Why doesn't Clopyralid damage cool season lawn grasses?

Auxins are a class of phytohormones involved in plant growth and behavior. Auxinic herbicides, such as clopyralid, induce an overinduction of the auxin response in susceptible plants (kelly & Riechers, 2007). From the Kelly & Riechers 2007 article I quote:

  [Auxinic herbicides] cause various growth abnormalities in sensitive dicots, ranging from leaf epinasty and/or cupping and stem twisting, to thickening of stems and roots, and ultimately chlorosis and necrosis [...]. Lack of phytotoxicity in grasses has been attributed to several factors, including anatomical differences in vascular structure and differences in ability to metabolize the herbicide [...]

Hence, grasses seem to be protected due to anatomical and metabolic differences. Specifically, auxinic herbicides seem to kill dicots and spare monocots (Song, 2014). Song explains, and I quote:

  However, the underlying molecular mechanism of how auxinic herbicides selectively kill dicots and spare monocots is not understood yet [...]. Early research has
  proposed that the selectivity of auxinic herbicide is because of either limited translocation or rapid degradation of exogenous auxin, altered vascular anatomy, or altered perception of auxin in monocots [...] The difference in vascular tissue structure between dicots and monocots may contribute to the selectivity of auxinic herbicides. In monocot stems, the vascular tissues (the phloem and xylem) are scattered in bundles, and lack a vascular cambium; in dicot stems, the vascular tissues are formed in rings and possess a cambium.

So in all, the exact mechanism of specificity between monocots and dicots is unclear, but may be related to structural and/or metabolical (pharmacokinetical) and/or different pharmacodynamical differences between monocots and dicots in general. Dicots are susceptible to auxin herbicides, while grasses, being monocots, are protected.

The complexity of the auxin hormonal system (Song, 2014) may explain why differences exist between grass species, but this is speculative.

References
Kelly & Riechers, Pesticide Biochem Physiol 2007;89:1–11
Song, J Integr Plant Biol 2014; 56:106–13


The green region will definitely not make an miRNA: It is not a part of a stem loop. See typical miRNA structures from miRbase.

EDIT

Bulges can sometimes determine which strand is chosen as mature miRNA. However, this green region is also is unlikely to form miRNA because the stem is just 15bp.


How much of my ancestry comes from each grandparent?

On average, 25%, because you have 4 grandparents, and all of your genetic material came from them as a collective. Of course it's possible to be more genetically similar to a particular grandparent by random assortment of chromosomes, but the average will be 25%.

Genetic tests can't tell you what your ancestry is (companies implying this are probably misleading you on purpose). At best, they can tell you how correlated certain features of your genome are with people from a certain geography. Even people who are currently live in Eastern Europe will not test as "100% Eastern European." There is far too much mobility and breeding of populations across geography and far too much variation within populations.


Why does organ transplant work although it seems organ's motor neuron isn't connected to recipient's CNS

Capillaries only transport blood for short distances, and within an organ. The blood supply to/from a major organ is generally carried over a few major blood vessels (usually one artery, one vein). Splicing such larger blood vessels are what surgeons earn their pay to do.

In terms of nerves, most transplanted organs function fairly well without being connected to the CNS.


How two genomes adopt when cell goes to recipient's body from donor's body?

My previous answer was to the original question which focused on red blood cells which do not contain DNA. Now the question has been revised to focus on tissue transplantation, where the cells do contain foreign DNA, my amended answer deals with a couple of the points raised, but only briefly with the question of identification.

Incorporation of foreign DNA into the human genome

It is extremely unlikely that any of the DNA from the tissue of the donor would be incorporated into the DNA of the cells of the recipient. The donor cells would have to be broken (i.e. die) to release the DNA, which is most likely to be degraded in the process. Even if it survived it would then have to be taken up by the host cells, which is unlikely as there is no specific mechanism to allow this. However if foreign DNA somehow got to the nucleus it would need specific machinery to be incorporated into the host DNA. This involves enzymes making staggered cuts in the foreign and host DNA to allow annealing and enzymes to ligate the two together. We know about this sort of thing because retroviruses and viruses that can exist in the genome in a latent state have specific mechanisms for doing this. It is unlikely to happen just by chance.

Even if foreign DNA did get incorporated, it still has to be in an environment that allows it to be expressed (appropriate promoters). A more likely possibility is insertion in a position that affects a host gene. This can result in uncontrolled division of cells, i.e. they become cancerous, and is a problem that has been encountered using viruses of the type mentioned to insert genes into genomes in gene therapy.

Do the differences in the DNA of transplanted tissue matter?

Obviously differences in the DNA of different individuals has an effect on the individual. It is genetic differences that cause people to differ in size, shape, features, hair colour etc. Oh, and some are girls and some are boys. But when the tissues and organs have finished developing it probably doesn't matter if a piece of transplanted liver is from a male or female donor. The genetic programme that causes sexual differentiation and function isn't the one being expressed in the adult liver. The genes that are being expressed are those for the enzymes the liver needs to play its metabolic role (too numerous to list), and if they work, they work, even if the proteins differ in amino acid sequence by the odd amino acid that doesn’t impair its function.

The problem of identification by DNA

I would have thought that this would not really be a problem. After all, if you want to take a DNA sample from a person you can do it with hair roots, white blood cells or scrapings from mouth skin. You wouldn't need to resort to liver biopsies and the like.

Doctor of Philosophy

Finally, I can see there is a general philosophical concern over who one is if one has tissue or organs from another donor, but until we have brain transplantation I’m not going to worry about that. (And when that comes, I won’t be answering questions on the subject.)


Intracellular recordings of action potentials always show the same format with which you are familiar. There is polarisation which the stimulus reduces, a threshold is reached, there is a positive spike, then repolarisation, hyperpolarisation, a refractory period an a return to the baseline polarisation.

The term "negative spike" applies to extracellular recordings. These measure the potential between a point close to but outside the cell and a reference point. The inflow of cations into the cell causes a drop in extracellular potential, which appears as a negative spike in the recording.


I think we may be missing a piece from Darwin's original hypothesis.

An outline of the first 4 chapters of Origin of Species form the kernel of the Theory of Evolution:

1: Variation under Domestication
2: Variation under Nature
3: Struggle for Existence
4: Natural Selection

Really you can't reduce evolution to less than variations; competition (struggle) ; selection.  that's about as far as you can go and still call it evolution.  Even genetic algorithms which don't use living organisms at all have these 3 steps.

Most people don't have an issues with Variation any more.  At one time it was thought that individual variations were not important, but now most people understand that one water bug might have significant individual differences from other water bugs and its not just people who look at each other and marvel at individual traits.

The struggle for existence was difficult for people to accept at the time, but its simply that most living things don't make it.  Darwin had noticed that each spring that a typical bird pair might have 3-4 eggs in their nest but if you do the numbers it tells a story of how much of a struggle life can be even if we don't see it on a walk in the woods.  If all eggs reached maturity and reproduced, a single pair of birds would generate enough birds to cover England in about 40 years.  That's just a squeak under 3.5^40 without death from old age.

The struggle for existence hints how competitive Selection is.  In their breeding lifetime, to have a static population of birds, a breeding pair produces 2 breeding offspring out of perhaps 14 eggs lain.

It's a given that genes don't know that they have to do anything, but if they don't work well they will not be seen again. Their host dies from a developmental issue, falls and hurts itself doesn't display the right plumage, isn't fast enough to catch its food, is so slow that it gets eaten, its seed falls on soil it cannot germinate in, etc etc.

The list is endless as to the things that can go wrong in the wild and would cause an individual to be removed from the gene pool and they don't produce offspring. All of the important qualities that genes need to have is mysteriously embedded in what we call the environment - the earth, the air, the water the behavior of other living things decide whether most genes make it or not.

If you need any more evidence that intelligence has nothing to do with evolution, then look at human beings... not getting along well with other living things well now - is that smart?

An example of selection
Since it was requested, let me expand and give a very simple example of random selection that I've always liked (Disclaimer: maybe because I made it up as far as I know!).

Take a box of 100 coins.  We want all 100 coins to be heads up, but we can't individually flip any of the coins over: we can only shake the box.  Note that when we shake the box - nothing is thinking or acting consciously.  Genes do permute randomly and, for all reasonable approximations of infinity, infinitely, but they tend to stick around when something works.  This makes evolution seem unnaturally quick to respond.

Method 1: shake the box, looking every time. There are 2^100 combinations.  Getting terribly lucky we'd have to shake the box 2^97 times before we accidentally caught a box of all heads up coins.  That's random chance.

Method 2: if we remove the coins that are heads up every time we shake the box, we'll be shaking the box 8 times or so.  That is similar to a strong selection case in evolution: the coins which are heads up are like traits which have an advantage so they stay around.  Its striking how efficient this can be and how many tremendous changes can happen in a short time if there is selection and advantage.

Note that we have plenty of bad traits here (tails up); they show up all the time - with great frequency.  They just don't stick around because the struggle for existence is so challenging.

You can further get an idea of weaker selection if you can imagine that instead of the heads always staying heads, you have a little stickiness on the tails of the coins.  80% or 60 or 52% of the time these coins stick and stay as heads.  It still will not be long before you find that the coins are mostly heads.  10 20 or 30 shakes of the box rather than 8.

Where do new traits come from then?
So taking all this and thinking about how new traits like eyes which had not been
seen before, the same blind and random process applies.  It is better not to think of humans and human traits - we're the product of over a billion years of selection and evolution!   Think how primal traits at the bacterial level emerge.

Below is a picture of salt pools in the San Francisco Bay.  Evaporation increases the salt concentration in the pools and as they become inhospitable, halophilic (salt loving) bacteria take over.

The pools are colored because these bacteria have an ancient mechanism which allows them to harvest light to pump the salt out of their bodies and help create energy as well.  The light is harvested in one well documented case by a retinol molecule which absorbs blue light.  Retinols are a variation on vitamin A and must be quite ancient.

