Is exon order always preserved in splicing? Are there any cases in which the splicing machinery constructs an mRNA in which the exons are not in the 5' -> 3' genomic order? I'm interested any such cases, whether they involve constitutive or alternative splicing.

After performing a quick literature search, I am, as with GWW, unable to provide any literature against this occurring, although this paper by Black (2005) states that exons in multi-exon pre-mRNAs are always maintained in order.

 Black DL. 2005. A simple answer for a splicing conundrum. Proceedings of the National Academy of Sciences of the United States of America 102: 4927–8..

Separate components of the spliceosome recognise sequences at the the start and end of each intron, along with a branch point adenine and some other conserved (highly in the case of yeast) regions upstream of the 3' end. The components seem to assemble in a particular order, which is 5' to 3' directional.

The general consensus seems to be that the spliceosome moves along the pre-mRNA from 5' to 3' removing the introns and splicing the exons together to form the mature transcript, ready for translation. The introns are subsequently degraded. In the case of eukaryotes some processing is required to transport the mRNA out of the nucleus to the ribosomes in the cytoplasm.

The mRNA would have a start codon near the 5' terminus and stop codon near the 3' end, at the boundaries of the CDS, and it isn't clear to me how this structure could be maintained if exon order didn't follow the 5' to 3' assemblage. I should imagine that the protein could be affected in much a similar way to exon skipping, possibly resulting in a truncated, inactive or ineffective protein. As protein folding is determined by the interactions between the amino acids, any change in exon order (secondary structure) is likely to result in a different tertiary structure.


What is the female equivalent of the morning erection that some men experience? There was question about what causes "morning wood." It was answered that the erection in the morning is caused by decline of norepinephrine during REM sleep. Which in part allows to prevent uncontrolled urination.

My question is: How does the decline in norepinephrine affect women? They obviously don't get erection.

Women have erections too! These erections are called clitoral erection. Clitoral erections are usually accompanied with vaginal lubrification.

Just like men (see here), the absence of norepinephrine during the REM phase of the sleep causes erections. In women, this phenomenon is called Nocturnal clitoral tumescence while it is called Nocturnal penile tumescence in men. In women, not only the clitoris get engorged with blood but the vagina too.


Why can't we breed watermelons without any remaining seeds in the flesh? Watermelon is just starting to come in season in the northeastern U.S., and having a seedless watermelon is convenient.  The only downside is, the "seedless" almost always still have the immature, sterile white seeds in them.

What is the mechanism for breeding these watermelons so that only these white seeds remain?  What is the genotype that results?  Could the genetics be modified so that there are virtually no seeds (short of any minor aberrations) left in the flesh of the fruit?

The seedless watermelons, like bananas, are a crop that are specifically bred to be trisomic (three copies of a chromosome). The consequence is the seeds are non-viable.


Is every cell competent? I would like to know if every cell is competent or if there are any cells that are not competent.

Assuming that you are asking about E.coli cells being made competent for transformation using plasmid DNA, an answer is cached here from this source:

  Hanahan, D. & Bloom, F.R. (1996). Mechanisms of DNA transformation. In F.C. Neidhardt (ed.). Escherichia coli and Salmonella : Cellular and Molecular Biology. (pp. 2449-2459). Washington D.C., United States: ASM Press.

The source (and it is perhaps worth emphasising that Hanahan is/was a transformation guru) states that treatment with divalent cations can achieve 10% of cells rendered competent, whereas treatment for electroporation can achieve transfer into 95% of cells.

This information was, of course, published in 1996 so it is conceivable that advances have been made in the case of the former method.


Worm inside a millepede I found a dead millipede lying on the ground in Wayand, Kerala (India). I put it in a bottle and brought it home. After around 5 hours a worm came out of it. It is about about 1.5 cm long and segmented.
Any idea if its a larva of some sort?

Edit:
It's been about five days since I posted the picture of the larva , and it seems to have pupated last night. The pupa is approximately 0.5 cms in length. All that's left is to see what happens next.

Definitely some sort of fly (order Diptera). Specifically, you found the legless larva, or maggot, of a fly that then developed into a pupa.

 Source: Univ of Florida IFAS
The above picture represents the life-cycle stages of the common house fly (Musca domestica).

M. domestica is one of the most common and widespread flies in the world:

This common fly originated on the steppes of central Asia, but now occurs on all inhabited continents, in all climates from tropical to temperate, and in a variety of environments ranging from rural to urban. Source

According to Wikipedia, M domestic larvae take 2-5 days to metamorphose into a pupa.

Although the OP mentions that a housefly emerged from the pupa, I'll caution the OP that many flies look like house flies to the untrained eye. Houseflies typically deposit their eggs in fecal matter or dead flesh, so finding a maggot deposited into the body of a living millipede seems unlikely behavior from the common house fly. (Edit: Though I see now that the OP said the millipede was dead, so this is not an unlikely candidate).
IF the larva was deposited when the millipede was still alive, then other genera would be more likely.
One example would be a Sarcophagid (or flesh fly; family Sarcophagidae), which some species being known to be internal parasites.
As for proper ID, according to Wikipedia:

Generally, only males of this family can reliably be identified to species, and then only by examination of dissected genitalia. The literature is incomplete or scattered for all regions

Here are some images for a fairly widespread species, Sarcophaga crassipalpis (which is very unlikely to be your species, but demonstrates general appearance of this family):

 Source: Univ of Florida IFAS
Your specimen might still belong to another group of flies, the tachinids (family Tachninidae), which very often parasitize other arthropods.
It'd be very difficult to differentiate most of these taxa without up-close examinations of specimens.


20/20 vision translated to resolution What resolution and or DPI would a TV or VR headset need to be to equal 20/20 vision? and 20/10? With even the 4K TV it does not seem as sharp as my own vision.

To measure acuity, it's important to have a measure that considers visual space rather than physical world space (it doesn't make any sense to talk about "millimeters" because that says nothing about how far away the object is), so one would normally talk in terms of "degrees or arc" where 360 degrees is a whole field in all directions. Within degrees of arc, you can refer to "arcminutes" which are 1/60th of a degree of arc. If you could see everything in front of you, but nothing behind you, then you have 180 degrees of visual field in both horizontal and vertical dimensions (humans actually have a much smaller visual field than this), or 10,800 minutes of arc.

Your visual acuity greatly depends on where on the retina an image falls; the 'fovea' is the center of the retina where your vision is most sensitive. In the fovea, the maximum acuity is somewhere around 0.5-1.0 minutes of arc (see for example Rossi, E. A., & Roorda, A. (2010). The relationship between visual resolution and cone spacing in the human fovea. Nature neuroscience, 13(2), 156-157.), which corresponds nearly to cone density in the fovea.

A good "rule of thumb" (no pun intended, since we won't be using the thumb here...) is that the width of your fist at arms length is about 10 degrees of arc, your pinky finger is about 1 degree of arc. To get 0.5 arcminute resolution, then, you would need a screen the size of your fist (600 arcminutes) held at arms length to be 1200 pixels wide. Modern cellphones held at a moderate distance likely come near this limit, whereas TVs and monitors typically do not; however, you probably view your phone much closer than arms length and your TV much further.

Realistically, however, pixel counts far below this are sufficient for most scenes, because acuity measured this way is referring to the ability to separate points of light. In real natural vision, we aren't usually separating points of light, but rather organizing visual representations into salient objects, so the actual pixel density required to get a smooth image is less. Pixel limitations are more likely to be apparent when displaying text, since contrast is much higher with text than with natural scenes.

References

Rossi, E. A., & Roorda, A. (2010). The relationship between visual resolution and cone spacing in the human fovea. Nature neuroscience, 13(2), 156-157.


Why should you use an annealing temperature about 5°C below the Tm of your primers? Why should you use an annealing temperature about 5°C below the Tm of your primers?

According to my current research, I think it has something to do with the other reactents in the PCR, but I am not sure.

You want to have primers which bind under the conditions of the reaction only to your sequence of interest. If you go too far off the optimal annealing temperature (5°C below the Tm is indeed a relatively good choice in my experience), your will affect the PCR efficency and thus the yield of your reaction.

An annealing temperature, which is much too low allows annealing of your primers to other sites than your intended target with partial annealing or internal base mismatches. This leads to unspecific amplification and lower yields.

If the annealing temperature is too high no primer binding can happen and you will get not PCR product. Alternatively, partial binding can also lead to misprimed products, although this is much less likely than getting no product at all.


What is Luc Montagnier's research on electromagnetic signals from DNA about? After reading a Youtube comment, I started reading on Luc Montagnier's research on electromagnetic signals from DNA. I haven't been able to find a source that would clearly explain what it's about. I would like to know, if possible,

what the claims are exactly;
what experiments were carried out;
whether the results have been replicated independently;
whether the results contradict anything considered firmly established scientific knowledge (it seems Montagnier says they do) and, if so, how;
what the criticism is.

I know it's a lot to ask, but if you could make your answers accessible, it would be great. Please don't refrain from using technical language where it's necessary, but do try to give a general picture for those (including me) who might not understand it.

I think that ymar poses an excellent set of questions that should be discussed on these forums.  It brings back memories (sic) of the memory of water controversy.
I'll quote from Andy Coghlan's excellent article published in New Scientist in 2011
Draw your own conclusions.  (The emphases are mine).

