Why do typical acetylcholinesterase inhibitors (like carbamates) have a greater parasympathetic effect than a sympathetic effect? I understand that the post-ganglionic neurones of the sympathetic system are adrenergic, but surely these neurones will be excited to the same extent as the parasympathetic post-ganglionic neurones (due to the ganglionic synapses being cholinergic), and thus target organs/tissues will be receiving equal and opposite sympathetic/parasympathetic stimulation, or rather equal and opposite activation of the muscarinic/adrenergic receptors. (Sub-question: Why does caffeine, a perhaps atypical acetylcholinesterase inhibitor have a greater sympathetic effect than parasympathetic effect?).

We were taught that ganglionic receptors have very high thresholds. So we need a very high concentration of the drug to produce the sympathetic effects. We even solved a hypothetical problem in class, where a patient presented with a pinpoint pupil (typical insecticide poisoning) and increased secretions but an increased heart rate (usually they present with bradycardia). We would still treat the patient with atropine since the combo of pinpoint pupil and increased secretions would be exclusively explained by insecticide poisoning (either organophosphate or carbamate). The increased heart rate could be explained by ganglionic action leading to sympathetic activation of the heart.

But as said this was only a hypothetical case and patients of organophosphate or carbamate poisoning always present with bradycardia. To elicit ganglionic responses the person has to consume a dose way higher which would certainly lead to sudden death.

Hope that helps :)


What is this arachnid? I came across a photo on Wikipedia depicting an Oreocereus celsianus with what looks to me like some kind of harvestman on it. The photo was taken at the San Francisco Botanical Garden.  Can anyone identify the arachnid in the photo?  (See link below for full-size image.)

Source: https://commons.wikimedia.org/wiki/File:Oreocereus_celsianus_1.jpg

The latin name for this animal is Leiobunum rotundum and Nelima fuscifrons, order Opiliones.

examples:
link


Microscopy of moving white blood cells Is there a way to get white blood cells to move while on a microscope slide? I want to try to get some microscope images of them moving, but so far I have only found them stationary.

Not an experimentalist, so take this with a grain of salt.  But for motility you often need some external factor, e.g. a chemokine or chemoattractant (FMLP is a common one for white blood cells).  Also some cell types may not crawl on bare glass, and might need a protein or gelatin coating.

White blood cells on slides can look like this: https://www.youtube.com/watch?v=JnlULOjUhSQ

Unfortunately, I don't know the conditions used there.  My recommendation is to look through Google Scholar for white blood cell motility or neutrophil motility, and see what turns up.  For instance, the first paper I found was: C S Spada, A L Nieves, A H Krauss and D F Woodward, J. Leuk. Biol. 1994 (PDF) which gives some details about how they got their assays to work, including a gelatin coating for the slides.  However, the details probably depend on the origin of your cells and the type of white blood cell you're looking at.


Why does the number of mutations per individuals follow a Poisson distribution? I was reading this review. On page 11, left column, first paragraph, one can read:

  [..] there is a Poisson distribution of the equilibrium number of mutations per individual, if fitness effects are multiplicative.

with no further explanations. In other words, let the variable $X$ be the number of (deleterious) mutations found in one individual (irrespectively to whether the mutation occurred in the parents gonads or is older back in the lineage). The variable $X$ is Poisson distributed.

Why is this statement true? I suppose that the statement also assumes that all mutations have the same effect on fitness, is that true?

A Poisson process follows these postulates:

$\lim\limits_{h\to0+}\frac{P(N_h=1)}h=\lambda$  i.e. the probability of occurrence one event in a very small interval of time is equal to the macroscopic rate or intensity ($\lambda\,$).
$P(N_h\geqslant2)=o(h)$ i.e. the probability of occurrence of more than one events in an infinitesimal interval is essentially zero.
Events are independent.

If you consider a single individual (for simplicity assume a single cell), then the DNA will undergo mutations at some fixed rate (which we assume to be uniform for all loci). Now each mutation event is independent of the previous event and in a very small interval of time the chance of two or more mutations is negligible. Considering all these facts and assumptions, it can be said that mutation in a single cell would behave like a Poisson process.

From the Poisson postulates you can derive the expression for the Poisson distribution which describes the probability of $k$ number of events in a given time interval, $t$. Hence, the number of mutations in an individual for a fixed time window ($t\,$) follows a Poisson distribution.

$$P(N=k)=\frac{(\lambda t)^k e^{-\lambda t}}{k!}$$

You can find the derivation of Poisson distribution from the postulates from many sources. I referred to this book:

Hogg, Robert V., and Allen T. Craig. Introduction to mathematical statistics. New York: Macmillan, 1978.

EDIT

The effect of deleterious mutations, in the mentioned section of the linked paper talks about Muller's ratchet that describes the accumulation of deleterious mutations and its effect on the population (i.e. extinction). Like any mutation event, accumulation of deleterious mutations will also follow Poisson distribution. Muller's ratchet just says that beyond a tolerance limit, deleterious mutations will cause extinction of asexually reproducing organisms. Perhaps if each deleterious mutation had a strong effect on the fitness, then sampling from the population may lead to non-Poissonian estimates.


What does it mean when a protein has a different excitation spectra than wildtype, but the same emission spectra? We have a GFP mutant that displays a different excitation spectra with emission at 510nm than the WT. However, their emission profiles with excitation at 490nm are the same, and we do not observe the same trend.

We're confused as to what might be happening.

Let me start from short description of fluorescence (since we talk about it here).

Fluorescence is one of the processes through which excited molecule can relax, lose its excessive energy. That is, quantum interaction between atoms in molecule (organic dye or complex GFP) create permitted energy levels. There is "ground state" $S_0$, for example, and excited state $S_1$. You "pump" your molecule with excitation light from $S_0$ to $S_1$. All this can be nicely illustrated as absorption in Jablonski diagram (look at a for now):

via http://micro.magnet.fsu.edu/

"Loss of energy" here is some process via which molecule returns to ground state. In case of GFP energy is released as an emission photon. Nature of fluorophores is that they tend to return to ground state as the state of less energy, and almost all systems tends to go to state with lesser energy.

Now, to your question. Why GFP can has different excitation profile but same emission? Notice, how in (a) molecule get pumped to highest state, then relaxes a bit to lowest of $S_1$ states and then go all the way to $S_0$? That initial relaxation is thermal relaxation. Some energy is lost, essentially, to water molecules around GFP. That is why emission is always "more red", i.e. has lower energy than excitation. Initial relaxation is why your GFP spectra also broad. There are many levels GFP can emit from, as well as be excited to. In crystals of GFP transitions will be very narrow, because much less of excitation energy will go not into fluorescence.

So, my point is following. Nobody prevents one from engineering a mutant molecule of GFP that could be pumped to some even higher level $S_2$, which then relaxes to $S_1$ via non-irradiative process (e.g. gives energy to water, but not into fluorescence!). Only requirement is that for mutant direct pathway from $S_0$ to $S_1$ would be forbidden (see b and c).

Another point is that whether your spectra are different in shape or only intensity. Different shape of spectra means there are differences in those levels and transitions.


Definition and example of Gene Variant Could someone clearly define what a gene variant is with an example. I am totally confusing myself with SNPs, alleles, variants and how the major and minor allele are defined. An example with gene names would be really helpful.

A fairly easy-to-understand example is that of the ABO blood group system. In this case, there is a single gene involved - ABO, which codes for an enzyme that modifies sugar groups on the surface of red blood cells. This ABO gene has three variants or alleles — i, IA, and IB. i (coding for Type O blood) is recessive, which means that its phenotype can only be observed if there are two copies of it – ii – one from the mother and one from the father. IA and IB are co-dominant, meaning that both can be expressed at the same time, and their phenotypes can be observed even if there is only one copy of that allele — for example, IAi would give Type A blood (as would IAIA), IAIB would give Type AB, and so on.

Major and minor alleles (at least in my mind) simply refer to the frequency with which an allele is found in a given population: a minor allele is one that is expressed less-often than a major one. The term minor allele frequency is sometimes used as a numerical representation of expression — a certain allele is only expressed in 3% of the population, for example.

These terms are all from classical genetics — talking about genes and variants without really knowing (or needing to know) what exactly the gene was made up of. Of course, we now know that genes are composed of sequences of DNA nucleotide base pairs (A, T, C, and G), which are then translated by 3bp-codons into proteins, where each codon corresponds to one of 20 amino acids, plus START and STOP sequences. It is in this context of DNA sequence analysis that terms like SNP or Single Nucleotide Polymorphism are used. If you were to compare two alleles, say IA and IB, any single-nucleotide difference between the two could be termed a SNP. Frequently, SNPs are often notated based on the changes the difference would bring to the translated protein sequence — for example, a AAG codon codes for the amino acid lysine, while GAG encodes glutamatic acid. In other cases, a SNP would make no difference to the protein sequence — for example, TTA, TTG, CTC, CTA, CTG, and CTT all encode leucine. You can find the DNA codon table here.

You should keep in mind that SNPs are not the only source of variation in genetic sequences — deletions, translocations, repetitions, inversions, frame shifts, and other mechanisms can all alter the DNA sequence at a particular locus or site. Taken together, all of these differences are often referred to as mutations, which simply means "changes."

I hope this was helpful, please let us know if you still have questions.


What is the function of spongin in sea sponges? Sea sponges (Porifera) use different types of skeletons to support their structures. Some skeletons are built from minerals, some are built from proteins like spongin, and some use both.

My question is about spongin. What is the benefit of having a skeleton made exclusively of spongin? (What advantages does it have compared to other types of skeletons?)

If you have ever used a natural bath sponge, you know that the structure of a sponge's spongin skeleton is great for absorbing water and squeezing that water back out.  The sponge's skeleton contains millions of tiny holes, all connected in a massive network of internal tunnels, through which the sponge takes in food and eliminates waste.  It feeds by use of cells that wave tiny cilia to push water into the sponge.  Nutrients are absorbed by the animal and spent water and waste are expelled by the help of similar cells, spinning their flagella to force the water out of the sponge.  A third class of cells, comprising a basic immune system, move around the organism engulfing microbes potentially dangerous to the animal.

