What chemical conversions are involved , and what's the name for the process, when the muscles use lactate as an energy source? I understand that muscles do anaerobic metabolism, specifically, "lactic acid fermentation", which I understand produces lactate. I'm not asking about that process.

What chemical conversions are involved , and what's the name for the process, when the muscles use lactate as an energy source?

I'm aware that it can happen as    This paper, is tellingly and usefully titled, "Lactate as a fuel for mitochondrial respiration"   (though I only have the abstract)

And aside from that paper i've also heard

  "lactate produced during exercise can be reused as fuel by the muscles
  by turning it into glucose".

But I'm interested in what chemical conversions are involved

I see you've already got an answer in the comments, so this is rather a collection (with more proper formulation) of comments. As is known, lactate is produced by muscles (generally) during exercise due to absence of oxygen. However, the lactate produced can be used again in following two ways:

Conversion of lactate to glucose in the liver via a process known as Cori's cycle. Basically, the lactate produced from the muscles is released into the bloodstream, through which it reaches liver. There, it is converted back to glucose and again released into the bloodstream, through which muscles can use it again as fuel. The basic cycle looks like:

Conversion of lactate to pyruvate is the one you are concerned about. However, this process does not have a special name, because this reaction can be catalyzed both in forward and reverse direction. In the absence of oxygen, an enzyme lactate dehydrogenase convertes pyruvate into lactate, consuming 2 H+ during the process. However, when the envrionment is rich in oxygen, or the concentration of lactate is high, the same enzyme converts lactate into pyruvate, producing 2 H+ in the process. The reaction can be shown as: $$\ce{CH_3COCOO^- + NADH + H^+ \leftrightharpoons CH_3CH(OH)COO^- + NAD^+}$$

Thus, when the concentration of lactate increases, the enzyme lactate dehydrogenase catalyzes the (above) reaction in the reverse direction. After this, the pyruvate produced can be used in the TCA cycle.

PS: there have been studies which now suggest that indeed lactate, not glucose, is the primary energy source of neurons. As per the lactate-shuttle hypothesis, the glial cells neighboruing neurons convert glucose into lactate, which is then used by the neurons. This fits with the observation that the extracellular fluid immediately surrounding the neurons is richer in lactate as compared with blood and cerebrospinal fluid, as shown in microdialysis studies. These studies suggest that glucose is not the actual primary energy source of neurons.

EDIT: As you see, the first reaction in both the cases is $\ce{lactate \rightarrow pyruvate}$. However, the main difference arises after this reaction. In muscle cells, this pyruvate is used in Krebs cycle, for which the first enzyme is pyruvate dehydrogenase converting pyruvate to acetyl-coA. However, in gluconeogenesis i.e. formation of new glucose molecule (a part of Cori's cycle), the first step is conversion of pyruvate to oxaloacetate, and is catalyzed by the enzyme pyruvate carboxylase. Thus, although the first step in both processes is the same, the end product is quite different.

References:

Lactic Acid - Wikipedia
Lactate Dehydrogenase - Wikipedia
Cori's Cycle - Wikipedia


Reason behind formation of positive supercoils during DNA replication/ transcription When a twist is unwound without cutting the DNA strands or is removed by cutting the strand(s) and resealing, negative supercoils are introduced in the DNA.

From Cell and Molecular Biology -Karp

But strangely enough unwinding of DNA by helicase cause the DNA ahead of the primosome to form positive supercoils. Why is it so?

From: Molecular cell biology -Lodish

My speculations: Underwinding cause the adjacent DNA to overwind and as the DNA overwinds the associated stress developed cause the DNA to form positive supercoils (which would have happened naturally had new twists been introduced in the DNA (Time:1:54) ).

I think removal of twist creates negative supercoils initially but when the unwinding causes too much overwinding of adjacent DNA, the strain developed cause the already negatively supercoiled DNA to form positive supercoils.

It's hard to explain in text, so here's a video:

https://www.youtube.com/watch?v=J4YlcD59-yw

Imagine the shoelaces are two DNA strands in a double helix. They are topologically constrained at each end. As the pen (helicase) moves through the helix, it creates overwound DNA in front of it and underwound DNA behind it.


Role of the pupil response in night vision What are the things that affect the reaction time of pupil light reflex? What I mean to say is, if you are in a bright room, and the light suddenly turns off. The time you spend to see things in the room (i.e.., night vision) is the reaction time.

Short answer
Pupil responses have little effect on dark adaptation. It is the retinal processes that govern the bulk of the dynamic range of the eye's light sensitivity.

Background
You are referring to dark adaptation of the eye, which is, according to the Universty of Calgary:

  This change is called dark adaptation and refers to the process by which the eye becomes more sensitive to light under conditions of reduced illumination. [C]ones are primarily responsible for resolving fine detail (acuity) and colour vision in good light, while rods allow us to see more effectively in dim lighting conditions. The recovery of sensitivity in dark adaptation involves the regeneration of photoreceptor photo-pigments as well as neural changes.

See figure 1. The rods are way faster in gaining sensitivity than the photon-hungry cones.

In a typical clinical setting for diagnostical purposes of e.g. rod function, a typical dark adaptation period is about 20 minutes or so, which fits the below graph quite well. At the end of dark adaptation, the eye is about 100,000 times (i.e., 5 log units) more sensitive than it was at the beginning of the test, a level called dark adapted sensitivity (Universty of Calgary).

In contrast, the pupil response has only a minor effect on light sensitivity in  dark adaptation. It does change its diameter in the dark for sure, but the amount of light that passes through doesn't change too drastically. Pupil diameters range between about 2 and 8 mm (Spector, 1990), say a factor of four. In terms of surface we are talking about 3 and 50 mm2, respectively using (pi*r2), hence a factor of 16, as opposed to 5 orders of magnitude in the process of retinal adaptation.

Fig. 1. Light sensitivity adaptation of rods and cones. source: Uni Calgary

Reference
- Spector. The Pupils. In: Walker et al. (eds.) Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd ed. Boston: Butterworths (1990)


What makes teeth feel sticky after drinking Coca-Cola? I asked some of my friends and we all agree that teeth feel funny after drinking Coca-Cola. Other similar soft drinks also cause this effect, but this one most noticeably. It's like teeth become sticky and moving them against each other (by moving jaw) creates rubbery feeling.

What ingredient in this soft drink makes teeth like that?

Glucose and other ingested sugars have a natural affinity to bind to surface proteins on teeth (as well as many other proteins in tissues). This process is called glycosylation, and is expedited both by acidic environments (such as provided by the acidic soft drinks as indicated by The Last Word) or metabolism of adherent bacteria on the tooth surface (see one example). A discussion of oral cavity lubrication and how this influences tooth surfance glycosylation and biofilm formation has also been reported. The fuzzy feeling is a result of plaque formation. Plaques form as a byproduct of metabolism of bacteria on the tooth surfaces, that ingest and break down dietary sugars, and also secrete acids as a byproduct of this metabolism. The result, if left long enough, is plaque formation and eventually tooth decay. You can also notice this fuzzy feeling after a day or so of not brushing your teeth, as the bacteria have had a long time to metabolize the sugars ingested over that period to produce a plaque.


variation in antigen binding site of antibodies Antibodies or immunoglobulins are proteins made by the immune system in response to alien(!) molecules. Each antibody binds to its specific antigen. This great diversity and specificity is cause of diversity in Antigen Binding Site of heavy chain and light chain of antibody. Although other sections of Antibody are highly stable, Binding sites are very mutant. What is the reason for this difference in mutation rates in different parts of antibodies?

The processes are called gene rearrangement and somatic hypermutation, and are used by maturing B-cells to generate very (very) large amounts of diversity in the antibody repertoire. If your institution has access, this great article in Annual Reviews in Immunology has all the details, or you can read about it in Janeway (slightly outdated edition). Essentially, the genes encoding the B-cell Receptor, or BCR, have many fragments of several different types in them, and through the process of gene rearrangement the final Complementarity Determining Regions, or CDRs (the antigen-binding sites), are generated into one mature sequence for each individual B-cell.