... So what have
Montagnier and his team actually found? Full details of the
experiments are not yet available, but the basic set-up is as follows.
Two adjacent but physically separate test tubes were placed within a
copper coil and subjected to a very weak extremely low frequency
electromagnetic field of 7 hertz. The apparatus was isolated from
Earth's natural magnetic field to stop it interfering with the
experiment. One tube contained a fragment of DNA around 100 bases
long; the second tube contained pure water.
After 16 to 18 hours, both
samples were independently subjected to the polymerase chain reaction
(PCR), a method routinely used to amplify traces of DNA by using
enzymes to make many copies of the original material.
The gene
fragment was apparently recovered from both tubes, even though one
should have contained just water (see diagram).
DNA was only recovered
if the original solution of DNA - whose concentration has not been
revealed - had been subjected to several dilution cycles before being
placed in the magnetic field. In each cycle it was diluted 10-fold,
and "ghost" DNA was only recovered after between seven and 12
dilutions of the original. It was not found at the ultra-high
dilutions used in homeopathy.
Physicists in Montagnier's team suggest
that DNA emits low-frequency electromagnetic waves which imprint the
structure of the molecule onto the water.
This structure, they claim,
is preserved and amplified through quantum coherence effects, and
because it mimics the shape of the original DNA, the enzymes in the
PCR process mistake it for DNA itself, and somehow use it as a
template to make DNA matching that which "sent" the signal

I always knew there was something suspect about genetics!  Stick to biochemistry, that's what I say :-)


What happens to our umbilical cord internally as we age? I was always curious as to if or how much of the internal structure or workings of the umbilical cord are still in existence as we age.  What happens to it over time?

The wikipedia article naval almost exclusively describes physical appearance and only touches on some disorders that affect physical appearance.

Then the wikipedia article on umbilical cord explains what happens briefly after birth, and only touches on it becoming part of the circulatory system.  What does it actually do in later life, as part of that system?

The umbilical cord, which contains the umbilical arteries and vein so important for nutrient, oxygen and waste transport before birth, becomes useless pretty much the moment the lungs start working (the kidneys already started before birth). As the baby breathes, the two arteries constrict to stop flow from the newborn to the placenta. The Wharton's Jelly, a structural element in the cord, causes collapse of the vein on cooling to outside temperature. Within a matter of a few minutes, the whole system is shut down.

Within the infant, the umbilical vein and ductus venosus (which carried blood to the liver and the inferior vena cava) close up and degenerate into fibrous remnants known as the round ligament of the liver and the ligamentum venosum respectively. The round ligament basically just divides the left part of the liver into medial and lateral sections. The ligamentum venosum does basically the same thing on the posterior surface of the liver. Both ligaments maintain their attachment to the umbilicus. (The small paraumbilical veins are unimportant except in the case of severe portal hypertension, where they act as a portacaval anastomosis.)

The parts of the arteries closest to the navel degenerate into what are known as the medial umbilical ligaments (which basically serve no purpose whatsoever and are buried in the abdominal wall), while the more internal remaining sections are retained as part of the circulatory system as the umbilical artery.

The umbilical artery in adults is a branch of the anterior division of the internal iliac artery. The umbilical artery is found in the pelvis, and gives rise to the superior vesical arteries (supplying the superior part of the bladder, and parts of the ureters. In males, it also gives rise to the the deferential artery which supplies the ductus deferens.


Why do Indian Major Carps spawn in running water? I think running water serves as a cue necessary for hypothalamus to release GnRH into hypophyseal portal system which initiates a cascade of hormone actions ultimately leading to release of gametes.

I have looked up in Internet with no results. I guess no work has actually been done to discover the reason. But as it's an assumption I would like to here from anybody more specialised.

Some fish spawn in running water for a simple reason: There eggs need oxygen and survival rate will be low under hypoxic conditions. Running water has a much lower change of becoming hypoxic than standing water, so that is why many fish spawn in running water. Some fish of standing water, like sticklebacks, wave fresh water over the eggs to achieve the same.

How they sense oxygen level is another matter. In fish, the neuroepithelial cells (NEC) have been implicated as the major oxygen sensing cells. See wikipedia above and specifically this if.you want to know more.


What are the (correct) terms for these flagella-arrangements? I came across the following diagrams depicting two kinds of arrangement of flagella over cells.

Now according to my (very unreliable) school textbook, the arrangements are termed as:

A - Cephalotrichous (tuft of flagella on one end)
B - Lophotrichous (tufts of flagella on both ends)

Whereas another (equally unreliable) book states the exact opposite:

A - Lophotrichous (tuft of flagella on one end)
B - Cephalotrichous (tufts of flagella on both ends)

A spot of cursory Googling reflects this sort of confusion online (compare the images and their labels here) as well.

According to Wikipedia that arrangement A is lophotrichous, but it makes no reference to arrangement B though.

I tried to figure it out, going by the smattering of Greek I picked up as a Bio. student ( Cephalos = Something to do with the head ; Lophos = something to do with a peak/protuberance ), I arrived at:

  Hmm... so cephalotrichous probably means you find the tuft on one "end" (so arrangement A), and ipso facto lophotrichous is arrangement B.

But I guess, I ended up putting a little too much thought into it...

  Cephalotrichous is probably used to indicate you have a tuft on the "head" in addition to another tuft on the "tail" (so arrangement B), and ipso facto lophotrichous is arrangement A.

 At this stage I'm not sure what's more serious: my inability to find an authoritative answer to my question... or my tendency to overthink stuff

I'm in a fix.

Could someone clarify, citing (multiple, if possible) authoritative sources, on the distinction between a "cephalotrichous" and a "lophotrichous" arrangement?

A good source on this subject is Tortora's Microbiology. Unfortunately, it uses a different terminology.
Have a look at this image (click on it for a bigger size), chapter 4, page 81:

As you can see, the lophotrichous arrangement is the one with the flagella at one end of the bacterium (which agrees with the arrangement at the Wikipedia page).
However, the opposite arrangement (flagella at both ends) is called amphitrichous (which, by the way, makes more sense), not cephalotrichous.
The text below that image says:

Lophotrichous: a tuft of flagella coming from one pole;
Amphitrichous: flagella at both poles of the cell;

If you assume that "amphitrichous" is synonym of "cephalotrichous", then the correct book would be your second one, which says:

A - Lophotrichous (tuft of flagella on one end)
B - Cephalotrichous (tufts of flagella on both ends)

However, there is no evidence that one should consider "amphitrichous" and "cephalotrichous" as synonyms. Besides that, things seem to be way more complicated: if you search those terms at Google Books, you'll see that most books say that amphitrichous bacteria have only two flagella, one at each end. And, indeed, some have completely opposite definitions.

Source: Tortora, G., Funke, B. and Case, C. (2010). Microbiology. San Francisco, California: Pearson Benjamin Cummings.


What is Meriva Phytosome Curcumin? What is Meriva Phytosome Curcumin other than being a food supplement?

Is it a plant? A type of plant extract?

I googled it but still couldn't figure out exactly what it is.

The reason I'm asking is because I came across the following list in a site selling vitamins and other food supplements:

Meriva Phytosome Curcumin
Turmeric (Curcumin)
Turmeric Formulas

It wasn't clear to me if Meriva Phytosome Curcumin is a specific kind of curcumin since it seems to be sold under a few different brands.

Well, http://meriva.org states that

Meriva® is a patented formulation of curcumin, a dietary phenolic, with soy lecithin (non-GMO)(1). The two compounds form a non-covalent adduct in a 1:2 weight ratio, and two parts of microcrystalline cellulose are then added to improve formulation, with an overall contents of curcumin of 20%

A phytosome is

[...]  a complex of a natural active ingredient and a phospholipid.
It is claimed that phytosome increases absorption of "conventional herbal extracts" or isolated active principles both topically as well as orally.
The complexation with phospholipid has been applied to many popular herbal extract or active molecules including [...] curcumin isolated from turmeric [...].

And Curcumin is

[...] is a diarylheptanoid. It is the principal curcuminoid of turmeric, which is a member of the ginger family (Zingiberaceae). Turmeric's other two curcuminoids are desmethoxycurcumin and bis-desmethoxycurcumin. The curcuminoids are natural phenols that are responsible for the yellow color of turmeric. Curcumin can exist in several tautomeric forms, including a 1,3-diketo form and two equivalent enol forms. The enol form is more energetically stable in the solid phase and in solution.

So, Meriva Phytosome Curcumin is a phytosome of curcumin developed by Meriva.


What exactly happens if during translation, an amino acid is not present? Lets say that the cell wants to make a particular protein. Transcription of the appropriate gene is done and the mRNA is made. mRNA attaches to the ribosome and the translation is initiated in a "normal" way.

What exactly would happen if an amino acid required in the protein is absent ? I know that the protein would not be manufactured properly but I want to exactly know what would happen to the ribosome and the mRNA. Are they destroyed? Are they simply separated? Who regulates this?

Point to know : aminoacyl-tRNA binds to mRNA its not just t-RNA..

So if there is no Amino-acid there is no aminoacyl-tRNA of that aminoacid.. so if there is no aminoacyl-tRNA, the anticodon of tRNA doesn't form a bond with mRNA, so the protein production halts (until the Amino acid produced).

If the protein is not formed within a certain long time, the premature protein folds itself and breaks. Then a molecule (example: ubiquitin for certain type of bacteria) attaches to this premature protein and marks it for degradation.

But there are still chances of protein production with slight mutations.

Mutation: tRNA with the same anticodon and different aminoacid can easily bind to the A site of the ribosome in the absence of the correct aminoacyl-tRNA, so the protein production doesn't stop in this case but the protein has a mutation with different aminoacid.


Applying Constraint Programming to sequence alignment/analysis My Masters program is focused on formal methods such as SAT solving and constraint programming. I am interested in applying such techniques to problems in sequence alignment and sequence analysis, areas that have been dominated by statistical methods.

So can you give me examples of some research problems suitable to be approached as constraints satisfaction problems?

Note: By constraint programming I also include more flexible paradigms like weighted constraint programming, where a solution may violate some of the constraints.

First read how local and global alignment differ from each other. Then decide an objective function, i.e. how to measure the similarity between two sequences? Maybe use Hamming distance? Or Levenshtein distance? After this the optimization part probably comes out quite naturally.

Be sure to check the existing softwares. Easy things have been tried out already. (And by the way, for some reason biologists call n-grams as k-mers.)


Gene located on Which strand? Want reference. Update: Initially my question (below) was appropriately marked as duplicate/overlapping  with two other questions; This and this ; among them a specific part of an answer of the second duplicate/overlap ; appropriately answer my question.

