in an irreversible agonist Competitive antagonists increase the ED50 while the Emax remains the same. Irreversible antagonists do not change the ED50 while decreases the Emax.

Katzung pharmacology, says that the irreversible antagonist may change the ED50 when spare receptors are present. How is that? What difference would it make? Could anyone explain the change graphically?

Spare receptors are said to be present when the Kd (dissociation constant, from the drug-receptor binding curve) is more than the ED50 (from the dose-response curve). This may happen due to

prolonged effect of a drug-receptor interaction or
when the receptors are actually in excess of the drug

ED50 = effective dose at 50% of maximum effect, Kd = Dissociation constant.

Irreversible antagonism is like removing receptors.

If there are spare receptors, maximum effect, or any effect level, can be recovered with more ligand (because displacing the irreversible ligand is not necessary, when there are other sites to fill).

$$K_D = \frac{R*L}{RL}$$

A given effect level corresponds to a given $RL$, but with less receptor $R$ available, more ligand $L$ is needed. That is by definition a change in ED50.

If you have no spare receptor (or there is enough antagonist to prevent full effect even with spare receptors), then maximum effect cannot be recovered. There is a new Emax, lower than without antagonist; but without shifting the dose-response curve to the right.

Here is an example in Rang&Dale (8th ed., p. 12, fig 2.6). Curves are labelled with time of incubation with a given quantity of irreversible inhibitor, that is equivalent to varying concentration of irreversible inhibitor at steady state. First two show the situation with spare receptors, and last two show what happens when the original Emax cannot be reached because there are not enough receptors left to elicit maximum response.


How does a prophage leave the host cell's genome? I understand that, unlike a prophage, a provirus never leaves the genome, but I don't understand how the prophage "leaves".

This is explained reasonably well at the Wikipedia entry for phage λ, which is the prototype lysogenic phage. Basically, integration occurs by site-specific recombination between the attP region on the phage genome and the attB region in the host genome. This means that in the prophage form the phage DNA is flanked by direct repeats. Excision involves the reverse process - recombination between these direct repeats. Excision is promoted by the phage-encoded Xis and Int proteins in combination with the host protein Ihf. The regulatory cascade which links cellular stress to this recombination event is detailed at the linked page.


Behaviour of neuron when membrane potential is maintained at threshold potential or more Via an external electrode the membrane potential of a neuron or group of neurons can be increased from resting potential of -70 mV to -50 mV or more. This will cause them to fire an action potential. What happens if the electrode maintains the membrane potential at -50 mV or more for say 1 minute? Initially it should fire once, but then it will not reach the resting potential, will it stop firing or keep on firing continuously since it is above threshold potential? Will this kill the neuron or make it malfunction permanently?

Before I start, I should point out that in order to change the membrane potential (known as the Vm) of a neuron you really need an internal electrode - so that you can pump current in to it, so increasing the potential above the resting membrane potential (RMP). The RMP is simply the Vm of a neuron at rest, without any external meddling by pesky scientists (or synaptic inputs).

When you depolarise a neuron - in other words, make it less negatively charged, it will fire an action potential once it crosses the spike threshold. This value is different for different neurons, but -50mV is usually not enough to trigger an action potential - normally it's more in the range between -30 and -40. But let's say it does, as it doesn't change the thrust of the question.

The major part of what happens during an action potential is that sodium channels open, allowing the spike to fire. Once closed, these channels have a 'refractory period' - essentially a time out, during which they are less likely to open again. So even though your neuron is still above spike threshold, it can't fire because the channels can't open. (For the aficionados, you can actually think of this as the spike threshold becoming temporarily more positive - going up to, say, -20mV).

So your neuron doesn't fire again for, say, 10ms, until the sodium channels reactivate. Then it does. So you get a train of regularly spaced action potentials at a certain frequency. The more you depolarise the neuron, the faster this frequency becomes until a point where the channels just become totally inactivated and the neuron stops firing. If you hold the cell at this voltage for more than a few seconds, in general it will die.


Can you vaccinate against bacterial diseases? Are there existing vaccines for such diseases? I have the (maybe wrong?) preconception that we only vaccinate against viral diseases, and that there can only exist vaccines against viruses. I think the idea comes from the idea that only for viral diseases are you becoming immune after contracting the disease, not for bacterial. The question Is there a vaccine against the plague (Yersinia pestis)? made me think that I don't really have a justification for that, seeing that the mechanisms for combatting viral diseases and bacterial diseases should be the same (is that right?).

So, is it possible to vaccinate against bacterial diseases? Do we have existing vaccines for any bacterial disease?

Of course we can - and do - vaccinate against bacterial diseases, as these are some of the dangerous infectious diseases.
Among these are:

Tetanus (although here the vaccination is targeted against the toxin, not the bacterium itself)
Tuberculosis
Diphtheria
Pertussis
Haemophilus influenzae type B
Cholera
Typhoid
Streptococcus pneumoniae
Meningococcus: against the strains ACWY, B

A list of the vaccines against bacterial diseases can be found here.


Finding Rna-Seq dataset for C. Elegans (Caenorhabditis elegans) I want to find a RNA-Seq dataset for C. Elegans to use it in RNA-Skim software. For those who does not know RNA-Skim let me explain it a bit. It is a tool which is used to quantify RNA-Seq data using sig-mers(special kind of k-mer). Firstly RNA-Skim clusters protein coding genes and find substrings that are special to cluster of that gene. After this preperation stage, it takes an RNA-seq data as an input and tries to quantify transcripts in it. So, I need to find a dataset in fasta file format for this step. Since I'm pretty new in this area, is there anyone who could provide me information about how could I find it?
Complete information about RNA-skim can be found here : RNA_SKIM

EDIT
The type of a dataset I'm looking for is something like that: http://codepad.org/n3ioT3nj .This dataset is for mouse, I need to find such a dataset for C. elegans as I said before

Go to NCBI-SRA or GEO and search for RNAseq data. Set organism as C. elegans and optionally any other keywords that you are interested in. This search term will give you all RNAseq data in SRA from C. elegans: ("caenorhabditis elegans"[Organism]) AND "strategy rna seq"[Properties]

You will generally find files in fastq format which you can easily convert to fasta. There are many tools that do that; you can also do it with your own script. Following awk command will do the job:

awk 'NR%4==1{print ">"substr($0,2)} NR%4==2{print}' data.fastq > data.fasta

Apart from SRA you can also look at ENA (European Nucleotide Archive) and DDBJ


Did radial symmetry evolve twice? In the history of animal evolution, both the Cnidarians and the Echinoderms have radial symmetry, according to this cladogram:

Source: http://www.cpalms.org/Public/PreviewResourceLesson/Preview/45851

Do both groups having this feature mean radial symmetry evolved twice?

Good question! I had never really though about it, so thank you!

Echinodermata have a pentaradial symmetry

Echinodermata actually don't have a radial symmetry like jellyfish do. They have a pentaradial symmetry as they systematically have 5 arms.

Parsimony

Even if Echinodermata were radially symmetric, then it would actually be unlikely that bilateral symmetry evolved, was then lost and evolved again. It is much more parsimonious that bilateral symmetry evolved once and was later lost in the echinodermata lineage.

Developmental and Genetics of pentaradial symmetry

As one would expect modifications of hox genes are involved into the evolution of this peculiar body plan. From Lowe and Wray 1997

  Here we report the expression domains in echinoderms of three important developmental regulatory genes ( distal-less, engrailed and orthodenticle ), all of which encode transcription factors that contain a homeodomain. Our findings show that the reorganization of body architecture involved extensive changes in the deployment and roles of homeobox genes. These changes include modifications in the symmetry of expression domains and the evolution of several new developmental roles, as well as the loss of roles conserved between arthropods and chordates. Some of these modifications seem to have evolved very early in the history of echinoderms, whereas others probably evolved during the subsequent diversification of adult and larval morphology.

Here is the whole abstract of Mooi and David 2008

  The strangeness of echinoderm pentaradiality results from superposition of radial symmetry onto ancestral deuterostome bilaterality. The Extraxial-Axial Theory shows that echinoderms also have an anterior/posterior (A/P) axis developed independently and ontogenetically before radiality. The A/P axis is first established via coelomic stacking in the extraxial region, with ensuing development of the pentamerous hydrocoel in the axial region. This is strongly correlated with a variety of gene expression patterns. The echinoid Hox cluster is disordered into two different sets of genes. During embryogenesis, members of the posterior class demonstrate temporal, spatial, and genetic colinearity within the extraxial region. We suggest that displacement of genes from the more anterior Hox classes toward the 5′ end of the chromosome leads to control of the later-developing, radially symmetric axial region. Genetic disorder is therefore another way of using colinearity to build the unique echinoderm symmetry.

As insinuated above, note that (in most echinodermata species at least) only adults have a radial symmetry. Larvea have a bilateral symmetry. Here are a bunch of picturesand schema.

