Genetic information storage and the extent to which it controls appearance/structure So there are often articles about cloning from a small piece of tissue etc.

My question is (two actually) Is the Complete information about entire organism's structure stored (as in duplicated) all over the body? And is everything actually stored/based on DNA information, such as number of hairs you have including their position and texture. That would be a lot of information, I mean just taking hair as an example and its quantity and position, but there are also things about every aspect of structure, from bone composition, to position of organs, veins etc. None of it is random (ignoring mutations aspect) and all of it has to be "programmed" in initially. How can this be possible when the number of specifications is so huge?

The common phrase I've heard is "DNA isn't a blueprint, it's a recipe". More specifically, the nucleotides in DNA correspond to which proteins get made (coding DNA) and when and where (regulatory DNA). Just like a recipe doesn't specify the exact color of a cake or the position of each raisin, but does say "cook the cake for this long" (which will, in interaction with the heat of the oven, determine its color) or "put in this many raisins, at this general point in this general area", DNA doesn't contain the exact information of how you end up looking (hence why identical twins aren't really identical), but it does say how to make you how you are.

It also illustrates how much has to be "programmed" initially; how we are really needs to be understood as an interaction between DNA and the environment through the process of development, just as you can't completely understand a cake just from the recipe, you also need to know how chemistry and physics cause the things in the recipe to have the effects that they do. A lot of what goes on in development is cells growing, changing or dying depending on the chemical environment they're in, which includes what their neighboring cells are. The information in DNA basically consists of affecting that via what proteins get made when and where during development.

As for whether complete information about the entire organism's structure is stored all over the body, yes and no (but mostly yes). Yes, by default every cell in your body inherited its whole genome from the original zygote that started things, and you can indeed in theory clone a whole person from many random cells in the body. However in practice it depends on the cell: some cells lose their nucleus entirely, like red blood cells, so of course they don't contain the body's whole genome. Other cells could theoretically multiply or eliminate certain genes in a similar way as they specialize for the specific task they need to do, meaning they won't end up with the same genes as all the other cells in the body, but this isn't thought to be a common phenomenon especially in humans (cells will vary more in the expression pattern of their genes without necessarily changing the DNA sequence itself). This is also ignoring the ordinary mutation rates in DNA as the cell divides, which will yield differences between different cells of a given body even without that being a deliberate process. Hence cancer !

Some references on the possible variations of DNA in somatic cells (i.e. not ova or sperm)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3497787/

  It is commonly assumed that all healthy cells that arise from the same zygote possess the same genomic content, with a few known exceptions in the immune system and germ line. However, a growing body of evidence shows that genomic variation exists between differentiated tissues.

Elimination of actual DNA in nematodes and lampreys :

https://www.ncbi.nlm.nih.gov/pubmed/23123092

https://academic.oup.com/mbe/article-abstract/33/9/2337/2579241/Characterization-of-Somatically-Eliminated-Genes?redirectedFrom=fulltext

Quote from the first abstract:

  Chromatin diminution is the programmed elimination of specific DNA sequences during development. It occurs in diverse species, but the function(s) of diminution and the specificity of sequence loss remain largely unknown.

I have found no mention of it happening in humans however.


Are these birch or aspen trees? I was just wondering if anybody could help me identify the trees in this image? I am confused as to whether they are aspen or birch, a mix of the two, or whether the brown/reddish trees are some other species I don't know about? Thanks!

Turns out this is harder than it seems from just the picture...

The three candidates I think one could most argue for are:

Quaking Aspen (Populus tremuloides)
Paper Birch (Betula papyrifera)
Grey Birch (Betula populifolia)

Here is a picture of Populus tremuloides from the USDA:

Notice the smoothness of the above Aspen bark (identical to that of the picture in the OP's question). Now compare it to the peely nature of typical birch bark (here pictured B. papyrifera or paper birch):

Though not all birch species have peely bark: (my emphasis below)

Grey birch (Betula populifolia) typically remains fairly smooth. From Viginia Tech's tree guide:

  Bark: Reddish brown with numerous lighter lenticels on very young stems, later turning gray to white and very chalky; remains smooth and generally does not peel.

B. pendula (European white birch) bark is also described as being smooth and only somewhat peely. From Virginia Tech:

  Bark: Reddish brown with light lenticels when very young, later turning white, generally smooth but does peel a bit; the base of the tree develops thick bark which splits into narrow, vertical furrows which are nearly black.

However, the branches in the OP's picture are not drooping as is also common for B. pendula (AKA the European weeping birch). So this is not our tree!

Also, some sources describe paper birch as simply being smooth (vs. emphasizing the peeliness). See here for an example.

Here are images of European white birch (left) and gray birch (right) :

But Gray birch remains smooth, even at the base of the tree (though see here)...

Pay attention to the bottom of the trees in the OP's picture. The bark at the base of the trees is becoming furrowed:

Zoomed in OP picture:

This base furrowing is a characteristic of P. tremuloides:

According to the Virginia Tech Tree Guide (my emphasis):

  Bark: At first smooth, creamy yellowish-white to very light green; later developing thick furrows and becoming dark, especially near the base.

And according to The Sibley Guide to Trees  (my emphasis):

  Bark color from white to greenish, grayish, or bronze. Bark smooth, pale with dark scars that persist for many years; base of trunk becomes coarsely ridged grey on old trunks.

And from the NDSU Agriculture webpage (my emphasis):

  Bark Color - Varies from chalky white to olive-gray, and becomes rough furrowed on the lower trunk of mature trees.

[Note: I give all 3 sources to demonstrate the inconsistency in description of P. tremuloides bark color].

Here is a close-up of furrowed aspen bark from the USDA website (yes, this is still aspen):

However, this furrowing can also occur in paper birch.

From V tech (my emphasis):

  Bark: Reddish brown with light lenticels on very young stems; later turning chalky to creamy white, peeling in horizontal papery strips; brown to black and may be furrowed at base; orange inner bark.

From Field Guide to Trees of North America (my emphasis):

  Bark white papery; older trees have rough black bark near base.

I will comment that I have never seen paper birch with furrowed bark at the base. Further, I was unable to find visual evidence from any reputable sources by searching on Google.

So what about tree shape and form?

Again, according to The Sibley Guide to Trees:

  [P. tremuloides has a] single main trunk with relatively stout , jagged twigs (unlike more slender and graceful twigs of birches).

  [B. papyrifera] branches begin lower on trunk than in aspens; more graceful, ascending, and regular with slender straight twigs. Mature tree has oval habit, few strong branches, clumps of fine twigs in the crown.

  [B. populifolia has] typically multiple leaning, crooked trunks and narrow crowns. Bark of mature trunks grayish white, nonpeeling.

Citing a different source (Field Guide to Trees of North America) to address different language to differentiate the species:

  [P. tremuloides:] Small to medium-sized tree. slender trunk; pyrimidal to round crown of spreading branches with sparse foliage.

  [B. papyrifera:] Medium-sized tree. One to several slender, straight trunks; narrow to broad crown; branches upraised in youth, often becoming horizontal or drooping in age

  [B. populifolia:] Small tree. sometimes shrubby; One to several trunks; narrow, conical crown.

The smaller trees in the front left of the OP's picture demonstrate a more birch-like architecture and have branches growing along the stem as the description for B. papyrifera describes. These qualities are reduced or eliminated in the larger trees in the OP's picture.

For visual clarification, the typical pyrimidal crown shape of P. tremuloides is shown below (from Oregon State Department of Horticulture). The trees in this image appear more slender (pyrimidal) than the trees in the OP's image, but aspen trees can also have "round" crowns as stated above.

The following photo from Michigan State University Extension's Tree ID Key attempts to demonstrate a difference between paper birch and aspen crown coloration:

The crown branches/twigs visible in the OP's picture seem to be lighter colored, and so this line of evidence points to aspen.

Ok, so what about size? According to Field Guide to Trees of North America the typical sizes of the species under question are fairly similar, but with gray birch being smaller than the other two species:

Quaking Aspen (Populus tremuloides) = 30-70' tall, 1-1.5' diameter
Paper Birch (Betula papyrifera) = 50-70' tall, 1-2' diameter
Grey Birch (Betula populifolia) = 20-30' tall, 0.5-1' diameter

The relative sizes of the trees in the OP's picture don't seem to preclude any of these species.

Both birches and aspens develop yellow leaves in autumn, so this characteristic additionally is not useful for differentiating the two genera (or 3 species).

Though @fileunderwater is correct in stating that birches have horizontal lenticels that are helpful in identifying birch trees, the OP's image is far too zoomed out to make out any lenticels (even when zooming into the OP's picture). Those black spots are not lenticels; they are scars (generally from lost limbs). Regardless, other species (including some aspen species) also develop lenticels.

Here is a close-up of lenticels. The little slits are birch lenticels (here from B. papyrifera):

Names on files and webpages are notoriously incorrect so using that as a line of evidence is dangerous. I saw a number of misidentified species in pictures while I was searching myself.

So thus far it seems as though aspen is a pretty good choice, but paper birch could also be potentially correct. The distance of the picture makes this distinction difficult, but I will point to the two lines of evidence that have convinced me that some of the trees are in fact paper birches.

The girth and shape of the larger trees are more consistent with the growth form of birches vs. the usually slender, single-stemmed aspen.
In the OP's picture, you cannot see peeling or lenticels, but this might be due simply to the distance from the trees. However, you can see a brownish/orangish coloration on a number of the trees, which is consistent with numerous descriptions of paper birch trees that have already started peeling revealing brown/orange bark.

Conclusion = Hard to tell, and likely actually a mix of Paper Birch (Betula papyrifera) and Quaking Aspen (Populus tremuloides). I think you're looking at taller aspen and mostly wider paper birch.


If I graft two trees together while young, will they grow as one plant? If I were to graft two apple saplings together --  by bending the tops toward each other and lashing them together --  will the plants grow as one and benefit from one another, or will they be fighting each other for root space and light? If they would grow with each other, then I could theoretically grow a line of closely spaced fruit trees to any length, and they would be strengthened by each other in bad conditions.