  The convention is that in indicating any sequence feature† in a protein-coding gene on double-stranded DNA, a single strand‡ is represented — the one from which the amino sequence could be read using the genetic code (conceptually, with T substituted for U). Like any other nucleic acid sequence§, it is always written in the 5ʹ to 3ʹ direction in the same manner as the mRNA transcribed from it, without this being explicitly stated.

But what it does not mention (but I'm still looking for); is whether there is a standard and universal documentation for this particular convention (IUPAC/ IUBMB/ ICBN/ ICZN/ anything such); because "conventions" are human-made rules, and without "declared, universally followed, and accessible" documentation; the conventions does not make a sense.  It rather feels like a rumor or viral phenomenon.  I visited the IUPAC and IUBMB website home pages but I could not locate the documentation from there. Also google keyword search did not found the helpful.

So I specify my question that I want to get the standard/ official source of this convention. I would be highly grateful if anyone kindly mention the source hyperlink.

My Initial Question

I'm stuck at a very basic convention on notation on reading Gene sequence. *Specially when a  book (or question paper or anything) does not mention whether a  nucleic acid (usually DNA), uses a single stranded DNA

The problem appears because similar region of the 2 opposite strands of a DNA can contain different gene, i.e.

(So it is possible that if we note a stretch from gene-1 with its complementary sequence, that complementary sequence could be confused with gene-2.)

In some cases, a sequence to a stretch of nucleic acid, indeed mean the sequence directly.

For example; In the wikipedia image about Reading Frame (Permalink)

the 5'to 3'Left to Right indicates the sequence of the template strand directly whereas

But at the more and more "interior chapters" I've seen a rather complicated and indirect notation (although I could not found  clear mention of a convention anywhere in books or web)... when they mean a sequence of a stretch of a gene (or a regulatory sequence), they writes the "nontemplate" or "sense-strand" sequence of the respective gene.

In the Wikipedia image on TATA Transcription Box (Permalink);

it must be a sequence from the nontemplate strand because if it was the template strand,  the "Promoter" location on the "template" strand must be on 3' side otherwise RNA polymerase would not be able to synthesize the nontemplate strand mRNA strand from 5' to 3' time-order. But it would become impossible to infer for me if the given sequence lacked labelling for relative locations of promoters and structural genes.

Now my question is If an article  provides me a single stranded  "Gene Sequence"; How can I infer it is directly the sequence of the mentioned gene stretch or it is the complementary ("sense") strand of the gene? What is the convention about it?

Assume that you are given the gene in the "forward direction"; the one where the starting ATG is on the left, that the sequence you are looking at is what the single stranded RNA will be.


Why can cones detect color but rods can't? I don't know if this question applies to only humans but why can cones see much greater detail than rods? Is it possible to have a rod that can detect light intensity and color?

The spectral sensitivity of photoreceptors expressed is the key to color vision. See figure below for the sensitivity of three-types of cone cells (S, M, L) and rod cell (R, dashed line).

From this figure, one can say rod cells provide information about the "blue-greenness" of vision, however, despite their spectral sensitivity, it seems that in human vision rod cells do not contribute to color vision, because they are highly sensitive to intensity, and thus they are mostly saturated in their response (does not induce firing of downstream bipolar cells) during normal daylight conditions. Rod cells specialize for night vision (scotopic conditions) which is crucial for survival, and under this condition the cone cells are pretty much useless.


Water-bird that can take off vertically from the water? If you look at ducks taking off, they take off at a pretty flat angle, building up speed before they finally get some altitude. This takes a lot of distance, it seems, for them to get high in the air.

But this lead to a question. Are there water birds that, sitting on the water, take off at a more vertical angle without the long run-up?

The best I can think of are flamingos, who cheat by having their feet on the ground, in the shallow waters. Some birds will dive into the water, grab a fish, then fly out at a high angle, but that's a bit different from sitting on the water then taking off.

Many birds are able to perform a vertical or near-vertical takeoff, on dry ground. Can any birds do this while sitting on the water?

Yes. A duck can be observed taking off near-vertically from the water's surface in this video. Watch the first duck to take off (from about 0:08). Immediately after take-off, the duck has a very low horizontal speed, and works to gain speed by a combination of flapping and vertically beating its tail. The full process is as follows:

Beat 1: The duck gives a sudden start. Both wings are beaten once on the water's surface to take advantage of the extra resistance the water provides, compared to air. The duck presumably also pushes down on the water with its feet below the surface in order to gain extra lift, but this is not visible.

Beat 2: By the start of the second downbeat, the duck's body is clear of the water, but the feet are obscured by spray.

Beat 3: The whole duck is clear of the water, and is gaining some horizontal speed. This wingbeat is accompanied by a clear vertical flap of the tail.

Beats 4 onwards: The duck continues to accelerate horizontally, remaining clear of the water.

Because the duck comes near-vertically off the water's surface, and remains airborne thereafter, I'd define the take-off as vertical, and the subsequent flight as transitioning into a duck's normal near-horizontal flight. Similar take-offs by terns can be seen in this video (but starting from a dive under the water's surface, see from about 1:02).

More generally, many waterbirds can take-off vertically from the water's surface, without requiring a run-up. All that is generally necessary is to face into the wind, and spread their wings. If the sea-surface is basically stationary, but there is wind, then any difference in speed between the air and the water can be exploited to generate lift.

If there is no effective wind (i.e., the water and the air are moving at the same speed), then the birds have to generate the lift for take-off by expending energy. Some species can do this, but it gets harder with increasing body-mass and wing-loading. I have personally observed a juvenile frigatebird (a species that generally weighs around 1 kg, but with very low wing-loading) lifting off vertically from the water's surface on a windless day. Note that frigatebirds would not normally land on the water (their feathers are not waterproof), and trying out a water landing seems to have been a play behaviour on the part of the juvenile.


How can you band wheat chromosomes using Giemsa dye? I am working with wheat chromosomes and trying to stain the chromosomes. However, during staining with Giemsa dye chromosomes appear totally dark. I'm not sure why this might be. Anyone have any ideas?

The Wright or Giemsa-stains can be influenced by the pH of the rinsing solution after the incubation in the dye-solution. The lower the pH the more pink will be the result. The higher the pH the more blue will be the result. Usually Giemsa-stains are differentiated at an approximately neutral pH. (Weise buffer pH 7,2 or acidified water pH 6,5). To lower the pH you can add few drops of acetic acid. This will also enhance the speed of differentiation.

Giemsa-stains are also sensitive for too long rinsing in diluted ethanol. The color turns blue and more faint.

Also it might be the trypsin that can digest some region rich in C or G. It's not condensed so appears light but the other region is very condensed so the trypsin can't enter and digest this region, which appears dark or the opposite.


How would the result of Hershey and Chase experiment been different if protein was the genetic material? Please answer in simple terms im only in 9th grade.

Hershey and Chase did two experiments to prove that DNA is the carrier of the genetic information.
First, they grew phages (viruses which infect bacteria) in a medium containing radioactive sulphur (35S). This marked all the proteins of the phage (the hull) radioactive. They then used this phage to infect bacteria. To do so, the phage attaches to the surface of the bacteria and injects its genetic material. This looks like in this picture from the Wikipedia page on Bacteriophages:

The bacteria with the attached phages are then blended, so they will loose the attachment to the bacterial surface. The mixture of bacteria and phages is then centrifuged, this makes the heavy bacteria sediment at the bottom of the tube, the lighter phages stay in the supernatant. Hershey and Chase then measured where the radioactivity from the marked phage proteins had gone, since they found it in the supernatant, they knew, that no proteins had entered the bacteria.
If proteins would have been the carrier of the genetic information they would have entered the bacteria and had been found in the sediment inside the bacteria.

In the second experiment (the proof if you want to say so) they marked the DNA of the phages radioactive (with radioactive phosphorus, 32P). They repeated the experiment and found the radioactivity in the sediment with the bacteria, proving, that the DNA had indeed entered the bacteria.
If the DNA wouldn't be the carrier, it wouldn't have entered the bacteria and would have stayed in solution.

The whole experiment is nicely shown in this Wikipedia illustration:


Is sex linked inheritance independent of dominance? I have a little challenge with what my lecturer said in class. I disagree with explanation but don't know how to convince myself. Please review and tell me your opinion.

Eye-color in drosophila is a sex-linked trait in which a white eye male was crossed with a red eye female. The F1 generation consist of 54 white eye and 49 red eye female; and 47 white eye and 50 red eye male. Explain.?

He said and I quote

  "the white eye male will transfer the white eye allele to the F1 female generation while the red eye female will transfer her red eye allele to the F1 male generation"

I disagreed because his explanation didn't account for the red eye f1 female generation and the white eye f1 male generation.... I proposed that the female parent was heterozygous for the eye color trait..... Hence a cross shows that the phenotypic ratios for either eye colors for any sex is 1/4...In response he acclaimed there's no dominance since it's a deviation from medellian principle.

Drosophila follow the same sex determination as in humans, XY for males, XX for females. The eye colour is sex linked, that is, the genes for eye colour are only carried on the X chromosone in this case, not the Y (there are other linkages that are only carried on the Y, but that's not the case here). The wild-type colour, red, is dominant over the white eye colour. When speaking of inheritance of eye colour in drosophila males specifically, you don't need to consider dominance or recessiveness as males only get one copy carried on the X - either the wild type red, or white, there is no interaction between alleles. The dominance and recessiveness only comes in to play with the eye colour of females, as they get two copies, one on each X they get from the parents, in which case the heterozygous will appear red eyed, as will the homozygous for the red eye allele.

For the image: In this cross we have a heterozygous red eyed female (XWXw) crossed with a white eyed male (XwY). In the offspring you see that half of the females would be heterozygous for red eyes, thus presenting as red eyed, and half would be homozygous for white. In the males half would be red eyed and half white eyed as there is no dominance or interaction between alleles as they only have the single copy on the single X chromosome they have inherited.