A mature IgG molecule (the soluble, secreted version of the BCR) contains four chains - 2 heavy (each of which are identical to each other) and 2 light (also identical). There are Constant or C regions in each chain that essentially don't vary much, and are not really involved in the process of antigen binding. On the "business end" are three regions (or types, from above) called V, D, and J in the heavy chain, while the light chain just has V and J. Those letters are from Variable, Diversity, and Joining, if you're interested.

Figure 4.3 from Janeway shows the number of "fragments" or gene segments of each type in humans. So, when the heavy chain is being made, 1 fragment out of 65 Vs is picked, 1 of 27 Ds, and one of 6 Js, then each is joined together in a process that can also introduce an additional amount of randomness at the joins. Combine this with an only slightly less complex process in the light chain (as there is no D region), and the fact that a single insertion/deletion of a base pair can drastically effect the resulting protein sequence, and you get a protein with a huge number of possible sequences, potentially in the range of 1011.

This process of gene rearrangement typically generates immunoglobulins with relatively low affinity for their antigens. During affinity maturation, a process called somatic hypermutation randomly changes individual base pairs (translated to amino acids) in the CDR in cells that are descendents of, and bear the same base sequence as, the original. Cells expressing antigen receptors that are of higher affinity are then positively selected and clonally expanded by the immune system, allowing your body to tailor its response to an infection or other exposure to what it sees as foreign material.


ID bug found in Mojave county, USA What is this? I found it under a bed sheet. I live In Mojave county, AZ, USA, in the middle of the desert. It was probably 1/8 inch long. And narrow.

Initial guess based on mouthparts, coloration and small size:

Neuropteran larva. Possibly a green lacewing (family Chrysopidae).

See:

 Source: Bugguide.net

 Source: Cedar Creek Ecosystem Science Reserve

According to here, green lacewings are found in Arizona deserts.

I will update in the morning with more detail...


Is this case Histoplasma capsulatum? A 62 year-old male was admitted to the hospital complaining of shortness of breath. His chest X-ray showed a rightsided cavitary lesions. His medical history indicated he had smoked one pack of cigarettes per day for past 40 years and has had cavitary tuberculosis in about 20 years ago. Recently he is receiving cytostatic therapy for his acute myeloblastic leukaemia. A biopsy specimen of the lung was obtained. Biopsy from lesion shows tubular eukaryotic septated hyphae with diameter of 510 μm that are infiltrating the lung tissue. Culture on Saboraud’ media shows conidia with spores in radiating columns. Which is the most like cause of the findings?

The disease is systemic - affecting lungs.
Organism has septated hyphae with conidia.
Is there any other possibilities for the disease?

Is there any other possibilities for the disease?
Yes.  At 37°C, Histoplasma capsulatum usually doesn't form hyphae.

Were the hyphae branching, like this?

If "conidia with spores in radiating columns" means the pictures below,
We have enough to say that this is not a case of Histoplasma capsulatum and there is definitely another possibility for this disease.
Conidia with radiating chains of spores is pathognomonic for aspergillosis.


phylogenetic Independent contrasts with unresolved tree I have a dataset containing morphological and performance measures of species from various groups, including insects, lizards, frogs, spiders etc, and want to analyse the relationship between these measures and the animal's body size  via regression methods, while controlling for common ancestry, similar to what has been done in this work:

Peattie, A. M. & Full, R. J. Phylogenetic analysis of the scaling of wet and dry biological fibrillar adhesives PNAS, 2007, 104, 18595-18600

http://www.pnas.org/content/104/47/18595.abstract

For most of my species, statistically supported branch lengths are lacking, and I was thus wondering what the best way to conduct my analysis would be, and I would be grateful for any hint.

Look also into PGLS. Either way, one thing you could do--it would be ugly--would be to set all branch lengths to 1. Additionally, you could smooth the tree with penalized likelihood, e.g. chronopl() function in ape package in R. Again, this is an ugly solution and look into PGLS (it won't solve the ugly phylogeny part).


What is the difference between transformation and transfection? What is the difference between transformation and transfection? How do both of these methods work?

If you are interested in the history of molecular biology this is an interesting question.

Basically transformation came to be used to describe experiments in which the phenotype of an organism was changed by the uptake of DNA, and because of the way this developed in  bacterial systems this DNA was usually a plasmid. Then it became possible to use purified phage DNA to infect cells, whereupon the 'transformed' cells produced phage particles - for obvious reasons this was called transfection.

When efforts turned to getting the same techniques working with cultured animal cells many of the vectors were based on viral genomes (e.g. SV40) and these workers referred to this as transfection. At this point the distinction between the two terms became meaningless, and usage tends to be for historical reasons. Interestingly in molecular manipulations of yeast, where there are no viruses, the transfection word is rarely used.


Why do we exhale after we hold our breath? I tested this out with my friends, and I find that after they hold their breath and can't hold it anymore, they exhale air, instead of inhaling air.

Interestingly, they all try to inhale in as much air as possible before starting to hold their breath. When I told them to exhale as much air as possible before starting to hold their breath, they inhaled air after they can't hold it anymore.

It's understandable that when one exhales then holds his breath, he needs air and thus he inhales afterwards. But when one inhales then holds his breath, shouldn't he inhale again after "using up all that air he inhaled before holding hi breath"?

This is more about basic physics than biology. When you hold your breath, you normally take in one last long breath and keep it in as long as possible, Your lungs are therefore already full of gas (remember that the oxygen used by our lungs is only ~22% of the total volume of air you inhale). Therefore, when you release that breath and want to take in a new one you need to first empty your lungs out in order to refill them.

In addition, you need to have your lungs empty in order to be able to expand them and draw in more air. There is no biological reason for any of this, it is the same principle as trying to use a turkey baster:

If you use it once and pull up some liquid into it, you will have to let air out before you can use it again. Your lungs work in the same way. Test this by exhaling all the air from your lungs and then holding your breath without inhaling. When you want to start breathing again, you'll be able to breathe directly in without needing to exhale first.


Death by exsanguination not painful? Several places on the internet seem to purport that animal sacrifice is painless because exsanguination causes no pain. That sounds unscientific to me and an attempt to appease culture than than using science. For instance this question on the se and others like it on the internet. Is there a difference between pig and cow anatomy that makes religious slaughter of the latter less painful?

Could someone comment on the validity of this research?

Schulze W, Schultze-Petzold H, Hazem AS, Gross R. Experiments for the objectification of pain and consciousness during conventional (captive bolt stunning) and religiously mandated (“ritual cutting”) slaughter procedures for sheep and calves. Deutsche Tierärztliche Wochenschrift 1978 Feb 5;85(2):62-6.

This is of course a controversial topic with there being supporters for both methods of slaughter. First of all, The research paper that you have mentioned is a highly cited one and it is the foremost study that supporters of exanguination use to support their method of slaughter. However, the author himself (Wilhelm Schulze) has stated and I quote

  "objective results presented for the captive bolt application in sheep
  indicates that the captive bolt device used is suspect" and that these
  initial "scientific findings and the results presented are only a very
  first contribution" and that they "need to be followed as a high
  priority by further investigations in the continuation of the
  scientific clarification of the issues of loss of pain and
  consciousness during slaughter of this kind with and without stunning
  using the same experimental approach with a representative number of
  grown cows of various breeds." (reference)

Since stunning methods have advanced (reference) from the time this paper was published (1978), it would probably be a bit unfair to hold onto this paper as proof for supporting exsanguination. Moreover, in another study, in which measurements were done with an electro-corticogram it was found that

  Captive bolt stunning followed by sticking one minute later resulted
  in immediate and irreversible loss of evoked responses after the stun.
  Spontaneous cortical activity was lost before sticking in three
  animals, and in an average of 10 seconds after sticking in the
  remaining five animals. The duration of brain function after shechita
  was very variable, and particularly contrasted with captive bolt
  stunning with respect to the effects on evoked responses. These were
  lost between 20 and 126 seconds (means of 77 seconds for somatosensory
  and 55 seconds for visual evoked responses) and spontaneous activity
  was lost between 19 and 113 seconds (mean 75 seconds) after slaughter (reference).