There are a couple of answers to this question.  Especially where trees are concerned, you can graft two or more trees onto the same rootstock, or even a single limb into a tree.

But if the graft takes, it won't behave too much more differently than just more branches of the same tree.  Structurally intertwining them will not be different than if you had just taken a single tree's branches to support each other.  The graft will usually only have a single set of roots, from the host tree.  They will not compete.  The tendency will be for the branches to grow apart so that they can independently get their own light.  This is very much like any other single tree.  Not sure about fusing two halves of a tree together - exposing the roots would tend to kill the tree or unsettle it.


Is genetic purging based on random shuffling of the genes of an individual or is it more intentional way of removing deleterious recessive alleles? Inbreeding depression may be reduced by selection against deleterious alleles, which eliminates, or purges, them from the population. I have two questions:

Is genetic purging based on random shuffling of the genes of an individual or is it more intentional way of removing deleterious recessive alleles?
Do the individuals/couple with deleterious alleles that breed together, pass down the purged genes EACH AND EVERY TIME they produce offspring? Does it happen every time they mate or just some times?

Is genetic purging based on random shuffling of the genes of an individual or is it more intentional way of removing deleterious recessive alleles?

There is no intention in evolution. Purging refer to the action of selection at removing deleterious alleles. This term is specifically used when a population goes through a demographic change under which purifying selection becomes more efficient (such as an increase in inbreeding coefficient).

  Do the individuals/couple with deleterious alleles that breed together, pass down the purged genes EACH AND EVERY TIME they produce offspring? Does it happen every time they mate or just some times?

Purging is a population-level process so your second question does not make much sense

Rephrasing the above a bit differently, purging refers to the reduction in frequency of deleterious alleles in the populations. Individuals will transmit whatever allele they can transmit.


what is meta-sympathetic nervous system? I always knew about the sympathetic and para-sympathetic nervous systems, and today I was told about the meta-sympathetic nervous system, but I didn't understand well the man who told me about it and I didn't find enough or reliable information about this system, and if it's accepted in the scientific world or it's arguable.

As @mgkrebbs says, metasympathetic nervous system is still a matter of debate and is not fully accepted in the scientific world due to lack of research and evidence.

Metasympathetic nervous system, just like sympathetic and parasympathetic nervous system, is a part of Autonomic Nervous System.

  On the basis of a number of structural and functional indices, application of pharmacological analysis as well as recording of neuronal activity, the autonomic nervous system is subdivided into the sympathetic, parasympathetic and metasympathetic parts. The metasympathetic system includes the complex of microganglia situated in the walls of visceral organs and having marked motility activity (the heart, ureters, intestine, stomach). According to the localization, separate areas of this system can be defined by its site (for example, the cardiometasympathetic area in the heart). The metasympathetic system attains the features of true autonomy. Its cells have no direct connection with the high centers: this connection is established through mono- and polysynaptic sensory and afferent units of sympathetic and parasympathetic nature.

Source

Full article here

How is it different from sympathetic & parasympathetic systems?

One major difference is in the location.

The Metasympathetic system

  includes the complex of microganglia situated in the walls of visceral organs and having marked motility activity (the heart, ureters, intestine, stomach).

while Sympathetic system

  consists of cells with bodies in the lateral grey column from T1 to L2/3. These cell bodies are "GVE" (general visceral efferent) neurons and are the preganglionic neurons. There are several locations upon which preganglionic neurons can synapse for their postganglionic neurons:

and Parasympathetic system

  consists of cells with bodies in one of two locations: the brainstem (Cranial Nerves III, VII, IX, X) or the sacral spinal cord (S2, S3, S4). These are the preganglionic neurons, which synapse with postganglionic neurons in these locations:

For detailed location, see this image:


How does a smoker's pleasure work? I smoke. For some reason, I've always had this idea that the pleasure of smoking works more or less like this: from the lungs, the nicotine reaches the blood, with which it travels to the brain, and there it does some difficult chemical stuff to make me feel all good. But that's also never made sense to me. I mean, the gratification is instant. I don't even inhale very deeply, and, momentarily, I feel the feeling for which I do the thing. I don't know how fast the blood travels -- I only know it varies -- but it seems impossible for it to travel this fast. Or is it?

Could you explain to me, a non-biologist, how it works?

20-30 seconds is all it takes to reach the brain, then levels continue to increase with a peak at around 15 minutes and normal levels by about 2 hours (hence the craving). Smoking increases your heart rate directly and also indirectly through reducing the oxygen levels in your blood so your body compensates by increasing heart rate as well as makes each beat stronger, so it pumps more blood with each beat. Nicotine itself is really soluble, it goes straight through the lungs (alveoli) because the lungs get an incredible amount of blood (which they need to do their job) so massive surface for the nicotine to go through so enough nicotine gets into the blood and concentrations are really rapidly high enough for you to feel the nicotine. Carrying on from that, the blood rapidly gets back to the heart and around the body with the brain being practically a direct connection away. Consider the classic cyanide capsule death seen often on TV. The reason people seem to lose consciousness within 30 seconds is because they inhale the cyanide.

Nicotine replacement therapy used to stop smoking uses similar mechanisms to give the same speedy delivery of satisfaction without the massive risks of smoking, stopping cravings and really improving one's quality of life.


What organism has the longest Hayflick Limit? Assuming I am understanding the concept correctly, Hayflick Limits are reflective of a cells capacity for stable division. Additionally, the Hayflick Limits of various organisms differs.

My question is, what organism has the longest Hayflick Limit? I know humans have one ranging from 40-60, just to give a bit context.

The Hayflick limit is generally associated with telomere length. Human telomeres are a little on the long side as species go, but are not extraordinary. Many species of mice, and other rodents, have far longer telomeres than humans, for example, and obviously have much shorter lifespans. There's also such a thing as a "mega-telomere", found in a number of bird species, which can hundreds of times longer than human telomeres.

There's only a vague correlation between telomere length and a species' lifespan.  See Comparative biology of mammalian telomeres: hypotheses on ancestral states and the roles of telomeres in longevity determination for a starting point.  Telomeres are a part of the longevity story, but probably a fairly small part.

That said I don't see an explicit statement that those species with very long telomeres have a higher Hayflick limit. I assume this is because the Hayflick limit is an ultra-simplistic and not very useful description of a very specific set of conditions, but I don't know that for sure.


Multiplex PCR, shorter amplicon inhibiting longer amplicon? I want to run multiplex PCRs for my genotyping, with a primer pair targeting my construct and a primer pair targeting some housekeeping gene (sort of a built-in control).

I designed the control amplicon to be very short (I tested 3 primer pairs with ~120, 85, and ~50bp amplicons respectively). The main rationale behind this being that usually my amplicons are ~200-400bp, and I want something clearly distinguishable, but shorter rather than longer (I want to keep my options open for longer target amplicons).

In any case, regardless which control primer pair I use, whenever I try to multiplex I only end up seeing the shorter amplicon. See the gel picture below for an example (lanes: 1-ladder, 2,3-target+control, 4,5-control, 5,6- target).

I see that lanes 2,3 have a very faint additional smear compared to 4,5, but I want a band for my target amplicon. Also, my shorter bands are quite blurred.

Also, just for reference, my amplicons do not overlap at all.

So, I guess my questions are:

Why is the longer band disappearing?
Why is the shorter band so blurred?
What can I do to prevent this form happening?

It turns out that the $T_m$ was in fact the issue, or rather, that the computation algorithm overestimated the $T_m$ of the primer pair for the longer amplicon (or underestimated that of the shorter one). At any rate, it seems that at 60°C the shorter amplicon primers hijack the polymerization mechanism.

Setting the annealing phase temperature to 55°C solved my issue, and now I consistently get better results:


Is there a difference in cytoplasmic pH between prokaryotes and eukaryotes? The cytosolic pH in human cells is around 7.4, but fluctuates as the cell is replicating. Prokaryotes and eukaryotes are vastly different in many ways. One thing they share is cytoplasm. Is there any general difference in the pH between these two cytosolic spaces? Any pointers to a previous investigation into this would be hugely appreciated. Ideally I'm after a quantified numerical comparison from a peer reviewed reference, but given the obscurity of the question that might be a tall order!

Googling was to no avail. It's swamped with pH survival data.

In the article "pH of the Cytoplasm and Periplasm of Escherichia coli: Rapid Measurement by Green Fluorescent Protein Fluorimetry", by Jessica C. Wilks and Joan L. Slonczewski, the pH of E.coli cytoplasm was mentioned as 7.2 - 7.8. I just took E.coli's pH range as a common example of prokaryotes.

Reference link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1951819/


Chromatin shearing: what is it and what are the effects of high-sensitivity? I am reading a paper  which discusses a complex (MSL-DCC) involved in dosage compensation of the drosophila X-chromosome. Descriptions of the complex's structure and function are given in the papers introduction.

To start with, could someone explain what is chromatin shearing? what is happening during the process?

Secondly, the authors then say:

  "Our data suggest that the complex is particularly sensitive to shear
  forces on transcribed chromatin so that only the direct interactions
  on MSL-3 with nucleosomes are retained" - discussion section (subheading: interaction of the MSL-DCC with target gene bodies)

Could someone explain what is meant by 'particularly sensitive to shear forces'? In comparison to what? And what are the consequences of it being more sensitive?

Shear forces are experienced by all molecules, and molecular complexes when they are treated roughly. So, for example, if you have a solution of high molecular weight DNA it will be very viscous, but if you treat it roughly by pipetting up and down through a narrow aperture the DNA strands will suffer shear forces strong enough to break covalent bonds and the solution will become less viscous. Another example of the use of shear forces in biology is lysis of yeast cells using small glass beads. As the slurry of beads and cells is vortexes the cells experience intense shearing forces (forces tending to pull different parts of the cell in different directions) and they break open. They are not being physically ground by the beads.

In the specific case that you quote, you apparently have a multimolecular complex (MSL-DCC) held together by weak (non-covalent) interactions and interacting with the nucleosomes through a component called MSL-3. Without looking at the paper, it seems that this complex is prone to falling apart (during isolation?) as a result of shear forces strong enough to overcome the non-covalent binding interactions. Think of a helicopter with a man hanging on to the undercarriage with both hands. Then imagine a second man hanging on to the first man's boot lace with his thumb and finger. Who will fall off first due to the shearing forces experienced as they are buffeted by the wind?