Hope this makes sense!

With all that in mind, you are right, you will only get white eye males in the F1 generation if the mother in a cross is heterozygous for the eye colour trait.


How to prevent protein precipitation? I'm trying to label a protein with fluorescent dye (TMR succinimidyl ester), but having trouble getting the protocol to work.

The protein seems to be stable in distilled water at a the recommended concentration of about 2mg/ml (determined by OD280 with an absorption coefficient calculated from its sequence).

However, the protocol calls for the addition of 1:10 1M sodium bicarbonate to raise the pH to ~8.5. When I perform this step the solution immediately turns cloudy. I have also encountered this precipitation problem when dialyzing against PBS.

What steps can I take to get around this? I assume a lower concentration of protein might prevent precipitation, but I have read that the labeling reaction becomes very inefficient below 1mg/ml.

Alas, the great problems with protein formulation. I assume that the labeling chemistry forces you to use the 8.5 pH. (I don't think this is necessarily true since succinimidyl chemistry does work at pH=7.2 and the NHS ester is fairly unstable above pH=8.6)

We usually tackle this problem entirely by brute force ie. testing multiple buffer condition with different bases and different salt concentrations. First attempt would be to try out all of the Good's Buffers notablely HEPES, TRIS, MOPS, Tricine, Maybe you should look at both zwitterionic buffers and non-zwitterionic buffers. In your case, the succinimidyl is vunerable to primary amines so avoid things like Tris/Glycine.

The second thing to test would be various salt concentrations. Since you're already dumping in Sodium Bicarb, NaCl should be great. Unfortunately, this is where things get tricky since it is hard to know if your protein precipitates at low salt or high. A test from 20 mM, 50 mM, 100 mM, 150 mM, 200 mM, 500 mM should cover most of the interesting regimes.

Alternatively the sudden change in the ionic environment around your protein may be causing it to precipitate. You probably should dialyze or purified your protein in PBS to allow it to refold appropriately.


How does translational immunotherapy work? I skimmed an article on a recent experiment which suggested that it was effective to inject induced colon cancer tumors with an attenuated salmonella variant. According to the article, this stimulated an immune response which suppressed metastasis of the cancer. How exactly does this work?

Tumors are commonly infiltrated with lymphocytes, including T cells, macs, DCs and B cells. The crux of the paper is that their attenuated virus secretes TLR ligands (Toll-like receptor) that resulted in an activation of tumor-suppressive M1 macrophages, a concomitant reduction in immune-suppressive M2 macrophage activity, and an influx of immune infiltrate to the tumor.

So M1 macs are activated typically by IFN-y and LPS stimulation, which is typically through TLR4. Their salmonella is attenuated and causes no disease, check one. It's gram-negative and thus has LPS, check two. It's engineered to secrete bacterial flagellin, a TLR5 agonist, check three.

M1 macs secrete IL12, important for polarizing T cells to TH1/TC1 phenotypes that are oncolytic, and IL10 which can elicit anti-tumor immunity though it's reputation is that of an immunosuppressant. M1 macs can also kill tumors of their own accord by producing nitric oxide which is cytotoxic to tumor cells. TLR4 agonsim on it's own accord also activates T cells in an NF-kB-dependent manner.

Whats also interesting is the inflammatory signal actuated by the macrophages actually tells other immune cells "hey come check this out," and potentially makes for a more robust anti-tumor response. The idea is that inflamed tissues secrete signalling or chemotactic molecules called chemokines which are picked up by chemokine receptors on leukocytes, telling them to enter the zone of infection (and thus the malignancy).

You'll also find, however, that despite immunological advances, modulating cells is a challenge due to the nature of each type of cancer's TME (tumor microenvironment). And so in your paper they tested it in a murine system in bladder cancer, but will it work in a human melanoma must be qualified, for example.


Why are mammals not very often (never?) toxic? Often reptiles or insects have poison to defend themselves or to offend their prey. But I don't know any mammals which are toxic. So are there any mammals using poison and why aren't there so less/any?

Answering the first part of your question: The cuban solenodon has venomous saliva. It's a mammal -- rather shrewlike in appearance. But yes, venomous mammals are rare!


Is the increased/decreased enzyme activity (tyrosinase) caused by an environmental factor (UV radiation) considered to be gene expression? My AP Bio assignment asks that I research the effects of UV radiation on melanin production, but the directions and questions suggest that UV radiation influences gene expression. From what I could find, such as on this university site or this abstract on NCBI, it seems that UV-B radiation directly affects the enzyme tyrosinase, which is responsible for producing melanin from tyrosine. So here is what I'm wondering: is our lesson wrong in stating that UV radiation affects gene expression, since it seems that it actually affects enzyme activity?

Unless there's a feedback mechanism shutting off gene expression (which controls the proteins made by a cell), activation or deactivation of an enzyme is not in itself a matter of gene expression, it's a matter of external factors controlling the enzyme's activity. You need to decide on what exactly causes skin pigmentation: the enzyme or cell proliferation, and what is under the control of gene expression and what isn't.

Most of what you find on ultraviolet light and melanin will be somehow related to melanomas, the formation of which does involve gene expression, so it's important to keep the two separated.

Ultraviolet light does cause proliferation of melanocytes, which cause the skin to darken. Melanocytes impart melanin to keratinocytes; these cells then are what give you a tan. The keratinocytes undergo constant turnover, so are eventually shed, and in the absence of continued exposure to UV radiation, there is no need to keep producing melanin-heavy keratinocytes.

  The keratins and proteins within the stratum corneum act mainly by scattering and absorbing the UV. UV-R sets in action an integrated mechanism for the formation and delivery of melanin within melanosomes from melanocytes to keratinocytes. This mechanism is probably triggered by keratinocytes, which respond to UV-R with bursts of mitoses and with increased production of ET-1 and POMC, thus creating a new demand for melanosomes. The mitotic rate of basal keratinocytes increases a day after UV exposure, reaches a maximum 2 days later, and maintains this level for ∼1 wk. It then declines, and the skin regains its original thickness after 1–2 months if there has been no subsequent exposure.

Continued exposure to UV light stimulates the melanocytes to grow. This increases the chance of the development of melanomas. Since skin cells containing melanin are shed (there's no getting around that), in light-skinned individuals, keeping a tan is to keep injuring the skin and risking carcinogenesis.

Melanin Pigmentation in Mammalian Skin and Its Hormonal Regulation
Human skin pigmentation: melanocytes modulate skin color in response to stress
Mechanism of UV-related carcinogenesis and its contribution to nevi/melanoma


What are the structual differences between DNA and RNA? How is the structure of DNA different from that of RNA?

DNA and RNA are similar, but different molecules. Both are made up of nucleic acids attached to a backbone made of phosphate and a sugar forming a nucleotide. DNA uses the nucleic acids Guanine, Cytosine, Adenine, and Thymine, while RNA replaces Thymine with Uridine.

The nucleic acids can form pairs due to hydrogen bonding, which allows the DNA/RNA to store information, if one strand has a C, the other must have a G and vice versa. Same applies for A and T.

While both molecules are capable of forming double helices by hydrogen bonding between G and C or A and T/U, the types of helix tend to be different. DNA prefers to form what is known as a B type helix, while RNA prefers the A type.

The left most helix is A type, the middle is B type, and the right helix is Z type, a highly unusual form found only under certain conditions.

DNA is almost always found as a double stranded molecule, and is primarily responsible for storing the information for making proteins and RNA and regulatory functions in cells. RNA is made by copying information from DNA through a process known as transcription and performs a variety of roles. Messenger RNA, or mRNA, carries information from DNA to ribosomes where it is used to build proteins through translation. Transfer RNA, or tRNA, carries amino acids to ribosomes to build proteins. The ribosome itself is made of RNA, known as rRNA, with proteins to help it function. Even through RNA is usually made up of only 1 strand, it can fold up and form complex shapes, such as the characteristic tRNA structure shown below. Some RNA molecules can even act as catalysts, carrying out chemical reactions such as cutting up other RNAs. These catalytic RNAs are known as ribozymes.


Will amylase inhibitors affect the colorigenic reaction between starch and iodine? I'm doing an experiment for my IB bio EE involving colorimetry. I'm not experienced at all with colorimetry, so I'm having some trouble planning it. The experiment is on enzyme kinetics, and I'm testing the effect of an inhibitor on the rate of digestion of starch by alpha-amylase. Currently, my plan is just to use a starch solution with an iodine indicator, add the amylase and inhibitor and measure the change in absorbance of a certain wavelength over time with the colorimeter, however, I'm worried that when I add the amylase and the inhibitor it'll affect the colour of the solution quite a lot. Will this be an issue, and if so is there a better method I could use to control for it?

Any help would be appreciated, this is my first time actually planning an experiment and I'm finding it difficult :)

To measure your amylase activity, you will monitor the disappearance of amylase’s substrate, starch.
Starch reacts with iodine (which is yellow) to form a blue compound (Amax 620 nm). This reaction is
the basis of a colorimetric assay for amylase activity. You should be very careful about the volume of the final solutions so it won't effect your results. For example you will add inhibitor to one of them and you won't add that to the other but you should add water instead of the inhibitor so dansity won't be a problem. (final volumes should be same since starch amount at the beginning will be same) You can use some acid like HCL to stop enzyme activity so it won't change the colour and won't effect your results. After the acid stops the enzymatic reaction and the iodine
reacts with the starch to produce the blue color. Any starch that has not yet been hydrolyzed by the
 amylase will turn blue color being proportional to the amount of starch
remaining. The intensity of the blue color can be by measured by its absorbance at 620 nm. The greater the change in absorbance between a sample containing the initial
amount of starch (without enzyme) and the hydrolyzed mixture containing the enzyme, the greater the
amount of starch degraded by the enzyme, therefore the greater the activity of the enzyme being
measured. Make sure you give the enzyme enough time and heat to catalyse the reaction. Sorry for grammar errors. I hope this was helpful!