Larvea

Adults


Is cell-free Life possible? I think most of the people on this site know about the famous Baltimore paper describing the ability of the poliovirus to replicate itself without the need of cells but I want to expand on the issue and ask could it be possible to have truly "cell-free" Life-e.g. life forms that do not have cells in any form according to modern biology but yet can be considered "alive" by its standards? This is the first paper in historical context describing the possibility of creating a self-replicating molecule in the laboratory. Well, it's about a viral genome and it only can self-replicate so it's not like it's alive according to what we consider "true" living organism, but nevertheless it triggers an interesting chain of assumptions in my mind. What if we could design a system where nucleic acid can evolve outside of cells? Then, what if we managed to provide an energy source t drive this evolution outside of the context of cells? Would such nucleic acid evolving on its own in a test tube depending only on the energy source we provide and on the specific conditions in the test tube be considered equal to a gene evolving in a "true" living organism? What if then we managed to add more nucleic acid's molecules to the system, just enough to have all the components involved in the replication of the evolving nucleic acid molecules synthesized by the system itself? Then can we consider this system analogous to a living organism, e.g. truly alive? What if we continued adding nucleic acid molecules to the system to the point when it was able to produce ATP from organic molecules used by what we commonly consider to be "alive", e.g. entities we prescribe the name living organisms, like glucose, for example. Then what would be the difference between this chemical reaction system and a genuine living organism? What if we continued building up this "in vitro metabolism" to the point when we have a genuine "molecule laboratory" testing the fitness of new nucleic acid molecules to itself. A true evolving, replicating and self-organizing molecular "machinery" we could "grow" in a test tube. Would we then consider such a thing a genuine living organism and if so why?

Yes, I know it's a "fringe question" and out of the scope of almost all branches of biology but nevertheless I think it's one of those questions that can "capture our mind". So, do you think there could possibly be such a thing that we could deem "alive" but have no cells at all? Something organized in such a way that we can readily call it a life form but yet not organized in the "way we think" about Life in general? If this is possible, when do you think this system of reactions could be called genuine living organism?

To the moderators-my question is different than the question "Why isn't a virus alive?" because it has a much broader perspective than it-a cell free form of Life can be anything-from a self-replicating "grey goo" to an evolving tornado. Viruses are only one small particular subset of possible answers. Plus the question you are referring to isn't about synthetic biology and the possible diversity of life forms as is mine but is only about a particular aspect of what we call a virus-its pertaining to the set of life forms or not. My question has both different direction and different set of objects it's aimed at. How can the two be identical, then?

Your updated question, as I said in a comment is much more precise but also describes a biologically and thermodynamically absurd scenario that betrays deep misconceptions about how cells work and what they need to work. Having said that I've realized it has an answer, so I'll give it:

  Would we then consider such a thing a genuine living organism and if so why?

As in every case in science where previously-sharp categories become fuzzier through the discovery or creation of entities that fall in previously-empty intermediate zones, "we" would debate ardently about whether those things should be considered "genuine living organisms" or not. There would be several possible outcomes to these debates:

1) All of the new intermediate entities demonstrate that in the space of characteristics things can have, the old category as previously defined no longer forms a sharp cluster, but a sharp cluster still does exist that is pretty close to that old category; in that case the old category gets a new definition, and as a result some entities might change their classifications, or not. Real-world example of this kind of definition change (though not necessarily caused by the appearance of intermediate steps): how stars and planets went from their antique definitions of "stays put in the sky vs moves around" to their current very-different definitions.

2) The new entities demonstrate that what was thought to be a sharp cluster in the space of characteristics is just... not. A clear, universal, unambiguous definition is thus impossible. One possibility is that the cluster dissolves entirely; the category as a whole is thus abandoned (many abandoned taxonomic terms can be seen as examples of this).

3) The old sharp boundaries no longer exist, but there is still a definite cluster in the space of characteristics that can be pointed to, it just has fuzzy borders. Like colors, which blend into each other but we still know there is "red" and "blue" and they're not the same. In that case, like with colors we might abandon the edge and focus instead on doing like we do with colors; defining the entity by looking at what "a good representative of this category is" and "what an ambiguous representative of this category is", thus giving a reliable idea of where the cluster is, where it isn't, and where the boundary is, even if it's fuzzy.

4) Sometimes you do need sharp definitions though, especially in science. In that case there are two possibilities:

4a) Use different definitions in different contexts, depending on which characteristics of the cluster interest us at any given point. "Species" is an excellent example of this; a paleontologist, a vertebrate biologist, a plant biologist, and a bacteriologist will use the same word to talk about similar concepts (a grouping of organisms with specific ecological and evolutionary significance), and they will use different criteria to determine what a species is in each case, meaning they have different definitions.

4b) Settle on an arbitrary boundary based on certain criteria that cuts through the fuzziness, with the understanding that it is arbitrary, other criteria would have yielded a slightly different boundary and different classifications for given entities that exist in the fuzzy zone, but it is useful for whatever purpose to have that boundary and thus a boundary will be chosen. Debate might continue a long time over where the boundary is, and potentially involve different people using different boundaries as in 4a, or not. Classic recent example is the definition of planet, and the process that led Pluto to no longer be considered one. This can also involve the creation of new categories, like "dwarf planet" in the case of the redefinition of "planet".

So to answer your question "would this be considered genuine life?", the answer will be "yes", "no", "it depends" or "neither" depending on which of those outcomes the debate ends up settling on. And we cannot know which outcome it will be, because the choice that will be made will entirely depend on what the space of characteristics will be like that makes a currently-sharp boundary fuzzy... And obviously we do not already know what the space of characteristics is like because those discoveries or inventions that will prompt us to revisit what we think of as "life" hasn't happened yet ! (well, not the ones you posit. Obviously the definition of "life" itself has already undergone the processes I describe many many times as it got better understood !).

(note I'm not even getting into the vernacular, and whether it will follow scientific usage or not and at what rate if so. It's interesting to note it still in many ways hasn't caught up with (or is just unrelated to) today's biological definition of "life" !)

(I will also add that I cannot posit an outcome even based on the specific scenario you describe, for two reasons: first, the decision would be a communal one made by professionals in the field, and I am a single person and not a professional biologist. Second, the specific scenario you describe already goes against everything we currently know about life, so, yeah.)


Why eukaryotes have three different types of cytoskeleton filaments? Ok: IF, microtubules and microfilaments serve different purposes. But whats the biological advantage of having these three types over other organisms? I don't know if I'm being clear.

While eukaryotes contain tubulin-containing microtubles and actin filaments, prokaryotic homologues do exist.
For example FitZ protein, the most common bacterial Tubulin homologue[1], is involved in cell division. Genes for this protein are actually present in eukaryotic nuclear DNA and the protein facilitate the division of the mitrochrondria and chloroplast organelles which were created by endosymbiosis[2].

Similarly, MreB, functions as the most common prokaryotic analogue of actin.

Regarding IF filaments, certainly subsets such as nuclear lamins are uniquely found within Eukarya, however a paper published by Bafchi[4] has suggested that IF-like proteins are present within bacteria.

Bi, E., & Lutkenhaus, J. (1991). FtsZ ring structure associated with division in Escherichia coli. Nature, 354(6349), 161-164. doi:10.1038/354161a0
Margolin W. FTSZ AND THE DIVISION OF PROKARYOTIC CELLS AND ORGANELLES. Nature reviews Molecular cell biology. 2005;6(11):862-871. doi:10.1038/nrm1745.
Gunning, P. W., Ghoshdastider, U., Whitaker, S., Popp, D., & Robinson, R. C. (2015). The evolution of compositionally and functionally distinct actin filaments. Journal of Cell Science, 128(11), 2009-2019. doi:10.1242/jcs.165563
Bagchi S, Tomenius H, Belova LM, Ausmees N. Intermediate filament-like proteins in bacteria and a cytoskeletal function in Streptomyces. Molecular Microbiology. 2008;70(4):1037-1050. doi:10.1111/j.1365-2958.2008.06473.x.


Is viral protein expression important for peptide vaccine? I would like to know if proteins expressed in higher quantities, such as DNA polymerase, would be better vaccine candidates for a T-cell based vaccine.

To find candidate proteins which can be used as peptide vaccine, these need to fulfill some criteria:

The most important is that the peptide (or protein) used for
vaccination shall not have a closely relate sequence in the organism
in which the vaccination shall occur. Otherwise either no reaction
(due to immunologic tolerance to self) or an autoimmune reaction
might happen.
The peptide/protein need to be expressed on the surface of the
microbe (either virus or bacteria) since otherwise it will not be
recognized by the immune system. Also domains of a potential vaccine
candidate which are inside of membrane are not useful.
The epitope needs to be stable enough to be used as a vaccine and
also be present on the microbe (otherwise there is no immune
reaction).