This unique system is facilitated by the structure of the spongin skeleton.  The skeleton needs to be strong enough to retain this complicated microstructure, while also having enough give and flexibility that its network of delicate tunnels don't buckle under the force of water pressure, deep currents, or fish and other matter bumping against it.  Notice that, when you squeeze the water out of a sponge, it snaps back into place, the tunnels still open for business.  Given that these tunnels are how the sponge eats, this is very important.  To build a complex tunnel system with millions of tiny little tubes running through it out of something hard and brittle would make it very easy for tunnels to collapse, cracks to form, and other damage to be sustained.  Some sponges, as you mention, have hard, brittle "spicules" in addition to the spongin, but these sponges tend to live in deeper regions and need extra strength to deal with the pressure.


loops in neuron synapses If we see at the connectome of c.elegans, it is easy to find "loops", in the simplest case, a neuron that synapses to another and this one backward to the first.

By example, neuron RIAR has 13 synapses to SMDVL (pre-synaptic is RIAR, post-synaptic is SMDVL) and this one has 8 synapses backward to RIAR (pre is SMDVL, post is RIAR).

Which is the scientific term to denote theses structures? Moreover, main hypothesis about its purpose?

"Recurrent" might be the term you are looking for, i.e.:

running or turning back in a direction opposite to a former course —used of various nerves and branches of vessels in the arms and legs

https://www.merriam-webster.com/dictionary/recurrent

If you observe a recurrent network within a single pair of neurons, you could also refer to this as a reciprocal connection, in that a pair of neurons are both post-synaptic and pre-synaptic to each other.

More generally, you could also talk about feedback as a general motif in neuronal circuits.

The function of recurrent connections likely depends on the specific network you are talking about, but they can be used for predictive coding, pattern generation, computation, and more. In organisms with 'simple' nervous systems like C. elegans, however, these connection patterns can be even more complex, because they have evolved to perform a lot of behavior with very few neurons.

Try searching Google scholar for recurrent neuronal circuits for some more information.


Why is chemotherapy-related hair loss temporary? Chemotherapy kills cancer cells by targeting rapidly growing cells. That is why patients lose hair as well. Why is chemotherapy-related hair loss temporary?
The doctors say it is because healthy cells are able to repair themselves. But, if that is true, then people should not even lose their hair, as the damaged hair cells would repair themselves before patients lost their hair.

Most chemotherapy drugs targets DNA replication in some way, which damages not only cancer cells but normal replicating cells as well. But normal cells are typically more resistant, and stand a better chance of survival. It is thought that this is because normal cells respond to DNA damage by "arresting" the cell cycle, and not dividing until the damage can be repaired. Cancer cells, in contrast, have lost these safety mechanisms, and will continue to divide despite having damaged DNA, which can cause serious problems and lead to cell death. This difference is exploited in chemotherapy.

There are of course large variations between individual cells. Some normal cells will die of chemotherapy, and some cancer cells will survive. But statistically, normal cells stand a better chance, and so chemotherapy dosage can be adjusted to a level where the drug effectively kills most cancer cells, but spares at least some normal cells. (Provided the cancer is sensitive to the particular drug used, of course; in many cases this strategy unfortunately does not work.)

After a course of chemotherapy, many normal proliferating cells will also be damaged, causing problems like hair loss and other unpleasant side effects. But given some time, normal cells will recover and repopulate hair follicles and other tissues.


Enzyme kinetics; what happens at the peak of the Gibbs energy graph? At the very peak, the energy is in a state of activation energy. Here, is the substrate just attaching to the enzyme, or is is substrate already breaking?

Enzymes are catalysts that lower a reactions activation energy (Ea), and thus increases the rate of the reaction. The diagram above is a Gibbs-Free energy landscape/pathway, where the top of the diagram is the transition state between the substrate and the product. Enzymes speed up chemical reactions by stabilising the transition state, and in effect, lowers the activation energy (Ea) required to transform the substrate into the product. The active site of enzymes are thus specifically 'designed' to be as energetically favourable as possible for the transition state.

To understand enzyme kinetics it could also be a good idea to look at (understand on a general level) the Arrhenius equation and reaction rate constants (k), to more completely understand what we mean by activation energy and reactions rate.
This whole topic is taught in basic biochemistry, and thus well described by many educational websites, all biochemistry text books, and even found in  educational youtube lectures (which is perfect for a basic understanding before you read more heavy theory). My earlier biology SE question Enzyme kinetics: recommended literature to grasp the concepts better also has some good book recommendations.
Following are also some webpages you can look at.
Khan Academy:

With the catalyst, the activation energy is lower than without. ...
That's because enzymes don't affect the free energy of the reactants
or products. Instead, enzymes lower the energy of the transition
state, an unstable state that products must pass through in order to
become reactant (...)

Chemistry LibreTexts: General transition state stabilisation is also a nice keyword that would give you a lot of information, e.g. from Chemistry LibreTexts:

Linus Pauling postulated long ago that the only thing that a catalyst
must do is bind the transition state more tightly than the substrate.
That this must be the case can be seen from the diagram (...)

Wikipedia: It could also be a good idea to generally read about catalysts, here from the wikipedia page where they use the classical example chymotrypsin and its oxyanion hole (active site that binds the substrate) that contains the Asp-His-Ser catalytic triad:

In the presence of chymotrypsin, (...), a nucleophile is used in the
form of the catalytic triad - Asp 102, His 57, Ser 195 side chains.
Moreover, the oxyanion hole, which consists of the backbone -NH-
groups of Gly 193 and Ser 195 of the enzyme, have the N-H groups
positioned in such a way that they will donate strong hydrogen bonds
to the substrate's C=O oxygen, given that the carbon atom is
tetrahedral as found in the transition state. This strains the bonds
of the trigonal planar C=O of the original substrate, helping the
reaction to proceed to the transition state. The hydrogen bonds also
stabilize the formal negative charge on the oxygen atoms. In this way,
the activation energy of the reaction is lowered and the rate of
reaction thus increases.


Why do biologists judge intellect based on brain size? I have seen many times, that scientists will say Species A is smarter than Species B due to a higher brain-to-body ratio.  I've even seen similar arguments made by comparing the sizes of specific regions of the brain.  For example, "Species A must have a more developed linguistic ability than Species B because it has a larger language center in its brain."

This doesn't make sense to me.  I don't think we can make these judgements because we don't know what "software" is being run in each brain.  I can run a merge sort algorithm on a weaker computer just as fast as a brute force sort on a stronger computer.  The raw computation ability of a computer doesn't necessarily correlate to how quickly it can solve problems.

What am I missing here?

Your are confusing yourself with your analogy, brains are not like computers. The complexity of the "software" a brain can have is determined by how many cells and therefore connections it can have. In particular flexible (learned) thinking as opposed to instinctual "programs." Brains that are flexible need more cells to allow for more possible connections. Computers are not great analogies for brains they are just the best we have. but to use them a brain is like a solid block of ram, yes a large mass is not necessarily fast but it Can do a a far larger variety of tasks, intelligence is not a measure of speed (flies react way way faster than humans) but generally a measure of how many things you can be computing at the same time. the human brain is basically built to model the entire worlds around us including the brains of other humans, which is many many tasks happening simultaneously. Which is one reason brain size can also be used to predict how social an organism is, (at least in non-kin selected social behavior) social interaction requires modeling many complex things. You also run into the problem with defining intelligence, which is problematic to say the least.

And as another poster has pointed out natural selection will quickly eliminate unused brain mass, (neurons are super expensive to maintain, our brain eats about a third of the calories we consume) so they are strongly optimized for weight, so portions of the brain that are larger should, in general, be doing more to offset the cost, otherwise they will be quickly shrunk. So a portion of the brain that is large must be being used, and must be offsetting the caloric cost, also note many the parts of the brain are fairly basal to the groups being compared like mammals so the so the chances of drastically different fundamental ways of operating are fairly slim.  so if the same portion of the brain is very different in size between two related organisms chances are it is becasue that portion is doing more or less. It is even easier to see with sensory processing portions of the brain, if the olfactory bulb of the brain is huge it has to be due to an increased function in the the sense of smell because it really doesn't do anything else and how the sense functions has not changed. this is backed up by observation the brains of animals with poor senses of smell (like cetaceans) have tiny olfactory bulbs while animals with excellent senses of smell (blood hounds)have huge ones. Intelligence is associated with enlargement and complexity only in specific portions of the brain, not the brain as a whole.

That said brain mass is only a rough estimation.  It more done to control for body mass (which effects brain mass directly) as things like how folded the brain is can drastically alter the complexity without changing the mass much. No one assumes brain size is a prefect predictor for intelligence.


Is the fixation rate always equal to the mutation rate for neutral alleles? Background

A classical result of population genetic is that the rate of fixation of netreual alleles is the mutation rate $\mu$. The reason is that each generation $PN_e\mu$ mutations enter the population, where $P$ is the ploidy number (e.g. 2 for diploids) and $N_e$ is the effective population size. The probability of each neutral mutation to reach fixation is simply its frequency $p$. When the mutation occur $p=\frac{1}{PN_e}$ and therefore the rate of fixation is:

$$\lambda = PN_e\mu \frac{1}{PN_e} = \mu$$

This result s typically very much used in phylogenetic, as assuming a constant mutation rate only, one can estimate the divergence time between two extant lineages.

The above is also explained on wiki>fixation_rate

Question

How robust is the result $\lambda = \mu$?

I understand that the result $\lambda=\mu$ is independent of the effective population size but is it also independent of..

changes in population size?
background selection?
selective sweep?
population structure?
selfing rate?
etc..

The answer to your headline question is that no, fixation rate is not always equal to the mutation rate for neutral alleles. For instance:

Fixation rates for neutral alleles are affected by changes in population size, given a constant mutation rate. In general, fixation rates are lower in growing populations (Waxman 2012).