Yet a similar molecule, retinal, is used in human eyes as the light sensor there.  A similar protein holds those light sensing molecules in both human and halophile as well. While the structure of the eye and the nervous system that processes information into the brain all came later, you can see at one point the interaction with a bacterium with light became so useful that once it evolved, it has stayed in the gene pool since the days of bacteria to be the light sensor.  Vitamin A is the product of a biosynthetic pathway that very easily makes a variety of molecules.  The light sensing genes that used them evolved once, but variations on it sense light in our eyes today.


I would say that anisogamy, the different gametes such as sperm and eggs, is itself, a form of sexual dimorphism. However, you've since stipulated that you want to know the prevalence of sexual dimorphism beyond sex organs/gametes.

Sexual dimorphism occurs in a vast plethora of traits, at a variety of levels, and in almost all known dioecious species. It occurs even at the level of gene expression in, for example, mice, birds, mosquitoes, fruit flies, nematode worms, humans, and much more. Sexual dimorphism is prevalent and obvious in morphology such as peafowl, red deer, mallards, humans, guppies, fruit flies, horned flour beetles, and much more. It also occurs in physiology, behaviour, and life history traits (e.g. lifespan, ageing).

Simply put, sexual dimorphism is extremely common. It is hard to put a number on it, any studies of sexual dimorphism are likely to be focussed on sexually dimorphic traits (so a meta analysis will likely suffer from publication bias), and not all traits can be easily measured. However, gene expression is a good place to look because many traits (expression level of each gene is a trait) can be sampled simultaneously. This study found that 18% of genes were significantly sex-biased in any one tissue, while this suggests that at various developmental stages it was between approximately (based on table 1) 13% and 61%. Note again, there's not much literature which actually puts numbers on the general frequency and extent of sexual dimorphism. That is generally because, in the relevant research community, the gonads and gametes are included as sexual dimorphisms.*

Also, despite the frequency of sexual dimorphism, it is thought that the evolution of sexual dimorphism is severely constrained by the sexes working from the same genome (links: 1, 2, 3, 4, 5, 6, 7) and sexually antagonistic selection could readily favour further evolution of sexual dimorphism.

In terms of your report, I don't think you would need firm numbers or a citation; it's a well accepted fact that sexual dimorphism is common.* You would be more than fine to say something along the lines of:

  "Sexual dimorphism is extremely prevalent in nature, found in a
  range of taxa, and found in a variety of traits."

* These points are based on my experience, I did my phd thesis on the evolution of sexual dimorphism so I've read quite a substantial component of the relevant literature.


Requirement of energy for metabolic processes

The first reaction is catabolism. It does require some energy input in the beginning ("energy investment" of glycolysis) but ultimately leads to net energy release through "energy payoff" of glycolysis, citric acid cycle, and finally electron transport chain and oxidative phosphorylation.

The final result is oxidation of glucose, and reduction of oxygen.. At various points, electrons transfer to NAD+ and FAD. Then, the reduced forms of these 2 electron carriers (NADH & FADH2) go to the electron transport chain, where electrons transfer to oxygen at the end (reduction of oxygen). Meanwhile, protons were pumped into the intermembrane space to create the proton gradient that drives ATP synthesis.

The second reaction is anabolism. The Calvin Cycle requires energy from ATP and NADPH to create the necessary bonds to build up sugars.

In terms of bioenergetics, degradation of a molecule is exergonic. This is favorable if you think about the second law of thermodynamics: there is more entropy when there are multiple, separate sub-units, while there is more order when one molecule made up of those sub-units. Synthesis of a molecule is endergonic (requiring energy). It IS favorable in the sense that we get sugar to eat and burn in the future.

In summary:

Breaking down a molecule = catabolism = release energy from chemical bonds
Building up a molecule = anabolism = absorb energy to FORM chemical bonds (think of the resources needed to construct a new building)

Note my answer leaves out specific details about the processes, but I hope this is basic enough to answer your question!

Source: Lehninger Principles of Biology, David Nelson & Michael Cox


How do PrP mutations lead to prion disease?

If the amino acid sequence of both proteins is the same,
  what determines whether the synthesized protein will take the
  disease-causing tertiary structure or the normal one?

PrP-C and PrP-Sc do indeed have the same primary structure. However, they differ in secondary and tertiary structure. The protein can take more than one shape (conformation), where the likely conformation spaces taken by the protein are due to chemical and physical interactions. Many proteins can change their shape, often this is not well understood in detail. However, we know that the conformational space of some proteins allows for several, stable conformations of a single protein; the factors which stabilize it in a conformation or cause it to switch are difficult to understand in vivo.

PrP-Sc tends to accumulate in compact, protease-resistant aggregates. Circular dichroism shows that normal PrPC had 43% alpha helical and 3% beta sheet content, whereas PrPSc was only 30% alpha helix and 43% beta sheet. Although the exact 3D structure of PrPSc is not known, it has a higher proportion of β-sheet structure in place of the normal α-helix structure. The end of each fiber acts as a template onto which free protein molecules may attach, allowing the fiber to grow.

Prion proteins therefore propagate accumulation of more and more prion proteins.

  Is it due to post-translational modifications?

No.

  How do prions, which are void of nucleic acids,
  integrate into the genome of a newly infected host by reverse
  translation, and become a familial disease?

They do not enter the genome through reverse translation. The DNA sequence itself is mutated and the mutation drifts across generations for as long as it is being passed on through the germline.


why does translation occur more frequently than transcription?

The simple answer

Under the assumption that each mRNA molecule is translated at least once, by necessity translation will happen more often than transcription. This is because the only way to get a protein is to translate an mRNA.

In other words, as long as there are more protein molecules (translation products) than mRNA molecules in a cell, then the process of translation must have occurred more than transcription.

One estimate of the ratio of protein molecules to mRNA molecules given here is on the order of 100-1000 for E. coli. ("Under exponential growth at medium growth rate E. coli is known to contain about 3 million proteins and 3000 mRNA (BNID 100088, 100064). These constants imply that the protein to mRNA ratio is ≈1000, precisely in line with the estimate given above.". [MP note: the numbers quoted are actually closer to ~400K and ~1.4K, so this is not completely accurate; the source paper itself estimates between $10^2-10^4$ for the same ratio of protein to mRNA. Note though that the yeast cell estimates are even higher.]) So there are likely between 100 and 10,000 times as much translation as transcription events.

The speculative answer

From the perspective of "why" this is the case in terms of why cells might "choose" to have this ratio of proteins to mRNA (accepting that it must be true based on the ratio of protein to mRNA), we might say that proteins are useful and mRNA is not. Therefore, it's better to have more proteins (implied but not stated by @mgkrebbs comment). Or rather, mRNA is only useful because it gets you proteins, which are useful.

So it "makes sense" for cells to minimize the amount of energy put into generating mRNA and maximize energy put into making proteins. But that's human logic projected onto the cell, we can't know that that is the logic for why cells do what they do (or evolved to do, or whatever).


Sexual Differentiation in Monoecious plants with unisexual flowers

I will be able to answer only a part of the question.

Sex determination in Zea Mays

Initially, all the flowers in the plant are perfect, ie they have both the male and the female
flowers. This is followed by abortion of stamen or pistil resulting in unisexual flowers.

Which part of the flower undergoes abortion is determined according to the location of the flower. The florets in the tassel undergo the suppression of the pistil primordia resulting in staminate flowers, while the florets in the ear undergo suppression of stamen primordia resulting in female flowers.

The hormone Gibberelic Acid seems to play a role in sex determination.

Source and other useful links :

Sex determination in Plants by CC Ainsworth.
Sex chromsomes in flowering plants
Sex determination in monoecious and dioecious plants
The sex determination process in maize


Why is 70% ethanol preferred for aseptic techniques?

70% ethanol is the minimum concentration when used in a lab setting for aseptic technique. You don't want to go lower, because it will not kill the microorganisms you are trying to kill.

However the solution requires water to be effective at doing its job. The 30% water is necessary to provide sufficient polarity to the solution.

EDIT

  A rough indication of a solvent's polarity is a quantity called the dielectric constant. The dielectric constant is a measure of the solvent's ability to insulate opposite charges (or separate ions) from each other...

  Water is the most effective solvent for promoting ionization, but most organic compounds do not dissolve appreciably in water. They usually dissolve, however, in alcohols, and quite often mixed solvents are used. Methanol - water and ethanol - water are common mixed solvents for nucleophilic substitution reactions.

Dielectric Constants

Water - 80
Methanol - 33
Ethanol - 24

-Organic Chemistry 11E T.W. Graham Solomons et.al.

Note

Dexter's answer provides experimental evidence for why 70% ethanol is used. My answer is based on my experience and understanding and the concentration that I have used in the lab. I would add that 70% was likely chosen as a balance between cost and effectiveness. If you are a little off on mixing the solution from 95% Ethanol stock, then you are still at a bactericidal level, where as if you err at 60% concentration, you could start to let a few bacteria survive.

70% ethanol is still flammable and should be handled with care. The issue with ethanol greater than 98% pure is that the only way to distill the last 2% of water out is to add benzene, and benzene is a known carcinogen. There will always be trace amounts of benzene in 100% reagent grade ethanol.


Why do some protocols require prewarming a liquid medium before inoculating?

It's because E.coli BL21(DE3) are competent cells. The competent is the key here as the cells were chemically treated so the transfection can be performed by heat-shock with high efficiency.

This means these bacteria are quite fragile, due to the chemical treatment, and therefore are very sensitive to both mechanical and thermal shocks.

Pre-heating the media simply avoids damaging the cells and maximizes the growth rate.


Referring to the six stages in your diagram as Stage 1 through Stage 6, let's look at Stage 3: At that point, there is one bidirectional replication in progress, having made it about halfway around the chromosome. So it has 2 copies of the first half of the chromosome, and 1 copy of the rest, which is yet to be copied.  To get to this state of replication took 20 minutes.

Now the cell starts two new replications, one at "origin of replication" on each of the two copies of the first halves of partially replicated chromosome.  This is the state shown in Stage 4.  There are now three replications going on: the original, which is working on the last half of the chromosome, and two replications, which are working on (their own copy of) the first half of the chromosome.  All three replications will continue working for about 20 minutes.