The helicopter is the nucleosome, the first man is MSL-3 and the second man is the rest of the complex.

added later in response to MattDMo
looks from this that I was wrong - it's actually a French press and other homogenizers that generate shear forces. I don't think I made the glass bead story up, but I can't remember who told me. The BeadBeater people also refer to "cell cracking" not shear. Apologies everyone, I think the rest of the post still holds up, and thanks to MattDMo for the challenge.


pfu Turbo DNA polymerase AD What is the duration (Life") of pfu turbo DNA polymerase AD. I am trying o Amplification a 3.3kb fragment and the PCR schedule is 6 hours long. The manufacturers notes just specify that its activity remains 94-99% in 1 hour at 95, nothing more.

I don't know the exact half-life of this special Pfu polymerase, but generally Pfu polymerases are pretty stable. This source gives a half life of 18-25 hours at 95°C, meaning you keep the enzyme at 95°C for the whole time a you still have 50% activity after that time. Since you don't do that, I wouldn't worry too much about the activity. To be safe, you can add an extra long (probably 10-15 minutes) single amplification step before cooling down.


What species is this turtle in Houston? This turtle was displaced by hurricane Harvey in Houston, Texas, USA (Buffalo  Bayou and Dunlavy). It appears to be a snapper. Can someone identify the exact species?

That's an Alligator snapping turtle, Macrochelys temminckii.

Here is another picture of it (from the same Wikipedia page linked above):

It should not be mistaken for the Common snapping turtle, which belongs to a different Genus.

There is a problem, though: in 2014 Thomas et al. divided the Genus Macrochelys (which originally contained only one species, Macrochelys temminckii) in three species: Macrochelys temminckii itself, Macrochelys suwanniensis and Macrochelys apalachicolae.

Therefore, narrowing this down to the exact species (according to the current taxonomy of the Genus) may be way more complicated.

Source:

Thomas, T, Granatosky, M, Bourque, J, Krysko, K, Moler, P, Gamble, T, Suarez, Leone, E, Enge, K, & Roman, J, 2014. Taxonomic assessment of Alligator Snapping Turtles (Chelydridae: Macrochelys), with the description of two new species from the southeastern United States. Zootaxa 3786 (2): 141–165


Oculus rift (or, what do other eye placements see?) I could be WAY out of line in the placement of this question, but here goes:

Everyone I'm sure has heard of the Oculus Rift or any of the several other VR headsets making their way around.

It reminded me of a friend who, when in art school, said, "Dali's eyes were crooked [whatever the opposite of crossed is], and it may have helped him develop a different sense of perspective, and we have been taught to practice letting our eyes go relaxed to recreate similar effects."

I don't know if he did it, and I never saw a representation. But now I am interested...

If an Oculus used a model with eyes pointing different directions...or on the "sides of the head" with a wider field of view like many non-predatory animals...

What would we see?

(And maybe if it's an interesting answer... a VR Dali or VR cow simulator might be in order...)

It would probably be quite disorienting, maybe even make you sick.

There is a much more limited fun classroom demo that my institution uses with kids, where they wear goggles that shift their view a couple degrees to the left (this demo is quite common, you can find many examples on YouTube as well). They stand a couple meters from a wall and throw a ball at a target: inevitably, they miss wide right for the first few throws, but eventually they adapt and hit the target no problem; then when they remove the goggles, they miss again to the left.

So, your visual system can adapt to some shifts in visual field. However, if the view was very skewed, oriented for example like the eyes of cattle, on the sides of the head, it would be much more difficult to adapt to where it feels natural. I would expect the strategy people would use would be to attend to only one visual field or the other, since there is no longer any binocular area of vision, sort of like if you would look as far to the right as you possibly can you see a lot of visual space with only one eye.

An important element to immersive VR is that you feel like you are actually having the experience - in VR when you have some sort of joystick or controller to manipulate, for example, it is really helpful to orient people by allowing them to see the controller in virtual space. Providing the eyes with very unusual inputs is going to make it much harder to maintain the illusion.


Biochemical coupling between two enzymatic reactions - Enzymes physically associated? I am wondering what the exact definition of biochemical coupling between two enzymatic reactions is. I know that these two enzymatic reactions have to

share the same intermediate(s)
one is thermodynamically favorable and the other is not.

So  the thermodynamically unfavorable reaction can happen when it coupled with the  thermodynamically favorable reaction. I just want to confirm that : Do these two enzymes have to be physically associated with each other? Since I do not have any evidence to support the physically interactions between these two enzymes, can I still use the term "biochemical coupling"?

Many thanks.

The enzymes don't need physical interactions to couple reactions. Some enzymes do share subunits which are physically associated, but this is a special case. The following review gives a sort of general example during glycolysis,

  For example, in the biochemical pathway that breaks down glucose for energy, two enzymes work one after the other to create a high-energy ATP molecule:

We can also look at the peptidyltransferase reaction during the elongation step in translation. Earlier, an aminoacyl tRNA synthetase catalyzed the covalent addition of an amino acid to it's associated tRNA. The energy from breaking this bond in the ribosome provides energy for the peptidyltransferase to link the two amino acids together. This isn't assuming the ATP/GTP needed by elongation factors, etc.


How the chaotropic agents help in purification of DNA molecule? Those plants which are rich in secondary metabolites and polysaccharides DNA isolation can be done using certain chaotropic agents? can any one explain how it works?

Chaotropic agents are cosolutes that can disrupt the hydrogen bonding network between water molecules and reduce the stability of the native state of proteins by weakening the hydrophobic effect. a chaotropic agent reduces the amount of order in the structure of a protein formed by water molecules, both in the bulk and the hydration shells around hydrophobic amino acids, and may cause its denaturation (biochemistry).
A chaotropic agent is often used in DNA isolation. It's purpose is

a. To degrade membrane lipids

b. To destroy the endoplasmic reticulum

c. To degrade mitochondria

d. To limit the amount of magnesium salts in the lysate

e. To destroy the three dimensional structure of proteins

To make it simple, a chaotropic agent destroys the 3D structure of a protein, thereby leading to subsequent protein degradation. It serves as a proteinase enzyme, cleaning the cellular proteins in your DNA isolation and purification process.

http://www.hindawi.com/journals/bmri/2009/574398/

http://www.ncbi.nlm.nih.gov/pubmed/16152629


does small different between 16s ribosomal DNA leads to diffrence into protein products? I have bacterium isolate after BLAST of its 16S  the different between its and the similar seq. on NCBI was 4 nucleotides my question is, does it lead to difference between whole genome seq. or I will obtain the same seq. consequently. does this also leads to  the same protein products from them.

The 16s ribosomal DNA does not code for any protein, it codes for the 16s ribosmal RNA, which is part of the (small subunit of the) ribosome.

The differences will most likely not affect the ribosome much, but to be sure you'd have to check the exact position of the mutations in a reference structure and see if they are at important positions (i.e. binding of the Shine-Dalgarno sequence)


Can insects or mosquitoes be astonished(shocked)? Can insects like mosquitoes get astonished by sudden happenings?

Background

I missed hitting a mosquito on a wall with great force. However even though I missed hitting it, it was dead.

So I wonder if insects can reach death or at least astonished by sudden happening, or lead to something like cardiac arrest.

Hope it isn't a noob question :)

I originally thought there was no way anyone had studied this - it felt like one of those questions we get here a lot where people seem to assume "scientists know (almost) everything" - but I decided to give a check anyways.

Short answer

There is in fact evidence that some insects could be scared to death. However, the process is a bit less dramatic than the one you suggest.

I didn't see much on mosquitoes specifically, but your question seems to allow extrapolation from other insects.

Longer answer

I found at least one paper, McCauley, et al. 2011, that studied whether the mere presence of a predator could cause fatal reactions, in this case in dragonflies. There are several others that show more generic stress-induced responses.

McCauley, et al. exposed dragonfly larvae to predators (either fish or a larger dragonfly) who were unable to actually eat the larvae because the larvae were contained within a 'cage' within a larger aquarium.

The larvae exposed to either predator type had substantially more mortality, and only about 30% as many survived to adulthood. This is not precisely insects being startled to death, but rather they propose that the chronic stress of predator exposure caused their growth to be impaired. An alternative explanation is that the larvae exposed to predators simply spent too little time eating to obtain enough nutrition, but they argue in their discussion that this is not likely to be the only cause in the case of the dragonfly predators, because unlike the fish those predators did not reduce their foraging behavior.

There are many other papers that talk about "non-consumptive mortality" more generally but these often include causes of death such as succumbing to injury from failed/incomplete predation, energetic expenditures, etc (Siepielski et al., 2014; Veselý et al., 2017) - few others actually use a highly controlled environment to prevent physical contact between predator and prey like in McCauley. Other studies do show that exposure to increased stress levels causes changes in gene expression and impacts on the immune system in insects (De Block & Stoks, 2008; Slos & Stoks, 2008).

On the point of mosquitoes, I did find one paper that showed reduced lifespan duration in adult mosquitoes exposed to increased predation as larvae (Bellamy & Alto, 2018) - again not exactly what you were looking for in terms of an acute event, but still somewhat related.

In summary

I think an important takeaway is that insects, like vertebrates, can be susceptible to stress.

References

Bellamy, S. K., & Alto, B. W. (2018). Mosquito responses to trait-and density-mediated interactions of predation. Oecologia, 1-11.

De Block, M., & Stoks, R. (2008). Compensatory growth and oxidative stress in a damselfly. Proceedings of the Royal Society of London B: Biological Sciences, 275(1636), 781-785.

McCauley, S. J., Rowe, L., & Fortin, M. J. (2011). The deadly effects of “nonlethal” predators. Ecology, 92(11), 2043-2048.

Siepielski, A. M., Wang, J., & Prince, G. (2014). NONCONSUMPTIVE PREDATOR‐DRIVEN MORTALITY CAUSES NATURAL SELECTION ON PREY. Evolution, 68(3), 696-704.