If you want to read further on this topic, there is an interesting Paper from the WHO available, which gives a nice introduction:

Guidelines for the production and quality control of synthetic
peptide vaccines

To answer your question: No, these proteins cannot be used for this purpose, as they are relatively closely related to the same proteins in the human body. This will probably lead to no immunologic reaction at all. Additionally, these proteins are located inside of cells and thus not exposed to the immune system.


Regulation in plants bearing cleistogamous and chasmogamous flowers In most plants bearing cleistogamous flowers, chasmogamous flowers are also borne by the plants. For example, Viola, Oxalis and Commelina contain both these kinds of flowers.( I am unaware of a species which bears only cleistogamous flowers, which would be very unfavourable for evolutionary success)

The Cleistogamous flowers help in reproduction with minimal energy and resource expenditure. It also maximises the chance of reproduction, which is an important factor where the agents of pollination are scarce. On the other hand Chasmogamous flowers provide variablity, hybrid vigour and generate better genotypes through recombination. Both of these strategies are useful in different environment. In adverse (less pollinators, energy stress) cleistogamy would be favourable, and in other cases where no energy stress prevails, chsmogamy is advantageous.

  My question is, How can plants, if they can, regulate which strategy
  is supported? Is the ratio of cleistogamous to chasmogamous flowers
  constant irrespective of the environment, or does the prevailing
  environment have a say in deciding which of these two kinds of flowers
  will be preferred over the other? If it does, what is the regulatory
  mechanism underlying this control of flowering startegies?

One other related question is whether there are any species which bear only cleistogamous flowers? That would seem very unfavourable for evolution to act on.

This is a very good question, but I think the reason that it's not being answered is because it is in a sense too broad: different plant groups maintain balances of cleistogamous and chasmogamous flowers, and they modulate that balance through different mechanisms. Many of these mechanisms (genes involved, environmental cues, developmental pathways) may not be fully understood.

Culley and Klooster (2007) categorize cleistogamy depending on the degree to which "the prevailing environment has a say":

In dimorphic cleistogamy CL and CH flower differ in the time or place
of production, with CL flowers produced in conditions (underground,
low light levels, early in the season) that are potentially
unfavorable for outcrossing.
In induced cleistogamy potentially CH flowers that experience conditions such as drought or low temperatures fail to open and self-pollinate, becoming, in effect, CL flowers.

You should check out the Culley and Klooster (available online if you make a jstor login) – they discuss complete cleistogamy which addresses your last question. They report several completely CL species in their Table 1, and give references.

More generally, many different plant groups maintain balances of self-pollination and outcrossing (i.e. "real sex"), through an even more diverse set of mechanisms.

Even more generally, many plants and some animals maintain balances of sexual reproduction and clonal reproduction, through an even more diverse set of mechanisms. For instance, vegetative reproduction (e.g., strawberry runners) is very common in many plant groups; facultative and obligate parthenogenesis in animals also occurs.

Culley, Theresa M. and Matthew R. Klooster (2007). The Cleistogamous Breeding System: A Review of Its Frequency, Evolution, and Ecology in Angiosperms. Botanical Review. Vol. 73, No. 1, pp. 1-30


Can humans ever directly see a few photons at a time? Can a human see a single photon? I am not asking the following question: Can humans ever see a photon in the same way we see a chair?

My question is: Can a human retina respond to a single photon? If so, how does this happen and why is the retina able to "sense" (detect) a single photon?

A single molecule of rhodopsin (actually the cis-retinal bound to it) can and actually does react to one photon (Purves et al. Chapter: Phototransduction in Neuroscience).

  It has been estimated that a single light-activated rhodopsin molecule
  can activate 800 transducin molecules, roughly eight percent of the
  molecules on the disk surface. Although each transducin molecule
  activates only one phosphodiesterase molecule, each of these is in
  turn capable of catalyzing the breakdown of as many as six cGMP
  molecules. As a result, the absorption of a single photon by a
  rhodopsin molecule results in the closure of approximately 200 ion
  channels, or about 2% of the number of channels in each rod that are
  open in the dark. This number of channel closures causes a net change
  in the membrane potential of about 1 mV.

Photoreceptor cells continuously secrete the neurotransmitter glutamate in dark; with light exposure glutamate release would reduce. This leads to activation of the next line of cells (bipolar, horizontal cells and retinal ganglion cells).

   Modelled relationship between glutamate release and rod membrane potential.  From Witkovsky et al. (1997).

From this model (Witkovsky et al. 1997) it appears that for a change in glutamate release rate, a larger change in membrane potential is needed. Moreover, the depolarization of the photoreceptors has to be sustained for a while so that downstream cells can react (light absorption is much much faster than biochemical processes). The lifetime of an activated rhodopsin molecule is ~40ms in mice (Gross and Burns, 2010) and ~400ms in salamanders (Lyubarsky et al., 1996). We can assume that human eye is more similar to that of mice. There are approximately 40,000,000 molecules of rhodopsin in a rod cell (BioNumbers). The most sensitive of retinal ganglion cells need ~0.04% of rhodopsin molecules per rod cell to be activated (Takeshita et al., 2017).

  (b) Absolute threshold of On and Off retinal ganglion cells

  Both On and Off RGCs carry rich information about the weakest light
  signals. Off cells are somewhat more sensitive than On cells but have
  a higher error rate in their gap-based coding. The absolute threshold
  for primate On and Off parasol cells in a two-alternative
  forced-choice task is extremely close to the limits posed by the
  quantal nature of light: On parasols reach 75% correct choices at a
  light level corresponding to approximately 0.0008 R* per rod per flash
  (mean, n = 6) and Off parasols at a light level corresponding to
  approximately 0.0004 R* per rod per flash (mean, n = 5).

A single activated rhodopsin molecule would be 0.0000025% of the total. This would be insufficient to activate an RGC.

So, I can make a reliable guess that you cannot actually "see" a photon although one of the retinal photoreceptor cells can sense it. However, I'm still looking for a solid reference that says how many photons are needed (and for how long) to produce a visual response.


What are the characteristics of a promising drug? The drug development industry is a multi-billion dollar economy powered by a multitude of research bodies from industry and academia. A big risk is that drug development costs are in the tens of millions of dollars when looking at the most successful drugs

Generally speaking, what makes a good drug for research for those researchers working on these projects? Why are some potential drug pursued and others not? What traits, according to the experts, justifies such a vast investment?

The specific characteristics sought after will vary widely, but that being said, there are a few key features many groups look for.  I've talked to and heard a number of individuals at a number of different companies, and there are a lot of different techniques and pathways looked for.  In general, however, the single, most important factor is value.  If the drug won't make money, it's almost never considered "promising."  Maybe that's a sad fact of the way the world works, but it's a fact.  The average drug costs around $1 billion (USD) to bring to market so the successful ones damn well better recoup that (Orphan drugs and companies actively pursuing them often have an easier time of this, as the FDA is understandably less restrictive and fast-tracks their progress).

That's not actually so simple.  It's a large, crowded market out there, and there is a lot of intellectual property floating around.  A wise businesswoman told me that her company focuses on the middle-ground.  A target that is too promising is probably already owned by Genentech, so they aim for the ones that are below the attention of the giants but still quite profitable.

After that, it's mainly what you might expect.  High avidity, long half-life coupled with low toxicity (more on this later), small size (if possible), and a realistic time frame.  A month can mean millions of dollars, so working for a decade is not necessarily a possibility.  Often, companies will use high-throughput screens of thousands, even millions of small molecules to look for an effect.  The screening process is usually extremely rigorous, and many potential candidates are eliminated as not good enough.  Sometimes they do some fancy stuff such as 3D modeling but it is definitely a field where brute force can still be successful.

Often those screens are used against primary cells to test for toxicity.  In fact, throughout the entire process, toxicity is a huge factor.  A full 20%-40% of drug attrition is due to safety and liability issues.  It's a constant balance: nothing can risk the health of healthy, control volunteers, but sometimes more risk is acceptable.  The first HIV/AIDS drugs were incredibly toxic, but that was okay because it was still better than the alternative.  These days, the toxicity requirements for HIV/AIDS treatments such as HAART are stricter.  Short-term antibiotics are allowed more risk since you only take them for five/seven days, whereas long-term medication for chronic illnesses are held to much higher standards.

Basically, loss of eyesight might be preferable to death, but it's unacceptable if treating the flu.  The mantra I've been told is three things:

Don’t treat one thing but cause another
Don't cause cancer
Don’t cause birth defects or alter the ability to have children

Toxicologists are conservative, willing to throw the baby out with the bathwater.  In short, Fail Early.


Where does Embryo Implantation occur? Where does the embryo get implanted? If it is in the uterus side wall, why is the embryo shown hanging from top in some pictures?

According to Minami et al. (2003)1 (open access) the early gestational sac can be located by ultrasound, and usually is high in the uterus, more often on the left or right than in the middle.  They provide an illustration of the distribution.