We then get to Stage 5: the original replication has finished and the septum forms to separate the daughter cells.  The two replications started in stage 4 are continuing, and are about halfway down the chromosome.

The cells separate, and we are at Stage 6.  But stage 6 is the same state for each daughter cell as we had in Stage 3: a chromosomal replication that is halfway through (thus having one and a half copies).  It took 20 minutes to get from Stage 3 to Stage 6, where we are ready to double again.  During that 20 minutes, only one half of a chromosome had time to be copied, so it takes twice that (40 minutes) for replication of the whole chromosome.  This works out because the cell is doing three replications at once.


Effect of light intensity on the frequency of stomata

You are misunderstanding photoelecric effect.

Intensity of light does not have effect on maximal kinetic energy of individual ejected electrons. Maximal kinetic energy of ejected electron is determined by energy it can get from single photon which is in turn determined by frequency of light.

However, intensity of light definitely does have effect on number of ejected electrons. More incident photons (higher intensity of light) result in more ejected electrons (and higher measured electric current).

In photosynthesis number of utilized photons is more important than their energy. Photon either does have enough energy for separating the electron (e.g. red or blue light) or it does not (e.g. infrared light). If a photon with energy higher than needed (e.g. blue light) is captured then the excess energy dissipates to heat.


Betaine HCl (trimethylglycine) was present in over the counter "stomach acidifiers" but the US FDA says there is no evidence for its efficacy and has banned its use for this indication (source: US FDA) - it may be freely available elsewhere, I am unaware of the regulatory status in other jurisdictions.

There is no biological reason to expect the "HCl" portion for most drugs to have any substantial effect on stomach acid. Lots of drugs are packaged in an acidic form as "drug HCl" - this is usually because the acidic form of the drug is more soluble. Drug doses are commonly in the microgram to milligram range (though obviously this varies for different drugs) - at those concentrations, the stomach acid is much too concentrated to be affected by the small amount of acid added from the drug.

The catch with Betaine HCl is it looks like websites are advocating for taking several grams to provide enough HCl to affect stomach acid. I suspect that supplement makers suggesting these high doses is what led the FDA to ban the drug OTC in the first place. Although betaine is produced as part of normal metabolism, there are some side effects reported, mostly mild.

Note that anhydrous betaine is prescribed (and approved by US FDA) for homocystinuria, and used as a supplement to animal feed, but neither application is related to stomach acidification (and the anhydrous form is not acidified).

One recent study supports use of Betaine HCl with patients who are being treated with acid-suppressing drugs such as proton-pump inhibitors, to be given along with other drugs that require an acidic environment to function/be absorbed. However, it is important to note that this study was in fasted patients: they consumed nothing but a little water with the betaine HCl. In this circumstance, the little bit of HCl in a moderate to large dose of betaine was sufficient to lower stomach pH. However, the results likely would have been very different if the patients had eaten a recent meal.


Why are some bodily fluids more of an infection risk than others?

This is just about where the pathogens can be found that are dangerous to people.

Vomit is highly acidic and less accommodating to microbe growth. Similarly saliva has many immune components in it as well as digestive enzymes that keep most microorganisms down.

Urine and CSF are actually quite sterile as they come from environments that are highly filtered - the kidney is an osmotic processor that essentially is a molecular filter and does not allow cells to pass, the spine is highly insulated from the blood and other direct exposure to microorganisms.

Compare that with the 'dangerous' list and you have organs that are open to human pathogens.  Venerial disease like HPV is so common that what - about 1 in 5 people under a certain age carry it.  That is a pretty high expectation of a biohazard.  most infections and viruses are blood bourne - influenza, cold, as well as any bacterial infections.

Feces is always a dangerous thing to handle as the digestive tract is rich in nutrients and essentially directly open to external bacteria and fungi.  (and its not acidified like the stomach).  Also parasites like tape worms and other multicelled animals! yum!

Diarrhea is often caused by an infection of some sort, so its just more likely a hazard, but feces is always a place where you might find a pathogen.

This is not to say that the 'safe' list is totally safe.  Its just less likely to bear disease causing agents.


How reversible is decerebrate posturing caused by brain stem damage?

The decerebrate posturing is a sign of major brainstem dysfunction.

The reversibility of this state (which is considered to be very critical and hardly reversible) depends upon the origin of the brainstem dysfunction.

The primary brainstem dysfunction means that the brainstem was directly damaged (by a bullet) and there is no way that this can be quickly reversed. This is exactly the case here and there are no chances that the brainstem might recooperate with time.

The secondary brainstem dysfunction may be caused by cerebral edema and thereby dislocation of the brainstem towards foramen magnum, where the brainstem is coned. The coning of the brainstem can be reversible if the brain edema is treated quickly and effectively (by administration of diuretics in the intravenal catheter.

With brainstem regaining its normal functions the decerebral posture will eventuall resolve and depending upon the residual brain injury the recooperation of the brain function (and compensation) may be almost entire.


What are the units of Q10 (temperature sensitivity)?

Figure. A schematic diagram showing the effect of the temperature on the stability of an enzyme catalysed reaction. The curves show the percentage activity remaining as the incubation period increases. From the top they represent equal increases in the incubation temperature (50 °C, 55 °C, 60 °C, 65 °C and 70 °C).

The $Q_{10}$ is a unitless number, that summarizes the effect of raising temperature 10°C on the rate of a chemical reaction. A $Q_{10}$ of 2.0 suggests that raising the temperature of a system by 10 °C will effectively double the rate of the reaction. This value would be expected for most chemical reactions occurring within normal physiological temperatures.

Mathematically, $Q_{10}$ can be represented by the following expression:

$$Q_{10}=\left(\frac{k_2}{k_1}\right)^{\frac{10}{t_2-t_1}}$$

$t_2$ = higher temperature
$k_2$ = rate at $t_2$
$t_1$ = lower temperature
$k_1$ = rate at $t_1$

Usually the temperature difference is about 10 °C, then you can simplify the equation

$$Q_{10}=\left(\frac{k_1}{k_2}\right)^{\frac{10}{10}}=\frac{k_1}{k_2}$$

Edit: You can easily calculate $k$ form Arrhenius equation

$$k=Ae^{\frac{-\Delta G^*}{RT}}$$

where $k$ is the kinetic rate constant for the reaction, $A$ is the Arrhenius constant, also known as the frequency factor, $-\Delta G^*$ is the standard free energy of activation ($kJ/mol$) which depends on entropic and enthalpic factors, $R$ is the gas law constant and $T$ is the absolute temperature.


Is Zymase, A Complex of Enzymes? Which ones?

This is all correct it seems, but maybe the term is more of historical interest rather than current science.

Zymase is a term which is no longer in use in the scientific literature.  It seems to have disappeared in the 1950s.   The latest reference I can see is 1970s.

The reason seems to be that Zymase was purifiable from yeast with 19th century techniques.  The term was coined in 1897.  This is probably because in brewers yeast the Zymase components are either in a protein complex or contained within a compartment in the cell that could be separated from the rest of the organism.  Here's an early reference - german isn't so great.

The Zymase activity was shown to vary from one strain of yeast to another, which makes the discovery seem more a manifestation of the physiology of that one strain of yeast.

Later work showed that Zymase activity was organizable into a more universal set of genes which are conserved in all living things and called the 'citric acid cycle' or the Krebs Cycle. Krebs performed his work without reference to Zymase, where biochemicals were added to a culture and their transformation tracked. So, Zymase seems more like a historical footnote...

Wikipedias' entry sounds as if the extraction was not very pure - its called a 'press juice' so I think it would be difficult to describe exactly which specific enzymes were in Zymase.  I'd naively assume that nearly all the citric acid cycle enzymes would be involved in Zymase activity, where observed.

Many of the enzymes in the citric acid cycle form large complexes with themselves and other of the enzymes, which might be responsible for the original discovery of Zymase.


Is it possible to trace of the ancestry of a person by only using his/her genetic information?

In short, yes, it is possible. There are companies that sequence part of your genome and then can trace it back to your ancestors. All human family trees can be traced back to their African origin 200 000 years ago, but the companies that sequence your genes do not do that. For example, 23andMe sequences only 1 million of your base pairs (single nucleotide polymorphisms (SNPs)). They trace your most recent heritage, which could lead to Europe, Africa, or Asia. They can basically trace which part of your chromosomes (and thus your ancestry) came from your mom or your dad:

  Unlike the sex chromosomes and the mitochondrial DNA, which are inherited as blocks, the 22 biparental chromosomes, known as autosomes, are scrambled during reproduction. Through a process known as recombination, each parent pulls his or her paired set of 22 autosomes into chunks, then reassembles a new single set using half the material from each pair. The two single sets of chromomes from each parent are combined into a new paired set when a sperm fertilizes an egg.

You can read more about 23andMe here. There are other companies that are specialized in tracing your ancestry: Genetic Genealogy, DNA Tribes, and Heirlines.


What is the difference between a bacterial artificial chromosome (BAC) and a plasmid?

BACs are a special kind of plasmid, based on E. coli's F-plasmid:

The BAC is based on a plasmid in Escherichia coli that is termed the F (for fertility) plasmid. The F plasmid (or F factor) contains information that makes possible the process called conjugation . In conjugation, two Escherichia coli bacteria can physically connect and an exchange of DNA can occur.
A BAC contains the conjugation promoting genetic information as well as stretch of DNA that is destined for incorporation into the bacterium.

Source
It isn't necessarily larger than a plasmid.


I'm not really sure, but it seems like a cross section of intestinal villi / intestinal glands from the large intestine.