The two questions that have to be answered in exsanguination are

-- Does the neck cut cause pain?

-- How long does it take for the animal to lose enough blood for insensibility to occur and for any perception of pain or suffering associated with slaughter to disappear?

With regard to pain, in the process of cutting the major blood vessels leading to and from the brain a number of other tissues are also severed by the extensive neck cut including muscle, skin, sensory and motor nerves etc. There is a chance that this might cause significant shock and fear to the animal. The time to lose consciousness is highly variable in  exsanguination. (reference)

Very good arguments are presented in this article and I highly recommend that you go through it.


How can a monocot get so massive? Some monocots (such as palms) are impressively thick and massive, yet botanists maintain that they don't have secondary growth. Why do botanists say this?  How can it get so big without secondary growth?

The vascular system is different in monocots and dicots. In dicots the vascular tissues are arranged in concentric circles; one of these rings is meristematic cells (undifferentiated cells that can differentiate into any cell type). This ring of meristem tissue is called the vascular cambium and is where secondary growth occurs - xylem grows inwards and phloem grows outwards.

Whereas:

  Monocots have a distinctive arrangement of vascular tissue known as an
  atactostele in which the vascular tissue is scattered rather than
  arranged in concentric rings. Many monocots are herbaceous and do not
  have the ability to increase the width of a stem (secondary growth)
  via the same kind of vascular cambium found in non-monocot woody
  plants. However, some monocots do have secondary growth, and because
  it does not arise from a single vascular cambium producing xylem
  inwards and phloem outwards, it is termed "anomalous secondary
  growth". (Wikipedia)

For palms specifically:

  Palm trees increase their trunk diameter due to division and
  enlargement of parenchyma cells, which is termed diffuse secondary
  growth. (Wikipedia)

Parenchyma cells are type of cells found in plant ground tissue, which makes up the bulk of plant mass.


Which protein complex is composed of the greatest number of different kinds of proteins, and how many types are involved? Why are some protein complexes composed of many different types of proteins? How many different types are they composed of? In particular, which protein complex has the greater number of different types of proteins in it?

For example, I've read that the ribosome consists of 70-80 different types of proteins.

How many different types of proteins are in the spliceosome for example?

I'm using the phrasing "types of proteins" to distinguish aggregates/complexes composed of many different copies of the same protein (i.e. some viral capsids) from those composed of many different kinds (i.e. ribosome, exosome complex, spliceosome).

In this paper detailed analysis has been made on spliceosome (U2-type) composition. It should be noted that this complex has dynamic composition. In the paper authors state that up to 170 proteins may associate to a metozoan spliceosome during its course of action. Individual assemblies contain approx 110 proteins (human). Similar complex of the yeast contains approx 60 proteins (precatalytic B complex), while C complexes have 50 proteins, altogether 90 different were identified in yeast. See the linked paper for details.


Paralogous genes in genome-wide association studies? Has anybody tested if paralogous genes are over-represented among the genes identified by genome-wide association studies (GWAS)?

For example, if a GWAS study finds 200 genes associated to the disease/trait, and a number X of those can be classified as belonging to Y different gene families, is there a test to see if X and Y are bigger than expected, given the total number of genes and gene paralogies in a genome? Here I am talking long established copies within a species, not CNVs in different individuals of the same species.

I am thinking there is an interesting question behind this: if a gene has duplicated during the evolution of a genome, and the different gene copies have taken specialized, yet related, roles, an unbiased analysis like GWAS should be able to find cases where different paralogous copies associate to different subdiseases/subtraits within the same global disease/trait.

There is no literature report saying such a thing. However, I did a cursory check for GWAS study on neuroblastoma.

Selected SNPs with p-value>0.05
Converted p-values to a score —  -log10(p-value)
Mapped the SNPs to genes while calculating cumulative score for a gene

I just sorted the genes based on their names, assuming that many paralogs have similar names. I know it is not the right way to go about it. However, I found many similar named groups in the list.

Now the next step is find actual paralogs and to score the cumulative score for a paralog-group. This is a little task:

Get sequences of the genes
Run a BLAST search to find paralogs
Assign genes to groups and find scores

I can share the file with genes and scores. I would, however, continue only if someone is actually interested in pursuing this — this could be a research paper.

PS: If you want the file just comment your email id. Some IT admin idiot has blocked rapidshare/4shared etc


Do we come to know which allele is dominant by seeing family genration tree only? I know that a Gene has Alleles (variation) and one is Dominant over Other i.e the Other Recessive.
Then I got a Thought that How can we tell whether an Allele is Dominant or Recessive...... and I came across this Site while Googling, and It says we can tell this by Observing Patterns in the Family Generation Tree.
So, my question is that can we only describe an Allele by observing pattern? Is there any other Method or by looking at the Molecular level and tell?
Please extend this "How can we tell whether an Allele is Dominant" to a Special Case where a Gene has 3 Alleles.....can we have 2 Dominant Allele?

Addressing Your First Question
We can tell whether an allele is dominant or recessive based on patterns in family trees, that is true, and it is very helpful! However, that is not the only way, since by looking at the molecular function of the alleles, the dominant and recessive relationship between alleles can be assessed without needing to look at family trees!
I think a deeper understanding of what it means to be dominant versus recessive would be helpful, because usually biology isn't just that simple! In most scenarios where there is a distinct recessive and dominant trait, it is because the dominant trait causes some specific activity/functioning protein while the recessive trait does not. Let's look at an example of this:
Let's choose eye color:1
There are multiple genes that affect eye color but let's just look at one: the one that codes for the brown pigment (melanin) to be produced in the iris [specifically the HERC2 gene]. As you probably already know, brown eyes are dominant and blue eyes are recessive.
Let's call the dominant allele B and the recessive allele b. The only way for blue eyes to be the phenotype is for the allele combination to be bb. Now think about why this would occur on a molecular level. Alleles are just forms of genes, which then in turn code for some protein. Think back to what we said earlier about how most of the time dominant alleles cause some certain activity within the cell and recessive alleles do not. We can now use that knowledge to uncover the molecular basis of this eye color scenario: The B allele codes for the brown pigment to be produced in the iris, while the b allele codes for a dysfunctional protein that does not lead to melanin being produced, leading to a blue-ish color seen. So, if the B allele causes the production of melanin and the b allele does not, it makes sense by the B allele would be dominant in this case. In the case of Bb, melanin is still being produced (even if it is because of just one allele), so there still would be brown eyes! Therefore this makes sense by bb is the only allele combination that results in the blue-eye phenotype, because it is the only combination with no allele still producing melanin. This is why brown eyes are dominant to blue eyes, because blue eyes can only exist without the presence of any B allele.
So, by knowing how an allele actually functions on a molecular level, that can help us to understand if it is in fact dominant or recessive to another allele. We should also acknowledge that genes do not necessarily need to be in this black-and-white relationship of recessive or dominant. There is also incomplete dominance and co-dominance!
Now to Your Second Question
When talking about three alleles, it is important to understand that allele dominance only is used when comparing one allele to another allele. So with three alleles, the dominance, recessiveness, co-dominance, or incomplete dominance is between two of the alleles.2 So if we are talking about alleles A, B, and C. We could say things such as:

A is recessive to B, B is dominant to C, C has in-complete dominance with A, etc...