 1. Minami, S., Ishihara, K. and Araki, T., 2003. Determination of blastocyst implantation site in spontaneous pregnancies using three-dimensional transvaginal ultrasound. Journal of Nippon Medical School, 70(3), pp.250-254.


Vision: what is the difference between on-off ganglion cells and lateral inhibition? Is 'lateral inhibition' just a term for the biological basis of the functioning of the on-center (or off-center) ganglion cells?
Or do these terms describe separate processes?

Short answer
Retinal center-surround receptive fields are an example of lateral inhibition. It occurs elsewhere in the nervous system too.

Background
Center-surround receptive fields are indeed an example of lateral inhibition, where the ON field suppress the OFF field through lateral inhibition. The center-surround connectivity in the retina (Fig. 1) is indeed the most well-known example of this kind of circuitry. However, lateral inhibition occurs in other sensory systems too, for example auditory and olfactory neurons (Bakshi & Ghosh, 2017). For more information on the retinal circuitry underlying center/surround inhibition see this answer.

References
- Bakshi & Ghosh (2017), Handbook of Neural Computation: 487-513.

Fig. 1. Retinal circuitry underlying On-OFF center-surround conncetivity in ganglion cells. source: New York University


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

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

I'm afraid I don't understand the "either ... or" contrast here. As I understand, antibiotic resistance genes are routinely introduced into GM plants with the sole goal: to check what cells have underwent transformation (got the neccessary foreign genes in their genome) and what have not.

I would be grateful to learn what are "initial gene constructions" here, and how does the method using "the control of plant promoters" differ from the first method. Is the purpose of introducing antibiotic resistance genes similar in both cases - to check what cells have underwent transformation? Sorry if the questions are too stupid. Please direct me to relevant Wikipedia pages or articles.

So basically, most plasmids that you buy have an antibiotic resistance marker, I think it's relatively standard, because you want to know which bacteria were transformed, right? Ergo, the initial cloning vectors being used. These markers are under control of a plasmid promoter like T7, for example, not a plant promoter (unless you contsructed it de novo to do this). But your plasmid is going to have a cloning site where you can make a cut, insert more DNA, and ligate it back together.

At least pursuant to the patent by Monsanto here, my assumption is that if you're looking to modify plants, your insert for the cloning site is probably a plant promoter, followed by a structural gene, and then a UTR sequence. I think what the authors are saying is that some groups put an antibiotic resistance gene into the insert as the structural part, and when you use something like an A. tumefaciens system to integrate that vector into the plant genome, you end up with an antibiotic structural gene under the control of a plant promoter. You should keep in mind that the whole plasmid gets integrated, but not all of it is transcribed by the plant, only that within the transcribed region controlled by a promoter the plant can utilize!!*

*I'll add, what they're worrying about in the linked OP article, is that whether or not the plant is actively producing antibiotic proteins, that the sequence for the antibiotic resistance has been introduced at any point in the plant's genome carries the risk that some bacteria will randomly obtain it through horizontal gene transfer.


Estimation of number of species at an earlier time The estimated number of species on Earth, as reported in this article is around 8.7 million. I am fascinated by how nature produces such a wide variety of species.

As per my understanding, many species have gone extinct, that is, were not able to adapt to changing conditions on Earth. Perhaps the number of species before few thousands of years were larger than today. Can we estimate the approximate number of species at a given point in the past, using available data?

according to the National Science Foundation press release"Species Have Come and Gone at Different Rates than Previously Believed" indeed show what Atl LED suggests, that the progression is not linear, with the study showing that:

  The previously thought exponential increase in diversity is not there.

Further, there is the "Palaeobiology Database, that

  seeks to provide researchers and the public with information about the entire fossil record.

The site also has links to further papers of the topic.


Are four-leaf clovers mutations, developmental errors, or something more complicated? What causes about 1 in 10,000 clovers to have four instead of three leaves? Will progeny(?) grown from its flower's seeds have a higher probability than that of also having four leaves?

From the Wired article The Mysterious Genetics of the Four-Leaf Clover

  A clover’s lucky fourth leaf is presumably specified in its DNA. But the clover genome is surprisingly complicated, and finding the genes responsible—and under what conditions—for the four-leaf mutation is a still-unsolved biological puzzle.

From the Wikipedia's Four-leaf clover: Cause  (emphasis mine):

  It is debated whether the fourth leaf is caused genetically or environmentally. Its relative rarity (1 in 10,000 clovers[ref]) suggests a possible recessive gene appearing at a low frequency. Alternatively, four-leaf clovers could be caused by somatic mutation or a developmental error of environmental causes. They could also be caused by the interaction of several genes that happen to segregate in the individual plant. It is possible all four explanations could apply to individual cases. This means that multiple four-leaf clovers could be found in the same clover plant.[citation needed] (emphasis added)

A recessive gene for four leaves has been identified (Tashiro et al., 2010). The clover is a tetraploid species and together with the fact that environmental conditions may also suppress the development of the fourth leaf, it indeed takes a lot of luck to find one. If it will bring you any is another question though.

In fact they are aiming at making a four-leaved cultivar (source: New Scientist).

Reference
- Tashiro et al., Crop Sci (2010); 50: 1260–8


What are embryophytes? And how are they characterized? What does it mean when it's said that plants are embryophytes?
What are the specific characteristics that help determine that?

The name derives from their innovative characteristic of nurturing the young embryo sporophyte during the early stages of its multicellular development within the tissues of the parent gametophyte.

source
https://www.revolvy.com/main/index.php?s=Embryophytes&item_type=topic

Similar definitions are in the New World Encyclopedia and Merriam Webster Dictionary.


Why don't humans typically drink human milk after infancy? Does any human culture routinely do this? Typically taboos have some evolutionary basis. So what would that be? Does any mammal drink the milk of its own species, besides nursing?

Giving a woman food for her to inefficiently convert to different food is a waste of time and energy; it only makes sense for infants that can't eat much else (and even there, plenty of people find substitutes so the woman can get back to work).

Turning grass, which people can't eat, into a food people can eat makes a whole lot more sense.


What conditions are necessary for HPL (human pancreatic lipase) to activate? What conditions are necessary for human pancreatic lipase to activate? Is there an optimal temperature or pH? How quickly does it take effect?

The protein referred to in the question is encoded by gene PNLIP, pancreatic lipase. From this annotation of the protein, I see that there is a signal peptide from amino acids 1 to 16. Thus, this signal peptide must be cleaved before the protein can be active in its digestion of emulsified triacylglyerides.

A paper describes the structural changes induced in human pancreatic lipase by lowering the pH. The secondary structure of the enzyme is stable within a pH range of 3.0 to 6.5. At this pH, a reversible opening of the lid controlling the access to the active site was observed. So, there is another aspect of activation - pH and the ability to open the enzyme lid so that the fat molecule enters the active site.


Does "squinting" make you concentrate better on a logic test? We have all had those moments of intense concentration on some tough exam, perhaps a college test or whatever...

Why is it that when we squint, it feels like we can focus and concentrate better on the test, and get answers more easily?

Do we actually get a better mental performance when we are squinting?  If so, why?

The phenomenon in question is probably related to people with uncorrected/undercorrected myopia.

This "ancient" phenomenon is called stenopeic slit effect (a case of pinhole effect): when the person squints the visual acuity becomes better because of smaller blur circles: the "slit" between the eyelids is the key point improving blurring.

One can check if it works by creating slit in paper or plastic:

Some "charlatans/witch-doctors/quacksalver/etc" can "treat" refractive error with pinhole/stenopeic glasses:

It is known that children with refractive errors have attention issues because they cannot see the objects sharply (this is why they can be mistakenly diagnosed with ADHD), thus your concentration improvement related mostly to your vision improve and not a better "understanding".

If you mean by squint using mimic muscles and corrugator muscle the answer should point out that not a "squint" improves your concentration, but your attempt to improve your concentration causes this type of "squint".


Complete list of touch sensitive plants I am not sure whether the word "touch sensitive" is precise enough. What I am looking for is a list of plants that respond to touch noticably  like Mimosa Pudica. I only know of Mimosa Pudica example. Is there any other such plant?