Here are some images:

Jubal Harshaw. Large intestine villi cross sectioned showing goblet cells_100X_CS0187 on ShutterStock
Jubal Harshaw. Large intestine villi shown in both longitudinal section and cross section on ShutterStock
Garry DeLong. Light micrograph of large intestine villi in cross section, showing goblet cells (Magnification x400) on Getty Images
Hill, M.A. (2014) Embryology Gastrointestinal Tract - Colon Histology. Retrieved September 24, 2014, from https://php.med.unsw.edu.au/embryology/index.php?title=Gastrointestinal_Tract_-_Colon_Histology

And this is one image from the last link:

  Crypts of Lieberkühn - (intestinal gland, intestinal crypt) [...] Transverse


The mechanical stability of a protein (I am assuming by strength you mean mechanical stability) depends greatly on the general context and there is no clear connection between alpha helix or beta-sheet content and stability. For example fibroin, one of the main components of spider silk and one of the strongest proteins known, consists mainly of beta sheets while keratin another very stable structural protein (the stuff hair and fingernails are made of) consists of four alpha helices alternating with three beta turns is believed to get most of its strength from hydrophobic interactions within its alpha helices. Also, actin and myosin muscle fibers consist mainly of alpha helices. The list goes on and on with no clear pattern which secondary structure forms more stable proteins.


First it is important to define what actually an error is. What you call misproduct is actually a right product for a different substrate. The enzyme has a low specificity; but you won't say hexokinase is error prone because it has wide substrate specificity. The question is — is specificity critical?

Coming to the example of DNA polymerase, you should note that DNA polymerase only adds a nucleotide to the DNA strand. Here the template DNA strand acts like a co-enzyme and it is the template DNA that provides specificity to the reaction. In this case the specificity is really critical and there are mechanisms that help in ensuring that.

Other enzymes also make errors and the probability of making errors depends on different parameters. Take the example of restriction enzymes that are supposed to cut at a specific site. When this specificity is lost we say that the enzyme is showing a "star activity" i.e. non-specific cleavage. This depends on different parameters such as buffer composition, enzyme concentration etc.

In general specificity is provided because of high affinity of binding towards one molecule compared to the other. These binding reactions are second order — a high affinity substrate will bind to the enzyme even at a low concentration, however if you increase the concentration of the low affinity substrate or the enzyme, then at some point the rate of binding may be significant enough to create a "wrong" product.

Sometimes there are cases where the enzyme can bind to a wrong substrate but cannot create a product. This is the typical case of a competitive inhibitor. It is also possible that a certain molecule is good at binding but the conversion rate is slower.

To conclude, these kinds of "errors" happen with many enzymes but it is very critical in case of DNA polymerization. You can get information on star activity of restriction enzymes (just google it).


Does a severed limb/finger experience pain after its separated?

Pain is a signal emitted from a nervous pain receptor cell (called a nociceptor) to the central nervous system (CNS, i.e. the brain). If I hurt myself causing a small cut in my finger, nociceptors around the cut will send the pain signal to the CNS, which in turn processes it and causes the physical feeling of pain in that region.

If a finger is severed, nociceptors just above the cut will be extremely active, interacting with the CNS and causing a lot of pain. On the other hand, nociceptors in the finger itself have nowhere to "push" the pain signal to, so in this sense they cannot measure any pain - there's not a CNS connected to the finger anymore that is able to process the signal emitted by any nociceptors in the finger.


Can you replace glucose with glycerol in cell media?

In most cases, it's not a good idea to replace glucose with glycerol in animal cell media. Animals do possess the ability to metabolize glycerol, via a pathway starting with the enzyme glycerol kinase. However, glycerol kinase is only expressed in certain cell types, such as liver cells and kidney cells.

References:

http://www.brenda-enzymes.org/enzyme.php?ecno=2.7.1.30
http://www.ncbi.nlm.nih.gov/books/NBK22591/


What is the function of nodes of Ranvier in axons?

Every signal rapidly fades out with distance if it is not amplified. So if the whole axon were covered with myelin, action potentials wouldn't reach their target. Each Ranvier node can be seen as an active signal repeater.


How could cyanobacteria survive the anaerobic conditions of ancient earth?

The first cyanobacteria were probably anaerobic, and this matter seems to be a hot topic of contemporary research. A recently published studya that performed a phylogenetic analysis of various Cyanobacteria genomes states:

  The most parsimonious inference from these data is that the last
  common ancestor of the Cyanobacteria did not use oxygen and that the
  three classes [of Cyanobacteria] acquired aerobic respiration independently after their
  divergence. The absence of aerobic respiration in ancestral
  Cyanobacteria suggests that abiotic oxygen sources on early Earth were
  insufficient to allow for its evolution until after the appearance of
  oxygen produced by photosynthesis.

Reference

a Soo, Rochelle M., et al. "On the origins of oxygenic photosynthesis and aerobic respiration in Cyanobacteria." Science 355.6332 (2017): 1436-1440 (http://web.gps.caltech.edu/~wfischer/pubs/Sooetal2017.pdf)


What happens in your brain when you receive information which causes you to bristle?

One thing is that we can't control the Goosebumps. It is an involuntary function caused by the Sympathetic Nervous System which is the major part of the Automatic Nervous System. The major function of the SNS is fight to flight response along with maintaining homeostasis in which case it internally will be alert maintaining body status from the background.

Before sending any response to target tissue when there is input to SNS it has to secrete neurotransmitters but before this to the sympatho-adrenal response of the body, as the preganglionic sympathetic fibers that end in the adrenal medulla (but also all other sympathetic fibers) secrete acetylcholine, which activates the great secretion of adrenaline (epinephrine) and to a lesser extent noradrenaline (norepinephrine) from it.

So whenever SNS senses (message flow is bidirectional) any stress it responds it in following action mentioned:

  At the synapses within the ganglia, preganglionic neurons release acetylcholine, a neurotransmitter that activates nicotinic acetylcholine receptors on postganglionic neurons. In response to this stimulus postganglionic neurons - with two important exceptions - release norepinephrine, which activates adrenergic receptors on the peripheral target tissues. The activation of target tissue receptors causes the effects associated with the sympathetic system.

Once the receptors receive the information then the response flows to the target tissue via neurons with the help of the neurotransmitters. To explain goosebumps technically:

  Properly known as piloerection, horripliation or pilomotor reflex, the bumps we get are stimulated by fear and cold and they are essentially just a temporary change in the skin. These stimulants cause a nerve discharge from the sympathetic nervous system (which is an involuntary portion of nerves we have) and the nerve discharges create muscle contractions called arrrectores pilorum that raise the hair follicles in our skin. It is the elevation of the hair that causes the Goosebumps.  The name Goosebumps actually comes from the fact that plucked goose feathers resemble the human hair follicles.

Goosebumps also occur when we listen to surprise songs, sad songs or some other kind of thrilling music. Researchers have tried to explain it and they call it "Frisson".
Check out this small video which talks about it. It is nice:

http://www.youtube.com/watch?v=-EA2eWZuYDs

Also refer to this website: Goosebumps


What is the difference between SNP and STR?

The solution is in the name!

SNP: single nucleotide polymorphism

The name tells us that it is a change that affect one single nucleotide and that there can be multiple of these (polymorphism could be rewritten as multiple forms)

From the SNP Wikipedia page:

  [A SNP] is a DNA sequence variation occurring when a single nucleotide — A, T, C or G — in the genome (or other shared sequence) differs between members of a biological species or paired chromosomes in a human.

So, for instance, if you take 8 individuals and sequence their gene XYZ, you may find, at a certain locus (=position) on the gene:

Individual 1: AAGGTG C AGCAGTC
Individual 2: AAGGTG T AGCAGTC
Individual 3: AAGGTG T AGCAGTC
Individual 4: AAGGTG T AGCAGTC
Individual 5: AAGGTG C AGCAGTC
Individual 6: AAGGTG C AGCAGTC
Individual 7: AAGGTG T AGCAGTC
Individual 8: AAGGTG T AGCAGTC

The position highlighted in bold is a SNP. In this case we only have either C or T (and this produces 2 different alleles for gene XYZ).

This page from University of Utah has a very clear animation on SNPs.

STR: short tandem repeat

These are short repeated sequences. They're in tandem, that is, one after the other.

STR consist of a few (2-6) nucleotides that are repeated several (5-100) times.
For instance this page from the University of Arizona gives the example of D7S280, one STR with sequence (GATA)n (that is, GATA repeated n times)

  1 aatttttgta ttttttttag agacggggtt tcaccatgtt ggtcaggctg actatggagt
 61 tattttaagg ttaatatata taaagggtat gatagaacac ttgtcatagt ttagaacgaa
121 ctaacgatag atagatagat agatagatag atagatagat agatagatag atagacagat
181 tgatagtttt tttttatctc actaaatagt ctatagtaaa catttaatta ccaatatttg
241 gtgcaattct gtcaatgagg ataaatgtgg aatcgttata attcttaaga atatatattc
301 cctctgagtt tttgatacct cagattttaa ggcc

In this case, variations between individuals reside in the number of times the sequence is repeated.


How are oranges in the US or anywhere made seedless?

Oranges and other fruits are generally not actively made seedless. Rather, seeds may fail to develop due to either lack of fertilization (pollination) or a natural tendency. The natural production of unfertilized and thus seedless fruit is called Parthenocarpy.

To quote the Scientific American article (3) mentioned by Oreotrephes:

  Fruit development normally begins when one or more egg cells in the
  ovular compartment of the flower are fertilized by sperm nuclei from
  pollen. In some plants, however, fruit develops without fertilization,
  a phenomenon known as parthenocarpy. Parthenocarpic fruit has
  advantages over seeded fruit: longer shelf life and greater consumer
  appeal.

  The most frequent reasons for lack of seed development are pollination
  failure, or nonfunctional eggs or sperm. In many plants,
  self-incompatibility genes limit successful fertilization to
  cross-pollination between genetically different male and female
  parents. This property is exploited by citrus farmers who grow
  seedless fruits, such as navel oranges and clementines. Because these
  cultivars are self-incompatible, they fail to set seed when they are
  planted in orchards of identical plants (clones). These plants have a
  high frequency of parthenocarpy, however, so they still produce fruit.