However, it is really up to the molecular function of each of the alleles and to determine how those interactions would take place. But to answer your question directly of "can we have 2 dominant alleles," the answer is sort of. Allele B and C can both be dominant to allele A, but that says nothing about the interaction between Allele B and Allele C.

1 This is a simplification of the actual molecular mechanism of eye color, but at a simplified level this works to illustrate our point. You can read more into the genetic/molecular basis of eye color here.
2 This article is very good at discussing alleles and clarifying the point that dominance is only between two alleles.


A strain of my hair has a grey spot in the middle, how is this possible? And why does it happen? My hair is usually brown and black, I haven't dyed my hair for two years and if I had this would be strange. A strand of hair went from black(roots) grey (middle) then light brown(bottom).

How does hair change color along its length? And why does this happen?

Your hair gets its color from a compound known as melanin, produced by special cells called melanocytes. There are two versions of melanin - one that produces dark pigmentation and the other that produces light pigmentation. If your natural hair color is brown/black, then it normally has a specific amount of dark vs light pigment. The middle section of this hair is grey because there was an absence of melanin production when the hair was still growing. There could be multiple factors (including stress , as described on the library of congress site), but it's nothing to worry about. Your melanocytes started to normally produce melanin again, which is why the newest hair growth (closest to the roots) is dark in color (dark brown/black).


Which organism has the sharpest vision? Which organism has the sharpest vision in terms of distance and spectrum. Please propose any other useful measure.

This paper suggests that bats have a comparatively high depth of focus.

It's believed that butterflies (depending on species) have the widest visual spectrum.


How the concentration of an antibiotic is chosen for YPD medium? I need to prepare YPD plates containing hygromycin, but I don't know which concentration I can use. I'll select transformants of Hansenula polymorpha.

According to this site,
for yeast (I assume this means Saccharomyces cerevisiae) you should use 50 µg/ml to 200 µg/ml; for fungi (!) use 100 µg/ml to 300 µg/ml. The site also stresses the importance of the pH of the medium.

I think that, unless a Hansenula expert comes along,  you will have to try an initial experiment to measure the sensitivity of untransformed cells across the range indicated. Then you can try selecting resistant cells at a concentration somewhat higher than that which kills untransformed cells. Finally, you can check to see how resistant the transformants are, to enable you to decide on a useful concentration for routine selection of transformants.


What advantage do dogs have in clearly disclosing whether they are afraid or unafraid in a conflict? Dogs are known to clearly show whether they are afraid or unafraid with the posture of their tails during a conflict.

How and why is this beneficial?

My limited understanding makes me feel that, in any social setting, disclosing whether an actor is afraid or unafraid would almost always be unfavourable for the actor. Is this incorrect?

Isn't it better for the less confident dog to try to bark out the stronger one and if it doesn't work then simply walk away, rather than broadcast that it is afraid of the stronger dog?

It is better for animals to broadcast their qualities, and size one-another up before risking injury in conflict. As pack animals, dogs are particularly sensitive to where they are placed in a hierarchy. So it is better for them to telegraph their qualities than to engage in conflict that may hurt them.


A way to measure ripeness of a fruit I'm doing an experiment how fast fruits ripen and decay

I'm wondering how to measure the ripeness of a fruit(banana, mango, tomato, kiwi etc.) so that I will get a quantitative results.

I have looked at using penetrometer to see how squishy it is. Is there any other ways to do it?

If not, I'm thinking of getting qualitative results. Is there any tips of making good qualitative results?

thanks

Sorry, I am not sure if this falls into Biology category

Asides from just eyeballing the change in color/consistency, Wikipedia suggests using iodine for a qualitative measurement (though without reference):

  Iodine (I) can be used to determine whether fruit is ripening or rotting by showing whether the starch in the fruit has turned into sugar. For example, a drop of iodine on a slightly rotten part (not the skin) of an apple will stay yellow or orange, since starch is no longer present. If the iodine is applied and takes 2–3 seconds to turn dark blue or black, then the process of ripening has begun but is not yet complete. If the iodine becomes black immediately, then most of the starch is still present at high concentrations in the sample, and hence the fruit hasn't fully started to ripen.

A quantitative method applicable to many kinds of fruit is going to be tricky. If you have a spectrophotometer you could measure the changes in light absorption as the fruit ages. You will probably want to measure the absorptions of control fruits as they age and then compare them to fruits from whatever experiment you perform.

Another possibility is measuring ethylene and/or carbon dioxide production. As fruits ripen they produce more of both these gasses, but this increase does not follow a neat linear correlation with time to put it lightly. Non-climacteric fruits, if you use them, may also be problematic here as they do not show such increase in gas production.

Merzlyak, M. N., Gitelson, A. A., Chivkunova, O. B., & Rakitin, V.
Y.    (1999). Non‐destructive optical detection of pigment changes
during    leaf senescence and fruit ripening. Physiologia plantarum,
106(1),    135-141.
Burg, S. P., & Burg, E. A. (1962). Role of ethylene in fruit
ripening. Plant Physiology, 37(2), 179.


Why bovine serum albumin is used in mass-spectroscopy and how to interpret such data? In the paper Network organization of the huntingtin proteomic interactome in mammalian brain, there is a description of a mass spectroscopy experiment where Bovine Serum Albumin (BSA) is added to a sample lysate and the same lysate without BSA was used as the control. I have a working knowledge of how mass spectroscopy works but I could not understand why BSA is used in this experiment. Can anyone help me?
This is probably a very trivial question. Excuse my ignorance, I am not a biology major. I tried google search to get an explanation for this but I didn't find anything satisfactory.

Their LC-MS-MS data was only semi-quantitative as gathered, meaning they could compare relative levels of one protein to another in the same sample, but not necessarily between different samples with a high degree of confidence. So, they spiked known amounts of BSA, an extremely well-characterized protein frequently used in the lab, into their samples and created a standard curve across different concentrations that correlated pretty well with the input amounts. They could then use this curve to better quantify the other proteins in their samples among all the different sample types. This in turn allowed them to say with greater certainty that, for example, Protein X was expressed at three-fold higher levels in Sample A than in Sample B. Otherwise, they would only have been able to say that Sample A expression of Protein X was higher than Sample B.


Is there anything that tells me how Lichens Grow? I've done a lot o research about this matter but I could not find anything relevant. So I'm doing a Computer Science project where, using AI and Computer Graphics, we try to predict the growth and aging of lichens on a stone, and at this moment I need some "academic validation", so is there any way like a formula or something that tells me how lichens evolve and grow on stones? Thank you so much!

This image shows what I've accomplished:

In real Life:

http://i.imgur.com/NFo4A8Y.jpg

So is it possible to predict how are they going to spread along the stone in a period of time? Do they start by growing in small colonies and then tend to get together to create a bigger colony? I don't know if this makes any sense, anyway thank you for your patience!

Just from conducting a Google search using the phrase, "lichen modeling pdf", I was able to find several studies/publications that address your need(s). Though its dated 2004, this article seems extremely relevant to your application.

Simulating and Modeling Lichen Growth

  In this paper, we present a system for modeling lichens
  and simulating their propagation and growth in a virtual
  scene.

In the article, they mention:

Aging and Weathering
Ecosystem Simulation
Lichen Seeding and Propagation
Environmental Charateristics
Theoretical Aggregation
Complex Modeling

And here are (a few) examples of what they produce:


How does bacteriorhodopsin differ from the rhodopsin present in mammalian eyes? In my high school textbook, it is written that they are similar. So, I was just curious to know about this.
Thank you.

Although they are similar in both bacteriorhodopsins  and rhodopsins being retinal-binding proteins, the similarity in their amino acid sequence is very limited.