This makes instinctive sense if you consider the single-generation fixation probability of a neutral allele which only exists at all but one copy in the population, i.e., the common allele (A) exists at 2N(t)-1 copies, whereas the less common allele (a) exists at 1 copy. To simplify, let's assume complete random mating. Under negative population growth (say N(t+1) = 0.9N(t)), there will be 0.9*(2N) places that the rare allele could possibly exist at t+1, and it has a 1/(2*N(t)) chance of filling each of them. Under positive population growth (say, N(t+1) = 1.1*N(t)), the rare allele could potentially occupy 1.1*(2N) places at t+1, but still has 1/(2*N(t)) chance of filling each of them. It is clear in this case that A has a reduced generation-wise likelihood of fixation under positive population growth than under negative population growth, simply because the rare allele has an increased chance of doggedly persisting. The finding applies to any allele near fixation.

If I have understood Kim and Stephan (2000) correctly, then overall fixation rates are also reduced by background selection. The main mechanism for this is that background selection purges linked neutral alleles, decreasing overall heterozygosity and thereby reducing the chance that a new, rare allele will become established. The same surely applies to selective sweeps, given linked neutral alleles.


Why would a human female have a sexual display despite male biased operational sex ratio? why would a human female have a sexual display despite male-biased operational sex ratio?

In human society there is a male-biased sex ratio, due to female child rearing, which results from anisogamy. Human females sometimes expend great amounts of energy and resources performing display acts and doing things to attempt to improve their apparent quality to males. Human males tend to be eager, despite a certain level of socially imposed monogamy, and many males will mate with a low quality female. Why do human women do sexual display behaviors, when there are so many eager males to choose from?

Sexual arms race.

There is a fine and internally consistent theory that this strategy by females evolved to oppose the strategy of infanticide by males.  Males of many species including primates and possibly humans can increase their own genetic fitness by killing infants that are not their own.  This frees up attention and physical resources of the female to instead have the baby of the infanticidal male.  Lions are famous for this.  But this is in opposition to the genetic fitness interest of the female, who just invested a bunch of efforts gestating and rearing an infant who was then killed.

My favorite writer on this is Sarah Hrdy.  From the Wikipedia article on this\

  This is where the idea of sexual counter-strategies comes into play.
  Hrdy theorized that by mating with as many males as possible,
  particularly males who are not part of the colony, mothers are able to
  successfully protect their young, as males were unlikely to kill an
  infant if there was the slightest chance that it might be their own.

This explains why women have the sexual displays referred to in the OP.  Other aspects of female human biology match.  Humans keep big breasts so they always look like they are lactating (compared to other animals) - to keep males guessing.  There is no external sign to indicate when a human is ovulating.  Females of other species are receptive and mate when they are ovulating - humans can mate any time.

A strategy of keep the guys guessing.  If one time he had sex with a given female, probably he shouldn't kill the kid.  Maybe it is his?

An interesting (& extremely arguable!) corollary to this is the premise that human culture in its entirety is the male countermeasure to this prehistoric female defense against infanticide: that male dominated culture is a method to ensure paternity.


Method of figuring out how much of a certain mRNA is present in a bacterium I am trying to develop a method for figuring out how much of a certain mRNA is present in a bacterium. This is what I have so far:

Perform a mRNA extraction
Using Electrophoresis, to isolate the wanted mRNA strain (based off of size)

Now, I am not sure how I would quantify the amount of mRNA. I was thinking of using nano drop to test concentration, but I am not sure if that will give a good enough answer. What other methods could I use to quantify the amount of mRNA in my sample?

You should be running qPCR to quantitate how much of a certain mRNA sequence is present in a sample. Remember that there are thousands to tens of thousands of different mRNA sequences present in an RNA prep, not to mention ribosomal RNAs, transfer RNAs, etc. If you then run your RNA prep out on a gel, you're just going to get a smear. Even if you cut out a portion of the gel that corresponds to the expected size of your mRNA of interest, there are going to be lots of other sequences present in that portion as well, so doing a gel purification step then measuring concentration with Nanodrop (which is quite accurate within its working range) won't tell you anything.

Quantitative real-time PCR (qPCR), on the other hand, when run with appropriate controls and standards, can give you a very good idea of approximately how many copies of your sequence of interest there are per nanogram of total RNA.


Book recommendation on mammal (or just primate) behaviour, especially in relation to child-rearing I have a growing frustration with the lows 'new-age' parenting is reaching, along with asininity of so much of our public schools' (and summer camps') philosophies and policies in relation to our kids. Whatever the implications, this has continually lead me to the thought of

  what the natural precedent is for how primates (or other mammals) raise their young, collectively or otherwise -- how they're guided, rewarded, chastised, and conditioned.

May someone please recommend a book that delves in to some of this? (Humans don't necessarily have to enter the picture, but something that does compare and contrast with the human condition would be a bonus.) (Preferably not a text book, but, by all means, please recommend those too.)

Suggested Reads:

Evolutionary Psychology

By Lance Workman, Will Reader

Evolution of Human Behavior: Primate Models

edited by Warren G. Kinzey

Social Behaviour of Children: A Cross Cultural Assessment

By Ralph E. S. Tanner


Genetics - Is this hybridization possible? Suppose you hybridize two plants - One has a red flower and a long stalk, the other has a pink flower and a short stalk. This resulted in these 4 type of plants, with ratio 1:1:1:1

Long stalk red flower
Long stalk pink flower
Medium stalk red flower
Medium stalk pink flower

What possible genotype could the parents have that would result this way?

Flower Color

A Heterozygous (Rp) x Homozygous recessive (pp) cross can produce the distribution:

         p      p

   R    Rp     Rp  = Red, Red

   p    pp     pp  = pink, pink

Stalk Length

To me, there appears to be another allele involved or a lack of allele, and definitely Co-Dominance. The only way I could think of a way to get the ratio of stalk lengths in the question after a few minutes thought is if one of the plants are missing a gene before the cross (akin to Turner Syndrome) - the example that follows puts the missing gene on the Short-stalked parents:

SS = Short
TT = Tall
ST = Medium
SX = Short
TX = Tall
X = Missing Gene / Nothing

         S      X

   T    ST      TX = Medium, Tall

   T    ST      TX = Medium, Tall

So ultimately the cross would look like this:

        Sp     Xp

   TR   STRp   TXRp = (#3), (#1)

   Tp   STpp   TXpp = (#4), (#2)


What is this tiny thing on the branch I noticed a tiny spot with weird shape on the shoot of a plant (Variegata), and there are many others on other branches. I wonder what is it, this is a cropped picture of it, Thank you!

This is a female of yet another scale insect (Coccoidea). We have discussed one recently.

I guess we can identify this one rather precisely as Ceroplastes sinensis or its close relative. Species of this group are of South American origin, but Ceroplastes sinensis has today an extremely broad distribution. So, if you found this plant ("Variegata" is a specific epithet, by the way: it would be of some help if you provided the generic name as well) in Europe or Asia it's likely sinensis itself.


Redundancy of the genetic code One particular codon codes only for one amino acid, but an amino acid can be coded for by several different codons. Now according to the genetic code, the codon UUU codes for the amino acid phenylalanine and UUA codes for leucine. But, according to the Wobble Hypothesis, the base on the third position of the codon and that on the anticodon need not be complementary (which helps explain why there are very few types of tRNA molecules, inspite of there being 61 codons). If this hypothesis is true, then we could have a phenylalanine placed in a position which was meant to be for leucine, and vice versa (since the codons coding for them differ only in their third base). The same holds true for pairs like aspartic acid & glutamic acid and serine & arginine. So how does translation of a particular mRNA molecule result in the right polypeptide sequence?

Wobble pairing is just a phenomenon and not a hard and fast rule. There are some justifications for why it should exist and that is why it is still called a hypothesis. And this statement is not true:"the base on the third position of the codon and that on the anticodon need not be complementary". The anticodon residue corresponding to the third residue of codon can be a promiscuous base which can pair with two or many different bases.  The tRNA for Phenylalanine has an anticodon - GAA which can pair with both UUU and UUC but not UUA.

So the statement of wobble hypothesis is that the first base of the anticodon (often is a modified/atypical nucleobase) can show promiscuity of binding.


Why do zoologists classify sponges as animals rather than plants? Sponges are fixed, do not move settle at one place, do not have a reproductive apparatus, respiratory apparatus, or organs, and live in marine environments. Why then zoologists consider that sponges are animals? In the past, zoologists considered them as plants and then considered them animals. What is the principe that zoologists have adopted to classify sponges are animals rather than plants?

Organisms are classified, not by their behavior, but by their phylogeny (evolutionary relationships). Sponges have unique and complex molecules in their intracellular matrix that developed in a common ancestor of sponges, and are shared with sponges and all other animals. These molecules include collagen, proteoglycans, integrin, and adhesive glycoproteins. These molecules are made by the cells, exist outside the cells, and fill the space between them.


Unknown animal - What could it be? It's the first time I use this website and I really need help
because I'm totally stuck

Now I'm in school, but I'm trying to prepare for the Olympics
During the preparation, I found the issue on the anatomy of the animals, but it's something new for me - I can't even determine what it is!

What kind of animal is it? Could you determine some, the most vital and major of highlighted points? If you can help me to determine the kind of it, i will be able to use more specific books to find out.

I will be very grateful for any help!

The animal is very suggestive for Dog whelk-like mollusc removed from its shell.

I try to mark the organs, do not rely on these marks as an absolut.

Testis
Renal vein
Gill
Mantle
Prostate
Osphradium

10 and others - digestive and reproductive systems, cannot mark precisely.

Digestive gland

source for comparing etc


Why does Hunger lead to the aggressive behavior? I have observed that frequently when people are hungry; they tend to get angry more easily on pointless issues. Does this mean that our fight or flight response is more active when a person is hungry? What is a possible reason for this? Is this phenomenon linked with our cell signaling pathways? If it is, then what would be the pathway that leads to the aggressive behavior?