Parthenocarpic varieties may arise from a lack of pollinators. From the Wikipedia page on Parthenocarpy:

  Plants moved from one area of the world to another may not always be
  accompanied by their pollinating partner and the lack of pollinators
  has spurred human cultivation of parthenocarpic varieties. Some
  parthenocarpic varieties have been developed as genetically modified
  organisms.

To preserve the seedless trait, parthenocarpic trees can be propagated by grafting. It is possible that more kinds of seedless fruits will be engineered in the future (3):

  Plant biologists have learned that if the plant hormone auxin is
  produced early in ovule development, parthenocarpic fruit can grow on
  plants that do not usually exhibit this property. Thus, genetic
  engineering will most likely give consumers parthenocarpic fruit in
  many other species in the near future.


Can bats echolocation discern what insects they are preying on?

Yes, some bat species can distinguish the species of insects by echolocation. One of the better studied species is the greater horseshoe bat (Rhinolophus ferrumequinum).

Echolocating greater horseshoe bats (Rhinolophus ferrumequinum) detect insects by concentrating on the characteristic amplitude- and frequency modulation pattern fluttering insects impose on the returning echoes. This study shows that horseshoe bats can also further analyse insect echoes and thus recognize and categorize the kind of insect they are echolocating.
von der Emde, G. & Schnitzler, HU. J Comp Physiol A (1990) 167: 423. https://doi.org/10.1007/BF00192577

Further reading:

Hans-Ulrich Schnitzler, Elisabeth K. V. Kalko; Echolocation by Insect-Eating Bats: We define four distinct functional groups of bats and find differences in signal structure that correlate with the typical echolocation tasks faced by each group, BioScience, Volume 51, Issue 7, 1 July 2001, Pages 557–569, https://doi.org/10.1641/0006-3568(2001)051[0557:EBIEB]2.0.CO;2

Ulanovsky, N., & Moss, C. F. (2008). What the bat’s voice tells the bat’s brain. Proceedings of the National Academy of Sciences of the United States of America, 105(25), 8491–8498. http://doi.org/10.1073/pnas.0703550105

Roverud, R.C., Nitsche, V. & Neuweiler, G. J Comp Physiol A (1991) 168: 259. Discrimination of wingbeat motion by bats, correlated with echolocation sound pattern https://doi.org/10.1007/BF00218418

Hearing by Bats (edited by Richard R. Fay)


What metabolically happens when an egg fuses with the nucleus of a somatic cell

Somatic cell nuclear transfer is a method for creating a viable embryo from a somatic cell and egg cell. A somatic nucleus is inserted into an enucleated egg, where the somatic nucleus is reprogrammed by egg cytoplasmic factors to become a zygote (fertilized egg).
This requires the use of eggs in metaphase II of the cell cycle. Somatic cell nuclei must be in interphase (G0/G1). Interphase is the portion of the cell cycle that is not accompanied by observable changes under the microscope.
What determines the success rates of cloning
Oct-4 and other yamanaka factor expression is essential for somatic cell nuclear transfer success (Pay-wall).
Outlined here:

"...we now think that the oocyte cytoplasm might reprogramme the somatic cell nucleus too strongly, or that the somatic cell nucleus is more sensitive to oocyte reprogramming factors than are sperm cell nuclei."

Thus, Reprogramming and cloning success is unlikely to be influenced by somatic nucleus polymerases and RNA.


This is basic epidemiology. When medical professionals notice that a group of people with some characteristic in common, are being seen for a similar disease, they ask if there's a connection. In this case, several people in Wuhan were diagnosed with severe pneumonia, and the doctors noticed that they worked in the same location.

  Three adult patients presented with severe pneumonia and were admitted to a hospital in Wuhan on December 27, 2019. ... Her occupation was retailer in the seafood wholesale market. ... He had been a frequent visitor to the seafood wholesale market.

--A Novel Coronavirus from Patients with Pneumonia in China, 2019

You're more likely to follow up when the disease is unusual or severe, and when the connecting factor is unusual or suspicious. In this case, the severe pneumonia was presumably unexpected, and live animal markets always have potential for disease transmission.

(In fact, it's quite possible that the virus had been circulating in the region for weeks before this cluster was noticed, and that previous cases had not been surprising enough to trigger the research needed to identify a new virus; though it's also likely that the medical personnel in Wuhan had noticed that there were an usually high number of pneumonia cases and were already looking for a connection.)

See also the answers to How did scientists discover HIV?. Old-fashioned epidemiology is always critical.

The same article explains how the virus was sequenced:

  Bronchoalveolar-lavage fluid samples were collected in sterile cups to which virus transport medium was added. ... RNA extracted from bronchoalveolar-lavage fluid and culture supernatants was used as a template to clone and sequence the genome. We used a combination of Illumina sequencing and nanopore sequencing to characterize the virus genome.

And isolated:

  ... supernatant from bronchoalveolar-lavage fluid samples was inoculated onto the apical surface of the cell cultures. ...  After three passages, apical samples and human airway epithelial cells were prepared for transmission electron microscopy. ...

So briefly, they took patient samples, grew them on cultured cells, used electron microscopy to check the kind of virus. They sequenced fluid (not cells, since the virus would be secreted into the fluid, making it a relatively pure source of virus RNA) and then sequenced using a standard high-throughput sequencing approach; knowing the likely kind of virus would make this easier but isn't essential. There would have been lots of human RNA in the sequence, but it's easy to bioinformatically separate that out and limit your analysis to the viral sequences. The virus isolate was also not essential for the identification; knowing the sequence is the critical information today. But having a virus isolate certainly makes all the subsequent work much easier.

This is pretty standard modern molecular biology, not an esoteric skill.


Why does the intensity of an action potential once generated at the trigger zone remain undistured throught the axon?

Actually, it would be better to say that action potential does not travel but is regenerated anew in a sequence along the axon.

I would like to elaborate how this happens and why this is the reason why the action potential stays constant:

In rest state, there is an ion gradient across the membrane of each cell. This causes a small voltage between the outside and the inside of the membrane, the so called transmembrane potential.
Once the cell membrane becomes permeable for ions (normally this occurs when an ion channel is opened), the potential causes ions to flow across the membrane, the membrane becomes depolarized.

In the axon, the membrane contains so called voltage-gated ion channels. As soon as the membrane is depolarized at the trigger zone, the depolarization of the adjacent membrane causes voltage gated ion channels to open in that adjacent memrane as well, causing ions to flow also across the adjacent piece of membrane. This process continues in a wave along the whole membrane, this is what we call the action potential. Because the ion gradient across the membrane and the density of ion channels is constant along the whole axon, the amplitude of the action potential stays constant along the whole length of the axon.


Genetics is a very wide field of knowledge and many different areas of mathematics are being applied to genetics. Here is a probably not exhaustive list of the fields of mathematics that I have encountered in genetics (you will note that the elements of the list are not mutually exclusive)

diffusion equations
differential equations
markov processes
birth-death process
probability theory (a lot of it)
Bayesian probabilities
statistics
Math related to MCMC processes as well as HMC processes
Many fields of theoretical computer science are being applied and I guess theoretical computer science is a field of mathematics.
Graph theory
numerical integration
Analysis of dynamic systems

You say

set theory

Yes of course

group theory

Probably not so much or maybe I jsut don't really know what it is

ordinary and partial differential equations

I think pretty much any field of science applying mathematics will use differential equations.

But of course, not all geneticists are good mathematicians. Each geneticist specialize in a particular subfield. Some of them do a lot of mathematical modelling, others don't do any. Statistics and everything related to data science will always be useful though.


What kind of soil-dwelling flying insect is this?

Those look to me like fungus gnats. If you're looking to get rid of them, I've heard that putting a layer of rice hulls on top of the soil keeps them from reproducing. From what little I've read my identification doesn't go much deeper than superfamily, taxonomically, but it's a least a common name to work from.


How do I create a probe for in situ hybridization?

I dont understand what you mean by hydrolysis in this context.

The way to go about is:

Clone the DNA, that will give rise to the probe, downstream of T7 (or any other) promoter
Linearize this plasmid by digesting at (or ahead of) the 3' of cloning site
Set up an In-vitro Transcription reaction with T7 polymerase (or whatever corresponds to the promoter you used)
Precipitate and purify the RNA (you can use DNAseI to get rid of the DNA).
To check the RNA size: mix ~2$\mu$l of RNA (less or more depending on your yield) with equal volume of 2x RNA loading dye (contains formamide 95%, EDTA, SDS, and the dyes).
Heat at 85⁰C for 5min. Let it cool and run in 1% TAE/TBE-agarose gel (no need to make MOPS-Formaldehyde gel)
dsDNA ladder wont be very accurate but may be used for size estimation (if linear, the mobility of dsDNA and ssDNA/RNA wont be very different. Formamide treatment keeps the RNA linear). Use ssDNA or RNA ladder for better accuracy.

Btw.. the absorbance ratios mentioned are okay.. you don't need an RNA of supreme quality for this application (in fact this suffices for most experiments)


Is there a point in our life when ALL the atoms from our childhood's body get replaced?

Is there a point in our life when ALL the atoms from our childhood's body gets replaced?

No. There is no point where ALL atoms have been replaced.

This has been shown by tracing distinct carbon isotopes in DNA [which reflect upon atmospheric 14C at the year of their generation (which reflect the extent of human atom bomb testing)]; Bergmann et al. 2009, Science: Evidence for Cardiomyocyte Renewal in Humans.

for your other questions:

  Is that fact widely accepted by the scientific community?

The phrasing of Richard Dawkins, which you also list, uses "more similar" (rather than the absolute ALL). These words provide quite an accurate approximation to express that  most building blocks of cells undergo a constant renewal. The choice of words of Grand seems a bit unlucky, if read out of context.

  Are the processes that repair DNA damage operating only in damaged areas?

As a first approximation: yes. For instance the image below shows the localized detection of H2A.X histones upon damage at the DNA (red: H2A.X staining -> much stronger in treated cells which have high level of damage; blue: DNA staining)

  Or do they constantly "repair" also healthy areas leading to the constant replacement of the atoms

As one approximation this would be true, e.g.: proteostasis  (a process whose failure contributes to aging).

  that constitute the DNA?