The key difference between them is that rhodopsin is a G-protein-coupled receptor, and this is not the case with bacteriorhodopsin. A quick Google search on Bacteriorhodopsin vs Rhodopsin will send you to a Wikipedia article that says:

  Bacteriorhodopsin belongs to the microbial rhodopsins. They have similarities to vertebrate rhodopsins, the pigments that sense light in the retina. Rhodopsins also contain retinal; however, the functions of rhodopsin and bacteriorhodopsin are different, and there is limited similarity in their amino acid sequences. Both rhodopsin and bacteriorhodopsin belong to the 7TM receptor family of proteins, but rhodopsin is a G protein-coupled receptor and bacteriorhodopsin is not.

A very good paper if you would like to know more about the two is by H. Gobind Khorana on the Two light-transducing membrane proteins.


Plot coverage per base for BAM file I have a BAM file and a BED file for my own chromosome. I would like to get coverage per base and ideally construct a histogram of coverage across each gene.

The motivation is to visualise the coverage across each gene. If my experiment is good, I should expect uniform coverage. It's also important to compare the coverage near the boundary of the genes.

A R (bioconductor) solution is ideal, because I can directly visualise.

How to do it?

From your bam-file, you can generate a BED(-graph) of per base coverage with bedtools genomecov (use the -ibam, -d and if you want a BEDgraph also the -bg flags).

There are multiple R packages for bioconductor which read and visualise these, including sushi.


Will the sex ratio of chickens become favourable to females? As male chickens are killed after birth in mass farming. Will being male become a negative evolutionary trait, that is to say will females become more likely as male death is more likely.

Any chick has a mother and a father. Hence, the contribution to the gene pool of the following generation comes at 50% from males and at 50% from females. As a result there is no selection for biasing the sex-ratio among its offsprings. The variance in reproductive success might be higher among males than among females but that does not matter for the sex-ratio.

This is known as Fisher's principle. In the terms of W.D. Hamilton (Extraordinary sex ratios), copy-pasted from wikipedia:

  [..] given the condition that males and females cost equal amounts to
  produce:

  Suppose male births are less common than female.
  A newborn male then has better mating prospects than a newborn female, and therefore can expect to have more offspring.
  Therefore parents genetically disposed to produce males tend to have more than average numbers of grandchildren born to them.
  Therefore the genes for male-producing tendencies spread, and male births become more common.
  As the 1:1 sex ratio is approached, the advantage associated with producing males dies away.
  The same reasoning holds if females are substituted for males throughout. Therefore 1:1 is the equilibrium ratio.

To my knowledge, only kin/group selection can yield a sex-ratio different from 1:1 to be an ESS.


Why do we fall asleep when our eyes are closed? Why do we fall asleep when our eyes are closed? When we lie down with our eyes closed, eventually we'll fall asleep. Why is that? Is our eyes closing some sort of trigger to our brain that says it's time to sleep?

You're confusing the cause with the effect. The effect is closing of the eyes (and maybe some component of relaxing.) The cause is sleepiness. In other words, when you're falling asleep, the eyes close, not the other way around. You can close your eyes for 24 hours straight, and you might sleep longer out of boredom, but you'll still spend most of the time awake. Closing your eyes doesn't cause sleep.

The reason our eyes close when we sleep is to protect the eyes from drying out and insuring the oxygenation of the corneas.

Take for example truck drivers. They need to keep their eyes open or bad things happen, like death and destruction. Yet, as they tire, try as they might, their eyes flutter closed and off to sleep they go.

Driver drowsiness detection with eyelid related parameters by Support Vector Machine


Ultrasound during pregnancy In a hospital I can see a long queue of pregnant women waiting for their turn for ultrasound.  Is it safe to go through the ultrasound during pregnancy, especially during last few weeks?
Is ultrasound really required?  What if it is not done? How does ultrasound affect baby?

The U.S. Food and Drug Administration (FDA) has the following information regarding the risks of ultrasound imaging;

Ultrasound imaging has been used for over 20 years and has an excellent safety record. It is non-ionizing radiation, so it does not have the same risks as x-rays or other types of ionizing radiation.
Even though there are no known risks of ultrasound imaging, it can produce effects on the body. When ultrasound enters the body, it heats the tissues slightly. In some cases, it can also produce small pockets of gas in body fluids or tissues (cavitation). The long-term effects of tissue heating and cavitation are not known.
Because of the particular concern for fetal exposures, national and international organizations have advocated prudent use of ultrasound imaging. Furthermore, the use of diagnostic ultrasound for non-medical purposes such as fetal keepsake videos has been discouraged.

FDA > Radiation Emitting Products > Medical Imaging > Ultrasound Imaging
Further information

I had a bit of a look through PubMed and Scopus for any papers relating to ultrasound risk, but didn't find any.


How can there be a one-to-one correspondence between RNA and genes? From what I know, multiple strands of DNA make up a gene, so how can for each gene there can only be one RNA corresponding to it and vice versa? Is my knowledge incorrect?

Very few things are that clear cut in biology. There are three main things to consider here.
1. Gene to RNA
Most eukaryotic genes are spliced. This is basically a process by which a single gene can be transcribed to multiple, different, mRNAs each of which will then be translated to a different protein.
Therefore, there is usually (some genes aren't spliced) not a one-to-one correspondance between a gene and the mRNAs it can produce.
2. RNA to Gene
The next issue is that some genes exist in multiple, similar copies in the genome. For such genes, it is not always possible to know which of the duplicates was actually read to produce a given mRNA.
There is, therefore, not always a direct one-to-one correspondance between an mRNA and the gene it was transcribed from. This, however, is far less common than the splicing issue mentioned above and can, in most cases, be ignored.
3. Each gene is only on a single strand
Each gene is only on a single strand of DNA. Yes, DNA is double stranded, but each gene resides on only one of the two strands (the other strand will be the reverse complement of the gene).

Despite the points made above, it is actually usually possible to map an mRNA molecule to the gene that produced it. In the case of duplicate genes you'll just get multiple hits. The programs that exist to do this sort of analysis can mostly deal with splicing. So, for example, if you have the sequence of the human chromosome 21 and the mRNA sequence of the ERG gene, you can do (on a *nix system with exonerate installed):
exonerate -m coding2genome -t chr21.fasta -q dscam.fasta > out

Which will produce:
Command line: [exonerate -m est2genome -n 1 -t chr21.fasta -q erg.fasta]
Hostname: [oregano]

C4 Alignment:
------------
         Query: gi|609878487|ref|NM_001291391.1| Homo sapiens ERG, ETS transcription factor (ERG), transcript variant 8, mRNA
        Target: gi|528476536|ref|NC_018932.2| Homo sapiens chromosome 21, alternate assembly CHM1_1.1, whole genome shotgun sequence:[revcomp]
         Model: est2genome
     Raw score: 7669
   Query range: 0 -> 1546
  Target range: 39594417 -> 39332536

        1 : GTTTTCACTTGGTCGGAATGGGGAGAGTGTGCAAGAGATCGCTGCGGGACAGGT :       54
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39594417 : GTTTTCACTTGGTCGGAATGGGGAGAGTGTGCAAGAGATCGCTGCGGGACAGGT : 39594364

       55 : TCCTAGAGATCGCTCCGGGACGGTCGTGACGGCCCCCGAGGGACATGAGAGAAG :      108
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39594363 : TCCTAGAGATCGCTCCGGGACGGTCGTGACGGCCCCCGAGGGACATGAGAGAAG : 39594310

      109 : AGGAGCGGCGCTCAG  >>>> Target Intron 1 >>>>  GTTATTCCAG :      133
            |||||||||||||||++         76685 bp        ++||||||||||
 39594309 : AGGAGCGGCGCTCAGgt.........................agGTTATTCCAG : 39517600

      134 : GATCTTTGGAGACCCGAGGAAAGCCGTGTTGACCAAAAGCAAGACAAATGACTC :      187
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39517599 : GATCTTTGGAGACCCGAGGAAAGCCGTGTTGACCAAAAGCAAGACAAATGACTC : 39517546