Edit:you asked if inhibitor effects the experiment. I did say it above. If you use a colorless substance to denature or inhibit the enzyme it won't effect your results. If you can't do this you may add the inhibitor after the reaction is over so it won't effect the reaction but you may eliminate possible differences in color


Help identify this red/black Vietnamese insect I found this strange insect while on Son Tra, Da Nang in central Vietnam. It was about 4cm long and although it was on the ground, was obviously capable of flying. I've never seen anything like this and would like help identifying it, please. Thanks!

Dasypogon is a genus of robber flies in the family Asilidae.

Kingdom: Animalia
Phylum: Arthropoda
Class: Insecta
Order: Diptera ,
Family: Asilidae
Tribe:Dasypogonini
Genus:Dasypogon.

84 species belong to the genus Dasypogon. Among these, this one is Asilidae Dasypogon diadema.


Are SNPs and alleles the same thing? It seems to be quite difficult to find an answer to this. Are SNPs the same thing as alleles?

Alleles are variations of a same locus that codes for a protein (gene). These alleles can come in different forms, one of which is SNP. For example, sickle cell anemia arises from an allele of the beta-globin gene which has had a change from A to T.
Meanwhile, for the ABO gene that determines your blood group, the O allele has a missing nucleotide (G) that leads to a frameshift in the gene and a loss of function.
So alleles are caused by SNPs, but can also be due to deletions, additions, insertions and other genetic changes.
Note that SNPs not always lead to new alleles. Sometimes they occur in non-coding areas and nothing happens.

Edit:

SNPs do not need to be gene specific, but this was for simplicty.

@Artem added nicely to the answer, I'm quoting it here:

"Single Nucleotide Polymorphisms (SNPs) are Single Nucleotide Variants (SNVs) at a population allele frequency greater then 1%. Alleles are any variants of the same position of DNA, which includes SNVs, insertion/deletions, or structural variants and at any frequency." - @Artem


"Blood circulation". Why blood bleeds in atmosphere ? If our body's blood pressure is 120 mm-Hg then why blood goes out of our body in 760 mm -Hg pressure if we have cuts?

That's actually the gauge pressure that we measure. Gauge pressure is the amount by which the pressure measured in a fluid exceeds that of the atmosphere. So, when we say that our blood pressure is 180mmhg, it's wrong. In reality, the blood pressure is (180+760)mmHg inside the blood vessel, and our blood pressure exceeds atmospheric pressure by 180mmhg.


Variations in action potential threshold and temporal coding I would like to ask a few questions about things I'm not sure I understand in a paper Action potential threshold of hippocampal pyramidal cells (...).

(1) At the start the paper considers the possibility of irregular firing patterns of action potentials may be an argument to hold that the information processed by the CA1 neurons is a temporal code. I think it is hard to see the relation of final results (see the abstract) with these initial considerations. Do the results support the temporal coding hypothesis of CA1 neurons? How?

(2) At the end of the first page it says the following: "significant variations in action potential threshold would have implications for the precise timing of action potentials since the probability of initiating an action potential could not be predicted by only fluctuations in the membrane potential".

Does this mean that they aim to explain the irregular patterns by means of the fluctuations in the threshold?

I also don't see how from "the probability of initiating an action potential could not be predicted by only fluctuations in the membrane potential" follows that "significant variations in action potential threshold would have implications for the precise timing of action potentials".

Hi,
For what I read, the objective of the paper is in fact to study the neural code using methods that study the membrane threshold changes (as you said). They mention both rate and temporal code in the introduction and they do give more emphasis to the temporal coding because it explains better the irregularities of the neuronal transmission.
They did find some correlations between changes in the threshold, which influences the iniciation of the action potential, and the timing and rate of the firing or the firing pattern. That means that the firing pattern influences the iniciation of the action potential even if in an indirect way (which is by influencing the membrane threshold). Saying that the pattern of firing is important it means that the timing is also important, instead of only the rate the firing. Because this is the major difference between both neural codes theory, it does support more the temporal code.


Deducing synaptic strength from electron micrographs? There are several promising techniques for connectomics based on iterative sectioning and imaging of tissue with scanning electron microscopes (e.g. FIB-SEM and ATUM)

By looking at such micrographs, one can identify synapses:

Is there any way to measure synaptic strength using these types of techniques?

First of all, definitions. By synaptic strength let's understand ability of post-synapse to elicit current flow/depolarization in response to neurotransmitter appearance in the synapse. How can NT appear? By release from pre-synapse or through uncaging (optical activation of "caged", or inactive NT).
Second, post-synapse contain all sort of stuff, but main sources of current/depolarization are ionotropic receptors of NTs, e.g. NMDA-R or AMPA-R. This molecules are not just floating ion membrane but attached to extensive scaffolding just below of the membrane. Scaffolding includes actin, and more importantly PSD95 (in case of excitatory synapses).

I work in vivo and don't do any EM. But in vivo issue of observing molecules is that you can't label sensitive proteins without disturbing function. Some things are just too delicate to be labeled with fusing GFP.

PSD95 has been used for in vivo labeling with GFP. One paper I will point you to, is this knock-in work in mice: Live Imaging of Endogenous PSD-95 Using ENABLED: A Conditional Strategy to Fluorescently Label Endogenous Proteins, J Neurosc. 2014

This is the figure that shows strong correlation between brightness of synapse (aka number of PSD95 molecules) and current that occurs in cell body when authors uncaged glutamate at different synapses.

Figure description

Now, how does that relates to your image? PSD stands for "post-synaptic density" protein, because in EM synapse is very dark. I don't know links, but I would assume some correlation between brightness of synapse in EM and its strength.


Why do germs live longer on surfaces than on skin? After looking up how long germs live for on surface, I came across lots of resources that explain how long germs live on different surfaces.

A common pattern is that germs survive longer on cold/hard surfaces than on skin.

Why is that?

Wouldn't skin be a much more hospitable environment than something like a desk?

because some skin cells which are alive , secret fat and other materials , these materials make the skin acidic , and acidic environment is not good for many germs , on the other hand , there is an enzyme in  sweat (lysozyme)which destroy the wall of bacteria


Bug Identification: Tiny Bugs I have seen these on my hands recently and I am wondering what they are. Urban Setting. South Central Pennsylvania.

This appears to be a bird mite (or possibly rat mite) in the genus Ornithonyssus of the parasitic family Macronyssidae.

 Credit: user Aewills on bugguide.com

Identification:

From Central Exterminating Co.:

  The mites are distinguished from most other common, structural species by the very long legs and very long mouthparts. These long, pointed chelicerae and palps stick well out in front of the head region. The 8 legs are very long and well separated, allowing for good mobility by these mites. The body is oval, with the thorax and abdomen combined to a single segment without separation. The color is light grayish in unfed mites to reddish orange in mites recently having had a blood meal. The fowl mites often seem to have a patchy, mottled appearance of dark areas.

Distinguishing between species is difficult.

Blaine Mathison mentions the following features useful for identifying these mites to lower taxonomic levels under magnification [source: bugguide.com]:

chelicerae shape
dorsal plate breadth and degree of dorsal coverage
spiracle present between legs
genitoventral plate width
sternal plate shape and presence of setae

(see the linked post for pictures and more detail).

You can see videos of these mites crawling on people here and here.

Regarding their affects on humans:

From Penn State Extension:

  Bird mites have piercing mouthparts that enable them to take blood meals from their
  bird hosts. Although the mites will inadvertently bite people, they cannot reproduce without their bird hosts...

  As the mites search for an alternative host, they will crawl onto the skin and conduct an exploratory bite to test the appropriateness of the host. The mite will move on, possibly trying the host again, but will not feed. These bites are felt as a “prick” and a resultant rash and itching, sometimes intense, will occur. Some individuals are apparently capable of sensing the crawling of the mites on the skin. The irritation produced by the bite is enhanced by the injection of the mite’s saliva that can cause a localized histamine
  response.

Management:

Remove birds (and especially nests) from on or near the building. Check for any holes in your building that could be large enough to allow birds inside. Again, these mites need birds to reproduce, so if you eliminate the birds eventually these will disappear. See PSU Extension and Central Extirminating Co. for more suggestions.


I need help identifying a bug Basically this tiny bug plopped on top of my laptop keyboard. And as much as I disdained bugs, this one didn't look like anything I've ever seen. It had something that resembled bits of a dandelion on its back, and its body seemed like half a moth/ whatever insect. After closer inspection, I thought it was just a dying moth, the thing on its back being clipped wings and its body cut in half... but when i tried to shove it off the keyboard with my pen, it jumped about a hundred times its width onto my wall - instantly. Tried to get a second picture but it jumped again/disappeared... no idea where it went, or what it was... Here's the picture I took, and a quick sketch of what it looked like.

This looks like an immature passionvine hopper (Scolypopa australis).  They are informally known as fluffy bums.

Source: http://ketenewplymouth.peoplesnetworknz.info/friends_of_te_henui/images/show/1486-nymphs-fluffy-bums-scolypopa-australis

This is am image of the adult stage from the Encyclopedia of Life site:

More information can be found at the Encyclopedia of Life link above.  It appears that their distribution may be only in Australia and New Zealand and I'm not sure where this photo was taken so take this information into consideration.


To what group does coconut plant belong? I've tried looking it up but I couldn't find an answer. Could someone please tell me to what group of plants do coconuts belong depending upon the natural availability of water?

In terms of taxonomy and morphology:

  Although coconut trees display considerable morphological diversity,
  they are considered taxonomically a single species (and the only
  species) within the genus Cocos. Based on stature and breeding,
  coconut cultivars can be divided into two groups: tall and dwarf.
  The former typically grows up to 35 to 40 meters and is mainly
  outcrossing, whereas the latter can only grow up to 25 to 30 meters
  and usually is selfing. Dwarf coconuts, which are less common than the
  tall variety, are usually found growing close to humans and have
  traits that likely result from human selection.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0074736

I've found little information about whether or not they are halophytes, hydrophytes, xerophytes,or mesophytes - but according to a Google Book, a number of crops are widely cultivated in non-saline soils, including Cocos nucifera (coconuts). Another Google book with a lot of information about coconuts states this: Some experiments show that a small quantity of salt added to the tree roots is beneficial.