Some of the plants that respond to mechanical stimuli:

Dionaea muscipula

  'Venus’ Flytrap (Dionaea muscipula) accomplishes one of the more spectacular thigmonastic movements resulting in a swap of the role of predator with animals (Simons, 1992). Indeed, Darwin referred to it as ‘one of the most wonderful in the world’ (Darwin, 1893). The specialized bi-lobed leaves with needle-shaped tines on the leaf margins are generally spread open as invitations to visitors. When an unsuspecting insect crawls along the ventral leaf surfaces and bumps into the three small trigger hairs (Curtis, 1834), intercellular electrical signals are generated (Burdon-Sanderson, 1873; Jacobs, 1954; Jacobson, 1965; Simons, 1981) and are thought to trigger differential enlargement of lobe cells (Fagerberg & Allain, 1991), resulting in trap closure in less than a second. Generally, multiple stimulations of one or more of the trigger hairs are required for a response.1

Drosera rotundifolia

  Distinct touch-induced carnivorous behavior is demonstrated by Drosera rotundifolia, a species examined in detail by Darwin (Darwin, 1893). The mucilage on the ends of the Drosera's tentacles glisten in the sunlight (Fig. 2a,b) and give the plant its common name ‘Sundew’. Over 100 tentacles can cover the surfaces of its modified leaves. This showy appearance attracts insects, which upon alighting on the tentacle surfaces become trapped in the gluey substance. The tactile sensitive tentacles detect the presence and further movements of the insect as it struggles to be released. In response, neighboring tentacles bend towards the ones directly stimulated by the prey's presence.1

Utricularia (Bladderwort)

  The Utricularia trap, attached via a stalk to the rootless plant body (Fig. 3a), is a thin-walled hollow sac with a watertight trapdoor. When the trap is set, the outer walls are concave and the chamber is under negative hydrostatic pressure. Various appendages, some with mucilage-secreting glands, have roles in luring prey to the trap door entrance and others near the bottom of the door are the touch-sensitive triggers. Small creatures, such as water fleas, are examples of those that fall prey to Utricularia traps.1

Mimosa pudica

  Mimosa pudica, known as the sensitive plant, and some of its relatives are other well-known thigmonastic plants. A touch stimulation results in a very rapid folding up of the small leaflets composing the doubly compound leaves. Remarkably, the touch response is not restricted to the stimulated leaflet, but can propagate to all the neighboring leaflets of the leaf (Simons, 1981; Malone, 1994). A stronger stimulus, resulting in wounding, can elicit folding behavior at distantly located leaf petioles (Simons, 1981; Malone, 1994).1

Bryonia dioica

  Elmar Weiler and colleagues have found that an increased level of octadecanoids, in particular 12-oxo-phytodienoic acid (OPDA), correlates with touch-induced Bryonia dioica tendril coiling (Stelmach et al., 1998; Blechert et al., 1999) and that OPDA, and related analogs that cannot be converted to jasmonic acid (JA), are sufficient to cause tendril coiling with physiologically relevant kinetics in the absence of a mechanical stimulus (Weiler et al., 1993, 1994; Blechert et al., 1999).1

Monstera (Vine)

  The Monstera vine has an unusual technique for finding a host tree to climb. It travels by growing along the ground in search of the darkness of a tree's shadow; this movement towards darkness is called skototropism (Strong & Ray, 1975). The vine completes its journey when the vine apex senses arrival at the host tree by the resulting touch encounter. A dramatic change in growth direction then occurs. The Monstera vine begins an upward climb of its host tree (Strong & Ray, 1975), and leaf and stem development changes in anticipation of increased light and productive photosynthesis.1

Ficus costaricensis (Strangler fig)

  The strangler fig (Ficus costaricensis) has a more sinister interaction with host trees (Putz & Holbrook, 1986; Putz & Holbrook, 1989). Roots of the epiphyte form grow downward from its host tree and, in addition to wrapping around the trunk, roots that touch each other fuse together (Fig. 5). As the roots continue to grow and fuse, they eventually encircle and prevent further growth of the host trunk. Further differentiation of the fig's roots result in such constricting pressure that it damages and eventually kills the host in a manner befitting its name. In this way, the strangler remains alone without competition from its former host.1

Catasetum (Flower)

  Male flowers are poised to respond to visitors that contact antennae in the center of the flower by the release of stamen filaments held under tension by petals. The force by which a sticky disc with pollen sacs hits the chosen pollinator can be strong enough to knock a bee from the flower (Simons, 1992). This experience and the burden of the attached large pollen sac can be so traumatic that the bee will carefully evaluate potential future visiting sites and strongly prefer female flowers rather than the explosive male ones (Romero & Nelson, 1986). In this way, male Catasetum flowers may have evolved to compete for exclusive pollination rights of female flowers (Romero & Nelson, 1986).1

Arabidopsis

  When Arabidopsis roots encounter glass barriers, gravitropism appears to be compromised and thigmotropism occurs instead. The touch-stimulated roots neglect their propensity to grow towards gravity vector and instead grow away from the perceived point of mechanical contact. The interaction of touch and gravity may occur at the subcellular level; touch can delay one of the earliest known graviresponses, the falling of starch granules in the root columella cells (Massa & Gilroy, 2003).1

References:

 1) In touch: plant responses to mechanical stimuli [Janet Braam]

 2) Thigmomorphogenesis: a complex plant response to mechano-stimulation [E.Wassim Chehab ; Elizabeth Eich ; Janet Braam]


How can you tell if a protein-coding gene is nuclear or mitochondrial? New to genes, and have to read literature to find candidate genes for a particular study. I cannot for the life of my understand if all genes are placed into either the "nuclear" or "mitochondrial" category...are there more categories? Some are easy, like cytochrome subunit genes are always written as "mitochondrial" and then rhodopsin are written as nuclear...but other genes like ATPase etc. don't have those descriptions. When I search online further, it still does not clarify, so I am wondering now if there are just more categories to this?

I have limited my answer to refer to humans, but the advice generalises to other eukaryotic cells.

In human cells, almost all of the genes that code for proteins are located in the genome, which is located in the nucleus. The mitochondria have their own genetic material, however, the mitochondrial genes only encode for 14 proteins. The answer to this question also notes the existence of extrachromosomal circular DNA. There are also a number of proteins (1192) that are verified to exist but their genomic location is currently unconfirmed.

In your comments you mention ATP1 and note that it is called a membrane protein. The gene is located on chromosome 19 in the nucleus. The protein, that is encoded by the gene, can be found in a variety of places, including the nucleus and also the mitochondrion. The gene for Cytochrome c oxidase subunit 1 (CO1/COX1) is encoded in the mitochondrial genome and it localises to the inner membrane of the mitochondrion.

The links in this answer all point to Uniprot. This is what I use to get an idea of the basic functions of proteins. The database includes information genes but its primary purpose is to describe proteins and their functions. The information is roughly correct, it is not perfect. It includes a many species and links to a number of tools, including the gene ontology which attempts to characterise proteins using a controlled vocabulary.


Do disaccharidases require a cofactor or coenzyme to function? I'm doing research on lactose intolerance and am curious if disaccharidases (enzymes that break down disaccharides) require a cofactor or coenzyme to function? Reviews or references would be greatly appreciated.

Apparently not for lactase and β-galactosidase, as one might expect for this sort of hydrolytic reaction. There are also Wikipedia entries for maltase, sucrase and trehalase with references you can follow up to check yourself.


Is there life on other planets and if so how frequent? Some shed tears of joy as the news about the successful landing of the Mars Rover Curiosity came in. Then the most comprehensive 3D map of our observable universe was published. 2012 is literally an astronomical year.

As an layman I would like to know about scientists current understanding about the frequency models that life forms on other planets?

See also:

Drake equation

OK, so we know a couple of things about life in the universe. Note, however, that this is not really an answer and is also not very biological in nature.

So, we don't know how life began on the Earth. However, do know that:

The probability of life evolving on a planet in the universe is non-zero (since we exist) and,
So far, we have not found evidence for life elsewhere in the universe.

So this leaves us with two main possibilities:

Life is rare in the universe.
Life is common in the universe but for some reason we do not detect it.

This latter possibility is basically a restatement of the Fermi Paradox which says

  "The universe is very big and there should be lots of alien life out
  there. Where is everybody?"

In the case that life is common, we can speculate extensively on why we have not detected  it so far. For example:

We haven't been looking long enough (SETI has been running for only a few decades)
We haven't been looking hard enough (the budget of SETI etc. is not large)
We haven't been looking in the right way. We are currently looking mainly in the radio regime, maybe aliens broadcast in X (where X is part of the E/M spectrum or something else entirely, e.g. gravity waves, tachyons)
Life is common, but intelligent life is rare (this would be my guess)
Life is common and intelligent, and doesn't want to answer (why? ask a xenopsychologist)

OK, so these are just some examples of "solutions" to the Fermi Paradox. There are many more which are much more exotic. My personal favourite of these is that we live in a simulated universe and the coders have not included additional alien life in the simulation. It would explain some strange "coincidences" about fundamental physical constants, but what simulation, no matter how good, would ever come up with cauliflower cheese for example?

However, until we actually detect life on another planet we will still be in the dark. The next generation of telescopes will be able to do this for nearby exoplanets if life is present on them and has affected the biosphere in a detectable way.

Edit - You mention "frequency models", but all we can currently say is that the probability of life on other planets is not zero - due to our existence - as I mentioned at the start

Some references:

A joint analysis of the Drake equation and the Fermi paradox, 2012, arXiv, Prantzos, N.
The Fermi Paradox, Self-Replicating Probes, and the Interstellar Transportation Bandwidth, 2011, arXiv, Wiley, K.B.
Interstellar colonization - A new parameter for the Drake equation, 1980, Icarus, vol. 41, 193, Walters, C., Hoover, R. A., Kotra, R. K.