      188 : ACAGAGAAAAAAGATGGCAGAACCAAGGGCAACTAAAG  >>>> Target In :      226
            ||||||||||||||||||||||||||||||||||||||++         9093
 39517545 : ACAGAGAAAAAAGATGGCAGAACCAAGGGCAACTAAAGgt.............. : 39517505

      227 : tron 2 >>>>  CCGTCAGGTTCTGAACAGCTGGTAGATGGGCTGGCTTACTG :      266
            bp         ++|||||||||||||||||||||||||||||||||||||||||
 39517504 : ...........agCCGTCAGGTTCTGAACAGCTGGTAGATGGGCTGGCTTACTG : 39508374

      267 : AAGGACATGATTCAGACTGTCCCGGACCCAGCAGCTCATATCAAG  >>>> Ta :      312
            |||||||||||||||||||||||||||||||||||||||||||||++
 39508373 : AAGGACATGATTCAGACTGTCCCGGACCCAGCAGCTCATATCAAGgt....... : 39508326

      313 : rget Intron 3 >>>>  GAAGCCTTATCAGTTGTGAGTGAGGACCAGTCGT :      345
             130340 bp        ++||||||||||||||||||||||||||||||||||
 39508325 : ..................agGAAGCCTTATCAGTTGTGAGTGAGGACCAGTCGT : 39377955

      346 : TGTTTGAGTGTGCCTACGGAACGCCACACCTGGCTAAGACAGAGATGACCGCGT :      399
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39377954 : TGTTTGAGTGTGCCTACGGAACGCCACACCTGGCTAAGACAGAGATGACCGCGT : 39377901

      400 : CCTCCTCCAGCGACTATGGACAGACTTCCAAGATGAGCCCACGCGTCCCTCAGC :      453
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39377900 : CCTCCTCCAGCGACTATGGACAGACTTCCAAGATGAGCCCACGCGTCCCTCAGC : 39377847

      454 : AGGATTGGCTGTCTCAACCCCCAGCCAGGGTCACCATCAAAATGGAATGTAACC :      507
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39377846 : AGGATTGGCTGTCTCAACCCCCAGCCAGGGTCACCATCAAAATGGAATGTAACC : 39377793

      508 : CTAGCCAGGTGAATGGCTCAAG  >>>> Target Intron 4 >>>>  GAA :      532
            ||||||||||||||||||||||++         21741 bp        ++|||
 39377792 : CTAGCCAGGTGAATGGCTCAAGgt.........................agGAA : 39356027

      533 : CTCTCCTGATGAATGCAGTGTGGCCAAAGGCGGGAAGATGGTGGGCAGCCCAGA :      586
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39356026 : CTCTCCTGATGAATGCAGTGTGGCCAAAGGCGGGAAGATGGTGGGCAGCCCAGA : 39355973

      587 : CACCGTTGGGATGAACTACGGCAGCTACATGGAGGAGAAGCACATGCCACCCCC :      640
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39355972 : CACCGTTGGGATGAACTACGGCAGCTACATGGAGGAGAAGCACATGCCACCCCC : 39355919

      641 : AAACATGACCACGAACGAGCGCAGAGTTATCGTGCCAGCAG  >>>> Target :      682
            |||||||||||||||||||||||||||||||||||||||||++         19
 39355918 : AAACATGACCACGAACGAGCGCAGAGTTATCGTGCCAGCAGgt........... : 39355875

      683 :  Intron 5 >>>>  ATCCTACGCTATGGAGTACAGACCATGTGCGGCAGTGG :      719
            698 bp        ++||||||||||||||||||||||||||||||||||||||
 39355874 : ..............agATCCTACGCTATGGAGTACAGACCATGTGCGGCAGTGG : 39336142

      720 : CTGGAGTGGGCGGTGAAAGAATATGGCCTTCCAGACGTCAACATCTTGTTATTC :      773
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39336141 : CTGGAGTGGGCGGTGAAAGAATATGGCCTTCCAGACGTCAACATCTTGTTATTC : 39336088

      774 : CAGAACATCGATGGGAAGGAACTGTGCAAGATGACCAAGGACGACTTCCAGAGG :      827
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39336087 : CAGAACATCGATGGGAAGGAACTGTGCAAGATGACCAAGGACGACTTCCAGAGG : 39336034

      828 : CTCACCCCCAGCTACAACGCCGACATCCTTCTCTCACATCTCCACTACCTCAGA :      881
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39336033 : CTCACCCCCAGCTACAACGCCGACATCCTTCTCTCACATCTCCACTACCTCAGA : 39335980

      882 : GAGA  >>>> Target Intron 6 >>>>  CTCCTCTTCCACATTTGACTT :      906
            ||||++          867 bp         ++|||||||||||||||||||||
 39335979 : GAGAgt.........................agCTCCTCTTCCACATTTGACTT : 39335088

      907 : CAGATGATGTTGATAAAGCCTTACAAAACTCTCCACGGTTAATGCATGCTAGAA :      960
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39335087 : CAGATGATGTTGATAAAGCCTTACAAAACTCTCCACGGTTAATGCATGCTAGAA : 39335034

      961 : ACACAG  >>>> Target Intron 7 >>>>  GGGGTGCAGCTTTTATTTT :      985
            ||||||++         1911 bp         ++|||||||||||||||||||
 39335033 : ACACAGgt.........................agGGGGTGCAGCTTTTATTTT : 39333098

      986 : CCCAAATACTTCAGTATATCCTGAAGCTACGCAAAGAATTACAACTAGGCCAGG :     1039
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39333097 : CCCAAATACTTCAGTATATCCTGAAGCTACGCAAAGAATTACAACTAGGCCAGG : 39333044

     1040 : TACGAAAACACCCCTGTGTGATCTCTTCATTGAGAGACATCCCAGATGTCCTGC :     1093
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39333043 : TACGAAAACACCCCTGTGTGATCTCTTCATTGAGAGACATCCCAGATGTCCTGC : 39332990

     1094 : TGAGATCCGTGCCCTAAGTCACGTGATACAAAGAGAGCTGATCCCGGAGCTGAA :     1147
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332989 : TGAGATCCGTGCCCTAAGTCACGTGATACAAAGAGAGCTGATCCCGGAGCTGAA : 39332936

     1148 : GCCAGTCCCAGACAGTCTTATTCTGCCTCTGTTGATTTGGAGACTAAATCCACT :     1201
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332935 : GCCAGTCCCAGACAGTCTTATTCTGCCTCTGTTGATTTGGAGACTAAATCCACT : 39332882

     1202 : CAAACCATTTCATTCAAAGACCACACTAAAGGAATTAAGAGCAGATTAGCCCTT :     1255
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332881 : CAAACCATTTCATTCAAAGACCACACTAAAGGAATTAAGAGCAGATTAGCCCTT : 39332828

     1256 : TAACTAGCTTTTCAGAAAGACAGATGGGCAAAGAAGGCATCCTGGATGCCTGGC :     1309
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332827 : TAACTAGCTTTTCAGAAAGACAGATGGGCAAAGAAGGCATCCTGGATGCCTGGC : 39332774

     1310 : AGTTAGGAATAGGCCGACTTTTGAACTAACAGAAGGATCTGTCCCTCCTCGGGG :     1363
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332773 : AGTTAGGAATAGGCCGACTTTTGAACTAACAGAAGGATCTGTCCCTCCTCGGGG : 39332720

     1364 : GAAGAGCACAAAACAAGGACACTCCCCAGATTCACAGTGACCGATTATCAGTAT :     1417
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332719 : GAAGAGCACAAAACAAGGACACTCCCCAGATTCACAGTGACCGATTATCAGTAT : 39332666