Note that DNA molecules are vastly outnumbered by other molecules in a cell.

DNA is quite static (see above publication), although individual parts could possibly be repaired (see above image on H2A.X);

Also there might be a selective retainment of more "healthy" DNA strands with less mutations (the immortal strand hypothesis).


What color is the hemolymph of the Japanese giant hornet?

I was able to figure this out for myself by watching videos of the hornets being eaten by other insects. The answer is that the hemolymph is a pale yellow color, like I've heard other wasps and some bees have as well.


Termination  of  the synthesis of  the RNA molecule in bacteria is also signaled by  a sequence in the template  strand of the DNA molecule.
This sequence of nucleotide in the template strand is the RNA polymerase pause site. When the RNAP continues its transcription it reaches this site and pauses it's transcription activity over here. The longevity of this pause can also be affected by various factors like high $Mg^{2+}$ ions in some cases.

Meanwhile, rho factor which after binding to rut-site, continues it's translocation along the mRNA (supposing mRNA is synthesized here) in 5'-3' direction using its ATPase activity. The rho factor utilises this opportunity when RNAP has paused it's transcription activity at the RNAP pause site to reach this ternary transcription elongation complex. When it had reached this complex it starts it's ATP dependent helicase activity which separates the RNA-DNA hybrid helix, causing the release of the mRNA.


Genetic coding question, amino acid to base relationship

I don't think that's right.  I think 102 would make sense, because you want 99 nucleotides to code for 33 amino acids and more more triplet to code for stop.  Maybe the question writer didn't quite realize that the starting methionine counts as one of the 33 amino acids.


Why only female mammals have well developed mammary glands?

It comes down to investment in offspring. Males invest little in offspring only a little sperm whilst females have to develop the more expensive egg and the energy used through its development. In the mammalian line, this investment has increased in amount, initially through viviparity and then through the secretion of feeding fluids.

In species, such as humans, where there is a lasting pair bond and both male and female invest in rearing the young then I suppose there could be a situation where it makes equal sense for both males and females to nurse - although the cost of mammaries on other functions may favour specialisation anyway - but remember that, in many mammals, it is the mother alone that rears the offspring.

You may also find the answer to this question useful: Do any birds beside the family Columbidae (or any reptile or mammal) feed their young “Crop Milk”. What I hadn't realised is that there actually two species of bats where the male lactates.


Not an easy question, but I got some references about it.
Mouse LS cells are Fibroblasts growing in suspension culture, the paper in reference 1 has this paragraph in its Materials and Methods section:

This cell line seems to be in culture since the 1940s, as the reference to Sanford, Earle and Likely, 1948 suggests. Digging up this reference (number 2 below) tells a bit more about the isolation:

  The cells of this study were from Earle's strain
  L (6), which originated from normal, subcutaneous,
  connective tissue of an adult C311 strain
  mouse.

Reference 6 in the Sanford et al. paper is:

  EARLE, W. R.: Production of malignancy in vitro.
  IV. The mouse fibroblast cultures and changes
  seen in the living cells. J. Nat. Cancer Inst, 4:
  165-212 (1943).

which gives no further details. It is a methodic paper which analyzes the conditions necessary for cell culture - interesting on a historical point of view, since the techniques where developed at that time. The full PDF is linked in reference 3.

About the name I need to speculate a bit, but since the original cells where named "Strain L", and LS cells where derived from there to grow in suspension, it might translate into Strain L Suspension cells.

References:

The Uptake of Amino Acids by Mouse Cells (Strain LS) During Growth
In Batch Culture and Chemostat Culture: The Influence Of Cell Growth
Rate
The Growth in Vitro of Single Isolated Tissue Cells
Production of Malignancy in Vitro.


Skin

First, you are being misled by your wrong assumption that hippos have soft skin. Hippos have a 5 cm thick skin! For fun, here is a picture of a hippo skin.

They are big and pretty fast

An adult hippo weighs on average 1.5 and 1.3 tons for males and females respectively (with a record at 4.5 tons) and can run up to 30 km/h on land and up to 8 km/h in water (according to wikipedia > hippopotamus).

They have an aggressive nature

Hippos are aggressive animals (esp. males). Hippos kill about 500 people a year (against 1000 for crocodiles) according to this BBC article (but estimates seem to vary quite a bit from source to source).

They have serious teeth

Hippos have a big mouth with very long teeth. Lower canines are 50cm (19.7 inches) long (see wikipedia citing Estes 1991)!

Hippos live in herd

As suggested by @ChinmayKanchi in the comments, because hippos live in a herd, a crocodile that attacks a hippopotamus might have to deal with more than one enemy.

Videos

You can find here a video fight between a crocodile and a hippopotamus (thanks to @TahlaIrfan) and here is a video of a lion waking up a hippo. You will easily find other videos on YouTube.


You did right for most of the exercise, but you got confused on one of the (apparently) easiest things.
Try to reason in terms of chromosomes, and not merely of genotypes:
F1 inherit their chromosomes from two homozygous parents, so you know that they are AbC and aBc.
You can visualize the cross with the recessive homozygote as follows:
Ab C     ab c

-- -  X  -- -

aB c     ab c

The second parent will always pass abc, so in order to have an offspring with genotype aabbcc you only need that parent 1 passes abc.
Given that the parentals are Ab and aB and that RF is 12% (0.12), regarding the first two loci, the frequencies of the gametes are
Ab = 0.44
aB = 0.44
AB = 0.06
ab = 0.06

Including locus C, the frequency of the gamete abc is then simply 0.06 * 0.5 (because c is unlinked), and that corresponds to 3%.


All research on saliva tests I've found involve antibody detection which, as you suspected, can produce false negatives depending on the disease process or the presence of immune disfunction (such as due to AIDS). Thus, if you can isolate T. gondii gDNA from the saliva, a genetic assay may be more sensitive. However, Amato Neto et al. report:

  In 26 patients with AIDS, including six with tomographical evidence suggesting cerebral abscess caused by Toxoplasma gondii, no parasites were found in the saliva by the use of the mouse inoculation model. This trial [suggests] that the search for Toxoplasma gondii in the saliva is not an alternative method for the diagnosis of toxoplasmosis in patients with AIDS.

So perhaps the most difficult aspect of generating a gene based saliva test is actually isolating the parasite from the saliva. I was unable to find other isolation attempts, but my research was very brief.

As for which genes to detect, studies involving human blood samples have found that PCR amplification of B1 paralogs provides a sensitive and selective method for detecting T. gondii. Burg et al found that there are about 35 copies of the B1 gene in T. gondii and also state that:

  Because of its repetitive nature, the B1 gene is an attractive target for detecting T. gondii parasites through amplification of B1-specific DNA.

They were able to amplify and detect the gene from crude cell lysate as well as from purified DNA samples containing a 1:10 000 ratio of parasite to leukocyte. Furthermore, they could not detect the gene when assaying other organisms. Ho-Yen et al. later attempted PCR amplification of the same genes in human blood from patients with suspected toxoplasmosis and found that:

  PCR can be reliably used on human blood samples. For a reference laboratory, this is a valuable addition to its array of diagnostic tests, and provides a more rapid assay than animal culture.

Jones et al. compared detection of the B1 genes with P30 and 18S rRNA genes in aqueous humour. They were able to detect 50 fg of gDNA using the B1 assay, which is equivalent to a single parasite. They concluded that:

  The B1 PCR protocol appears to be the most sensitive protocol in the detection of T. gondii DNA and has been successful in identification of T. gondii DNA in ocular fluids and retinal sections.


Could someone recommend an introductory book on epidemiology?

There are two books I'd highly recommend for someone starting to dabble in Epidemiology. The first is Kenneth Rothman's Epidemiology: An Introduction, which I'm affectionately going to refer to as "Baby Rothman" from hereon out for reasons that will become obvious.

Baby Rothman is an excellent "getting your feet wet" book. It's simplistic, and clearly designed for someone with no background in Epidemiology, so it starts from things that, if you have a statistical background, you might find a bit dull. But it accomplishes two key tasks:

A basic treatment of the subject from a pre-eminent methodologist and advocate for the field that doesn't make some of the sloppy slight-of-hand mistakes many introductory books do.
An introduction to the "vocabulary" of Epidemiology as a field - what we call things, how we thing about effect estimates, etc.

The second book I would buy would be Modern Epidemiology: 3rd Edition by Rothman, Greenland and Lash. This is the definitive reference book for most epidemiological methods  currently used in the field. As I said on a related CrossValidated question, ME3 is the only epidemiology book that has always come with me, regardless of what project I'm doing, and which I have routinely found invaluable.

The other benefit of the book is that it's "platform agnostic". It's not going to try to teach you a statistics package - its going to teach you the science and philosophy of Epidemiology, the actual doing of the science, rather than the toolkit. Without that kind of methodological rigor, you can be a wizard at your language of choice and still do bad science.

If I were only going to buy one book, it would be ME3.


Are quaternary protein monomers unique to a particular protein complex?

If I understand the question correctly, you're thinking something along the lines of modular tertiary domains, but in a quaternary sense?

For a reversible interaction, heterotrimeric G proteins spring to mind. Once activated by a G protein coupled receptor (GPCR), the alpha subunit and the beta-gamma complex dissociate from the receptor and from each other. They can both go on to affect signaling by binding to various effector proteins, depending on the particular pathway in which they are involved, and their activities can be mediated by other proteins (e.g. the alpha subunit GTPase regulated by GAP proteins).

I spoke to my Protein Engineering professor, and she also directed me to a few examples, although I'm not sure they're quite what you're looking for in the strictest sense.