How to clean and preserve a cicada's molted exoskeleton (exuvia)? I found a good quality molted exoskeleton (exuvia) of a cicada, about 3-4 cm long on the ground. I'm amazed at the completeness and detail, the exit hole is in the center of the back and you hardly notice it. The "claws" on each foot are sharp and you can stick it onto any surface with a bit of roughness.

It had rained and there is some mud on it. I'd like to gently wash it and then keep it.

Are there any particular guidelines or techniques I should know about? Can I just gently swish it around in soapy water and then let air dry, or do I need to take some precautions, or even use some kind of fixative? Humidity is high where I live; anything that can possibly support mold will get moldy if you are not careful!

Sorry I can't add a real photo right now but it looks a bit like the emptying exoskeleton in this randomly chosen photo from here:

The exuvia is made of cross-liked chitin, and will not decay. You don't need any special preservatives as all. If you need to get the mud off, just rinse it as you said, in soapy water, let it dry, and you are done. Simple.


How can I pare down a PDB file in Python to only include specific residues? I'm trying to make a script that will take a MTZ file (reflections), convert it into a CCP4 map, then pare that map down to only encompass a desired area to cut down on the size of my PyMol session files so they're email-able (a.k.a. not 200 MB) and ease the burden on my POS computer.

I currently have a Python script that can fft (CCP4) to create the map and mapmask to fix unit cell tiling issues.  What I want to add now is something that can take a PDB file and strip out most of it except, for example, residues within 10 Å of #123.

I've been looking at ProDy, but not quite sure where to start.  I would also be open to using something in the CCP4 toolkit.

With the program RasMol, you can select, as Mad Scientist explained it for PyMol, everything in a specific distance around an atom. RasMol can be run from command line, using a script (with the -script option under UNIX).


Forming a cladogram from a table of information Can someone please give me some tips or help me build a cladogram from the following table of information? The outgroup is Lancelets and the first derived character is vertebrae, followed by Lampreys and jaws I believe.  It’s not until after jaws I have trouble figuring out where to link up the organisms and traits. I’m assuming you cannot repeat or remove traits. When I look online the simpler examples do not help me much for this branching issue...I hope that made sense. It’s probably simpler then I think but I’m having a mental block with it. Any help would be great, thanks

I think the clue is at each step to look for the trait that is shared by most of the remaining taxa.

In your example: 9 out of 10 taxa are vertebrae. So you are correct to pick this trait first and outgroup Lancelets.

Looking at the remaining 9 taxa:
8 have jaws, and a different set of 8 swim bladders or lungs
At this point you can pick one of those traits, as far as I know.
You chose jaws and outgrouped Lampreys.

In the remaining 8 taxa, the characteristic that is shared by most of them (7), is having swim bladders or lungs. Thus, you can outgroup Sharks here.

In that way, you can go on for the remaining traits and taxa.


Why is the Kakapo more attracted to humans than its own kind? The Kakapo can be seen in this video by BBC. It is said that the species is strongly sexually attracted to humans. Why could this be the case?

The male kakapo (Strigops habroptila) in that video is called Sirocco. Kakapo were (and still are) very close to extinction, so in the 1980s the Kakapo Recovery Programme was launched. As part of this programme, rangers monitor all known kakapo in the wild, visiting their nests and generally ensuring they are in good health. When Sirocco was a young chick, a ranger discovered him in his mothers nest with severe breathing problems. He was brought back to the Kakapo care hut and raised by humans. As a result of this, he imprinted on his carers (see his website!).

Imprinting is common in birds, and takes several different forms. The most well-known form is filial imprinting, where young birds (and some other animals) develop a strong fixated image of who their mother is. They then learn their behaviour almost exclusively from the animal they fixated on. This is well studied in geese, for example by Konrad Lorenz.

However, Sirocco was demonstrating sexual imprinting. This is where young animals (including humans, see e.g. Bereczkei et al., 2004) learn which characteristics are sexually desirable by fixing an image of their parent(s). In Sirocco's case, he imprinted on a human and subsequently saw humans as his species, and therefore potential mates.

The exact purpose of sexual imprinting has been widely discussed (e.g. see Immelmann, 1972). Lorenz suggested that it allowed animals to recognise their own species. However, some imprintable birds will show a preference toward individuals resembling the one they imprinted on, but when introduced to their own species will still recognise them as potential sexual partners. It may therefore be the case that imprinting allows a juvenile firstly to supplement a genetic predisposition toward its own species, but secondly to recognise closely related and less related individuals. Bateson (1978) suggested that this would enable a sexual strategy of choosing mates which are sufficiently unrelated so as not to cause inbreeding depression, but sufficiently related so as not to cause outbreeding depression, and he found an example which bore out the predicted behaviour in Japanese quails.

Sirocco seems not to have the genetic ability to recognise his own species, and according to his website does not associate with other birds.

 Bateson P. 1978. Sexual imprinting and optimal outbreeding. Nature 273, 659 - 660.
 Bereczkei T, Gyuris P, Weisfeld GE. 2004. Sexual imprinting in human mate choice. Proceedings of the Royal Society of London, Series B: Biological Sciences 271: 1129–1134.
 Immelmann K. 1972. Sexual and Other Long-Term Aspects of Imprinting in Birds and Other Species. In Advances in the Study of Behavior, Vol. Volume 4 of, pp. 147–174, Academic Press


What type of spider is this? VA, USA Spider found in Richmond, VA. Can anyone identify?

Sure, I can identify this for you!

That is an Argiope Aurantia, most commonly known as a "Yellow Garden Spider". They're quite well known for the design of the webs they spin, and because of this, they also go by "Sewing Spider" and "Writing Spider". They may try to bite if startled (which can be easy to do), but their venom is harmless to humans, so no worries.


What's the difference between Phage DNA and Recombinant DNA Genetic engineering:
In my textbook the following sentences describe the two, but to me they seem the same:

The new combination of bases in the DNA (vector DNA + DNA fragment)
is called recombinant DNA.
With bacteriophage vector, the bacteriophage will infect the bacteria by injecting its DNA into it. The Phage DNA (with the
desired gene in it) then integrate into the bacterial DNA.

Without going too much into it. What is the difference between Phage DNA and recombinant DNA?

Phage DNA is the DNA in a bacteriophage.

Recombinant DNA is synthetically combined DNA used in genetic engineering.

In your case, since the phage's DNA is used as a vector, the phage DNA is the recombinant DNA, but that does not mean every phage's DNA is recombinant, since phages occur naturally. The point is, the phage DNA was altered to become recombinant DNA.


What are the possible reasons to get extra unrecognized band in agarose gel electrophoresis? I ran 0.7% agarose gel electrophoresis of my plasmid DNA sample consisting of GFP vector, using NheI and HindIII restriction enzyme.
I used two types of plasmids, i.e., isolated by miniprep-alkali method, and another isolated by midi prep system (pure) of the same source E. coli.
The 4 and 5 lines show cut and uncut plasmid, respectively, isolated by midi prep system.
The 1, 2, and 3 lines show the 500 bp marker, cut, and uncut of miniprep isolated plasmid signal, respectively. In the attached image, we found an extra band in the plasmids isolated by alkali method (line 2 and 3), but in the pure samples (line 4 and 5) no such extra bands were found.
What are the possible reasons behind the result? How may I interpret this result? If anyone has experienced similar results, please share.

Looks like genomic DNA contamination to me.

More importantly, does it really matter? I certainly appreciate the curiosity but, if your objective is cloning, I would just keep going and then do some diagnostic cuts of your plasmid after transformation. You can clearly see your vector or insert in the gel.


Simple Mendelian Genetics Question here is my question:

In certain plants, tall is dominant to short. If a heterozygous plant is crossed with a homozygous tall plant, what is the probability that the offspring will be short?

My Solution:

Let T be the allele for the tall phenotype and t be the allele for the short phenotype.

Then the parental cross would be Tt x TT = 100% tall phenotype (1/2 Tt, 1/2 TT).

Hence the probability of having short offspring should be $\fbox{0}$.

However, the answer key for this question says the answer is $\fbox{$\frac{1}{2}$}$. How can this be??? It really bothers me when the answer key is potentially incorrect because it makes me very unsure, and I end up wasting time trying to figure out if the key is wrong or if I am. Can somebody please let me know if what I did was correct/incorrect??

Thanks

Assuming you have stated the question correctly, the answer key is incorrect for exactly the reasons you have given and your reasoning and consequent answer are correct.

I would double-check you have read the question correctly and then conclude the answer key is incorrect. It happens.


Understanding Genetic Dynamics of Specific Problem The following questions comes from International Biology Olympiad 2014, theoretical part B.