To summarize the question:

When a person is hungry and they get angry, is it due to a cell signaling pathway? If so, what pathway?

Brain's main energy source is glucose. It uses about 20% of total glucose [1]. Brain hypoglycemia causes depressive-like behaviors in mice through adrenergic pathways [2].
When it comes to humans, here is a study that claims low glucose leads to increased aggression in married couples (see this too):

Self-control requires energy, part of which is provided by glucose. For 21 days, glucose levels were measured in 107 married couples. To measure aggressive impulses, each evening participants stuck between 0 and 51 pins into a voodoo doll that represented their spouse, depending how angry they were with their spouse. ... As expected, the lower the level of glucose in the blood, the greater number of pins participants stuck into the voodoo doll, and the higher intensity and longer duration of noise participants set for their spouse [3].

However, the conclusion is disputed:

Bushman et al.'s study does not demonstrate that fluctuations in blood glucose affect individuals' self-control abilities. As an important consequence, there is no reason to assume that giving couples a sugary “boost to their self-control energy” (p. 3) will reduce intimate partner violence. Because the glucose model of self-control lacks empirical foundation, it does not qualify as a framework for scientifically based intervention strategies [4].

What is sure, is that hypoglycemia activates sympathetic nervous system:

... the neurogenic symptoms of hypoglycemia are largely the result of sympathetic neural, rather than adrenomedullary, activation [5].
Hypoglycemia increases plasma levels of both epinephrine and norepinephrine. These catechols are released primarily from the adrenal medulla. However, it is well documented that hypoglycemic increases muscle sympathetic nerve activity, and that both alpha and beta adrenergic activity increase [6].

And this leads to behavioral changes (at least in animals):

Noradrenaline is involved in many different functions, which all are known to affect behaviour profoundly. ... Part of these effects may arise in indirect ways that are by no means specific to aggressive behaviour, however, they are functionally relevant to it. Other effects may affect brain mechanisms specifically involved in aggression. Hormonal catecholamines (adrenaline and noradrenaline) appear to be involved in metabolic preparations for the prospective fight; the sympathetic system ensures appropriate cardiovascular reaction, while the CNS noradrenergic system prepares the animal for the prospective fight. ... It appears that neurons bearing postsynaptic alpha2-adrenoceptors are responsible for the start and maintenance of aggression, while a situation-dependent fine-tuning is realised through neurons equipped with beta-adrenoceptors [7].

References:

Wikipedia contributors, "Human brain," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Human_brain&oldid=615456836 (accessed July 6, 2014).
Park MJ, Yoo SW, Choe BS, Dantzer R, Freund GG. Acute hypoglycemia causes depressive-like behaviors in mice. Metab. Clin. Exp. 2012 Feb;61(2):229-36. doi: 10.1016/j.metabol.2011.06.013. PubMed PMID: 21820138.
Bushman BJ, Dewall CN, Pond RS, Hanus MD. Low glucose relates to greater aggression in married couples. Proc. Natl. Acad. Sci. U.S.A. 2014 Apr 29;111(17):6254-7. doi: 10.1073/pnas.1400619111. PubMed PMID: 24733932.
Lange F and Kurzban R (2014) Sugar levels relate to aggression in couples without supporting the glucose model of self-control. Front. Psychol. 5:572. doi: 10.3389/fpsyg.2014.00572
DeRosa MA, Cryer PE. Hypoglycemia and the sympathoadrenal system: neurogenic symptoms are largely the result of sympathetic neural, rather than adrenomedullary, activation. Am. J. Physiol. Endocrinol. Metab. 2004 Jul;287(1):E32-41. doi: 10.1152/ajpendo.00539.2003. PubMed PMID: 14970007.
Hoffman RP. Sympathetic mechanisms of hypoglycemic counterregulation. Curr Diabetes Rev. 2007 Aug;3(3):185-93. PubMed PMID: 18220670.
Haller J, Makara GB, Kruk MR. Catecholaminergic involvement in the control of aggression: hormones, the peripheral sympathetic, and central noradrenergic systems. Neurosci Biobehav Rev. 1998;22(1):85-97. PubMed PMID: 9491941.


Does our eyeball increase in size as we grow? Does the size of the eye increase as we develop from the stage the complete eye first forms to infancy and then to adulthood ?

First of all, I should quote the sentence from the MOST reliable ophthalmology sourcing in the world - American Academy of Ophthalmology:

Section 11 - "Lens and Cataract"

"The equatorial diameter of the unfixed human lens measures 2 mm at 12 weeks and 6 mm at 35 weeks. Both the growth and the maturation of lenticular fibers continue throughout life." The antero-posterior dimensions of the lens enlarge from 3 mm at infancy to 6 and even more in adult years.

"The lens continues to grow throughout life (page 7 the same source)

Secondly, the growth of the eye continues after birth - at the beginning the growth is fast and later the growth is much slower but still - there is GROWTH of the eye after the birth.


What are the disadvantages of myelin The myelination of axons has plenty of advantages. It increases signal speed in axons, and thereby reduces reaction times. This is, of course, very good for the survival of the animal in question.
Most invertebrates do not have such a myelin coating. I know, that evolution does not just evolve features, because they are useful, but it seems to me, that invertebrates are entirely outclassed by vertebrates, because of how important reaction times are to an animals survival. So if such a trait is not impossible to evolve, it would most likely have evolved multiple times in different animals. If it was as advantagious as I imagine, invertebrates without myelin would have been outcompeted by now.
So there must be a significant disadvantage to having myelin coating.
Can you explain to me, what that is exactly?
Is it just the associated energy cost?

Many invertebrates possess myelin. It is a misconception that invertebrates lack myelin.

The world speed record for a traveling bioelectric signal is held by the myelinated axons in the abdomen of the Penaeus shrimp!

Please take a look at this website or this review to find a highly recommended comprehensive website about invertebrate myelin from about a decade ago. Here you will find a list of references and additional readings if you are so inclined.

As an additional note: invertebrates also possess and very often make use of ensheathing glial cells, such as is the case with sensory neurons in lepidopterans (moths and butterflies) as depicted below. I've labeled the sheathing cells in pink and red. Please understand that it is currently still unclear whether these cells secrete myelin, though they are thought in some way to insulate the neuron. What you are looking at is a hair-shaped sensillum that is innervated by one or several sensory neurons; these are the basic functional units for sensing movement, proprioception, smell and taste and they exist across all invertebrates, often lining the cuticle and across the entire body, e.g. on legs, on the antennae, in genital tracts, etc. They are best studied in hexapod insects.


Enzymatic Protein Deglycosylation of TCL I've done O- and N- linked enzymatic deglycosylation of purified and lyophilized proteins. Following some modifications to the manufacture's protocol, I had great results.

I now want a student to deglycosylate some total cell lysates (TCL) of infected cells.  Can he just Vacufuge/vac-spin Triton-X  TCL's and then proceed with the deglycosylation?  The first step is often resuspend in water.  I'm wondering if ether the salts would need be removed by dialysis, or if it doesn't matter, if he can start just from the lysate.

The antibodies we have for western detection are excellent, so that is unlikely to be a limiting factor.

So we went ahead and did this.  The efficiency was much lower, which you might expect, and dehydration did aid the process.  We found that taking raw lysates and running them through the linked protocol, had about ~20% the efficiency of conducting it on purified protein.  I assume the majority of the loss was due to reagents being expended on proteins that were not of interest.


What is the speed of blood in when flows through the fingertip? What is the average speed of blood as it flows through the index finger on the right hand?

This reference gives about 10-20cm/s in the major arteries and 5 cm/s in the major veins of the index finger in 5 male subjects, though there was a lot of variation.

The answer is going to be highly dependent on the level of the vasculature you are talking: through the largest artery or capillaries you will get different results, and different results in veins as well, and it will depend on many other physiological parameters.

Because it will vary greatly, even within individual vessels, you can't use the speed to estimate volume per time because the vasculature does not maintain a constant diameter; in fact, changes in vessel diameter are the major contributors to changes in flow volume.


conservation of C-peptide sequence in the guinea pig Where can I compare the C-peptide sequence of guinea pig with human or mouse?
I am also interested in finding whether the guinea pig has insulin 1 and 2 to know whether I could use an anti-C-peptide 1 and 2?

The NCBI Nucleotide database can be used to search for coding sequences (mRNA and translated protein) of genes. You need to enter the name of the gene (INS) or protein (insulin) and then species (use either the common name, "guinea pig" or the scientific name, "Cavla porcellus").

Filter the results to show you only mRNA coding sequences (sometimes abbreviated as "complete CDS"). These entries are annotated with the regions that account for the signal peptide, mature peptide(s) and prodomain(s). In your case, the full proinsulin is annotated as mature peptide and the B and A chains. The C peptide connects the A and B chains, located between the only two dibasic sites (R55R56 and K88R89).

Another useful database is the UniProt Protein Knowledge Base which presents similar information in a slightly more graphical presentation. Here is guinea pig insulin in this database.

If you happen to compile a whole list of C-peptide domains from other mammals, then you can use an alignment tool like ClustalOmega to align the peptide sequences to look for commonalities.

As for guinea pigs, there is only a single insulin gene (like most mammals). Only mice and rats have a two gene insulin system, Ins1 and Ins2. Generally speaking, there is poor conservation of the C peptide domain across mammals, in part because it only serves to link the A and B chains together to form the necessary disulfide bridges.

If you are wondering whether an anti-guinea pig antibody will cross react with another species' epitope, that information is listed on the antibody specification sheet under species cross-reactivity. Some antibodies are more cross-reactive than others, and you will need to refer to the specific manufacturer's information to be sure.

Wang S, Wei W, Zheng Y, Hou J, Dou Y, et al. (2012) The Role of Insulin C-Peptide in the Coevolution Analyses of the Insulin Signaling Pathway: A Hint for Its Functions. PLoS ONE 7(12): e52847. doi:10.1371/journal.pone.0052847 A note on this paper, I would not take the conclusions that C-peptide has a physiological role in intracellular or endocrine signalling because it is still quite a controversial issue. I used this article because it was open access and to demonstrate in Figure 1 the variability of the C-peptide domain across selected mammals.