Slos, S., & Stoks, R. (2008). Predation risk induces stress proteins and reduces antioxidant defense. Functional Ecology, 22(4), 637-642.

Veselý, L., Boukal, D. S., Buřič, M., Kozák, P., Kouba, A., & Sentis, A. (2017). Effects of prey density, temperature and predator diversity on nonconsumptive predator-driven mortality in a freshwater food web. Scientific reports, 7(1), 18075.


What is the difference between how motor function is controlled in cerebrum vs frontal lobe? At least according to wikipedia, the frontal lobe houses the primary motor cortex, but in a different article about the cerebellum, it says the cerebellum controls motor function. So, do both parts control voluntary movement at once? What's the difference in the roles these two parts play in movement?

https://en.wikipedia.org/wiki/Cerebellum

https://en.wikipedia.org/wiki/Frontal_lobe

The motor cortex, basal ganglia, and cerebellum all contribute to motor control.

Cortex stores movement memory, basal ganglia is responsible for "chunking", or segmenting the memory, and cerebellum compares cortex memory and current movement to correct for errors and to update perception of movement. So to answer your question they all control different components/processes of learned movements at the same time and in conjunction.


At What Rate Do Ions Leak Out of a Plasma Membrane Segment That Has No Ion Channels? In reading about the purpose of myelin during action potential propagation, I came across a point of confusion.

From what I understand, one of the primary "benefits" of myelin is that it aids in increasing the transverse resistance of an axon...which, biologically, is equivalent to stating that it minimizes the extent to which ions move out of or into the cytoplasm of the axon.

However, I feel as though I have always been taught that "the plasma membrane is impermeable to charged particles" and am therefore confused as to what additional benefit is conferred on the axon by the myelin.

Consider the following two cases:

Case A) The action potential starts at the axon initial segment. The subsequent segment is myelinated. The action potential, through passive diffusion, makes its way down the myelinated section until it reaches the 1st node of ranvier, where the action potential is subsequently regenerated.

Case B) The action potential starts at the axon initial segment. The subsequent segment is unmyelinated but contains no ion channels (or pumps). The action potential, through passive diffusion, makes its way down this unmyelinated section that has no ion channels (the same distance as in Case A) until it reaches a dense collection of voltage gated sodium channels.

In case B, will the action potential be regenerated? Or has the passive diffusion event suffered from too much "leakage"? If so, is it really true that:

(the plasma membrane + myelin) transverse resistance >> (the plasma membrane) transverse resistance alone

I'm going to mostly skip over the title of your question and focus on the confusion in the body, because the question in the title is a bit of an XY problem. It doesn't make much biological sense to think about a membrane that is truly that resistive (that is, I am unaware of any example neuron, or even any other cell, that has that property).

If there were truly no channels of any sort, you could indeed consider the resistance to be very high, at least as high as one could measure in patch clamp. Additionally, what matters is not the resistance itself but the ratio of the transverse to axial resistance; relative to the axial resistance the transverse resistance is already very high.

  From what I understand, one of the primary "benefits" of myelin is that it aids in increasing the transverse resistance of an axon

Your understanding is not completely correct. The insulating benefit of myelin (ignoring other organizational benefits) is not only related to the transverse resistance, but importantly to a decrease of the capacitance of the membrane (see Moore et al 1978 or Richardson et al 2000 for some example simulations; also any reasonable neuroscience textbook will explain this). You can test this yourself in a simulation environment like NEURON.

Myelin decreases capacitance by effectively increasing the distance between the 'plates' of the membrane capacitor (see this answer).

In order to charge a long length of membrane with channels on only at short segments, you would need enough charges to come in within that short segment to charge the entire length of axon, and the potential would decay with distance.

Myelin does also affect resistance, but that's mostly important because the membrane does not consist only of a phospholipid bilayer and there is non-zero leak. For example, there are channels under the lipid bilayer that establish a resting potential (Chiu & Ritchie, 1984).

Chiu, S. Y., & Ritchie, J. M. (1984). On the physiological role of internodal potassium channels and the security of conduction in myelinated nerve fibres. Proceedings of the Royal society of London. Series B. Biological sciences, 220(1221), 415-422.

Moore, J. W., Joyner, R. W., Brill, M. H., Waxman, S. D., & Najar-Joa, M. (1978). Simulations of conduction in uniform myelinated fibers. Relative sensitivity to changes in nodal and internodal parameters. Biophysical journal, 21(2), 147-160.

Richardson, A. G., McIntyre, C. C., & Grill, W. M. (2000). Modelling the effects of electric fields on nerve fibres: influence of the myelin sheath. Medical and Biological Engineering and Computing, 38(4), 438-446.


Drosophila melanogaster eclosion Is there any published data which shows the number of Drosophila melanogaster fruit flies eclosing (hatching out of the pupae) against time since egg oviposition? I'm thinking there should be something like a "cumulative flies eclosed" plot showing the cumulative number of flies emerging per time interval after the eggs were oviposited (something like this dummy figure).

I expected to find this in the Ashburner et al Drosophila book but there was nothing. I am trying to see how much variance there is around the mean for an experiment design. It may be helpful to know (though I am not necessarily after specifics to this set up) we keep our flies at 25 degrees, 12:12 light dark cycle, 60% humidty on a yeast and sugar based food source. The flies are an African lab adapted population (Dahomey ca ~1970's?) and eggs in the experiment would be kept at low density so resource competition is not an issue.

Although I found this study, where mean and 95% CIs of median time to
eclosion (h) are provided for some strains of D.m. (with a resolution of 12 h) (in table 3), the moment of eclosion seems to be under circadian control: "in Drosophila melanogaster, the emergence of adults from their pupal cases (eclosion) is gated by the circadian clock such that it occurs during a window of approximately 8-10 h starting 1-2 h before lights-on in 12-h light:12-h dark cycles (LD)". In that particular study Canton-S flies eclosed within 4-5 days after pupation (LD 12:12, 25°C) with the following distribution over day (digitized from Fig. 1A [numbers are approximate, percents don't sum up to 100]):

Hours   % eclosed
Dark
12-14   0.5
14-16   0.4
16-18   0.6
18-20   1.1
20-22   1.4
22-24   5.6

Light
0-1     20.4
1-2     9.3
2-3     13.7
3-4     12.0
4-5     10.3
5-6     11.3
6-7     6.6
7-8     4.9
8-9     2.1
9-10    0.8
10-11   0.8
11-12   0.4


Could we detect GMO foods if there were no samples to compare with? In my understanding, there’s nothing “special” in how a GMO product is composed inside compared to a “natural” product. I mean, still, same principles apply to both: some DNA that controls protein building, and so on.

Now, having read about all existing methods of GMO detection, I still can’t understand how it works: e.g., given two potatoes, one GMO and one natural, would you be able to detect which is which without having any samples or knowledge about what parts of DNA to consider engineered by humans?

Once you change someone’s DNA, does it contain any signs that it was changed? Or do we need a database of “natural” products’ DNA to compare with in order to be able to detect DNA ones? Or do we need a database of GMO products to compare with?

[G]iven two potatoes, one GMO and one natural, would you be able to detect which is which without having any samples or knowledge about what parts of DNA to consider engineered by humans?

No, you can't distinguish them without knowing a priori the DNA sequence of the wildtype and of the GMO. There is no other mark left within a GMO in the general sense.

Of course, one particular GMO is created with one particular goal in mind. One particular phenotypic effect. If you detect the phenotype of a GMO, then you can recognize it. For example, if you make a GMO tomato that produces a new type of pigment, you can, of course, recognize it by the presence of this pigment! However, there is no general attribute of being GMO that you can recognize. You need to look for something specific that you know about a specific GMO (or specific wildtype).

There are also phenotypic traits that you find (quasi) exclusively in GMO such as Cytoplasmic Male Sterility (CMS) for example. If you find CMS in a plant, then you can be pretty sure it is a GMO. But if you can't find CMS though, you can't be sure it is not a GMO.


Protocol for measuring stamina of arthritic mice I am going to make some mice ill with arthritis. The medicine which I am testing as control is known to cause extreme fatigue. I think I've improved it. I'd like to humanly measure their stamina in the presence of something like morphine. How would I ethically do this?

I believe the standard is an graded-speed treadmill test.  An example pub:

Genetic variability in forced and voluntary endurance exercise performance in seven inbred mouse strains

If there is a particular ethical concern, you should always have your institutional review panel review it.  If you call up your department of animal resources (or what ever it is called in your institution) they will almost always give lists of preferred LOPs.

Another option would be to score time sleeping if you have them under behavioral surveillance.  The problem with this is the large amount of man hours needed, even watching tapes at high speed.  Instead I recommend you check this paper out:

Evaluation of two automated metrics for analyzing partner preference tests

Then to get accurate scoring, I would put a strongly colored bedding pad in a corner so the computer could pick it up.  Be sure to put the bedding in at least a week before so the mice get used to it and actually sleep on it.


Why is some scat in the form of little pellets? The scat I most often encounter when out and about is from coyotes, black bears, deers and rodents. The deer and rodent droppings I find are in little pellets, what is different about their digestive system or their food choices that produces these perfectly uniform little balls?

According to this article:

The material that cannot be broken down any further, such as
indigestible fiber, passes directly into the large intestine.  Here
water is reabsorbed and the material is passed, making up the round
droppings you see in your rabbit’s cage.  This indigestible fiber is
important in the diet of the rabbit as it helps to stimulate
intestinal contractions, which keeps the chyme moving through the
gastrointestinal tract.

While this article is specifically about rabbits, all herbivores require high quantities of fiber in their diets. Ruminants such as deer have different stomachs, but it is the large intestine, which is commonplace, that these pellets are formed. Fiber tends to clump together (either because the strands are attached or intertwined), and contractions in the intestine as the material is dehydrated cause these clumps to roll around similarly to pebbles in a rock tumbler, causing them to form round pellets.
Carnivores and omnivores have (and need) less fiber in their diets, so this phenomenon is not present in their feces.


In the vacuum of space would death be instantaneous? I was arguing with my colleague about this matter (I'm not going to mention which side I fall on).