Cocos nucifera also love sunlight, so they can be considered heliophytes.


Questions to ask to a panel of people that will be sequenced Some genes have been shown to be associated with left-handedness.

Working with some clinicians, I've recommend them to ask their patients (whose genome will be sequenced) if they are "right or left-handed".
It's a simple phenotype (without any ethical issue) that will be later fun/interesting to analyze through the sequencing data outside of the main study.

Do you know any other such kind of simple phenotype that we could ask to our patients ? :-)

23andMe is a company that provides sequencing. Before they sequence your genome, they ask you to fill in a couple of surveys, one of which is about your physical features. Here is a list of some of the questions they ask:

  How much hair do you have on your upper/lower back?
  When you walk, in what direction do your feet naturally face?
  Do you have a line or indentation (dimple) in the middle of your chin?
  Excluding any hair loss, does your natural hairline have a widow's peak (a V-shaped peak of hair at the front of the hairline)?
  Can you flip your tongue over so that the underside is on top?
  Can you lift one eyebrow while keeping the other eyebrow in place?
  Which is longer, your big toe or the toe next to your big toe?
  On your left hand, which finger is longer, your index finger or your ring finger?
  What is your shoe size in U.S. shoe sizes?
  How would you describe the arches of your feet?
  Can you bend down and place your entire palms on the floor while keeping your legs straight (see above image)?
  Which image best matches the natural shape of your face (with your hair pulled back)?
  ...

That's a small list of phenotype questions you can ask ;-)


Enlargement of thyroid gland Why does thyroid gland enlarge both in hypothyroidism and hyperthyroidism?
Hypothyroid goitre is due to lack of iodine in diet and hyperthyroid goitre (Exopthalmic goitre, Grave's disease) is due to oversecretion of thyroxine, or Thyroid stimulating Hormone. How does these two apparently opposite effects produce similar physical manifestation of the disorder (symptom) i.e is the enlargement of the thyroid gland?

The primary activity of the thyroid gland is to concentrate iodine from the blood to make thyroid hormone. The gland cannot make enough thyroid hormone if it does not have enough iodine. Therefore, with iodine deficiency the individual will become hypothyroid. Consequently, the pituitary gland in the brain senses the thyroid hormone level is too low and sends a signal to the thyroid. This signal is called thyroid stimulating hormone (TSH). As the name implies, this hormone stimulates the thyroid to produce thyroid hormone and to grow in size.
In Graves' disease one’s immune system produces a protein, called thyroid stimulating immunoglobulin (TSI). As with TSH, TSI stimulates the thyroid gland to enlarge producing a goiter. However, TSI also stimulates the thyroid to make too much thyroid hormone (causes hyperthyroidism). Since the pituitary senses too much thyroid hormone, it stops secreting TSH. In spite of this the thyroid gland continues to grow and make thyroid hormone. Therefore, Graves’ disease produces a goiter and hyperthyroidism.

Source: American Thyroid Association. What is a Goiter - Causes


When forming an enzyme-substrate complex in a spontaneous reaction, why free energy increases? We ate food, and then food was digested into proteins, carbohydrates...
Does not digestion break bonds within food macromolecules? and thus free energy decreases? why when looking to the curve we see an increase in the free energy and then a decrease?

This increase is the activation energy:

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


Least painful way to die There is a lot of talk about inhumane treatment of animals and how we don't kill them in the proper way. I wonder how much research is done on this subject. What is the overall least painful way for an animal to die?

I also wonder if this would be the same for a human. It is often said that its least painful to die in ones sleep and i wonder if this is true. I wonder what is the most humane way to execute a capital punishment (if that is at all possible)

The American Veterinary Medical Association (AVMA) has thought about humane methods of euthanasia quite a bit and has an extensive (102 p. PDF) set of guidelines for the euthanasia of animals. The guidelines are not the same for all animals. Some examples:

Companion animals (e.g., dogs and cats): injected barbiturates are recommended

Laboratory animals (e.g., mice and rats): injected barbiturates are acceptable as are inhaled agents (isoflurane, carbon dioxide).

As for humans, you might look into the physician assisted suicide literature. I think that these generally use a sequence of drugs. As far as natural deaths, kidney failure is supposed to not be very painful.


Do oral vaccines exist? Do edible vaccines exist, and if yes, what is their mode of action? Are there any edible vaccines commercially available now?

In short, yes.

A good example of an orally-administered vaccine is this Polio vaccine.


Why would deer continue to cross a river full of crocodiles even though some of them have been killed? I recently watched a clip on Discovery Channel, where I saw deer crossing a river full of crocodiles, ignoring the fact that some of them would have been killed doing so.

Is there a possible evolutionary reason for this behaviour?

The reason for their behavior is that exactly the fact that even though some of them do indeed get killed, most of them survive -- what you have said.  The deer cross the river because that allows for the better continuation of the species rather than if they had stayed on the original side of the river. You could think of it this way: If there was a crowd of 5000 people crossing a field of grass and aliens were abducting them one by one, the actual chances of them abducting you are rather little.


What are those patterns found on the surface of wooden furniture? Are those growth rings of trees? This image can give a suitable example for the above question.

Thees cut on any angle will reveal growth patterns; not all wood grows exactly the same. Some kinds grow straight and have a very even grain, at the other end is the "black gum", the grain of which seems to follow no organized pattern (it's almost impossible to split.)

Without a close up, it's hard to say exactly what's going on with your table.

Some woods, because of their grain and even density, take up stain very evenly and uniformly. An example would be oak. Some woods take up stain more irregularly, an example being maple.

Your table, though (all this is speculation since there's not a close up or head on view) looks like an example of blotchy stain uptake.

This is an example of blothcy staining wood:

If you look carefully at the grain, you can see that's not the only cause of uneven uptake. Some blotchiness is due to not sanding the table down finely enough. Some is due to the uneven density of the wood. See that diagonal scratch? It takes up color regardless of the grain. As do the ends of the boards.

Your table is made up of younger trees (you could see growth rings on the edge) which will give you more uneven uptake, plus it's a blotchy job. So, the answer is yes and no. Or, a qualified yes.


How can I perform virus neutralization assay for influenza? How can I perform a Virus Microneutralization assay for influenza virus using serum from mice vaccinated with this virus?

There are a number of different protocols, but the canonical one is published at the WHO Influenza site:

SEROLOGICAL DIAGNOSIS OF INFLUENZA BY MICRONEUTRALIZATION ASSAY

It gives a detailed, step by step protocol.


Who discovered DNase? I was recently studying genetics in which  DNase had a crucial role in proving DNA to be the genetic material and I tried to find who discovered DNase (like the discoverer of DNA) but in vain.
Who found the DNA-digesting DNase ?

There are, of course, many different deoxyribonucleases (DNase), but the question has other implicit problems. It assumes that there was a single event that resulted in the realization of the existence of a new enzymatic activity. As the Introduction to this paper by M. McCarty on the purification of one such enzyme in the Journal of General Physiology in 1946, science wasn’t (and still often isn’t) quite like that:

The enzyme which breaks down highly polymerized desoxyribonucleic (sic) acid
has been known for many years under various names. In 1903, Araki (3)
reported that crude preparations of trypsin and erepsin brought about
liquefaction of gels of a thymonucleate prepared according to the
method of Neumann (4) Although Araki interpreted the effect as being
proteolytic in nature, his experiments represent the first observations
on the enzymatic breakdown of this type of nucleic acid. Two years
later Sachs (5) demonstrated that liquefaction of the nucleate gel by
pancreatic extracts is caused by an enzyme distinct from trypsin, and
further presented evidence indicating that trypsin rapidly inactivates
the nuclease. De la Blanchardière (6) confirmed the findings of Sachs,
and made several unsuccessful attempts to separate the nuclease from
the inactivating tryptic enzymes. This writer also devised a more
quantitative method of measuring the nuclease activity by following the
fall in viscosity of a dilute solution of thymonucleate during
digestion with the enzyme.

Araki, T., Z. physiol. Chem.,1903,38, 84.

Sachs, F., Z. physiol. Chem.,1905,46, 337.

De la Blanchardière, P., Z. physiol. Chem., 1913, 87, 291

[desoxyribonucleic acid and thymonucleate are older terms for DNA and its ionized form]
Many scientists have subsequent been involved in identifying different types of DNase and their roles in DNA metabolism, and anyone wishing to know about a particular DNase would need to research the literature.


Is "Cloning" exact or almost similar to parent? I was studying "Reproduction in Organism" as an interest of my own and there was a line

  offspring produced through single parent are exact copies of their parent. Also, they are genetically identical.

So, in here, it says, "genetically identical" (I assume that identical here implies exactly same) but then the next line quite confused me.....

  The term clone is used to describe such morphologically and genetically similar individuals.

Here, the term "genetically similar" is used.

So, clones (offspring produced through asexual reproduction- involvement of one parent) are "genetically exact" to their parents or genetically similar?

If "genetically exact", Then how is it possible since, there is 'No 100% efficient DNA Replication' that can be achieved?

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

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


What does the gene name "lexA" stand for? It is an important gene expressed in E. coli that represses the SOS response and also the expression of lambda lytic phase genes. UV light and damage to DNA is responsible for its breakdown and hence the expression of repair genes and, if present, lambda phage genes. However I couldn't find a reference for its original name.

I'd go with Lambda Excision A. Terms like lex or rec often stand for what'd be termed a mnemonic, where for example rec may stand for recombination, or umu for UV mutator. The naming conventions can be difficult.