Did spiders respond to light for building webs before artificial light was invented? I have noticed that during summer, beautiful spider colonies grow wherever a strong light is:

I'm wonder whether spiders evolved to seek naturally lighted areas where they build nests (before artificial lights) or if they always had the ability to seek places full of juicy insects - and in cities this ability just leads them to lights.

New Answer, following discussion in comments below.

Spiders are capable of choosing habitats based on the specific requirements of the species (reviewed by Riechert and Gillepsie 1986). Spiders move within and among suitable habitat for a number of reasons, including damage to existing webs, and life history changes that require new habitat types. They point out that spiders are probably choosing the proper habitat based on various cues from the habitat. How the spiders respond to the cues would have been shaped by natural selection. The specific cues used will vary among the different species of spiders but may include wind speed and direction, thermal regime (which affects dehydation foraging time), odor cues, density of competing spiders, and more. The many options are reviewed by Riechert and Gillepsie, which is freely available and not too filled with technical jargon.

Many species of spiders do select their habitat based on prey availability. Gillespie (1987)  lists a number of references. She also studied the long-jawed orb weaving spider, which lives along streams and rivers.  She found that this spider tends to build nests in open areas near water, which prevented dehydration, but the exact site chosen was determined by prey availability. Enders (1973) studied a different orb-weaving species. He found that the juveniles were most often in densely vegetation areas but that the adults were in more open areas at the edges of woods. He suggested that web site selection of adults is driven by light.

Heiling (1999) performed an interesting study on a nocturnal orb-web spider. The spider lives near the water so it will sometimes build its orb webs on the bridges crossing the water. She found that more spiders build their webs near the lights on one particular bridge compared to unlit parts of the bridge that were otherwise built the same. She found that there was more insect activity around the lighted area (no surprise there) and that the spiders that built near the lights caught more of those insects compared to the spiders that built away from the lights.

Perhaps the most interesting result is when she studied the behavior of these spiders in the lab. Spiders that were born and raised in the lab preferentially went to the artificial light source. These had never before been exposed to the artificial lights. She argued that the light-seeking ability of the orb-web spiders she studied is genetic.

These studies suggest that light may have functioned as a visual cue for web location long before humans lit up the night sky with house and street lights, at least for spiders that build webs in open areas. Spiders may identify open areas by light cues (lighter vs darker), perhaps along with other cues such as air movement and humidity. Lighter areas would presumably be more open and thus favorable to large numbers of flying insects. Natural selection would favor spiders that responded to light for web construction. Artificial lights may present a very strong visual cue that attracts spiders, as well as insects.

However, other cues such as olfactory cues (mentioned by Riechert and Gillepsie 1986) may attract spiders. If insect prey are found in high abundance in open areas or near artificial lights, then you would expect higher concentrations of chemical odors emitted by the insects, thus drawing more spiders.

Clearly, more studies similar to that of Heiling (1999) but across a broader range of web-building spiders are necessary to determine whether many web-building spiders are responding to light and if the response is genetically determined.

Citations

Enders, F. 1973. Selection of habitat by the spider Argiope aurantia Lucas (Araneidae). American Midland Naturalist 90: 47-55.

Gillepsie, R.G. 1987. The mechanism of habitat selection in the long-jawed orb-weaving spider Tetragnatha elongata (Araneae, Tetragnathidae). Journal of Arachnology 15: 81-90.

Heiling, A.M. 1999. Why do noctural orb-web spiders (Araneidae) search for light? Behavioral and Ecological Sociobiology 46: 43-49.

Riechert, S.E. and R.G. Gillespie. 1986. Habitat choice and utilization in web-building spiders. In: Spiders: Webs, Behavior, and Evolution (W.A. Shear, ed). Stanford University Press, California, USA.

Legacy answer

Spiders evolved long before street lights were invented. The oldest known spider fossil dates back to between 374-380 million years ago (Coddington and Levi 1991.  Street lighting of any type only goes back a few centuries. So, spiders were spinning webs long before humans evolved, and before we humans began lighting our streets and homes at night.

The spiders are simply taking advantage of the situation. The lights draw insects, the food for the spiders. Webs constructed near light sources may catch more insects than webs constructed away from lights.  Could this affect the current or future evolution of spiders? Perhaps. The spiders that build webs near the lights may get more food, which allows them to obtain more energy, and potentially produce more offspring. This would increase their fitness relative to spiders that do not build webs near lights, which could lead to evolutionary change occurring over the next several thousands of years. However, it may be that so many insects flying around the web end up damaging the web much more often than the spiders away from the lights, so the spiders near the light expend much more energy maintaining the web and removing insects they don't eat.  This is one extremely hypothetical example (of many; see comments) to illustrate the point. We can't actually predict what evolutionary changes might occur, or even if they will occur.

Some of the hypotheses stated in the comments below could be tested to determine whether natural selection is possibly occurring on spider species that build near lights, or if the observation is simply observation bias as noted by @Oreotrephes.


Why does applying pressure to a venipuncture site prevent haematoma? From what understand, when drawing blood, a phlebotomist puts pressure on the venipuncture site while withdrawing the needle to prevent a haematoma.

I'd like clarification;

How does this prevent a haematoma?
And why is it not necessary until withdrawal?
I assume it's not necessary, and counterproductive to apply pressure prior to withdrawal, besides complications or unusual procedures etc?

My best guess at a rough idea if what's happening is simply pressure restricts flow out of the vein, so slowing blood leaking into surrounding tissue, helping clotting? Or maybe it increases vein inner wall cell damage, releasing agents triggering faster clotting?

Thanks

Prevention of hematoma (as we say in the colonies) is by causing hemostasis within the vessel (here, a vein). Careful pressure during withdrawal, followed by firm pressure after withdrawal until primary hemostasis is achieved reduces the rate of hematoma formation.

Thorough mechanistic studies being absent, we can still confidently make some statements about what is likely happening, based on our knowledge of physics and hematology.

  Why is it not necessary until withdrawal?

Good venipuncture technique results in a single puncture of a vein that is no larger than the needle. With a single puncture, during the blood draw, all blood exiting the vessel enters the needle and the collection tube. This is why pressure is not necessary until withdrawal of the needle.  In fact, pressure at this point may cause the needle to damage the vessel at another site, allowing blood to exit into the tissue.

  How does pressure prevent a hematoma?

On withdrawal, external pressure to a punctured vessel that is greater than the internal pressure of that vessel will stop the flow of blood, preventing blood from entering the tissue.  At a standard venipuncture site, e.g., the antecubital vein, it takes approximately 2-10 minutes for primary hemostasis (in the absence of aspirin, or otherwise poisoned or disordered platelets). If you prevent flow out of the vessel during this period, you'll prevent formation of a hematoma. There are other mechanisms at work here that help, e.g., vasospasm, so you may still avoid a hematoma without pressure, but the rate of hematoma formation is higher when this isn't done

  Does it increase vein inner wall cell damage, releasing agents triggering faster clotting?

Possibly, but the primary mechanism is simple physics. Increase the pressure until a plug is formed, and you prevent blood from exiting the vessel into the tissues.


How do you derive steady-state conditions from the open-state differential equation of ion channels? My books describes this differential equation for the open state of an ion channel:

Where $k$ are the rate constants,

$k_1$ denotes a forward reaction

$k_{-1}$ denotes a reverse reaction in the Markov model

$O$ is the open state, $C$ is the closed state.

According the principle of mass conservation
 $ C + O = 1 $
where $ C $ denotes the closed state

"From here, it can simply shown that under steady-state conditions that $O_{\inf} = \frac{k_1}{k_1 + k_{-1}}$

and the relaxation time constant of the reaction $\tau = \frac{1}{k_1 + k_{-1}} $ "

My question is, how are $O_{\inf}$ and $\tau$ derived?

These are really math problems (algebra and basic calculus) rather than biology problems.

Oinf comes from solving algebraically the first equation you posted for steady state: i.e., when dO/dt = 0; just solve for O.

The time constant comes because this is a first-order exponential decay, which you get when you solve an equation (calculate an integral) of the form dO/dT = -lambda * O. The solution to that equation is an exponential decay of the form O(t) = O(0) * exp(-lambda*t)

tau is defined as 1/lambda and gives you the decay rate(relaxation time constant).


Link between pornography abstinence and hormone levels I have a question regarding abstinence from pornography, and also possibly celibacy, and how these two lifestyle choices affect hormone levels.

Trends such as No Fap have been emerging recently. An excerpt from their website states :

  No Fap held you to sharply increase your testosterone levels.

Is this true? From my research, I see no evidence to suggest this. Links to any studies would be appreciated. It is clear that people participating in No Fap have experienced psychological changes, but whether these changes are present on a hormonal level is an interesting proposition. If there is no hormonal change, what does this infer about what has happened to the minds of participants?

In the context of breaking a pleasure producing habit, such as masturbation (with or without pornography), testosterone plays very little part.

There are two factors at play here:

Habitualisation - the tendency for an orgasm to repeat behaviours that it has become accustomed to.
Addiction/Dopamine Response - it feels good so I'm going to carry on.

The first bullet point is obvious, if you've always done something, it's going to make you feel different if you stop. If generally in society it is perceived as being a bad thing (thus making you feel guilty for partaking, even subconsciously), stopping that habit will make you feel good. Especially once you've gotten over the relapse stage.

The second bullet point is more involved. Orgasms, along with the viewing of sexually stimulating material, release dopamine into the blood. Over time, the dopamine receptors in the brain become desensitised and require more and more dopamine to get the same buzz. This is exactly why drug addicts need bigger and bigger doses of their drug. Consequently, once one has stopped partaking in the dopamine producing behaviour the receptors gradually begin to return to normal levels of sensitivity. This results in a generally better mood and a potentially higher libido. To those that don't know the root cause, this increase in mood and libido may appear as though testosterone levels had increased, however, this is likely not the case.