     1418 : GTCACAAGAAGCCAGTCTTGCAGAGCAGAAGCATGCAACCAGTAGTATTTACAT :     1471
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332665 : GTCACAAGAAGCCAGTCTTGCAGAGCAGAAGCATGCAACCAGTAGTATTTACAT : 39332612

     1472 : CTGAATCTTACTGCCTGTCCTCCAAATGATTTAATTAGGTAATAAATTTACATG :     1525
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332611 : CTGAATCTTACTGCCTGTCCTCCAAATGATTTAATTAGGTAATAAATTTACATG : 39332558

     1526 : CCATTCATGCAAAAAAAAAAA :     1546
            ||||||||||||||| ||| |
 39332557 : CCATTCATGCAAAAATAAACA : 39332537

vulgar: gi|609878487|ref|NM_001291391.1| 0 1546 + gi|528476536|ref|NC_018932.2| 39594417 39332536 - 7669 M 123 123 5 0 2 I 0 76681 3 0 2 M 102 102 5 0 2 I 0 9089 3 0 2 M 86 86 5 0 2 I 0 130336 3 0 2 M 218 218 5 0 2 I 0 21737 3 0 2 M 152 152 5 0 2 I 0 19694 3 0 2 M 204 204 5 0 2 I 0 863 3 0 2 M 81 81 5 0 2 I 0 1907 3 0 2 M 580 580
-- completed exonerate analysis

Alternatively, you can use an online resource like the UCSC's BLAT page to align the mRNA against the genome. You can see the results here and in the image below:

As you can see, our query mRNA sequence (NM_001291391.1) overlaps perfectly with the ERC gene.


Compare and contrast "Rubisco activity" and "assimilation rate" (is there a difference, and if so, what is it)? I am confused about the variable "RuBisCO activity". How is it measured, and is it any different from the net assimilation rate?

Based on some background reading (e.g. Kling, 2008; Lambers et al 2011)  the only difference that I can find is the units. Both would have "carbon fixed per unit time", but RuBisCO activity is expressed per unit mass of the enzyme, while assimilation rate is per unit leaf area (or less commonly, leaf mass).

Both are measures of carbon fixation rate.

RuBisCO activity specifically refers to the rate at which the enzyme RuBisCO fixes carbon to RuBP, and is measured by isolating the enzyme from tissue samples and, usually, using radiolabelled CO2 to measure how much carbon is fixed in a set amount of time in controlled conditions and with controlled supply of substrate.

Carbon assimilation rate is generally a whole-plant or whole-leaf variable, measured on a larger scale. It is usually measured by measuring leaf sugar carbon before and after a set period, again using radiolabelling. Conditions may or may not be controlled, and it can be measured in the field (unlike RuBisCO activity).

RuBisCO activity might differ from net fixation in the short term in plants which have an intermediate carbon fixation step, such as in CAM or C4 plants, if the net fixation measurement includes the intermediates - the pool of intermediate carbon-containing molecules have technically been fixed but not by RuBisCO. However, over longer time periods this effect will disappear, as ultimately all CO2 is fixed or re-fixed through RuBisCO.


Why does an electrical shock freeze up muscles? Why is it when someone comes into contact with an electrical supply that their body freezes up and is unable to move away from the electrical source?

Can someone explain this through a physiological perspective?

Interesting question!

An important factor here is the let-go phenomenon, which is defined as the current level in the arm that will cause the hand to involuntarily grip the current source. When the fingers are wrapped around a large cable, most adults will be able to let go with a current of less than 6 mA. At 22 mA, however, more than 99% of adults will not be able to let go.

Nearly all cases of inability to let go involve alternating current. Alternating current repetitively stimulates nerves and muscles, resulting in a tetanic (sustained) contraction that lasts as long as the contact is continued. If this leads to the subject tightening his or her grip on a conductor, the result is continued electric current flow through the person and lowered contact resistance.

Given that the current flow in the forearm stimulates both the muscles of flexion and extension, it seems surprising that one cannot let go. However, the muscles of flexion are stronger, making the person unable to voluntarily let go (similar to the fact that a crocodile's jaws can be kept shut with your bare hands, but one should better not attempt to keep them open like that...).

Direct currents below 300 mA have no let-go phenomenon, because the hand is not involuntarily clamped.

Several different outcomes may occur when a person grasps a conductor giving 10 kV AC hand-to-hand voltage. Within 10 to 100 milliseconds, muscles in the current path will strongly contract. The person may grasp the conductor more tightly. However, mostly subjects are propelled away from the contact, likely due to generalized muscle contractions.

Reference
- Fish & Geddes, J Plastic Surg (2009); 9: 407-21


What is the effect of self envenomation on reptiles? If a venomous lizard bites its own tongue will it die?
I've searched the whole internet and I am unable to find a reliable answer on self envenomation.

TL;DR
No, it won't die. Lizards/snakes are usually immune to their own venom.

Since I couldn't find a good answer to this recurring question on this site, I will try to summarize it here. I found more research on snakes than on lizards, but for now we will just assume that similar mechanisms can be found in lizards.

First, the question is how the venom kills the prey. What does it do in the body?

A common mechanism is a block of acetylcholine receptors at the neuromuscular junction. Simplified, these receptors activate muscle contraction upon a neuronal signal. When the receptor is blocked by the toxin, the neuronal signal cannot be transmitted to the muscle, which paralyzes the animal. Research has shown, that some snakes and lizards have evolved different acetylcholine receptors, that can still bind acetylcholine (and activate muscles), but not the toxins (source1, source2). This makes them immune to the most common neurotoxins found in reptile venom.

Another mechanism is hemorrhagic activity of the toxin, which is a disruption of blood vessel integrity resulting in bleeding and death. This was linked to a proteolytic ("destroying proteins") function of venom compounds (source3, source4, source5). The blood serum of snakes can contain factors that block the hemorrhagic function of toxins, possibly by neutralizing the mode of action (inhibiting proteases). This could be specific antibodies/inhibitors or an adaptation of serum proteins (source6, source7, source8).

Further research has implicated phospholipidases (destroying phospholipids like used in cellular membranes) as the mode of action for snake venoms. Again, phospholipidase inhibitors can be found in the blood serum of the snakes themselves. There were also reports, that the expression of these inhibitors changes from younger to older snakes (source9, source10) and can be induced by venom injection (source11). It is therefore hypothesized that venomous snakes or lizards are repeatedly exposed to small amounts of their own venom, building up immunity over their life span.

Other modes of action include myotoxicity (destroying muscles), edema-formation or blood thinning. Again, it depends on the specific mechanism and how snakes and lizards have adapted to be immune to these.

Since similar toxins are found in several species, snakes and lizards are often not only immune to their own venom, but also to bites of other members of the same species or other related species.


What is the outcome of a human population starting with only 2 individuals? Starting with a human population N = 2, is there any way the genetic variability seen today could have come about? I don't know that much about meiosis, but isn't there a very limited number of alleles that could be passed on by the parents? Without a population to start with, wouldn't the lineage eventually turn into clones of each other like the cheetahs are now?
Are there any known mechanisms besides mutation that replenish the variability in alleles?

Indeed natural selection decrease variability and therefore decrease information and mutation recreate this information. You can think of a bunch of pens of different colors. If you select
for the red pens you will decrease the variability in pen colors as the other colors will slowly disappear. If you allow for mutation to occur you will recreate blue and black and purple and yellow pens to occur again in your population of pens.

Is it an accurate statement that less variability means less total information?

Yes, less variability means less information. Information is a concept that increases as predictability decreases. If no variability exist, you can predict at 100% what allele a given individual is carrying. You may want to have a look to shannon's theory of information here on Khan academy. Note: this has not much to do with biology but it has to the mathematical definition has to do with mathematics, probability and computer science.

Are there any known mechanisms besides mutation that replenish the variability in alleles?