Would death be immediate in the vacuum of space? For example, if I was suddenly teleported into the vacuum of space would I die straight away? Or would I experience a suffocating sensation?

Nope, you wouldn't die instantly. While explosive decompression has never been tested on humans (for obvious reasons), the dangers of a vacuum have mostly to do with the pressure differential between your body and the now pressure-less void around you. The most fragile parts of the biological system would be the lungs and ears, and the instantaneous transportation would cause a severe case of the Bends if you were rescued quickly enough. You would pass out within a few seconds stated by NASA when an experiment went awry, and death might be from lack of oxygen to the brain, although after a few minutes everything bad starts to happen so nobody really knows what you would die of:

  At NASA's Manned Spacecraft Center (now renamed Johnson Space Center) we had a test subject accidentally exposed to a near vacuum (less than 1 psi) in an incident involving a leaking space suit in a vacuum chamber back in '65. He remained conscious for about 14 seconds, which is about the time it takes for O2 deprived blood to go from the lungs to the brain. The suit probably did not reach a hard vacuum, and we began repressurizing the chamber within 15 seconds. The subject regained consciousness at around 15,000 feet equivalent altitude. The subject later reported that he could feel and hear the air leaking out, and his last conscious memory was of the water on his tongue beginning to boil.


Regarding apoptosis and inhibitors If there is an apoptosis shut-off mechanism of any kind, one could call it a null-apoptosis mechanism.

If this is possible, could there be a null-apoptosis inhibitor? Something that inhibits an apoptosis inhibitor?

Apoptosis is very tightly controlled for obvious reasons. Setting it off without proper control would result in the uncontrolled loss of cells. Apoptosis is one of the major pathways which are either mutated or shut-off in cancers, preventing the body from eliminating malingnant cells. These two papers are interesting in this context:

Apoptosis: A Review of Programmed Cell Death
The role of apoptosis in cancer development and treatment response

In this context it makes no sense to have a shut-off mechanism once the apoptosis cascade has started. It is only set off when there is a real reason (and is well controlled), so I don't think there a "null-apoptosis" mechanism. It would of course still be possible to artificially make substances, that inhibit parts of the activation cascade. But besides for apoptosis research I don't see any use for it. There is actually some research going on to find out how to activate apoptosis again in cancers.


Why does white light viewed through optical chopper appear purple/blue? I looked at a light like the one shown here through a fidget spinner (I believe I was observing near where the "blades" meet the inner portion) and noticed that it appeared purple/blue, particularly when viewed for a prolonged period (I looked at the reflection of sunlight from snow and observed this as well.).  I believe this is either an optical effect (the spectrum is convolved with the Fourier transform of the "chopping function or pulse" ) or has something to do with the eye/my perception.

So what's going on here?

I totally wasn't expecting to immediately duplicate this with a fidget spinner and the fluorescent light in my office.  What a neat effect!

My technique: I hold the spinner quite close to my eye, so that it occupies nearly all of my field of view, and look through the spinning part at my ceiling light.  If the spinner is very fast or very slow, I don't see any change in the hue of the light.  However there's an intermediate rate where the back part of the fluorescent lamp takes on a patchy blue tint with colored edges. The tinted region is irregular and unpredictable in the same way as a pressure phosphene, if you're familiar with that better-documented effect, and has kind of the same "feel" to it.

Trying to photograph the effect just gives the rolling shutter problem, so that's no use.  (No color change in the photo, either.)

At the rotational speed where the color change effect is the most pronounced, I estimate the frequency at which the spinner blocks nearly all of the light to be 10-20 Hz.  (How? I let the thing hit a fingernail and listened to it tap; it sounds like thirty-second notes, four to a click, at a good presto tempo.)  I've read elsewhere that the human eye can process images at 10-15 Hz. So some sort of biological stroboscopic effect, where the eye has just enough time to begin to respond to the reduced light before the light returns, seems plausible to me.


What initiates primase to add an RNA primer to a DNA strand and what makes it stop? What initiates primase to add an RNA primer to a DNA strand and what makes it stop adding RNA nucleotides? Is there tags added to the DNA back-bone?

Prokaryotic primases are activated by DNA helicase [1, 2] while the eukaryotic ones are triggered when they form a complex with DNA polymerase alpha and its accessory B subunit [2].

I couldn't find too much information about what exactly triggers activation, but according to De Falco M et al. (2004):

  [...] synthetic function (of the prokaryotic primase) is specifically activated by thymine-containing synthetic bubble structures that mimic early replication intermediates. [3]

It stops when it finishes reading a DNA template:

  The Sso DNA primase utilizes poly-pyrimidine single-stranded DNA templates with low efficiency for de novo synthesis of RNA primers [3].

References:

Wikipedia contributors, "Primase," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Primase&oldid=593928284 (accessed December 1, 2014).
David N. Frick, and Charles C. Richardson. DNA PRIMASES. Annual Review of Biochemistry. Vol. 70: 39-80 (Volume publication date July 2001). DOI: 10.1146/annurev.biochem.70.1.39
De Falco M, Fusco A, De Felice M, Rossi M, Pisani FM. The DNA primase of Sulfolobus solfataricus is activated by substrates containing a thymine-rich bubble and has a 3'-terminal nucleotidyl-transferase activity. Nucleic Acids Res. 2004 Sep 30;32(17):5223-30. Print 2004.


What is Growth and how can we define it to be a defining property of life? I was reading a book and it said that internal/intrinsic growth is defining property of life and not extrinsic growth as saying accumulation of dust on a book makes it a bit bigger, even if it is by a few mm but since it's just a deposition of material and it can be removed, so it's not living. Now, if we see intrinsic growth then I had a doubt. Say we took a piece of log and dipped it into the water. Then the log will also grow in size and this growth is from inside, but the log of wood isn't living. So, I was in doubt that how can I define growth for a living.

If you are just asking what does growth mean in the context of living systems then it almost always means replication of a unit: cell or genetic material (cell division, DNA replication etc).

Note that increase in cell volume or the inter-cellular space (accretionary growth) also happen in living systems and they are also considered growth. However, at a gross level these processes are indistinguishable from what is happening to wood that is dipped in water.

So growing is not an exclusive feature of living systems but still one of the defining features.


What's the name of this flower? I photographed this flower in Central Europe. I looked in online databases but can't really identify the actual flower, since there are so many that look quite similar. Can you help me? What's the name of this flower?

It looks like the common Geranium sylvaticum (also called wood cranesbill or Mayflower), and it is at least a close relative (member of the Geranium genus). This plant is commonly found across Europe and in parts of Asia (see map below), and it is sometimes planted in gardens. It is a perennial herb that grows in many types of habitats (woods, meadows, road sides, mountain areas), and the flowers are most commonly violet to blue, but can also be white. Geranium pratense is very similar, but usually has more narrow leaf lobes and bent flower stalks. However, it might not be possible to separate these two species based on your picture.

There are also similar relatives found in North America (e.g. Geranium maculatum) and Asia (e.g. Geranium himalayense) and many hybrids of plants from within this genus are cultivated.

(picture from Swedish Wikipedia)

(distribution map from the Swedish Museum of Natural History: Den virtuella floran)


How many times did terrestrial life emerge from the ocean? Evolution is often mistakenly depicted as linear in popular culture. One main feature of this depiction in popular culture, but even in science popularisation, is that some ocean-dwelling animal sheds its scales and fins and crawls onto land.

Of course, this showcases only one ancestral lineage for one specific species (Homo sapiens). My question is: Where else did life evolve out of water onto land?

Intuitively, this seems like a huge leap to take (adapting to a fundamentally alien environment) but it still must have happend several times (separately at least for plants, insects and chordates, since their respective most recent common ancestor is sea-dwelling). In fact, the more I think of it the more examples I find.

I doubt we know the precise number, or even anywhere near it. But there are several well-supported theorised colonisations which might interest you and help to build up a picture of just how common it was for life to transition to land. We can also use known facts about when different evolutionary lineages diverged, along with knowledge about the earlier colonisations of land, to work some events out for ourselves. I've done it here for broad taxonomic clades at different scales - if interested you could do the same thing again for lower sub-clades.

As you rightly point out, there must have been at least one colonisation event for each lineage present on land which diverged from other land-present lineages before the colonisation of land. Using the evidence and reasoning I give below, at the very least, the following 9 independent colonisations occurred:

bacteria
cyanobacteria
archaea
protists
fungi
algae
plants
nematodes
arthropods
vertebrates

Bacterial and archaean colonisation
The first evidence of life on land seems to originate from 2.6 (Watanabe et al., 2000) to 3.1 (Battistuzzi et al., 2004) billion years ago. Since molecular evidence points to bacteria and archaea diverging between 3.2-3.8 billion years ago (Feng et al.,1997 - a classic paper), and since both bacteria and archaea are found on land (e.g. Taketani & Tsai, 2010), they must have colonised land independently. I would suggest there would have been many different bacterial colonisations, too. One at least is certain - cyanobacteria must have colonised independently from some other forms, since they evolved after the first bacterial colonisation (Tomitani et al., 2006), and are now found on land, e.g. in lichens.

Protistan, fungal, algal, plant and animal colonisation
Protists are a polyphyletic group of simple eukaryotes, and since fungal divergence from them (Wang et al., 1999 - another classic) predates fungal emergence from the ocean (Taylor & Osborn, 1996), they must have emerged separately. Then, since plants and fungi diverged whilst fungi were still in the ocean (Wang et al., 1999), plants must have colonised separately. Actually, it has been explicitly discovered in various ways (e.g. molecular clock methods, Heckman et al., 2001) that plants must have left the ocean separately to fungi, but probably relied upon them to be able to do it (Brundrett, 2002 - see note at bottom about this paper). Next, simple animals... Arthropods colonised the land independently (Pisani et al, 2004), and since nematodes diverged before arthropods (Wang et al., 1999), they too must have independently found land. Then, lumbering along at the end, came the tetrapods (Long & Gordon, 2004).

Note about the Brundrett paper: it has OVER 300 REFERENCES! That guy must have been hoping for some sort of prize.