Cyclin-dependent kinases, as @Armatus mentioned, bind to all sorts of different cyclins. (I get the sense that subunits found in multiple protein complexes will probably be more common in signal cascades. I don't have any real data on that, but it makes sense that a signal protein could interact with two or more protein complexes and even have slightly different functions in each.)
Alcohol dehydrogenase (ADH) is an example of a protein with different quaternary structures between species. According to my professor, it occurs as a homodimer in mammals, but as a tetramer with some slightly different residues in budding yeast. I can't say whether the sequence changes are what affect the oligomerization, although my prof also mentioned "oligomerization domains" that could mediate protein-protein interactions.
She also directed me toward a slightly more interesting example (in my opinion), though, again, it's also more along the lines of oligomerization. Small heat shock proteins (sHSPs) undergo something called "dynamic subunit exchange" and can take on a wide variety of oligomeric architectures. Binding is transient, but it's still kind of neat. There's a review here: http://www.sciencedirect.com/science/article/pii/S0968000411001903. Figure 3 shows different oligomeric architectures from the one monomer.

It seems that pretty much any protein that interacts with two or more separate protein complexes could be considered an answer. Neither I nor my professor have managed to come up with an example of an irreversible assembly of common subunits, but she is of the opinion that, in all the different possible protein structures, there is probably at least one example of everything, no matter how outlandish it seems.


Why does an electric shock contract the muscle?

Nice Question! Lets first introduce ourselves to the topic i.e. Electrical Muscle Stimulation.

  Electrical muscle stimulation (EMS), also known as neuromuscular electrical stimulation (NMES) or electromyostimulation, is the elicitation of muscle contraction using electric impulses...The impulses mimic the action potential coming from the central nervous system, causing the muscles to contract.

Now, lets come to the main point. Its actually not about flow of electrons or ions, but the change in voltage that plays the pivotal role in muscle stimulation. See this:

  Crystallographic structural studies of a potassium channel have shown that, when a potential difference is introduced over the membrane, the associated electric field induces a conformational change in the potassium channel. The conformational change distorts the shape of the channel proteins sufficiently such that the cavity, or channel, opens to allow influx or efflux to occur across the membrane. This movement of ions down their concentration gradients subsequently generates an electric current sufficient to depolarize the cell membrane.

In short, when you touch a wire, you become a part of the circuit i.e. any 2 points on your hand (or your hand and foot, if you're barefeet) act as part of the circuit i.e. there is potential difference between them, which generates an electric field. This electric field causes the voltage-gated channels in neurons/muscles to open which, in turn, generates an action potential and causes the muscle to contract.

References:

Electrical Muscle Stimulation - Wikipedia
Voltage-gated Ion Channel - Wikipedia


No, it is not a "Deathstalker". The members of the Genus Leiurus are what are commonly referred to as the "Deathstalkers". I do not like using vernacular or common names as they can be too broad in iverlap for multiple species and so to avoid confusion and for clarity utilize Genus and where can be determined species and subspecies. The scorpion you found appears to be a member of the Genus Mesobuthus. While superficially similiar to Leiurus sp., the pedipalps in Mesobuthus are shorter and more bulbous...among several other features.
In 2018 there was a good paper on Mesobuthids in that region. A quick google scholar search should provide you sites for the paper to be viewed at.

Revision of the Mesobuthus caucasicus Complex from Central Asia, with Descriptions of Six New Species (Scorpiones: Buthidae)


They only tested 3 heat treatment regimens: 56C/30min, 60C/60min, 92C/15min (6 if you consider the "with BSA" and "without BSA", but only 3 combinations of temperature and time). They didn't measure the time required at certain temperatures to get to a certain level of inactivation. It seems they chose some of these particular protocols because they have been recommended in the past for other viruses.
They don't really have sensitive enough data to compare the 56C/30min to the 60C/60min or really enough to do any sort of statistical comparison whatsoever (as far as I can tell they only tested a single sample of each); yes, you can say they were roughly as effective, but it would be a leap to say 56C is the same as 60C.


Reducing the Proportion of Phenotype in Hardy Weinberg Population through Selection

The theory

You have to use the diploid selection equation (see here). Let $p$ be the the frequency of the recessive allele of interest, you get

$$p' = \frac{p^2 W_{aa} + p(1-p)W_{aA}}{\bar W}$$

, where

$$\bar W = p^2 W_{aa} + 2p(1-p)W_{aA} + (1-p)^2W_{AA}$$

You can simply iterate over with this equation. Do no forget to recompute $\bar W$ at each generation as the allele frequency changes, so does the mean fitness $\bar W$. Also, do not forget that we are looking for the generation where the frequency of sick individuals is lower than $0.05$, that is the generation where $p<\sqrt{0.05}$.

I don't think this recursion equation has any general solution unfortunately. This would mean that iteration is the only way to got.

The practice

I am a bit too lazy to compute everything by hand so here a short R code that will do the calculations for us.

frequencySickIndividuals = 0.16
p = sqrt(frequencyHomozygoteRecessiveMutants)
waa = 0.5
waA = 1
wAA = 1
for (generation in 0:10)
{
    frequencySickIndividuals = p^2
    cat(paste0("Generation ", generation, " frequency sick individuals = ", frequencySickIndividuals, "\n"))
    p = (p^2 * waa + p*(1-p)*waA) / (p^2*waa + 2*p*(1-p)*waA + (1-p)^2*wAA)
}

It outputs

Generation 0 frequency sick individuals = 0.16
Generation 1 frequency sick individuals = 0.120982986767486
Generation 2 frequency sick individuals = 0.0935350533786218
Generation 3 frequency sick individuals = 0.0738632061510922
Generation 4 frequency sick individuals = 0.0594638505565122
Generation 5 frequency sick individuals = 0.0487003101360286
Generation 6 frequency sick individuals = 0.0404940467744661
Generation 7 frequency sick individuals = 0.034123112395776
Generation 8 frequency sick individuals = 0.0290951856295452
Generation 9 frequency sick individuals = 0.0250680151553009
Generation 10 frequency sick individuals = 0.0217991643532054

So, it actually takes 5 generations to reach an allele frequency lower than $\sqrt{0.05}$.

Source of information on hardy-Weinberg problems

Note by the way, you might be interested in having a look at a tutorial on how to solve Hardy-Weinberg problems on the post Solving Hardy Weinberg problems.


Why marker and control are loaded in the beginning or ending lane of the gel?

No important reason. It is for esthetics, and also for ease of description in figure legends. One could argue that it might be confusing to have the markers or the control in the middle, but since the relative locations of these wells would be recorded, it does not matter where you put them. In publication, it would be easier to say, for example, "The control is in the far right lane, and the ladder is in the far left lane" Rather than saying, for example "Third from the left".


What are the minimum conditions required for "open-ended evolution"?

In principle open-ended evolution can occur with condition one violated. Because evolution is simply a change from one generation to the next (see answers here, here, and here), the is no requisite for a "non-trivial minimal criterion". Such a minimal criterion (e.g. survival to sexual maturuity) would imply that evolution is occurring by drift or selection, because being non-trivial implies that some members of the evolving population will fail to reproduce. However, evolution also occurs by mutation (and migration).

For example, we can have a population at generation $1$, and each individual within that population produces one offspring, present in the next generation. This means no variation in reproduction exists. If generation $2$, the offspring of generation $1$, carry new mutations then the characteristics of generation $1$ and $2$ can differ, and the descendant generation has evolved from the ancestral state. This can be seen in mutation accumulation lines as an example:

  "In a typical mutation accumulation experiment a single inbred and
  highly homozygous line is replicated.  Each of the replicated lines is
  maintained at a very small population size (usually brother sister
  mating, or in plants, selfing).  These lines are maintained for many
  generations.  During that time mutations accumulate, and the lines
  generally decline in fitness, and the variance among lines increases." - UVM Blog

So the answer to your question, these conditions are not necessarily met in nature. However, that doesn't mean evolution can't be open ended - the conditions outlined in the paper are flawed when trying to compare to nature. Evolution can occur when the "minimal criterion" is trivial (when all individuals are capable of meeting the criteria). The existence of a non-trivial MC only implies drift (e.g. some don't reach survival to sexual maturity by bad luck) or selection (e.g. some don't reach sexual maturity because they carry a genetic disease which kills them first). A trivial MC says that there is no drift or selection, but says nothing of mutation. I have since spoken with one of the authors who describes a non-trivial MC as the same thing:

  "Regarding nontriviality, it should at least be possible that some
  individuals do not meet the MC"

Note: I have only focussed on condition 1, because this condition is not necessarily met in nature, thus your question is answered (are all conditions satisfied in nature)


"...in a single generation of species, the most fit individuals tend to survive.".  This is not correct. "Fitness" in an evolutionary context refers to how many offspring you produce. It has nothing to do with how many pushups you can do.
Yes, individual organisms are selected, and the selection process involves differential survival (to reproduce).

"The process by which, over many generations, the genotypes that result in highest fitness tend to to be selected for. "

This is largely correct.

"The "things that are being selected" are the genes..."  Yes and no. It is individuals that are selected. They live or die, depending on their traits, which are encoded by genes.

Darwin noticed the extreme physical variations that humans could create in dogs, and pigeons by selective breeding. He thought that the same process could occur in nature, and termed it "Natural selection".


Capture recapture for only two visit assuming a open population model

In a classic closed population model, you can estimate population size with k=2 (where k is the number of events) but it's impossible to separate survival from recapture probability.

Seeing this formula you could expect to be able to estimate recapture probability dividing R by S but it would be an error since S = M*survival (ø) *probability of recapture (p) . Therefore it's imposible to separate p from ø when k<2.

Hope it helps !

Cheers


Can life forms exist from simple structures not made of the four bases?

So this question is difficult to answer because it has some errors in it, in that lifeforms being dependent on rarely used elements is a different question than lifeforms using different DNA bases, but I will answer both.

So for the question about whether or not organisms could exist that use DNA bases not found in organisms on earth, the answer is certainly yes.[1,2]

The above reference shows a very elegant example of completely synthetic DNA bases being incorporated into E Coli and propagated in culture without providing any noticeable negative effects. This provides strong support that life on Earth developed around the same 5 bases (CTGAU) by chance.

As for whether or not organisms could rely heavily on elements other than H,C,N,O, and P, this is certainly possible and evident already here on Earth. Extremophiles are a general class of organisms that have some pretty interesting properties to them. Some metabolize sulfur or metals, others live in really extreme temperatures or in areas of high radiation.