Edit: A 1981 study by Roger Brent and Mark Ptashne notes some data from initial studies that showed the lexA repressor downregulated a number of genes including himA, which they note to be required for integration of lambda phage.

http://www.pnas.org/content/78/7/4204.full.pdf


What is the mechanism behind cats' geolocating homing behavior? Some cats, which are separated from their home, have the ability to travel back to their original home - even over long distances and land that they haven't encountered before. E.g., see the Time article on the mystery of the geolocating cat or the following blog entry.

Based on the material above there seem to have only been some suspected mechanisms a few years ago.

It is explained with path integration in behavioral neuroscience. Not only cats, but other mammals, birds and even insects use path integration to return to a starting point.

Here is a relevant excerpt from the book Beyond the Cognitive Map: From Place Cells to Episodic Memory (by A. David Redish):

  Path integration is the ability to return directly to a starting
  point (sometimes called a home base or reference point) from
  any location in an environment, even in the dark or after a
  long circuitous route (Barlow, 1964; Gallistel, 1990; Maurer and
  Seguinot, 1995). Sometimes called dead reckoning, this ability
  has been shown in gerbils (Mittelstaedt and Mittelstaedt, 1980;
  Mittelstaedt and Glasauer, 1991), hamsters (Etienne, 1987, 1992;
  Chapuis and Scardigli, 1993), house mice (Alyan and Jander,
  1994), rats (Tolman, 1948; Alyan et al., 1997; Whishaw and
  Maaswinkel, 1997), birds (Mittelstaedt and Mittelstaedt, 1982;
  von Saint Paul, 1982), and even insects (Wehner and Srinivasan,
  1981) and arthropods (Mittelstaedt, 1983), as well as dogs, cats,
  and humans (Beritashvili, 1965).

  Path integration in animals has been the subject of argument
  for more than a century, including a notable debate in 1873 between
  Alfred Wallace and Charles Darwin in which Wallace suggested
  that animals find their way back via sequences of smells
  and Darwin argued that animals must be using dead reckoning
  (see Wallace, 1873a, 1873b; Darwin, 1873a, 1873b; Nature, 1873;
  Forde, 1873; Murphy, 1873). The carefully controlled experiments
  of Mittelstaedt and Mittelstaedt (1980) and Etienne (1987) have
  demonstrated conclusively that this ability is a consequence of integrating
  internal cues from vestibular signals and motor efferent
  copy.

emphasis mine

Cats, dogs and rodents can use taxon navigation as well along with path integration. Here is a relevant excerpt from Neural compass or epiphenomenon?
Experimental and theoretical investigations into the
rodent head direction system (by Matthijs van der Meer):

  “Internal allocentric” navigation. This type of navigation relies on a mapping of praxic commands to an allocentric spatial representation, allowing the animal to make a direct return to a home base after a complex outward path in the absence of cues, an ability referred to as path integration, discussed in detail in the next section. Returning by following an odour trail back, or navigating to a cue indicating the home base would be taxon navigation, but behavioural experiments have provided convincing evidence that rodents are able
  to do this without using external cues. As mentioned above, this ability requires some mechanism of continuously updating at least one’s directional heading (a “homing vector”) relative to the home base. This is an allocentric representation which does not need to be related to any external cues, unlike the next class of strategies; the reference point or direction can in principle be set to any location the animal desires.

emphasis mine

Further reading:

A connectionist model of path integration with and without a representation
of distance to the starting point (ROLAND MAURER, University of Geneva, Geneva, Switzerland) - Copyright 1998 Psychonomic Society, Inc.


Hemiptera sp preimago? Which species of Hemiptera is this preimago, seen in 2015 in Rome?

I think this is an Aphid because it has long, thin legs and two-jointed, two-clawed tarsi and resemble the Russian wheat aphid very much. They are very common in temperate zone and is a major plant pest.

Here's how the Russian wheat aphid looks:

Source:Website of tasmanian government


Confusion regarding Lindeman's law I came across Lindeman's 10% law at school. It states that 10% of the total energy entering a trophic level is available for transfer to the next trophic level.

I was reading Ecology: Principles and Applications
By J. L. Chapman, M. J. Reiss and they mentioned two contradictory statements:

The 10% law, i.e. the trophic efficiency is always 10%
The trophic efficiency increases with trophic level (which was substantiated by data).

This is the statistics:

What is right? Is Lindeman's 10% law actually valid?

Lindeman's "law" is not a true "law" like the laws of thermodynamics, it's more of a catchphrase for a concept.

The true, valid concept from Lindeman is that "lots of energy is typically lost as you go to the next trophic level, especially at early stages...but there might be exceptions." This is characteristic of most of the "laws" of biology: there is always a lot of flexibility and leeway in biology.

The data in the chart you provide support this generalized version of the law: namely, most of the energy is lost at each trophic level, and a rough average or rule-of-thumb is that it's about 10%.

The usefulness of the 10% number is that it presents a nice benchmark: when you look at these data, you should notice and remark on the relatively high 22.3% level for secondary consumers on the Cedar Bog Lake: you should wonder "what features of this ecosystem or these consumers mark the relatively high energy transfer here?" Without the "10% law" you wouldn't know which numbers should stand out and which are unremarkable.


How do animals/plants change for each season? The question pretty much sums it up. How do animals/plants change for each: Spring, Summer, Autumn, and Winter?

A detailed explanation on distinct behaviour and appearance changes would be nice.

There are various parameters that describe change of seasons such as day length, temperature, humidity. But it can be assumed that most of these parameters ultimately depend on one parameter- day length.

The response of plants towards the length of day/night cycle is called photoperiodism (which dictates spring flowering).

This article explains the effect of a gene called CONSTANS(CO) on spring flowering. CO is post transcriptionally regulated by cryptochromes and phyochromes.

  The circadian rhythm in CO mRNA abundance was proposed to represent a photoperiod response rhythm, in which exposure to light coincides with CO expression only under LDs (Long Day) and thereby triggers flowering.

  ......

  We propose that early in the day phyB promotes the degradation of CO whereas in the evening cryptochromes and phyA antagonize this degradation and stabilize CO protein,

However, my knowledge of plant molecular biology is not that great and I would advise that you refer the mentioned article and the cross references cited in that.


How do astronauts eat in space? If there is no gravity in space how does the food enter the stomach?
My guess is that it is due to the movement of the esophagus.Am I correct?

swallowing of food or water from mouth to stomach is done with the help of peristalsis action of esophagus

Then rhythmic, unidirectional waves of contractions will work to rapidly force the food into the stomach. This process works in one direction only and its sole purpose is to move food from the mouth into the stomach.

In earth it also happens but it is assisted with gravity but in space Peristalsis action is the only process by which food or water is taken to stomach .


What do you call a virus when it's cured? When a cure has been found for a virus, can it be called such anymore?

Virus implies it's something you've contracted that you just have to live with until (hopefully) your body can overwhelm and destroy it.

But say someone found a cure for the Common Cold tomorrow, would we still call it the cold virus or would it just be known as the "cold infection" or something to that effect?

Is "Virus" just a nomenclature we've adopted for a bug that has no cure, or is it used to describe a certain type of organism?

Lets start with the definition of a virus (from the Wikipedia page on viruses):

  A virus is a small infectious agent that replicates only inside the
  living cells of other organisms. Viruses can infect all types of life
  forms, from animals and plants to bacteria and archaea.

So basically speaking you have a piece of genetic information (DNA or RNA) which encodes proteins which are important for the function of the virus and a hull (not always, but mostly). These invade a cell type, take over the cell (litarally, after an infection the cell will mostly only make viral proteins and DNA/RNA). Finally new viruses are built inside the cell and released to infect more cells. In principle this works like in the figure below (from here):

There are two possibilities for cures: The first one are vaccinations. Here you either use dead or attenuated viruses (or parts of viruses) to train the immune system. When this has happened, the immune system "knows" this specific agent and can rise a fast and highly specific immune answer against it, before the virus can replicate in high numbers and infect a lot of cells. This happened for example for the small pox virus which could be eradicated from the human population.

The other would be drugs which either target a virus (or some of it functions) specifically or prevent them from spreading. The immune system usually does the final cleanup here.

Both methods only work for people which either take the drug or are vaccinated, so they have no influence on the virus in people which are not protected. For further information have a look on the Wikipedia page on Viruses.


What errors can occur during DNA replication? When there is an error in copying DNA (a mutation), what exactly goes wrong?

If G goes with C and A goes with T, I don't see how that part can mess up.

Is the idea that when the double helix is split, an A gets ruined and replaced with a G by mistake, which then pairs with a C in one of the copies? So something that was supposed to be AT is now GC.

There are many way in which DNA can be damaged. As already pointed out in the comment by @skymninge, the Wikipedia page on DNA repair, as well as the mutation page detail some of the things that can go wrong.

You say:

  If G goes with C and A goes with T, I don't see how that part can mess up.

This, however, would imply that the four bases are completely different so that mispairing cannot exist. This is (may I add luckily?) not true.
Indeed the chemical structure of the bases is very similar, and changes between one base and another (transversions and transitions) are common.

These can result for instance from exposure to external agents such as ionizing radiation and alkylating agents, or from exposure to endogenous products such as reactive oxygen species.

Furthermore, the enzyme synthetizing DNA, called DNA polymerase, can insert the wrong base, although most of these errors can be corrected by its "proof-reading mechanisms". However, it is estimated that

  the frequency at which human DNA undergoes lasting, uncorrected errors range from $1 * 10^{-4}$ to $1 * 10^{-6}$ mutations per gamete for a given gene.

Source: Nature Scitable

So, in summary, the system is not perfect, and mutation can be introduced even endogenously. This may seem bad, but, at least for relatively small rates of mutation, is not, as it allows change in the population, which is the basis for evolution.


How is evolution possible in contemporary humans? I would like to know if evolution is continuing to happen in modern humans, assuming things like existence of the nuclear family structure, fidelity to one partner, etc. It seems to me the answer would be NO because evolution depends on differential reproductive rates, but in the modern world, all male humans have roughly 2.5 (or whatever the number) kids. Add in the process of culturally modified selection pressure, and it seems to me that even an "unfit" male would end up having a couple of offspring. The fittest male (or female) is no better off than his or her contemporaries because of this "leveling" effect.