References

 Battistuzzi FU, Feijao A, Hedges SB. 2004. A genomic timescale of prokaryote evolution: insights into the origin of methanogenesis, phototrophy, and the colonization of land. BMC Evol Biol 4: 44.
 Brundrett MC. 2002. Coevolution of roots and mycorrhizas of land plants. New Phytologist 154: 275–304.
Feng D-F, Cho G, Doolittle RF. 1997. Determining divergence times with a protein clock: Update and reevaluation. Proceedings of the National Academy of Sciences 94: 13028 –13033.
 Heckman DS, Geiser DM, Eidell BR, Stauffer RL, Kardos NL, Hedges SB. 2001. Molecular Evidence for the Early Colonization of Land by Fungi and Plants. Science 293: 1129 –1133.
Long JA, Gordon MS. 2004. The Greatest Step in Vertebrate History: A Paleobiological Review of the Fish‐Tetrapod Transition. Physiological and Biochemical Zoology 77: 700–719.
 Pisani D, Poling LL, Lyons-Weiler M, Hedges SB. 2004. The colonization of land by animals: molecular phylogeny and divergence times among arthropods. BMC Biol 2: 1.
 Taketani RG, Tsai SM. 2010. The influence of different land uses on the structure of archaeal communities in Amazonian anthrosols based on 16S rRNA and amoA genes. Microb Ecol 59: 734–743.
 Taylor TN, Osborn JM. 1996. The importance of fungi in shaping the paleoecosystem. Review of Palaeobotany and Palynology 90: 249–262.
Wang DY, Kumar S, Hedges SB. 1999. Divergence time estimates for the early history of animal phyla and the origin of plants, animals and fungi. Proc Biol Sci 266: 163–171.
 Watanabe Y, Martini JEJ, Ohmoto H. 2000. Geochemical evidence for terrestrial ecosystems 2.6 billion years ago. Nature 408: 574–578.


Why do skinny people live for shorter than the norm even though calorie restriction extends life expectancy? If I understand correctly, calorie restriction may extend life expectancy slightly (not proven exactly how much for human). But according to the statistics, skinny healthy people have even shorter life expectancy than healthy, slightly obese people. Could you explain why this is not considered as contradictory?

This is an interesting point you raise, and as the study you linked to states, "the link between physique and life expectancy is not clearly understood," which is certainly true at the moment. The relationship between BMI and lifespan in humans is a very different story to controlled dietary restriction in model organisms.

Dietary restriction is defined as "undernutrition without malnutrition" [1], and by definition model organisms live in controlled environments. In contrast, humans have confounding factors that may reduce weight and health (for instance smoking status, early-life diseases, malnutrition, etc) that are not modelled in these experiments.

In addition, the relationship between BMI and mortality is complicated in older humans, known as the 'obesity paradox'; overweight and obese elderly hospital patients have a lower mortality risk than low-normal weight patients [2]. There are a number of hypotheses regarding this, but the favoured one appears to be that the association is not actually paradoxial, but that higher BMI only appears protective because losing weight is associated with many diseases of ageing, so after accounting for many of these confounding factors (e.g. dementia, cancer, etc) high BMI no longer appears protective.

Therefore the study you found only appears to be contradictory to the dietary restriction experiments; in human populations the situation is much more complicated. Additionally, there is conflicting evidence as to whether dietary restriction even works in primates [3], let alone in humans (the largest effects are observed in worms and drosophila).

Weindruch et al. The retardation of aging in mice by dietary restriction: longevity, cancer, immunity and lifetime energy intake. (1986) J Nutrition; 116(4):641-54
Yamauchi et al. Paradoxical association between body mass index and in-hospital mortality in elderly patients with chronic obstructive pulmonary disease in Japan. (2014) Int J Chron Obstruct Pulmon Dis; 9:1337-46
Maxmen. Calorie restriction falters in the long run. (2012) Nature; 488, 569


Molecular simulations without capping n- and c-terminus of polypeptide When running molecular simulations, what is the consequence of not capping the n- and c-terminus?

I have been following gromacs tutorials and haven't come across any that deal with capping the termini, so is it important?

Interesting question. I have to admit, that I haven't really come across it, but for the moment it seems to me that this mechanism is used mainly to protect short alpha helices and stabilize them.
See this articles: "Helix stop signals in proteins and peptides: the capping box." and this one: "Helix capping."
A lot of research is done in combination with actin filaments, where the capping plays an important role in stabilizing the filament strands - either prohibiting the addition of new monomers and on the other hand preventing the removal of elements from the polymer strand.
This review gives an overview:"F-actin capping proteins."
This research article might also be interesting when doing simulations:"N- and C-capping preferences for all 20 amino acids in alpha-helical peptides." As always, if you have some problems with access to the articles, let me know.


In percentage, how much is the human genome (DNA) similar to the mouse genome? Some guy argued with me against evolution theory, and he claimed that human and mice share 98% just like human and chimpanzee.
I've tried to search online for a simple and accurate answer, but I couldn't yet.
In simple words, how much is the human genome (DNA) similar to the mouse genome?

Please use numbers as much as you can and provide references.

This question cannot be answered as simply as you put it, but it's not too much to elaborate on.

The order of the base pairs will be drastically different, but the same proteins and amino acids will be coded for in genes, just at different points along the DNA. For example, you may find the same sequence to code for a protein in a mouse as in a human, but they will not be found in the same place along the DNA code (although they will still be read and eventually produce the same protein).

http://www.nature.com/nature/journal/v420/n6915/full/nature01262.html
Additionally, this article shows that, if we take your question literally, "at the nucleotide level, approximately 40% of the human genome can be aligned to the mouse genome", that is, if human and mouse DNA was lined up side-by-side, and a percentage of identical match-ups was calculated.

However, taking a 'looser' approach, it is worth noting that about 5 percent of both of genomes consist of protein-coding genes (https://www.genome.gov/10001345), and the remaining 90%+ is non-coding. If we only count the protein-coding genes, the average similarity of genes between humans and mice in only protein-coding genes is 85%. The link above says that some are 99%, and some are 60% - there is a clear similarity here between humans and mice, albeit not 100% identical.

If you wish to know the explanation, simply it is because mice and humans both have a common ancestor (the last link also explains this) about 80 million years ago. Due to these similarities, and the striking similarities, scientists simulate genetic changes in mice that can occur to humans, and have used computers to analyse the similarities in mouse genome.

I hope this is understandable, if you need any clarification on terms, please ask :)


Beta oxidation of saturated fats In my text book there is an example of a 18 carbon long fat and it says that it can run 8 laps of oxidation. I don't understand why it doesn't run 9? 2 are removed each cycle?

Thanks.

I believe your textbook is referring to the fact that you only perform the complete beta oxidation eight times.  Because there's a carboxylic acid at the terminus of a fatty acid chain, the cell takes a slightly different route and reacts it with ATP, which generates a fatty acyl adenylate and pyrophosphate (PPi).  This AMP can subsequently be displaced in an attack by CoASH, at which point the beta oxidation process can proceed in full to begin cleaving off acetyl-CoA.

Here's a visual representation of this activation process, too.


Is the innate immune system capable of identifying all foreign antigens? I've been studying immunology on my own lately and I would like to know if the macrophages and the other components of the innate immune system are capable of identifying all foreign antigens.

As far as I understand the innate immune system is responsible for activating the adaptive immune response that will produce antibodies. So the innate immune system should be able to identify new antigens, antigens that the body has never seen before.

If that's the case, how does it work? Does everything "alive", from virus to bacteria, present the same molecular pattern that is responsible for triggering an innate immune response?

Thanks!

TL;DR the huge block of text:

The innate immune system only recognizes certain antigens, called PAMPs.
The activate immune system usually requires the immune system, but it can get around this in some cases.

You're on the right track.
Pathogen-associated molecular patterns (PAMPs)
Innate immune cells such as macrophages and denritic cells (DCs) only recognize certain pathogen-associated molecular patterns (PAMPs), and this occurs primarily through membrane-bound receptors called Toll-Like Receptors (TLRs). Diversity of PAMPs is extremely limited compared to the extraordinary diversity in recognition by the active immune system. However, they include many molecules and classes of molecules that are essential for certain pathogens, such as flagellin, lipopolysaccharide, and viral double-stranded RNA.
To answer some of your question right away, the immune system can't adapt, but it can recognize antigens that the body hasn't seen before, because the set of antigens it can recognize (the PAMPs) are dictated by the genes associated with Toll-Like Receptors and other "Pattern-Recognition Receptors".
Exception 1: T cell anergy
The major link between the innate and active immune systems that you mentioned is through the presentation of antigens to T helper cells in lymph nodes by DCs: DCs present antigens (digested parts of pathogens) to T helper cells through a process called antigen cross-presentation.
When this happens, the T helper cell is activated through a series of chemical exchanges between the DC and the T helper cell, with two that are important to mention here: 1) the T cell recognizes the antigen–MHC class II complex on the DC (called T cell stimulation), and 2) the T cell receives a signal (called co-stimulation). The first signal only requires cross-presentation and recognition by a T cell. But for the DC to release the co-stimulatory signal, Toll-Like Receptors (TLRs) on its surface need to have recognized a PAMP.
With these interactions (plus some more), the T cell will begin proliferating. However, immunology is very nuanced; you can probably find exceptions to every sentence I just wrote (I see a lot even while writing this). It turns out that a T cell can still be activated even without co-stimulation if its own stimulation is strong enough. This occurs through a process called T cell anergy. Activation of an anergic T cell—that is, one that was activated but did not receive a co-stimulation signal—has to do with the autocrine and paracrine nature of a signal called IL-2, which T cells normally produce only small amounts of but produce much more when fully stimulated.
Exception 2: B cells T-independent activation
But T cells are only half of the active immune system. It turns out that B cell activation follows similar rules, though not through DCs. B cell activation usually occurs with help from activated T helper cells (only one that recognizes the antigen the B cell is specific for). However, B cells can become activated without T cell help in two situations: an antigen binds to the B cell receptor and to a TLR, or 2) the B cell receptors become saturated with highly repetitive epitopes. Situation #2 technically occurs without help of the innate immune system.
So you're mostly correct that the active immune system requires innate immune system help, except that there are these two exceptions. And since immunology has so many exceptions, there are likely to be more.