Advantage of being deuterostome We know that most of the so called "Advanced" organisms are deuterostomes (i.e., development of gut starts from anus). Is there any evolutionary advantage of that? If not, why and how did it evolve?

I would speculate that there is no direct advantage imparted by the deuterostomic development process over that of protostomes with regards to the evolution of more complex species. Instead, I would guess that sometime after that split, a series of novel alleles arose in various genes which were eventually fixed and laid the groundwork for future increased complexity. Given the trait in question (increased organismal complexity), I would be certain that these alleles were in mostly unrelated genes and were selected for some other function (in other words, there is no gene encoding a protein that imparts organismal complexity; that trait is, by definition, a complex one!). Perhaps the genes involved in the deuterostome/protostome split were part of this groundwork, given their activity at the base of development, however it would be very difficult to know at this point.

I don't know why I didn't think about this before, but the more likely explanation for the difference in complexity between deuterostomes and protostomes is actually unrelated to that difference. Most of the complex deuterostomes that you're probably thinking of are vertebrates. Vertebrates went through a couple of rounds of genome doublings (tetraploidizations) during their early divergence. The extra copies of all the genes provided fertile ground for evolutionary novelties that seems to have led to some wonderfully complex creatures. It's still possible that the tissue groundwork laid out by the deuterostome developmental process somehow contributes to that complexity, but it would be rather indirect, I think.


Does the term 'protein expression' refer to the production of proteins only or also their regulation? I am learning about molecular biology and I have come across the term 'protein expression' in a research paper. I have searched the definition of this term online and on the Thermo Fisher Scientific website it states that "Protein expression refers to the way in which proteins are synthesized, modified and regulated in living organisms". However, on the National Cancer Institute website it states that protein expression "Refers to the production of proteins by cells".
I was wondering, between these two definitions, which one is more correct? Can protein expression also be used to refer to how proteins are regulated (e.g. can you use the term protein expression when discussing how one protein regulates the activity of another)? Any insights are appreciated.

There are no formal definitions accepted in science for ambiguous
phrases such “protein expression”.

If you wish to know what a particular author who uses such a shorthand phrase means you need to examine the context. If you wish to write scientific reports that are comprehensible to others you must express yourself precisely, defining any shorthand phrases that are necessary to avoid clumsiness.
In the context of the question, all that “protein expression” means to me is “expression of protein” — the synthesis of the protein from some entity that has the potential to do so. It a fundamental level that would be a gene or mRNA that encodes a protein (or proteins — that too is unclear), in which case this might be less ambiguously expressed as, for example:
“…expression of protein from gene X inthe plasmid construct Y…”
“…expression of proteins from mRNA in vitro…”
(I would generally retain the preposition. Be kind to it, poor little thing!)
To indicate that one was interested in the potential of tissues to synthesize proteins, then (with all due respect NCI, who are probably simplifying for the layman) one would need to write something like:
“…expression of protein in liver cells (after prolonged starvation etc.)…”
Under no circumstances would I imagine the term “expression” to imply or include “regulation” or “post-translational modification”. To illustrate why, consider the following example of a perfectly valid use in this sentence:
“A problem with expression of mammalian proteins in bacteria is that the required post-translational modification does not occur.”
If I wished to indicate I was also writing about regulation I would say so specifically:
“The expression of haemoglobin in reticulocytes and its regulation”
(and expect others to do so too.)
The fact that, as a professional molecular biologist, I disagree with @MattDMo, who is likewise a professional scientist, only demonstrates that the term is ambiguous. We would both like the context.


Does opponent process happen in the retina or in the brain? I understand that both the Trichromatic Process and the Opponent Process take place in human vision.
Trichromatic Process is widely accepted to happen in the retina,
however I heard differing accounts of where Opponent Process happens - in the retina or in the LGN.

Opponent process happens BOTH in the retina, and in the brain (Lateral Geniculate Nucleus).

Here is the excerpt from Vision Science: Photons to Phenomenology by Stephen E. Palmer:

In the brain (LGN):

  Physiological psychologist Russell De Valois (1965) and his colleagues (De Valois, Abramov, &
  Jacobs, 1966) measured responses in the LGN of macaque monkeys and
  discovered color-selective cells whose responses to wavelengths of
  light were incompatible with trichromatic theory but conformed roughly
  to the pattern predicted by Hering's opponent process theory. Some
  were excited by red light and inhibited by green (R+G- cells). Others responded in the opposite way,
  exciting to green and inhibiting to red (G+R- cells). In addition,
  they found cells that were excited by yellow and inhibited by blue
  (Y+B- cells) as well as ones showing the reverse pattern of responses
  (B+Y- cells). Together, these LGN cells can reasonably be interpreted
  as a neural implementation of Hering's opponent process theory.

In the retina:

  Further research has shown that these patterns of response are also
  present in the bipolar and ganglion cells of the retina. Output of R+G- opponent cells can be derived by combining excitatory
  input from the L cones and the inhibitory input from M cones,
  essentially computing the difference between the output of these two
  cone systems (L - M).


Trying to identify a beetle seen in Ontario, Canada...and its babies, or parasites? I'm trying to identify a beetle I took video of in July (around 2010) in the Muskoka region of Ontario, Canada. Attached below is a still frame.
I've done some googling and was thinking this was a Milkweed Leaf Beetle because of the orange and black stripes. This beetle however has an interestingly marked green head, and Milkweed Leaf Beetles appear to only have a black head.
I'm especially curious to know if the smaller insects on this beetles back are its young, or some type of parasite.

I've just posted the original video to youtube. It's right here: Beetle Video

Thanks to pascal's answer, I looked at the genus Nicrophorus and agree that this is some member of that genus. (The spelling Necrophorus has been used in the past but is now deprecated.)  The 60+ members of this genus are commonly known as burying beetles or sexton beetles from their behavior of burying dead small animals to serve as nourishment for their offspring.
However, instead of N. vespillo, I think the species might be N. tomentosus:
(Photo: Judy Gallagher via Wikimedia Commons)
The most distinguishing feature seems to be the green or gold hairs on the thorax as seen clearly in the large version of OP's photo. These hairs or setae Wikpedia mentions as separating N. tomentosus from other members of the genus.  A common name for the species is "gold-necked carrion beetle". Two other photos of this species are here and here.


What to look for when buying a light microscope? I am a science lover and want to buy a microscope to explore things around me. Like studying cell structures, microorganisms, blood and plants. It would be great if there is way to photograph slides. Just curious to know and explore things around me.

I want to know which features I should consider while buying it?

Well it depends on the application. First you have to determine what it is that you want to view under the microscope e.g. an organism such as Drosophila or you want to see microscope slides? In the first case you need to by a dissecting microscope, otherwise you need to by an upright light microscope with the appropriate objective lenses, again depending on the application. If you are viewing cells in a flask/dish/plate in a cell culture setting or if viewing a haemocytometer (although not necessarily in the case of haemocytometer), you need to buy an inverted light microscope with phase contrast since you wouldn't be able to view the cells very well with an upright microscope since the goal is to reduce the distance between the objective and the sample for a better view of the samples in cases of dishes or plates. Again the choice of equipment depends on the application. But as correctly said above you need to clarify what you mean in the question.


Simulating Cell differentiation I'm a computer programmer deeply interested in Biology.

I wish to write a computer simulation for cell differentiation. I understand there will be seemingly impossible challenges in doing this. But first I am looking for  answers to some basic questions.

I've learned that a zygote turns into 'embryonic stem cells' which results in the organism. How does the zygote turn into embryonic cells ?
What are the factors that determine the specialization of embryonic stem cells into more specialized types of cells and how does this transformation take place physically ?
Where is the data stored which acts as the "guide" for all these processes ? Is it stored in the DNA ? If it's stored in the DNA , is it known how the cells interpret the information in the DNA?
What are some textbooks I should be referring for this project ?

PS : Pardon my ignorance if these questions sound stupid, but I'm willing to commit time for learning anything needed to do this. Also , I understand all these questions cannot be answered in a few lines. Please provide references/pointers . Thanks !

Trying to answer this question in a few lines is a tedious task. Mostly I'm not sure that as of today we know all there is to know about it.

I'll try to give you some hints though.

The process is called embryogenesis. The zygote (or ovum) undergoes rapid mitotic divisions with no significant size growth which will lead to the development of an embryo. This process is called cleavage. Blastomeres are created during this process. On the third day - time may vary but not significantly - cleavage reaches the state of 16 cells. Cell divisions always occurs by parallel division (1 -> 2, 2 -> 4, 4 -> 8, 8 -> 16). Study the links I gave you and come back with more specific questions.
Again that's kind of impossible question to answer without explaining the entire process from fertilization to fetal development, because creation of tissues (cells) and organs happens along the way, not at once. However, it's documented.
Not sure.
Start with the wikipedia links and try to come back with more specific questions. I have a couple of text-books but I'm afraid they are not as detailed as you would want :-)

Good luck!


What direction is a sequence in databases written? In many databases, the DNA sequences for proteins are given as a string of a,t,g,c without specifying whether the starting is from 5' or from 3'.
Also it is not specified if it is the coding or non coding strand.

Is it because all the sequences are written from 5' to 3' of coding strand only?

Directionality

It is indeed the convention to represent nucleic acid sequences in the 5ʹ to 3ʹ direction.

This is implied in the IUPAC/IUB document on Abbreviations and Symbols for Nucleic Acids, Polynucleotides and their Constituents, although not stated explicitly — presumably because this was written in 1974, before the large nucleic acid databases were established.

Strand

In general you can assume nothing about which strand a particular feature is located on. You need to refer to the context or documentation for the particular database that you are using.

I prefer the term ‘sense strand’ to ‘coding strand’ as explained in another post. However this only has meaning in a restricted set of circumstances relating to mRNA, particularly considering cDNA copies of eukaryotic mRNAs. Only if the context indicates that this is the case can you assume the strand presented as a ‘sense strand’.