It states:

  Earlier research suggested that the red flower pigment of plant species was the result of a
  chemical pathway including multiple steps and that all intermediate pigments were white. Three
  pure-bred lines with white flowers (White 1, 2 and 3) of this species were crossed with each other
  and the following ratio of colors were obtained among the progeny:

The question was how many genes control flower color. I completely botched it. Here are my thoughts:

Looking at F2 generation, there are 9 reds + 7 whites = 16 total. (I know it's a ratio.) Generally, having 16 suggests at 2 genes controlling the phenotypes. For example, cross AaBb x AaBb, you'll get 16 phenotypes.

Turns out 2 is incorrect, and I have no clue as to how colors are inherited in this problem. Any suggestions?

First of all, since two is incorrect, and one is not possible, three is the most probable answer. It is also supported by the format of question that three different types of white purelines are given. Let the genes be A, B, C. Now, there are three possible ways:-

1) Each one has two homozygous dominant genes and one homozygous recessive.

2) Each has one homo dominant and two homo recessive.

3) Any one has all homozygous recessive and the rest two can have any of the above two.

The problem with (2) & (3) is that they do not explain the red F1. Red will require a dominant allele of each gene. But in crosses of (2) or (3), at least one gene will be left out.   For example, AAbbcc x aaBBcc will give all progeny with cc. So none can be red. Same problem with aabbcc x aaBBcc or AABBcc

So lets go with (1). Let

W1 AABBcc

W2 AAbbCC

W3 aaBBCC

W1 x W2. => all AA Bb Cc (Red F1 of cross 1)

F1 x F1 will be like a cross of BbCc with AA in front of all the genotypes. This will give you exactly 9:7 phenotypic ratio as mentioned in question.

Now, lets solve the question.

A) Three genes. So false

B) F1 were homozygous for one gene and heterozygous for other two. So false

C) F1 of cross 1 = AABbCc and W3 aaBBCC
Since it is evident that it is possible to inherit dominant alleles of each gene (eg. AaBbCc or AaBbCC) so red colour can come. So false

D) F1 cross 1 = AABbCc

F1 cross 3 = AaBBCc

It is evident that one segregation of gene alleles of “a” and “b” will have a dominant allele no matter what. So for a white colour, only chances are from cc. So in cross Cc x Cc there is 1/4 probability for cc. So all in all, 1/4 probability for white (since aa and bb genotypes are not possible here).

So D is True.


What is this giant insect that just bounced off a second-floor glass door? At about 11 pm, I heard a loud impact on the nearby glass door to a second-floor balcony. I thought it might be an acorn but it'd be a very unlikely angle - it'd have to be thrown from below or be a very strange ricochet.

So I looked and encountered this rather impressive creature recovering on the balcony:

Those planks are six inches wide.

I've never seen one of these before. What is it? Are those giant serrated appendages on the front mandibles or antennae?

I expect it's not as hazardous as it looks, but is there any risk of it biting people or pets?

Do they routinely launch themselves two stories into the air, or would it have crawled up and then just bounded from the balcony floor?

Location: Southern Oregon, USA.

Searching the Internet again this morning, I think I may have identified it as a California (Giant) Root-Borer Beetle (https://www.insectidentification.org/insect-description.asp?identification=California-Root-Borer-Beetle). Yes?

They fly, and are active at night.

The disturbing serrated appendages are antennae (whew!).

It looks like I have nothing to fear from it unless I or others panic at its appearance, but it or its progeny may be bad news for nearby deciduous trees.


Flow cytometry issues I'm having problems with data analysis here.

I have flow cytometry data being collected on a Fortessa, and when I import them into FlowJo 8.7, all of my fluorescence values are systematically 10X lower than they are on the cytometer. No idea what's going on here, anybody can help? If you want screenshots and photos of the data, I'm happy to post them up.

I have this issue too with data from a Partec PAS III. I don't consider it a problem, as it's really just the x-axis which is one order of magnitude higher. At the end, all values coming from the machine are arbitrary values, so as long as the change is systematic, there's no problem.


Finding a reaction from a KEGG map I have come across a map and a part of it looks like this:

Now I have not been able to locate the reaction that converts alpha D-Glucose to Glucono-1,5-lactone but was successfully able to locate the reaction that converts alpha D-glucose Glucose to Glucose-6P. Since an arrow exist from alpha D-Glucose to Glucono-1,5-lactone, i am assuming that such a reaction exist. But could not locate it. I clicked on the arrow marked in blue in the picture, but could not find the desired reaction.(alpha D glucose and beta D glucose are different compounds)  What is the reaction and how is it possible to find the reaction from the map?
NB: The arrows are clickable so are the circles that denote the compound.

It was a simple search. You could have easily searched for glucose oxidase in KEGG, and you would have got this reaction.

In fact if you had clicked the link for glucunolactone's compound page, you would have got a list of many different reactions that convert glucose to glucunolactone.

You can even click the arrow which opens the KEGG-ORTHOLOGY page. You can find a field called RN in the section called "Other DBs". The links corresponding to this field would give you the exact reactions, that the pathway uses.


Does the dissociation of serotonin receptors and their ligands really take hours? If I understand the principle of neurotransmission correctly, then after binding to a receptor on the postsynaptic side, neurotransmitter molecules must be dissociated from the receptor and removed quickly from the synaptic cleft (see this book).

This article states that the off-rate $k_{\text{off}}$ for the 5HT3 receptor and some ligand is approximately $43 * 10^{-6} s^{-1}$. If we ignore the binding process for now and denote by $C$ the complex formed by 5HT3 and the ligand, we can describe the dissociation process by the following simple differential equation:
$$
\frac{dC}{dt} = -k_{\text{off}} * C
$$
(see Wikipedia).
Using the $k_{\text{off}}$ from above, we get that the half time of this dissociation process is $\frac{\ln{2}}{k_{\text{off}}} \approx 16116s \approx 4,5h $. A similar $k_{\text{off}}$ rate for all other kinds of 5HT receptors binding serotonin can be derived from the dissociation constants found in the Ki Database.

But wouldn't that mean that, when serotonin is released from the presynaptic axon terminal and the 5HT3 receptor binds it, not even half of the neurotransmitter molecules are dissociated from the receptor after more than 4 hours? That seems to clearly contradict the statement from the beginning of this post - so is something wrong with my calculations or does it really take that long? Or have I understood something completely wrong about the principle of neurotransmission?

That paper is describing the binding between the 5HT3 receptor and some high-affinity ligand, not serotonin.

Numbers of serotonin probably vary according to the precise receptor (species, subunits, etc), but for a ballpark figure this source says 1.7/s, giving half time of ~400 ms. That estimate is based on solution changes, so I'd say it's an upper bound.

Remember from the other questions you have asked and I have answered, serotonin is a slower-acting neurotransmitter, and clearance of serotonin is not as fast as for other, faster-acting neurotransmitters. However you are correct that your initial calculation of a ~4-hour dissociation time is unreasonable.


What does it mean to be a fully human monoclonal antibody? I somewhat understand that some monoclonal antibodies are developed from the cells of mice, or a fusion of human and mice genes.

When something is a fully human monoclonal antibody does that mean it came from some person? What type of human cell did it come from? Will the drug always be from that original human?

I read that they're derived from something called a phage display technique. I'm guessing this is another type of way to fuse genes together, but with all human cells.

Where do the cells come from?

I found this small article that seems to cover all your questions:

https://www.sciencedirect.com/topics/medicine-and-dentistry/human-monoclonal-antibody

Summary:

Being considered a human monoclonal (many of the identical antibody, as opposed to different antibodies for the same target) antibody does not mean it is produced by a human body; it means that the fc-region of the antibody is human-like, which aims at avoiding immune reactions against that antibody if injected into humans.
So the human antibody can originate from animals (e.g. rats or rabbits) with humanized antibody genes or from immortalized human cell-lines (lymphocytes).


Does isolation have any effect upon mouse behavior? I work with a lot of mice. I don't do any behavioral analysis, I just inject DNA or RNA and do imaging assays. However, I have noticed some effect of isolation on mouse behavior. Normally, the mice are housed in our university's animal facility with no more than 5 mice to a cage. Sometimes, 1 mouse will be put in a cage by itself. When I go to get these lone mice from their cages, they seem more skittish, harder to grab, and more likely to bite me than mice kept in groups.

Additionally, our Office of Animal Resources, which is responsible for getting in the mouse shipments and putting them into cages, has recently changed how our mice are caged, with a group of 4 mice being normal, any leftover mice are put into cages with other mice, making a 5 mouse cage. This means I haven't seen a single mouse in a cage for a while. So I might not be the only one to have noticed an effect of isolation on the animal's health.

I have heard of studies on monkeys by B.F. Skinner, where he induced very severe depression and other psychological issues by isolating them, so I suspect similar studies have been attempted on mice using far more quantitative methods than I've been able to do.