Can you bleed from your bones? I was talking to my science teacher about the body specifically the red bone marrow.

She said that blood is created in the red bone marrow. Does that mean that if you were to cut a fresh bone open it would bleed?

Yes, bones too bleed if they get damaged (break or bruise). This is because bones are highly vascularised organs and breaking of bones will indeed rupture the blood vessels causing bleeding. Main artery which supplies blood to bone is nutrient artery , others are epiphyseal, metaphyseal and periosteal arteries. Skeletal system receives about 15.6% of cardiac output.
Since bones contain very low percentage of water ( about 31% ) comapred to others like skin(64%),brain and heart (73%) and lungs ( 83%). So the saying "as dry as bone " stills holds well.

Sources:

1-https://www.mananatomy.com/basic-anatomy/blood-supply-bones

2-https://water.usgs.gov/edu/propertyyou.html


Blood pressure in the blood vessels Why do the capillaries have a lower blood pressure than the arteries even though the capillaries lumen is much narrower. Wouldn't the narrowness of the blood vessel increase the pressure? Also the arterioles have an even larger lumen than the arteries so shouldn't the capillaries have a larger blood pressure than them as well?

Answer: You are right that if you had one big pipe that was getting progressively narrower, the pressure in that pipe would increase. In the vascular system, you have one big pipe emptying into exponentially more small pipes. The total lumenal diameter of the small pipes is actually greater than the single big pipe.

Even though each individual capillary has a smaller lumenal diameter than each artery, the sum lumenal diameter of all of the capillaries is much greater. This is because there are way more capillaries than there are arteries.

More detail: The following image plots total cross-sectional area and pressure in the pipe against the level of the circulatory system. The sum cross-sectional area of the vessels is highest in the capillaries, simply because there are so many capillaries. You can see the pressure decreases accordingly.


Can birds suddenly suspend in the air in one position? I don't know if it was my eyes fooling me or if it was real. I've seen birds suddenly get suspended in the air, flapping their wings but not moving. Like making non-locomotor movement on the air. Is there an explanation for this?

Doing a stationary flight is called hovering (as @kmm said in the comments).

With head wind

When there is a (relatively important) head wind, many birds are able to perform stationary flights. However, in the bird's referential the flight is not stationary. It is typically common to see that for see birds.

True hovering

In absence of head wind, most birds aren't able to hover. There are a few exceptions. Hummingbirds hover while feeding on nectar. Some birds of prey are able to hover (they do so for hunting purposes) such as the common kestrel for example. While fishing, the pied kingfisher is famous for its hovering behaviour.

Anatomy and metabolic cost

Generally speaking, hovering requires flapping its wings very fast and is therefore energetically very costly. From wikipedia

  Most birds that hover have high aspect ratio wings that are suited to low speed flying. One major exception to this are the hummingbirds, which are the most accomplished hoverers of all the birds. Hummingbird flight is different from other bird flight in that the wing is extended throughout the whole stroke, the stroke being a symmetrical figure of eight, with the wing producing lift on both the up- and down-stroke. Some hummingbirds can beat their wings 52 times a second, though others do so less frequently.

Videos

Here are some videos of birds hovering:

Hummingbird hovering
Common kestrel hovering
pied kingfisher hovering


Do hermaphrodites have more nerve fibers in their puendal nerve? Recently I have been thinking, both the glans penis and the clitoris are the most sensitive parts of the body. They contain a lot of nerve endings. Do hermaphrodites share the nerve fibres between the two organs, or do they have double the regular amount of nerve fibers?

Also, at which point does their nerve branch out? Do they have two sets of dorsal genital nerves coming out of the pudendal nerve or does the same set of dorsal genital nerve go into both organs?

Short answer
The genitals of true intersex individuals are not duplicated. Instead, their external genital features are hybrid structures. In turn, it's not a matter of duplicated neural innervations.

Background
Hermaphroditic phenotypes in humans are nowadays preferably described as  intersex phenotypes. In humans they come in different flavors, dependent on the underlying genetic causes, which are often caused by mosaics of X and Y chromosomes. Dependent on the exact genetic underpinnings, various types of intersex phenotypes occur, with different internal and external phenotypes of the reproductive tracts.

To proceed to the most extreme case, namely the true intersex individuals - these people display both male and female external genital tissues. However, this doesn't mean they have fully developed male as well as female genitals.

Now taking a step back to the normal male/female situation - you have to realize the clitoris and glans penis develop from the same tissue (Fig. 1). In true hermaphrodites, the external genitalia are not duplicated, instead they form a hybrid, where it becomes unclear what exactly is present: a small (glans) penis, or an outsized clitoris (Fig. 2).

So in all it is not a matter of duplication, but a hybridization of similar feats.

Fig. 1. Male and female genital development. source: University of the Cumberlands

Fig. 2. Intersex external reproductive organs. source: ImageSlideShare


Stomach Virus : How does it affect the bacteria of the intestines? When you have a stomach virus and it causes extreme bowel movements to the point of almost pure stomach acid, does this kill off the bacteria in our intestinal tracks?

No, since the pH and the conditions are different in the different compartments (stomach, small intestine, colon) of the bowel.
See this figure (taken from this website) for the differences:

There are not that much bacteria in the stomach, so even even nothing else than acidic stuff comes out, the bacteria are not affected. And even when you have a severe diarrhea, there are still enough bacteria left to keep it colonized.


How can low cholesterol cause mortality? I am studying processes 1. stroke, 2. heart disease, and 3. cancer, and their mechanisms associated with low cholesterol which is a result of lowering cholesterol especially in elderly, Low cholesterol is associated with mortality from stroke, heart disease, and cancer: the Jichi Medical School Cohort Study.
Stroke's manifestation is primary intracerebral hemorrhage ICH confirmed by many exclusion articles of other factors such as liver disease).
In the heart disease, there CAD and ischemia.
In the cancer, metastasis.

I started to think what could be enough general for all of these.
In the energy sense, one possibility could be glycogen, since it is used as an acute energy storage in all those organs.
Mechanisms could be the macro/microstructures of storage which are mostly unknown, presenting roughly 80/20 proportions.
So I propose that the lack of energy causes those conditions.

I noticed that many authors use the word remnant cholesterol when speaking about the subject. I did not understand its biophysical meaning.
Remnant cholesterol is an independent factor of cardiovascular manifestations apparently through the larger triglyceride-rich lipoproteins' (TRL) remnant kinetics.
Remnant cholesterol does not seem to cover all aspects of low cholesterol.

How can you low cholesterol cause stroke, heart disease and cancer?

What you have asked for is a causal answer to correlated findings. There is no cause-effect evidence (at least from my searching) showing low cholesterol will indeed cause stroke. Associations like this are dangerous in the sense that we shouldn't think that one causes the other. But, we can speculate on how they are linked, which is always fun.

I'll be going off my understanding of cholesterol transport and will include the reference at the bottom. Essentially, cholesterol is used in the cell membrane to change the permeability of the membrane. The more cholesterol, the less permeable the membrane is to water. However, this also changes the physical properties of the cell membrane, making it more rigid and structured. If I had to guess (which is again PURE SPECULATION) I would think that decreasing the cholesterol to the point of a dangerous level would increase the cell permeability of vital cells, the most sensitive would be neurons who depend on ion based signaling to perform primary functions. Since ions are very small and easily pass through the membrane if the membrane is leaky, they might be the first indicator that the something is wrong and the membrane isn't strong enough. Again, purely speculative with no evidence. An experiment one could do is examine the amount of cholesterol required in a cell to keep ions from crossing the membrane and see if there are any other effects that occur within or around the cell before ion passing. If you aren't in this type of research yourself, maybe you can fund it!

Source= Cassarett and Doul's Essentials of Toxicology. Textbook, 12th edition


How can pasteurized milk last 7 days? In Estonia, the product bought from the shop lasts about 2-3 days, in Finland 3-5 days and In Oslo Norway 7 days.

The better infrastructure of transportation explains some for Finland and Norway.
But how on earth so big difference between Norway and Finland?

I heard today that some countries are fluoridating milk.
Ii is not in Finland and Norway.
However, it may be the case that some minerals are existing naturally more in Norway than in Finland. Also, more rain dissolves more minerals in Norway than in Finland.

How can pasteurized milk last 7 days?

I would rather think about regulatory differences instead of biological ones. (Edit, as also Rory M highlighted in a comment)

Extended shelf life can be obtained through microbial ultrafiltration. However in Europe, ultrafiltration labelling is not mandatory, so it is difficult to distinguish if a milk product was simply pasteurized or also ultrafiltrated. The converse case, biologically speaking, two milk products could be generally the same but one country could be more stricter than the other on shelf-life legislation. (The shelf-life relates more to the unsuitability for sale rather than for consumption).


Muscle force/energy relationship I found the Hill muscle model, which helps relate the force a muscle can generate to its change in length over time (its "contraction velocity").  Is there a similar model to get an idea of the energy consumed during a contraction as a function of the force generated?

You can calculate the energy consumption using basic physics formulas.

Work = Force x Distance

and the unit of work is the Joule. Therefore if force is a function of change in length then substituting this function in for force in the above calculation we have that work is a function of length.

If you want to talk about energy consumed in terms of calories rather than joules,

1 calorie = 4.184 joules


Mesosome - does it exist? This wikipedia page says that mesosomes are artifacts produced by chemical fixing techniques. Most of my textbooks still show a mesosome and describes it as having functions like - respiration, helping in DNA replication, etc.

Has the idea that it is an artifact been widely accepted by the scientific community ?