The problem arises from the fact that for all (or almost all) genomes, different genes are located on different strands of the DNA — the chromosome has no unique ‘sense strand’ or ‘coding strand’. Thus, for DNA sequences in a database such as Genbank, the following are possible:

The DNA sequence presented does not encode protein or structural RNA.
The DNA sequence presented contains genes on both strands.

An example of the latter is given in the Sample GenBank Record which should be consulted to understand the feature annotation in DNA sequence entries in GenBank. This 5028 bp yeast chromosome entry encodes two genes. The first, AXL2, is annotated:

 gene            687..3158
                 /gene="AXL2"

The second, REV7, is annotated:

 gene            complement(3300..4037)
                 /gene="REV7"

This indicates that, when presented in the 5ʹ to 3ʹ direction, the gene REV7 lies on the complement of the strand presented.


Why did we evolve to control our breath? I had this question in my mind and tried to think of why we would evolve to be able to control our breath. I remembered the Aquatic Ape Hypothesis, which makes a lot of sense and would explain it, though it is not a confirmed scientific theory (but that is another topic).
I also found this question, but it has not been answered properly. A Google search hasn't given me much either.

So my question is, what is the current scientific thinking on this topic (if there is one)?

edit I know that the Aquatic Ape Hypothesis is not a scientific theory. I did not ask anything about it, I only brought it up because it came up a lot when I was looking for an answer to my question. I do not want "maybe this is why it evolved", I was more interested in some creditable scientific paper or something similar.

From the abstract of MacLarnon & Hewitt, "The evolution of human speech: the role of enhanced breathing control", Am J Phys Anthropol. 1999 Jul;109(3):341-63:

  Evidence presented herein shows that modern humans and Neanderthals have an expanded thoracic vertebral canal compared with australopithecines and Homo ergaster, who had canals of the same relative size as extant nonhuman primates. Based on previously published analyses, these results demonstrate that there was an increase in thoracic innervation during human evolution. Possible explanations for this increase include postural control for bipedalism, increased difficulty of parturition, respiration for endurance running, an aquatic phase, and choking avoidance. These can all be ruled out, either because of their evolutionary timing, or because they are insufficiently demanding neurologically. The remaining possible functional cause is increased control of breathing for speech.


Expected time for a neutral allele to reach a frequency of $p_1$ when starting at frequency $p_0$ Kimura and Ohta (1968) showed that the expected time for a neutral allele to reach fixation (given that it will reach fixation) is

$$\bar t(p_0)=-4N\left(\frac{1-p_0}{p_0}\right)\ln(1-p_0),$$

where $p_0$ is the initial frequency and $N$ is the population size.

From their work, can we generalize this result to calculate the expected time to reach a frequency of $p_1$ (given that this frequency will be reached at some point), where $p_1$ is not necessarily equal to $1$?

Plain English Answer:

I have written a computer function which simulates neutral evolution to solve this problem. It's not an exact mathematical answer, but it is basically the same approach as Kimura and Ohta took in (the second half of) their paper, except that my computer is more powerful than their one, so I could get far more precise estimates by simulating more populations than they did.

Figure One is a lattice plot of the relationship between P0 and the expected time to reach P1, for different values of P1 (by column) and different population sizes (by row). It is clear that the same relationships between P0, P1 and expected time to get from P0 to P1 are seen in every population size, but with larger populations, you should expect a longer time to get from P0 to P1.

When P0 and P1 are close together, you generally expect a smaller time to get from P0 to P1 than when P0 and P1 are far apart. You might think of this as a rule like 'it takes a longer time to travel further'. Expected time taken to get from P0 to P1 is smaller when P0 and P1 are on the same side of 0.5 as each other and P1 is further from 0.5 than P0 is, than when P0 is further from 0.5 than P1 is. You might think of this as a rule like 'it is quicker to travel when you're closer to fixation or extinction, than when you're in the middle frequencies'.

Figure One: Expected time for a neutral allele to go from frequency P0 to frequency P1, given differences in P0, sub-plotted by P1 and population size. Modelled frequencies of P0 and P1 are 0.1, 0.3, 0.5, 0.7, and 0.9. Modelled population sizes are N = 10, N = 50, and N = 100. Each sub-plot represents one combination of P1 and population size, with P1 increasing from left to right, and population size increasing from bottom to top. All expectations are estimated from 10,000 simulated populations.

Some populations take longer than others to go from P0 to P1. Generally, most populations take a small number of generations to reach P1, and a smaller number take a long time – but a very few can take a very very long time.

I've attached my code, so if you know how to use R you can use it to estimate the expected time to get from P0 to P1 for any combination of P0, P1, and population size.

Additional details and assumptions for the technically inclined:

Relevant theory:

In a diploid, sexually-reproducing population of size $N$, there are $2N$ copies of a given locus. Each locus is occupied by some allele. All variation at our locus of interest is selectively neutral. For our purposes, we can consider that each locus is occupied either by our allele of interest ($A$), or another variant ($a$), ignoring variation in the 'other' alleles. The number of copies of $A$ in the population at the start of the process, $A | t=0$, is given by  $2N*P0$.

Let us assume that population size is constant ($Nt+1 = Nt$ for all $t$), and that mating is random. Let us further assume that generations are distinct. Let $t = 1$ be the first generation born, and so on.

The expected number of copies of $A$ at time $t+1$ then follows a binomial distribution:

$At+1$ is distributed $Binom(2N, At/(2N))$

Since we have a transition rule for $At → At+1$, it is a fairly simple matter to simulate populations undergoing this form of evolution. I have written the R function neutralFPT to carry out this simulation and estimate the proportion of all populations which reach $P1$ at some point in their history, the expected time for a neutral allele to reach $P1$ from $P0$, given that it will reach $P1$, and the distribution of lengths of time taken to reach $P1$, given that a population will reach $P1$. The script is given in the final section of this answer.

Probability densities of first-passage times:

Probability densities of first-passage times over plausible values of $P0$, $P1$, and $N$ follow a similar structure – unimodal near the left margin, with a long right-tail of longer first-passage times (Figure 2).

Figure 2: probabiltiy-densities of first-passage times from P0 to P1 under different values of P0, P1, and N. A: P0 = 0.5, P1 = 0.9, N = 50; B: P0 = 0.9, P1 = 0.5, N = 50; C: P0 = 0.5, P1 = 0.9, N = 500.

Function: neutralFPT, with examples of use.

 ## this function simulates the number of generations taken for a
 # neutral allele to go from a starting proportion, P0, to a final
 # proportion, P1, in a random population, given that it will at some
 # point reach P1. Allele frequencies are not modelled after the point
 # when P1 is reached.
## neutralFPT was generated in response to Stack Exchange user Remi.b, at
 # http://biology.stackexchange.com/questions/30812/expected-time-for-a-neutral-allele-to-reach-a-frequency-of-p-1-when-starting-a
## neutralFPT was written by Shane Baylis, 2015
 # for R version 3.2.2

neutralFPT <- function(P0, P1, N, niter) {

tOut <- c(rep(NaN, niter))
 # create a vector of blank t-values
statOut <- c(rep(NaN, niter))
 # create a vector of population status values (reached P1, or didn't)

if(P0 == P1) stop("P0 and P1 are set to the same value!")
if(P0 == 0 | P0 == 1) stop("P0 is set to zero or one, so its frequency
                           cannot change!")
if(P0 < 0 | P0 > 1) stop("P0 must be between zero and one")
if(P1 < 0 | P1 > 1) stop("P1 must be between zero and one")
## work out whether you're heading upwards or downwards
if(P1 > P0) { # i.e., our target is above us
    for (i in 1:niter) {
        NAllele <- round(2*(P0*N))
        Target <- round(2*(P1*N))
        t <- 0
        while (NAllele < Target && NAllele != 0 && NAllele != 2*N) {
            t <- t+1
            NAllele <- rbinom(1, 2*N, (NAllele/(2*N)))
        }
        if(NAllele >= Target) {
            statOut[i] <- 1 ## 1 indicates that P1 occurred
            tOut[i] <- t
        }else{
            statOut[i] <- 0
            tOut[i] <- Inf
        }
    }
}else{ ## i.e., our target is below us
    for (i in 1:niter) {
       NAllele <- round(2*(P0*N))
       Target <- round(2*(P1*N))
       t <- 0
       while (NAllele > Target && NAllele != 0 && NAllele != 2*N) {
           t <- t+1
           NAllele <- rbinom(1, 2*N, (NAllele/(2*N)))
       }
       if(NAllele <= Target) {
           statOut[i] <- 1 ## 1 indicates that P1 occurred
           tOut[i] <- t
       }else{
           statOut[i] <- 0
           tOut[i] <- Inf
       }
   }
}
successes <- sum(statOut) # the number of populations in which
                          # P1 was reached
propSuccesses <- successes / niter # the proportion of populations
                                   # in which P1 was reached
successTimes <- subset(tOut, statOut == 1)
expectedFPT <- mean(successTimes)
medianFPT <- median(successTimes)
outs <- list(successes=successes, propSuccesses=propSuccesses,
             successTimes=successTimes,expectedFPT=expectedFPT,
             medianFPT=medianFPT, trials=niter)
return(outs)
} # function close

## neutralFPT examples #################################################

sim <- neutralFPT(0.5, 0.9, 500, 10000)
sim$expectedFPT # Numeric. shows the expected (i.e., mean) first-passage
                # time from P0 to P1, in generations, given that a
                # population reached P1.
sim$medianFPT # Integer. Shows the median first-passage time from P0 to P1,
              # in generations, given that a population reached P1.
sim$propSuccesses # Integer. The proportion of simulated populations which
                  # reached P1. Other populations reached fixation
                  # or extinction of A without reaching P1.
sim$successTimes # Vector. The number of generations taken to reach P1,
                 # for all populations which reached P1.
hist(sim$successTimes, xlab="First passage time (generations)",
     main=paste(sim$successes, "successes from", sim$trials,
         "populations"))  ## histogram of first-passage times

PZero <- c(rep(c(0.1, 0.3, 0.5, 0.7, 0.9), 15))
POne <- c(rep(c(rep(0.1,5),rep(0.3,5),rep(0.5,5),rep(0.7,5),rep(0.9,5)),3))
PopSize <- c(rep(10,25),rep(50,25),rep(100,25))
FPTs <- c(rep(NaN, length(starts)))
testFrame <- data.frame(PZero, POne, PopSize, FPTs)
testFrame <- subset(testFrame, starts != ends)
for(s in 1:nrow(testFrame)) {
    sim <- with(testFrame, neutralFPT(PZero[s],POne[s],PopSize[s],10000))
    testFrame$FPTs[s] <- sim$expectedFPT
}  ## estimates expected first passage times from P0 to P1 for a variety
    # of values of P0, P1, and population size. Outputs the estimates to
    # a table called testFrame.

require(lattice)
with(testFrame, dotplot(FPTs~PZero|POne*PopSize,
   main="Expected First-Passage Time by P0, P1, and Population Size",
   xlab="starting frequency (P0)")) ## generates the lattice plot used as
                                     # Figure One.