However, the impression I get from the popular science media is that scientists think evolution is continuing to happen. I would like to know what the actual scientific consensus is, and why. Thanks.

It is certainly not true that "all male humans have roughly 2.5 (or whatever the number) kids". First of all, male and female humans have exactly the same reproductive rate. For obvious reasons, every time a male has offspring, a female must have had also. Last I checked neither male nor female humans are capable of parthenogenesis (certain popular religious beliefs notwithstanding).

Second, let's assume that the 2.5 number is correct. That would be the average number of children per couple. That does not mean that all couples will have 2.5, or even that most couples will have 2.5. It just means that the average will be 2.5. If, for example you have one couple with 6 children, one with 2 and two with 1, the average will be (6+2+1+1)/(1+1+2)= 2.5.

On to the main point. What does selection mean? In its simplest form, that the individual most likely to survive (the famous "fittest") is also most likely to reproduce. This is a very simple concept, the longer you live the higher your chances of managing to have offspring. If you die two weeks after birth it is going to be hard to manage to reproduce yourself. This has not changed.

So, what does "fitness" mean? It can mean many things. If you are a warm blooded creature at the beginning of an ice age for example, it could mean being better at regulating your temperature than your peers. If you are a 21st century human, it could mean being funnier on twitter than your peers. The two are not fundamentally different. They can both be selected for or against. As long as one mate is chosen over another, selection is happening and the "fittest" (in each particular context) is most often selected.

  Add in the process of culturally modified selection pressure, and it
  seems to me that even an "unfit" male would end up having a couple of
  offspring. The fittest male (or female) is no better off than his or
  her contemporaries because of this "leveling" effect.

"Culturally modified selection pressure", as you call it, is still selection pressure. Cultural factors can change what it means to be "the fittest" but there is no objective gold standard of "fitness". While it may be true that in modern human society, different characteristics are selected for than was the case with early Homo sapiens, this does not mean that "evolution is not occurring". On the contrary, it is occurring but perhaps it is moving in a new direction. In fact, this is essentially a circular argument. By definition, "fittest" means most likely to survive and reproduce. It does not mean strongest or fastest or prettiest. It just means whoever is better at reproducing. If that happens to be those individuals who are best at square dancing, then it is they who are the fittest.

Take the example of a modern human with diabetes. Medicine allows diabetics to lead fully productive and largely normal lives. So, perhaps diabetes is no longer a selective criterion. This does not mean that the diabetic cannot be selected for or against based on their fitness on other scales.

Whatever the selective pressure, whatever it may be that defines a "good mate", if selection is present then so is evolution. The only way to remove a species from the process of selection would be to have all (or none) individuals of each and every generation reproducing at the same rate. This is clearly not the case with humans. Surely not everyone around you has, or will have, children? There you go, selection!

UPDATE:

In answer to your comment, yes indeed, in order for a selective pressure to make itself felt and affect phenotype (at the species level), it needs to be constant across several generations. However, even the absence of selective pressure affects evolution. As others have mentioned below, active selection is not the only mechanism of evolution.

Your main question however seems to be the following: If modern society (medicine etc) allows individuals that would not survive in the wild to reproduce, how does that affect evolution? The main points in my answer, and all others here, are:

Even if we accept that modern humans have removed themselves from the purely "biological fitness"-based selection pressure (an assumption I am not at all sure is true), and assuming that this removal is constant enough over many generations (again unclear), even if all this is true, evolution is most certainly still occurring. It may even be faster since genotypes that would not survive in the wild persist in the gene pool, thereby increasing its diversity.
As you point out in your comment below, for such social pressure to make itself felt, it needs to be constant across many generations. We are probably not there yet.
Most importantly, as I said above, there is no such thing as an absolute biological fitness. When the ecosystem changes, so does the definition of fitness. Modern humanity's ecosystem, our habitat, is intimately connected with our culture and society. If an individual is better at reproducing in that context, then that individual is more fit.


Frequent urination caused by sound of running water I urinate at sound of running water when I brush my teeth or wash my hands . This only happens when I am home

Very simply put, its the power of suggestion. You urinate, flush, wash your hands umpteen times together each day. So when you hear the sound of running water, you naturally feel the need to urinate.

Apparently, the sound of running water also help patients with lower urinary tract symptoms urinate (reference)


A theory about the possible connection between protists and first animalia I learnt that organisms within Kingdom Animalia can be either microanimals or (nonmicro)animals.

a microanimal is any Kingdom Animalia organism that in general cannot be seen by a human eye without microscope

I understand that while it is controversial how a first cell was formed (or appeared) in earth, it is broadly accepted that archaebacteria was at one time formed in earth and multiplied and that with time cyanobacteria evolved out of these, multiplied and evolved by themselves (while on the way crating stromatolites) and by that time the first protist was formed and multiplied and evolved into various shapes (morphogensis) of protists.

I also learnt that the difference between a protist to a microanimal, is that the latter does have specialized cells, so that its body isn't seemingly just a cluster of cells in a given shape and can possibly do any other function that a protist can't do besides perhaps surviving by morphogensis (if either one isn't a function by itself).

Due to the similarity in shape and size of protists and microanimals, I ask if there is a theory and if it reflects a consensus, that microanimals were the first Animalia and were indeed evolved out of protists?

Short Answer:

Probably the most widely accepted (though certainly not fully accepted) theory of animal evolution is called the Colonial theory.

According to the Colonial theory of animal origins, the earliest animals (i.e., sponges) seem to have arisen from colonial protists called choanoflagellates forming an invaginated hollow, spherical colony.

However, other theories do exist: Syncytial Theory and the Synzoospore Theory (proposed by Mikhailov et al. (2009)1)

Regardless of these theories, no reasonable theory about the evolution of animals from protists would link such evolution to "microanimals" given that microanimals (as defined by the OP) is not a phylogenetic group but rather a term to describe microscopic animals from various taxonomic groups.

 Long Answer:

There seems to be strong morphological evidence that choanoflagellates are the closest protist relative to currently living animals -- specifically to the simplest group of animals: the sponges (phylum Porifera).

 Protist / Animal phylogeny, Source: Cengage 20132

Specifically, we can see very similar characteristics between a choanoflagellate and a choanocyte (or "collar cell") of a sponge.

The choanoflagellates often form colonies consisting of numerous protists adhering to one another using adhesion proteins.

Due to the morphological similarities between choanoflagellates and choanocytes of sponges (along with similarities in adhesion proteins and signaling proteins shared between both), and the regular colony-forming tendencies of choanoflaggelates, it has been long suspected that the evolution of multicellular animals arose from these protists.

Ernst Haeckel (1874) was the first to propose that colony-forming chonaoflaggelates were the precursor to modern animals in a theory he called the Gastraea theory and which is now called the Colonial Theory of animal evolution. This thoery is summarized simply by Mikhailov et al. (2009)1:

  According to Ernst Haeckel, the transition from unicellularity to multicellularity
  proceeded through two consecutive stages (Fig. 1A). First, unicellular flagellates aggregated to form a hollow ballshaped floating colony of identical cells. This hypothetical stage was named the Blastaea to reflect its similarity with the blastula, an early stage in animal embryogenesis....

  ...At the second stage, the homogenous cellular wall of the Blastaea invaginated to form a second layer, the precursor of the primary gut. After this important event the Blastaea acquired primary cell differentiation (=spatial cell differentiation).

  Haeckel named this hypothetical ancestral form the Gastraea, again to indicate its similarity with the gastrula stage in animal embryogenesis. According to Haeckel, extant
  cnidarians and sponges are the first direct descendants of the ancestral Gastraea,(11) because their body plans derive from two embryonic layers.

Below is an illustration of the Colonial Theory of animal origins:

Other Theories:

I've cited two additional theories at the start of this answer (i.e., the Syncytial Theory and the Synzoospore Theory proposed by Mikhailov et al. (2009)1). For the sake of breviy, I will exclude further discussion of either theory here. Please feel free to visit my links/citations to learn more. I certaily encourage other users to provide answers describing such theories in more detail if they find doing so necessary and insightful for this post.

Regarding Microanimals

The term "microanimals" is simply referring to the size of the organism (i.e., that they need magnification for viewing) and not to any phylogenetic or evolutionary connection between these microscopic animals. Put differently, microscopic animals actually belong to a broad range of animal phyla -- in other words, they are not immediately related.

the Wikipedia post the OP links to (and the one I also link to in the preceding paragraph) lists, for example, microanimals from the phyla Arthropoda, Rotifera, and Loricifera.

Given this information, I strongly doubt you will find a theory suggesting that "microanimals" (as defined) played a role in the transition from protists to Animals.

1. Mikhailov, K.V., Konstantinova, A.V., Nikitin, M.A., Troshin, P.V., Rusin, L.Y., Lyubetsky, V.A., Panchin, Y.V., Mylnikov, A.P., Moroz, L.L., Kumar, S. and Aleoshin, V.V., 2009. The origin of Metazoa: a transition from temporal to spatial cell differentiation. Bioessays, 31(7), pp.758-768.

2. Starr, C., Taggart, R. and Evers, C., 2013. Biology: The unity and diversity of life. Cengage Learning.


why can proteolysis only occur once on a enzyme? My texbook says that proteolysis can occur once in the lifetime of the enzyme? I know that proteases must cleave the zymogen at more or more specific locations, but why can't the process take place more than once?

Because you mention zymogens, I assume the proteolysis you are referring to is the conversion of the inactive to active form of an enzyme by cleavage. The reason this would only happen once is that there isn't any process to put the two cleaved halves of the protein back together, so once cut in half it stays that way until degradation.

The proteolytic enzyme that is doing the cleavage of the zymogen will repeat this process over and over with multiple copies of the zymogen: it is the zymogen itself, the target, for which this is a once-in-a-lifetime event.

It would certainly be possible for a zymogen to require multiple cleavage events, but each of those events could only happen once.