I've always wondered about mesosomes. They were controversial 35 years ago when I was working in a related field. I decided to check the current status of the term.
I checked for research activity in this area using a Web of Science search "mesosome" in Title: this gave just 54 hits. I list the most recent here (unless otherwise indicated, these are single hits per year).
2010; 2008; 2004 (human cell mesosome??); 1994; 1988 (geology); 1983; 1982 (2); 1980
So it doesn't seem to be a very active area of research. The 2008 and 2010 papers are from the same group. The earlier paper is:

Li, X et al. (2008) Mesosome formation is accompanied by hydrogen peroxide accumulation in bacteria during the rifampicin effect. MOLECULAR AND CELLULAR BIOCHEMISTRY 311: 241-247   DOI: 10.1007/s11010-007-9690-4
Abstract: Ultrastructural alteration and hydrogen peroxide localization were examined in Xanthomonas campestris pv. phaseoli during rifampicin effect using transmission electron microscopy. Bacterial cells were treated with rifampicin and then were examined by electron microscopy to observe the changes of ultrastructure or hydrogen peroxide accumulation in living cells that took place before lysis. Intriguingly, rifampicin treatment led to presence of an additional location of hydrogen peroxide accumulation within the cells. There was an association between the frequency and size of the additional location of hydrogen peroxide accumulation and the concentration of rifampicin. Furthermore, an additional ultrastructure, mesosomes, was also present in cells during rifampicin effect. The frequency and size of mesosome increased with the increasing concentration of rifampicin. Result of multiple linear regression showed that the size of mesosome plays as a key factor in the quantity of excess hydrogen peroxide accumulation in cells during rifampicin effect. Linear correlation was confirmed between quantity of excess hydrogen peroxide accumulation and the size of mesosome in cells during rifampicin effect. This finding intensely indicated that mesosomes are just the additional location of hydrogen peroxide accumulation in cells under cellular injury caused by rifampicin treatment. The mesosome formation is always accompanied by excess hydrogen peroxide accumulation in X. campestris pv. phaseoli during rifampicin effect.

This paper has been cited 7 times. One of those citations is from:

Saier, MH. & Bogdanov, V. (2013)  Membranous Organelles in Bacteria. JOURNAL OF MOLECULAR MICROBIOLOGY AND BIOTECHNOLOGY 23: 5-12   DOI: 10.1159/000346496

Free full text here.
The language used in this review seems to support the existence of mesosomes as some sort of intermediate in the formation of intracellular membranes in prokaryotes. This review is a polemic in favour of the idea that prokaryotes do indeed contain intracellular membrane-bounded compartments. It has no abstract, but the first paragraph gives a flavour of its stance:

The traditional view of life on Earth divides the living world into two major groups, prokaryotes and eukaryotes. These two groups were originally suggested to differ in very basic respects. While eukaryotes had complex cell structures including a cytoskeleton and intracellular membrane-bounded organelles, prokaryotes were believed to lack them. In fact, numerous textbooks and current sources still note this distinction and hold it to be true. For example, in Campbell’s Biology [Campbell, 1993, p. 515] it is stated without equivocation: ‘Prokaryotic cells lack membrane-enclosed organelles.’ In ‘Functional Anatomy of Prokaryotic and Eukaryotic Cells’ [Tortora et al., 2009, chapt. 4] it is similarly claimed that ‘Prokaryotes lack membrane-enclosed organelles, specialized structures that carry on various activities’. In the current Wikipedia, under ‘Prokaryote’ the following statement can be found: ‘The prokaryotes are a group of organisms whose cells lack a cell nucleus (karyon) or any other membrane-bounded organelles’. In the same online compendium under ‘Organelle’, one can read: ‘whilst prokaryotes do not possess organelles per se, some do contain protein-based microcompartments’. Proteinceous microcompartments will be the subject of a forthcoming Journal of Molecular Microbiology and Biotechnology written symposium, but this one will show that these generalizations, suggesting a lack of subcellular compartmentalization in prokaryotes, are blatantly in error [Murat et al., 2010a].


Genetic carrier Pedigree of Recessive Traits A human male and female couple with normal colored ears discover that, in both of their families, their fathers (who have normal ears) each had siblings with red ears.  Red ears is a rare autosomal recessive disorder.  None of their grandparents had red ears.  Assume that the red ears in both families were caused by mutations in the same gene, that there were no new mutations within the pedigrees, and that the mothers of the couple were not carriers of the disease gene.

A) based on the information, what is the probability that the male in the couple is a carrier of the red ear disease gene?

B) if the couple had 1 child, what would be the probability that child would have red ears?

I was discussing this problem over with a friend and we got different answers.

A)I think the answer is 25%.  I multiplied 1/2 and 1/2.
B)6.25%.  I multiplied 1/4 and 1/4.

Let's take Question A:

Both fathers have siblings with red ears, and red ears are an autosomal recessive trait. The grandparents did not have red ears, we know then that they were carriers of the recessive allele. Each grandparent was Nr (for Normal and red alleles respectively).

The fathers have normal ears, so they could be NN (probability 0.33) or Nr (probability 0.67).

The answer then is that each father independently has a 2/3 chance (0.67 probability) of carrying the red ears gene.

The male's mother, being RR, makes the male a carrier only if the male's father is himself a carrier. To put it mathematically, he has a 1/2 chance of being a carrier with 2/3 probability that he was a carrier to begin with. (2/3)*(1/2) = 1/3.

Therefore the male can be carrier with 1/3 chance.

Now Question B:

Short answer:

Since the male and female have symmetrical pedigrees, and we just solved the chance of the male being a carrier with 1/3 chance, then the chance of them having a child with red ears is (1/3)*(1/3) = 1/9.

Long answer:

The male's and female's fathers may each be heterozygous or homozygous normal, given the information, with both mothers being homozygous normal (NN).

If Father A is NN (crossed with Mother A, also NN), there is a 0 probability of passing on the red ears allele.

If Father A is Nr, then Person A has a 0.5 probability of carrying the red ear allele.

Person A can now be NN (with 0.25 probability) or Nr (with 0.5 probability).

Likewise with Person B.

Now lets consider all 4 combinations of genotypes that Person A and B can have when they have a child. I will write a table with one Person on each side of the table, with the probability of their genotype written in brackets beside. Each intersection will represent the frequency of carrying the red ears allele.

                Person B
             (1/3)     (2/3)
Person A      NN        Nr
(1/3) NN      0/4       2/4
(2/3) Nr      2/4       2/4

Carrying the red ear gene: (A more interesting example)
There are a total of 6 outcomes in which the child carries the red ears allele, but these must be weighted by the probability that each parent has the associated genotype.

Probability of carrying 'r' = [ (1/3)(1/3)(0/4) + (1/3)(2/3)(2/4) + (2/3)(1/3)(2/4) + (2/3)(2/3)(2/4) ] / [ (1/3)(1/3) + (1/3)(2/3) + (2/3)(1/3) + (2/3)(2/3) ]
 = 0.25

Having a child with red ears:
Probability of having red ears = [ (1/3)(1/3)(0/4) + (1/3)(2/3)(0/4) + (2/3)(1/3)(0/4) + (2/3)(2/3)(1/4) ] / [ (1/3)(1/3) + (1/3)(2/3) + (2/3)(1/3) + (2/3)(2/3) ]
 = 1/9 or about 0.11

It's left as an exercise to the student to derive the remaining probabilites.
Nr 4/9
NN 4/9
rr 1/9


In insects, does the Alanine repeat occur on the homeodomain sequence of the abdomen or does it occur on a different sequence? By "Alanine repeat", I am referring to the suppression of the formation of extra insect legs due to Ubx gene suppression through Distal-less repression.

Some background:

  The new work involved misexpression of the Drosophila Ubx protein in the presumptive thorax of transgenic fruitfly embryos. Limb development was suppressed because of repression of Dll. By contrast, the misexpression of onychophoran and crustacean Ubx proteins did not interfere with Dll expression and the formation of thoracic limbs. These results raised the possibility that the Drosophila Ubx protein is functionally distinct from Ubx in onychophorans and crustaceans. One study suggests that Drosophila Ubx has acquired an alanine-rich peptide that mediates the repression of gene transcription; this peptide is lacking in onychophorans. The other study provides evidence that the crustacean Ubx contains an additional peptide that modulates the activity of the alanine-rich peptide, and possibly other repression domains, in crustacean Ubx.

  Insect-restricted sequences include four regions N-terminal to the
  homeodomain (I1–I4), a peptide motif (QAQAQK), and an extended run of
  alanine residues C-terminal to the homeodomain

  The onychophoran Ubx protein might function as an activator of appendage development. When the onychophorans and arthropods diverged,
  Ubx acquired an alanine-rich repression domain near its carboxy
  terminus. This domain mediates constitutive repression in insects.
  But in crustaceans the addition of the regulatory peptide causes it to
  function in a conditional fashion. As a result, Ubx does not suppress
  limb development in crustaceans. But it eliminates abdominal limbs in
  insects, greatly reducing the overall number of appendages compared
  with crustaceans.

You can read about it here:

Levine, Mike. "Evolutionary biology: how insects lose their limbs." Nature 415.6874 (2002): 848-849.

Galant, Ron, and Sean B. Carroll. "Evolution of a transcriptional repression domain in an insect Hox protein." Nature 415.6874 (2002): 910-913.


Excretion of small kangaroos while in the pouch How is the excretion of small kangaroos done when they are in the pouch of their mother, fastened onto her teat? My question is what happens with the products; do they accumulate in the pouch?

Wow! What an interesting question!

I did a bit of searching around, and here's what I found. It looks like the baby kangaroos, or joeys, do in fact produce excrement while in their mothers pouch. The mother kangaroo uses her tongue to clean her joey and her pouch.

I found this information in a couple of differently places by doing a google search for "biology of marsupial reproduction pouch excrement."

One of the first sources I found was a New York Times article titled "Marsupail Maintenance." You can find this article at this link:
http://www.nytimes.com/2012/08/14/science/how-do-female-kangaroos-keep-their-pouches-clean.html?_r=0

The article was published in a reputable news paper, and used an interview with a curator of mammals from the Bronx Zoo as a source.

Another resource I found when researching this topic was an Australian wildlife sanctuary. This wildlife sanctuary has information web pages online to help visitors learn more about the animals that live in the sanctuary. You can find their entry on Eastern Grey Kangaroos at this link:
http://billabongsanctuary.com.au/native-animals/mammals/eastern-grey-kangaroo/

This web pages gives a pretty detailed overview of the Eastern Grey Kangaroo. The information on joeys and pouch cleaning can be found in the section called "Raising the Young."

I hope this fully answered your question!