Why is carbon dioxide produced in alcohol fermentation but not in lactic acid fermentation? From my understanding, alcohol fermentation takes place in yeast and lactate production takes place in humans.

These two pathways take place only when there is insufficient oxygen, because the other parts of metabolism (TCA cycle, ETC) can't take place as they happen in the mitochondria, which requires O2.

For alcohol fermentation, there is production of carbon dioxide while lactic acid fermentation does not produce carbon dioxide. CO2 is produced when there is an oxidation of one carbon molecule. So my main question is: since there is a lack of O2, how does yeast produces CO2 while humans do not?

Also, how does NAD+ recycle all the time when glycolysis is happening?

Thanks!!!

Glycolysis needs a steady supply of NAD+ to happen - this is the driver for the anaerobic oxidation to lactate and ethanol, although this is energetically much less favorable than the complete oxidation. But without oxygen there is no other way to keep the glycolysis active for at least some energy supply.

The difference is located in the enzymes available for the conversion of the pyruvate. This is the Lactate dehydrogenase in humans (and other mammals) and the Pyruvate decarboxylase in yeast. The first catalyzes the reaction from Pyruvate to Lactate, the second from Pyruvate to Acetaldehyde and CO2, the Acetaldehyde is subsequently converted to Ethanol. Only the second step produces NAD+.

See the illustration (from here) for further understanding:

The CO2 produced in this reaction does not occur due to oxidation, but is released from the decarboxylation of the Pyruvate. See the illustration below (from here):

In the production of lactate no decarboxylation is happening which allows the backreaction from lactate to pyruvate once enough oxygen is present again.


Is human zygote unicellular or multicellular Is the human zygote which is formed by fusion of sperm and egg a unicellular structure? Bcz at some places the 2 celled stage which is formed due to cleavage has been labelled as the zygote. So is the zygote 2 celled stage or the unicellular structure which is formed initially.

A zygote is produced when the gametes, a sperm and egg cell, combine with each other. This is unicellular. That one cell then duplicates into two cells, and then four cells. People don't really have a need to name this stage, but anyone would understand it if you just called it two-cell or four-cell within the context of zygotic development. As more cells are created (16+), the solid mass of undifferentiated cells is called a morula. This occurs around 3-5 days after fertilization. This then becomes a sort of hollow sphere of cells. These cells are now called blastomeres and the whole structure is called a blastula. When you hear a cell name with "blast" in it, it typically means it is a precursor to some other type of cell. In this case, those 16 or so cells are the precursor to a future human's entire body.


Are Richard Lynn's estimates of African IQ inherently innacurate on the basis that most Africans aren't mentally retarded? I've been looking at Richard Lynn's studies on average African IQ, and he seems to estimate really low IQs in the 60s range (e.g. http://www.sciencedirect.com/science/article/pii/S0160289609001275?via%3Dihub).

However, is this inherently wrong, as somebody who would score that low in a Western country would no doubt be mentally retarded (and this isn't the case for most African people)?

IQ is just a measure of how good you are at taking IQ tests, that's it. Those tests are usually culturally biased towards middle income first world citizens (among other things). Think of it this way, questions about mortgages, supermarkets, airplanes, or such thing presuppose the person being questions knows a reasonable amount about those things, this is not a reasonable assumption in many places around the world.

The classic "a train leave chicago at 10:00..." is a perfect example since the reader needs to know what a trains is, that chicago is a place, and what 10:00 means additionally they need to be familiar with reading exact measures of time and velocity, that they have already been taught basic math, are familiar with abstract questions, and that they are experienced readers, these are all fine assumptions for the New York suburbs but pretty bad ones for sub saharan subsistence farmers.

People who try to write the questions for said cultures often run into the reverse problem, we think of travels as a steady rate but to people who travel by boat know allowances need to be given for things like the speed the stream is moving, or the paddler taking breaks for lunch, information the writer may wrongfully assume or not understand. I recall a question about two people traveling along the same road that was consistently wrong because people in that culture thought is was proper for the faster person to slow down to match the slower for the safety of both (the norm in said society) so they constantly calculated their speed as the same, something the writers never anticipated.

There are millions of these differences across cultures and these cultural differences quickly snowball in to large differences when taking identical tests. So you are not seeing a real difference in intelligence just an artifact of culturally biased testing.


How are ions 'pumped' across a membrane during electron transport? A number of sites (including this one) that provide descriptions of photosynthesis state that high energy electrons 'pump' ions across a membrane. What is the actual 'pumping' mechanism? I've looked at Wikipedia and at a number of YouTube lectures/tutorials but so far have only found statements as to the where and when but not the how of this important process.

Short answer:
Electrons flow through membranes by floating through kind of channels made out of iron-sulfur clusters.

Long answer:
Let's take a look at the electron transport chain in the inner mitochodrial membrane. There is a proton gradient across the membrane building up a potential difference by pumping protons across the membrane as electeons flow through the respiratory chain. They (electrons) like to flow throught the respiratory chain because they can go from enzyme to enzyme each with a lower standart free energy. These enymes together form one big complex within the inner membrane with Fe-S clusters enabeling electrons to flow through the membrane by giving them a kind of a power stroke (see here).
This as an simplyfied answer on a example.


What causes leaves to be hydrophobic? In my garden, I'm growing broccoli. I was spraying it with water the other day, and I noticed that water bounced off the leaves. When I just misted it instead of a full-on spray, the water beads collected, but stayed as beads instead of spreading out. Some of them bounced off, but some accumulated. So what makes that happen? I know the leaf is hydrophobic, but I haven't found by searching Google if there's a coating of some type on the leaf or if it's something else that's making it hydrophobic.

This is due to presence of a hydrophobic chemical called as cutin present at the the aerial surfaces of plants.

  Cutin is one of two waxy polymers that are the main components of the plant cuticle, which covers all aerial surfaces of plants. The other major cuticle polymer is cutan, which is much more readily preserved in the fossil record,.[1] Cutin consists of omega hydroxy acids and their derivatives, which are interlinked via ester bonds, forming a polyester polymer of indeterminate size.

Source: https://en.wikipedia.org/wiki/Cutin


Does the cell have a mechanism to determine DNA sequence from protein? Something like a reverse genetic code.

"Reverse translation"

Translation is the process by which an mRNA is "translated" into a protein.

It is impossible to get the exact DNA sequence from the protein sequence because a large number different DNA strands could code for the exact same proteins. In other words, there is a loss of information in the translation process. See codon redundancy and I am not even talking about introns and UTR.

Now, it is theoretically possible to get one of the large number of possible DNA sequence from the protein sequence. I am not aware of any natural process that does this job.

"Reverse transcription"

Transcription is the process by which DNA is "transcribed" into a mRNA.

It is possible to get the DNA sequence from an mRNA. And it just so happen that such process does exist! A "reverse transcription" if you want. The enzyme that does this job is called reverse transcriptase. Reverse transcriptase is mainly found in retro-viruses but there are a number of non-retro viruses that have a reverse transcriptase.


Is it possible for a parasitic wasp to alter the behaviour of its host after emerging from it? I know that parasitic wasp larvae can live for a long time inside their live host (eg. caterpillar), but I always thought that they kill the host when they eventually get out of it. But I've seen a film, where it's shown that not only can a caterpillar survive the emergence of a wasp larva, but also the parasites infect the host with some kind of virus that changes the behaviour of the caterpillar to protect the wasp’s pupa. Is it possible and common among parasitic wasps? What species of wasps and viruses cause such effect?

The species of wasp in the video you link to is Cotesia glomerata. Furthermore, there is at least one other species, Glyptapanteles, which parasitizes other caterpillar species in the same way and induces the same behaviour in its host.

I'm not sure which virus it is.

http://www.newscientist.com/article/dn14053-zombie-caterpillars-controlled-by-voodoo-wasps.html?feedId=online-news_rss20

Is it possible? Of course, you have an example! Though, there is a small caveat. Some of the offspring sacrifice themselves to induce the behavioral change after the rest of the brood has emerged.

Is it common among parasitic wasps? No. While injecting offspring into host species is a common theme for parasitic wasps, and while there are a handful which somehow induce behavioral changes in the host animals - continuing the manipulation after leaving the host animal is extremely rare among parasites in general.


Hibernation in ectotherm and endotherm Both snake and weasel hibernate. Which of the following is correct?

  A. They will die when temperature decreases below the critical
  temperature.

  B. Weasel will die when temperature decreases below the critical
  temperature.

  C. Snake will die and weasel will wake up when the temperature
  decreases below the critical temperature.

  D. Weasel keeps low body temperature and slow heart rate during the
  entire period of hibernation.

I don't think any of them should die, they would have some adaptation to prevent that. So,is the answer (D) ?

What is the snake's adaptation in this situation ?

Weasels don't hibernate.  See http://icwdm.org/handbook/carnivor/Weasels.asp

Both will die when the temperature falls below a certain level.  The difference between snakes (ectotherms) and weasels (endotherms) is that the snake's body temperature will fluctuate more, depending on the surrounding temperature.