Yeah, it's not good:

  Social isolation (SI) rearing in rodents causes a variety of behavioral changes, including hyperlocomotion, anxiety, impulsivity, aggression, and learning and memory deficits. These behavioral abnormalities in rodents may be related to the symptoms in patients with neuropsychiatric disorders, such as attention-deficit hyperactivity disorder, obsessive-compulsive disorder, autism, schizophrenia and depression...

Also:

  Our findings suggest that [social isolation]-induced behavioral abnormality is a psychobehavioral complex relevant to various clinical symptoms observed in neuropsychiatric disorders, including ADHD, schizophrenia and depression, and that SI-reared mice are a useful animal model to study the pathophysiology/pathogenesis of these diseases.

There's this:

  In contrast, long-term social isolation is a model to study the behavioral and neurochemical consequences of depriving rodents of social interaction. Many of the symptoms caused by long-term isolation resemble those seen in depression and anxiety disorders. Furthermore, long-term isolation of male mice is known to induce offensive and aggressive behavior, such as attacks.

And this:

  These data suggest that long-term isolation may induce functional changes in the sensitivity of alpha 2 receptor in the noradrenergic system...

And this:

  In the present study, we found that social isolation elevated the anxiety levels of mice...

Emphasis all my own.

There's a lot more meat in those studies, and especially the paper they cite in their introductions.  Some of them, as well as others also explore the effect of isolation in addition to other substances.  It can absolutely affect your studies, in particular behavioral or expression-based studies.  Your mouse house is good to change their practices.


Are all tastes just a combination of sour, sweet, bitter, etc.? For example, can the taste of pineapple be isolated to just a certain amount of "salty-taste-triggering-molecules" and "sweet-taste-triggering-molecules" etc.? Can our current understanding of the gustatory system predict the taste of a new substance (for example we could predict it tastes like chocolate) just based on the amount and ratios of these molecules?

Interesting question.

  The brain perceives taste or flavor as a combination of input from taste buds, the olfactory system, and even pain receptors (spicy foods). Other food contents, such as metal, spice, fat, pH, and even dissolved gas content seem to contribute.

While there are 5 types of taste receptor, there are some 2000 olfactory bulbs encoded by 1000s of gene.  As such, it is not possible to predict how something will taste in a simplistic 5-taste combo.  However, this is an area of active research, such that structural models are used to develop taste enhancers, artificial sweeteners etc.

Sources:

http://www.sciencedirect.com/science/article/pii/S0976120913000041
http://health.howstuffworks.com/mental-health/human-nature/perception/taste.htm
http://www.livescience.com/17684-sixth-basic-taste.html


Validation of houskeeping genes in a mixture of cDNAs of two species I have a parasite sample (mixed with host blood) and I need to check gene expressions of parasite using relative quantification (RT_qPCR). For this, I need a good housekeeping gene. I chose 10 genes (suggested as housekeeping) that I need to validate and after choose the most stable one(s). My problem is that my parasite cDNA is mixed with host cDNA and it is impossible to separate them or count the parasite. I do not know how I could choose the best housekeeping gene in this case? I do not have the real amount of parasite cDNA used for qPCR, and I do not have any good internal control. Basically, it is circular problem: In order to validate my target gene I need a good housekeeping gene for internal control, but I do not have an internal control to make relative quantification of my housekeeping genes and to chose the best one. Could you please suggest any study or method that deals with such a case?

Two possibilities:

Design primers based on differences in the sequences of the gene for the same protein between the two organisms. (Suggested by @Artem)
Identify an aspect of the metabolism of your parasite that is not present in the host, then use enzymes from that pathway. If the parasite is a worm and the host a mammal, for example, you should surely be able to find something.


Why there is no typical cells My physiology book says that cell specialization is so great that no cell in the body could be called a typical cell.

I don't understand the above sentence, why couldn't there be typical cells? After mitosis don't we get two typical cells? Or what is meant by the sentence??

Thanks in advance!

Typical here means representative of the whole.

from the google dictionary

  typ·i·cal ˈtipik(ə)l/Submit adjective having the distinctive qualities
  of a particular type of person or thing. "a typical day"
  synonyms: representative, classic, quintessential, archetypal, model,
  prototypical, stereotypical, paradigmatic;

There is such a variety of cells in the body no one is really typical.  Like a typical human.  Who would that be?  Me?  Chinese lady?  Indian kid?  There are many of us and a lot of variety.  Maybe you could say "typical older Scotsman" or "typical arrogant Stack Question answerer".  You could definitely say "typical liver cell"; narrowing down the zone limits the variety possible and lets you more accurately characterize a call as prototypical or representative.


What does the (-) in the molecule name mean? I'm reading some text (purchase request) that has the following line in it.

  (-)-Norepinephrine

What does the minus sign mean in front that is in parenthesis? Is this some kind of standard way of describing charge of the molecule or something? Or is this someone's way of representing something else? Or does this mean nothing?

The minus sign in parentheses here indicates the optical rotation, (+) means the molecule rotates linear polarized light clockwise, (-) means it rotates counterclockwise. Typically you would also write exactly which stereoisomer is meant (R or S), which is generally the more useful information.

The following are all valid names for the natural stereoisomer of norepinephrine:

D-norepinephrine
D-(-)-norepinephrine
(R)-norepinephrine
(R)-(-)-norepinephrine

I'd recommend that you take a look at the concept of Chirality if you're not already familiar with it.


Do presynaptic neurons and postsynaptic neurons have different compositions of neurotransmitter receptors and transporters? For example if certain neurotransmitter is released, will there be neurons that won’t be even potentially affected, because it doesn’t have such type receptors?

Typical bouton-spine synapses are formed as an interactive process between the pre- and post-synaptic cells (Scheiffele, 2003). There is communication between pre- and post-synaptic cell through guidance cues, growth factors, and structural proteins, as well as neurotransmitter release itself. Therefore, as part of the normal developmental process, postsynaptic cells will usually have receptors for the major neurotransmitter released by the presynaptic cells: they find each other rather than connecting at random.

Synapses that become inactive or have lower activity than their neighbors can also degrade and disappear entirely (Purves and Lichtman, 1980) by a competitive process (Balice-Gordon and Lichtman, 1994). Because of this process, I would expect that even if some developmental fluke led to a formation of a synapse between mismatched pre/post neurotransmitter release/receptors, the result would be that the synapse would get no stimulation and would be pruned according to the normal process.

However, some neurotransmitters can be released more broadly into the extracellular space rather than at highly specialized synapses (including serotonin, dopamine, and acetylcholine - note: these neurotransmitters can also be released at synapses) (De-Miguel and Trueta, 2005; Trueta and De-Miguel, 2012) and call also 'leak' from synapses into the extrasynaptic space: in these cases, the neurotransmitter is not likely to have an effect (or the same effect) on all nearby dendrites, only those that express fairly high-affinity receptors that can detect the neurotransmitter at an extrasynaptic concentration.

References:

Balice-Gordon, R. J., & Lichtman, J. W. (1994). Long-term synapse loss induced by focal blockade of postsynaptlc receptors. Nature, 372(6506), 519.

De-Miguel, F. F., & Trueta, C. (2005). Synaptic and extrasynaptic secretion of serotonin. Cellular and molecular neurobiology, 25(2), 297-312.

Purves, D., & Lichtman, J. W. (1980). Elimination of synapses in the developing nervous system. Science, 210(4466), 153-157.

Scheiffele, P. (2003). Cell-cell signaling during synapse formation in the CNS. Annual review of neuroscience, 26(1), 485-508.

Trueta, C., & De-Miguel, F. F. (2012). Extrasynaptic exocytosis and its mechanisms: a source of molecules mediating volume transmission in the nervous system. Frontiers in physiology, 3, 319.


Why are spinal nerves considered a part of PNS while the spinal cord is a part of CNS? So from my common understanding, CNS consists of brain and spinal cord, and PNS consists of everything else. But the spinal nerves - the nerves connected to the spinal cord - why are those considered part of the PNS? And another clarification - spinal nerves are COMPLETELY DIFFERENT than the preganglionic neurons of the sympathetic nervous system?

Thanks for all your help.

CNS consists of brain and spinal cord, and PNS consists of everything else

That's really it. The distinction is slightly arbitrary, I'd think of them as the central (nervous system) and the peripheral (nervous system): that is, the most important part is that together they are parts of the nervous system, rather than being distinct systems; the central/peripheral difference is fairly minor, especially if you are thinking primarily of the somatic part of the peripheral nervous system (that is, not the autonomic part) relative to the associated part of the CNS.

The peripheral part of the nervous system is not protected by the bones of the skull and spine, does not have the protection of the blood-brain barrier (specialized endothelial cells and astrocytes that limit transmission of molecules between CNS and the blood circulation moreso than in other tissues), and myelination is mediated by cells with a different morphology: Schwann cells in the periphery vs. oligodendrocytes in the central. That's about it.