So really yes in both cases, life can really take numerous shapes and forms even when it seems completely impossible for them to do so.


Nice question! I've found a great article about fatty acid metabolism in heart muscle in healthy and disease conditions. As it is stated in this paper long chain fatty acids are utilized through beta-oxidation to meet the high energy need of continuous contraction. Beta-oxidation of long chain fatty acids produce far more ATPs than glucose. According to wikipedia:

For an even-numbered saturated fat (C2n), n - 1 oxidations are necessary, and the final process yields an additional acetyl CoA. In addition, two equivalents of ATP are lost during the activation of the fatty acid. Therefore, the total ATP yield can be stated as:
(n - 1) * 14 + 10 - 2 = total ATP or 14n-6 (alternatively)
For instance, the ATP yield of palmitate (C16, n = 8) is:
(8 - 1) * 14 + 10 - 2 = 106 ATP

While a single molecule of glucose produces 36 ATPs (under aerobic conditions)
Thus use of fatty acids (fats) in cardiac muscle is beneficial because of their higher energy concentration. Also it is noteworthy that this does not occur in isolation, so this is a response to contractile work and other competing energy sources (such as glucose, lactose etc). Also excessive uptake and beta-oxidation in disease conditions can even endanger cardiac functions. See details in the linked paper.


Is "Cloning" exact or almost similar to parent?

Biology is a lot messier than pure math, so if you insist on the same level of perfection and rigidity in definitions you are going to be very frustrated. You are correct that DNA replication is never 100% efficient, so "genetically similar" is probably a more literally accurate description of a clone.  However "genetically similar" is a very vague term, which we might apply (depending on context) to two cells from the same individual, clones and parents, two siblings, a child and a parent, two unrelated members of the same species, or even two members of the same biological kingdom. It is sometimes useful to distinguish different levels of similarity, even if we acknowledge that the boundaries of our definitions are fuzzy and arbitrary. Saying two individuals are "gentically identical" is really a short-hand for "in the context of the phenomena we're looking at, genetic differences are so small as to be irrelevant"

If you look at the level of DNA base pairs, it's estimated the average number of base pair differences between two humans is about 20 million or 0.6% of the 3.2 billion base pairs in the human reference genome. Clearly that 0.6% difference can generate a lot of variation in readily observable traits. During development some cells in an individual will undergo somatic mutations, so even two cells from the same individual may not be literally genetically identical. For the most part (excluding catastrophes like cancer), these differences will be in only a handful of bases out of the 3.2 billion, and won't cause any observable difference in the two cells. The difference between a parent and their clone will mostly be these somatic mutations, probably with some additional mutations caused by the cloning process.


Does the Michaelis-Menten equation take in account the non-enzyme formation of products?

In any study of enzyme kinetics it is essential to subtract all 'blank' rates and to ensure that the measured rate is due only to enzyme catalysis.

That is, in kinetic 'parlance', the velocity vs [enzyme concentration] should be linear and go through the origin.  Doubling the enzyme concentration should double the (enzymic) rate, and halving the enzyme concentration should halve the (enzymic) rate.

Failure to subtract blank rates may give rise to a variety of spurious kinetic effects such as downwardly-curving double-reciprocal plots (Lineweaver-Burk plots).

Downwardly-curving Lineweaver-Burk plots are diagnostic of negative co-operativity, but such a conclusion may be artefactual if blank rates are not subtracted.

A very good reference to this sort of this is Enzymes, (1979) by Dixon, M, Webb, E.C.,  Thorne, C.  & Tipton, K.F. (3rd Edn), Longmans,  in particular pp 461 - 462.


Spatiotemporal patterns in neural networks

Unfortunately, I haven't looked at this sort of literature for a long time, but here are some thoughts with which to start.

Your question is about "spatiotemporal patterns" of neural systems. One of the first things that comes to mind is neural oscillations (e.g. alpha waves). This is essentially looking for the presence of "frequency patterns" in the neural system. This has a huge amount of literature.

Another methodology that comes to mind is the graph-theoretic approach. In essence, functional or anatomical activity is used to build a graph, which can be analyzed for patterns (i.e. special properties of the graphs of neural systems that are, say, shared across species). One paper: Complex brain networks: graph theoretical analysis of structural and functional systems by
Bullmore and Sporns.

Separately, I might think about the neural correlations literature. Essentially, this is analyzing a neural population by examining the correlation structure of its members, and looking for patterns within it (i.e. that characterize the population code of the system). Two review papers: Neural correlations, population coding, and computation by Averbeck et al
and Measuring and interpreting neural correlations by Cohen and Kohn.
For a review on population codes, see Information processing with population codes by Pouget et al.
This notion is sort of orthogonal to the notion of sparse coding in neural networks, more prevalent in sensory perception.

Sorry if this is broad, but then again I feel the question is quite broad as well. If you have more specific questions, let me know.


Edit: Similar questions have been asked before: Textbook/lab manual for mammalian cell culture
Cell culture reagent/consumables suppliers can have good step by step recommendations for how to use their products. For example Thermo has some guidelines that you may find helpful. Specifically, cell culture maintenance would seem to be helpful.
These folks also have what superficially look like good resources.
Reviewing MC38 culture requirements is also always a good idea.
Good luck!


Why is it often the case that an enzyme is favorable only towards one direction of a reaction and not both directions?

Reactions have their set equilibrium constants, which are determined by the free energy of the reactants involved, and this cannot be changed by catalysts, including enzymes. Let's look at your example of peptide bond formation between two amino acids A and B,

A + B + energy $\leftrightharpoons$ H$_2$O + AB

This reaction might proceed in both directions; the rates of forward and reverse reactions depend on the free energy of A,B and the dipeptide AB, as well as how much "energy" we are talking about in the left-hand side. Let's ignore the energy term to start with, and just consider

A + B $\leftrightharpoons$ H$_2$O + AB

As it turns out, this reaction is not favorable: the $ \Delta G$ is about 10 kJ / mol (it depends a bit on which amino acids we're talking about). So this reaction goes in the reverse direction; dipeptides actually spontaneously decompose in water. But the rate of this reaction is very slow, because the peptide bond is quite stable. We say that there is an "energy barrier" between the substrates and products. Catalysts, including enzymes, lower this barrier, which increases the rate of reaction in both directions. It is physically impossible for enzymes to change the equilibrium by catalysis alone. There are plenty of enzymes that catalyze the above reaction, causing peptides to break down rapidly (peptidases, for example trypsin).

But enzymes don't just provide catalysis: an important role of enzymes is to couple two (or more) reactions together, so that a favorable one can drive an unfavorable one. This is how we obtain the "energy" term in the first reaction. The most common mechanism is to couple the unfavorable reaction to ATP hydrolysis,

ATP + H$_2$O $\leftrightharpoons$ ADP + P$_i$

which itself is highly favorable ($\Delta G$ around 40-50 kJ / mol). The coupled reaction is then

A + B + ATP + $\leftrightharpoons$ AB + ADP + P$_i$

which is now both favorable (due to ATP) and fast (due to catalysis). This is pretty much what ribosomes do (well, the actual mechanism is much more complex, but the principle is the same).

So, catalysts cannot change the equilibrium of a given reaction, but enzymes can couple reactions together to come up with something that is favorable. This is a central theme in biochemistry, allowing cells to drive reactions in the desired direction; but there is always a "price" to pay, often in the currency of ATP.


Indeed, many plants produce molecules which are poisonous to things that eat that plant (insect, mammal, bird) in the "hopes" of preventing that animal from eating them. In this sense, even eating the "right" fruit may be dangerous (if that individual plant happens to be an exceptionally vigorous producer of the poison, or because the eater is weakened for some other reason, or simply ate too much). I doubt insects would eat the wrong fruit that much, because evolution favors insects that can precisely recognize correct prey plants, at least in indigenous surroundings.

Indeed, many plant "flavors" that we humans enjoy (such as garlic and peppers) are likely such herbivore poisons that we happen to be immune to. In fact, almost every plant is actually poisonous - the question is, poisonous to which species?

Plant defense is a very actively researched topic these days, since it relates to things like agricultural efficiency and global food shortages (and besides, it's a very interesting phenomenon). Here is a review discussing what you ask about in more detail: http://www.plantphysiology.org/content/121/2/325.full

An addendum upon reading this question many months later: While evolution has perfected the ability of insects to recognize correct food, this has not been the case for man-made pesticides. I would guess that the caterpillar you saw is more likely to have eaten an artificial chemical (either pesticide or pollutant) than a "wrong fruit".


What is the benefit of using Gonoline-Euroline in combination?

Looking at your other question, I think there's some serious editing that needs to be done to clarify this question.

Still I think there is a quick and easy answer to your question.  Gonoline media makes an excellent transfer media.  If you are out in the field some where and want to take a swab for further analysis, you could easily choose a gonoline media for transport.  Then you would want to follow that up with some selective blood agars that might show a pathogenic species that you were looking for.  Thus to use gonoline media with any other medium, is merely to preserve your sample for plating on your diagnostic media/agar later.

Again, looking at your related question, I could only guess that you meant chocolate agar, because you might be hunting Neisseriaceae (which you should put in the question if you are).


What is the minimum water consumption for Arabidopsis and other plants?

The plant will intake water to keep constant internal water pressure to compensate for evapotranspiration. However, the evapotranspiration will not be a simple universal number.
The evapotranspiration rate strongly depends on temperature, air humidity, water tension inside the plant you want to keep (may it wilt?) and also the radiation received by the plant (PAR - photosynthetically active radiation) and also the air flow. In longer time that will also depend on the ventilation of air in your box. That means how fast water vapour escapes the air from your box and whether any of it condensates.
Also, how much water evaporates from the soil itself? That depends on soil properties, air temperature and also air flow.
A common model for evapotranspiration is by Jarvis and Stewart but is most often used for trees. You can read about interesting measurements of evapotranspiration at Whole plant open chamber to measure gas exchange on herbaceous plants.