No, there is nothing else than mutations that creates new alleles. "Mutation" means any kind of structural change of DNA. So by definition any change in the DNA is due to mutations, therefore only mutations creates new alleles. Note: that some people may use the word mutation in a more narrow sense including some kind of DNA change such as indels but excluding chromosome rearrangement for example. I used here the word mutation in the broad sense.

Segregation and Recombination

Two other concepts may interest you though: Segregation (See Mendelian inheritance) and recombination(also called crossing over).

For example if 2 individuals $AB$ (Allele $A$ on one chromosome and allele $B$ on the other chromosome) reproduce they can create the individuals $AA$, $AB$ or $BB$ thanks to segregation.

Two Genes set on chromosomes and if two genes are on the same chromosome, one might think that these two genes cannot segregate independently one from the other, they are linked! For example imagine an individual has the alleles $A_1$ and $B_1$ on two loci of one chromsome and alleles $A_2$ and $B_2$ on the two same loci but of the homologous chromosome. If this individual transmit the allele $A_2$ it must necessarily transmit the allele $B_2$ and can't transmit $B_1$ if recombination does not occur. But recombination does occur and allows for partially independent segregation of these two genes.

You will find more information about these two concepts on wikipedia. I don't want to go too much into details but in short these processes can in some conditions increase the phenotypic variance but in any case these phenomenon do not create new alleles. New alleles are created by mutations only.

Can 2 individuals carry as much genetic information than today's world population?

No! As a very simple argument, two individuals can only have 4 different alleles. But we know several loci (sing: locus, position on a chromosome) where there exist more than 4 different alleles. Therefore, mutations must have happened at some time.

And only to enjoy some further arguments: if these two individuals had together 4 alleles at all loci, it would be extraordinary unlikely that their variation would have remained in today's population. Let's imagine two heterozygote (=who has two different alleles on their two chromosomes for a given locus) individuals are $AB$ and $CD$ that have two offsprings. The probability that their 4 alleles are present in the two offsprings is $1/4$. I don't when Adam and Eve were supposed to exist but it very sound like their variability would have not been maintained through times. This random process which diminish variability is called genetic drift. To be a bit more accurate, in a population that do not change in size, the expected loss of alleles due to genetic drift at each generation $1/2N$, where $N$ is the population size. So the bigger is the population size, the lower is the loss of alleles due to genetic drift. In the above example $N=2$ and therefore the expected loss is $1/4$.

I don't know that much about meiosis, but isn't there a very limited number of alleles that could be passed on by the parents?

Yes, as said above, one individual can only have two alleles at a given loci and can therefore not transmit more than two different alleles.

Without a population to start with, wouldn't the lineage eventually turn into clones of each other[..]?

Yes, because in absence of mutations (and in absence of different special types of selection such as overdominance) the variability is slowly lost due to the randomness of segregation. This process is called genetic drift.


What is this Las Vegas area weed? This is a picture I took of my mystery weed out by Pittman wash in Henderson NV earlier this year. From my experience this last year, I assume that the plant turns red later in the year and loses the bottom leaves. The plant typically seems to grow no more than half a foot tall but can grow a couple feet wide at or near the top.
Edit: I wasn't able to get a background but here are more pictures

Alright, after a lot of searching, I have a proposed ID: Eriogonum deflexum known commonly as skeleton weed or little desert trumpet.  I feel pretty confident of the genus, less so on the species (there are several close candidates).  The family is buckwheat or Polygonaceae.

This plant has basal leaves as yours does, has pretty much leaf-less stems and relatively infrequent flowers, which look quite a bit like your picture.  Reading various descriptions it seems the plant is somewhat variable, it often looks like your pictures but sometimes has more flowers and sometimes the plant is more dense, rounded, shrubby and taller (it probably depends on the moisture and soil quality).  It is a desert species, preferring scrubby areas and washes, widely distributed in Western US deserts.

CalPhotos has a picture which looks to be a good match (credit: Jean Pawek; also, CalPhotos has many other photos).  This photo by Hank Jorgensen looks like a good match too and shows flowers which look similar to yours.

If you see the plant again, bring a picture on your phone and check the flowers carefully. Also the leaves should be hairy/wooly.


In my DNA sequence for one sampling site there're W's; Y's; R's and K's? I also just experienced the same thing with my DNA sequences, there are w's, Y', R', s' and k'. This is the very first time I've seen this. I am used to N but not these ones. Please kindly assist with knowing what might have caused these. Thanks in advance.

These are the so called "DNA ambiguity codes", when the sequencing result allows to bases at the position but it cannot be decided which. This can happen for example when you sequence genomic DNA and you have two different alleles present.

The code is the following (taken from this website):


How to inhibit formation of specific antibodies (to antisera)? Is there a way to inhibit an antibody response to a specific antigen using immunosupression? I am interested in reducing the anti-antibody formation to animal antibodies such as murine antibodies in antisera.

I have read that there are ways to decrease the immune response to antisera but haven't found a detailed paper on how they work.

Update 12/3/2014: Would this work? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2374127/pdf/0100491.pdf
Although it is streptavidin, could a similar process be used for antibodies?

If you are referring to reducing the titer in the immunized animal, you could give the animal a drug that has immunosuppressive properties. Velcade (PS-341) is a drug that effectively reduces plasma cell counts. There are many immunosuppressive drugs available.

If you  want to reduce the antibodies affinity, you are undertaking a much more delicate process. Affinity can be transiently affected by introducing a  unfavorable environment for the antibody. You can accomplish this by changing the temp, salt conditions, pH or introducing a denaturing agent like guanidine HCL.

Changing any of these conditions in just a little excess could also result in a permanent reduction in affinity.

If you are attempting to tailor the affinity constant of the Ab by changing the architecture of the antigen, you are correct this can be done using site directed mutagenesis. However I think it would be more effective to perform a random mutagenesis and then screen the mutants for the Ka value you want.

Lastly the antigen could also be post-translationally modified. After performing in vitro transcription and translation you could modify your antigen using different strategies such as ubiquination, phosphorylation, prenylation etc... All these could potentially affect Ka as well.

A Hybridoma system to produce a monoclonal antibody should also be explored. Here is a reputable company that produces monoclonal antibodies:

http://www.sdix.com/Products/Custom-Antibody-Services/Ab-Production-and-Services/mAb-Antibody-Development/Hybridoma-Development.aspx


What's the proper way to determine whether dose response curves +/- another variable (besides dose) are statistically different? I have an experiment wherein I measured uptake of a certain molecule into cells when delivered using Carrier A vs Carrier B. In other words, for example, I delivered 1, 2, 3, 4, 8, and 10 nmoles of DrugX to 6 wells of cells per dosage, HOWEVER in 3 wells DrugX was delivered using Carrier A and in the other 3 wells DrugX was delivered using Carrier B. I would like to statistically determine whether the dose-response curve I get when I used Carrier A for delivery is any different than the dose-response curve I get when I used Carrier B for delivery.

My initial thought was to run a paired T-test, but then I realized I would have to report results at each point and I would like to report on the curve as a whole. My next thought was to use a two-factor ANOVA, however from what it looks like, when it determines whether or not there is variance due to the change in carrier it looks at the average and variance of all the responses. Another thought I had would be to calculate area under the curve, but I'm not sure how. I finally settled on running a nonlinear regression on the Carrier A data, then on the Carrier B data, then as the dataset as a whole and compared the resulting fit curves. I got a nice p-value, however the $R^2$ values are lower than I'd like (about 0.9) because the curves didn't model especially well.

What would you do? What is the industry standard?

Good call on not using multiple t-tests. The reason being, assuming a 95% confidence interval, each time you run the test you are "allowing" a 5% possibility of making a Type I error - this means that you incorrectly reject the null hypothesis in favour of the alternative hypothesis. If you run one t-test, there's a five percent chance of making an error. If you run two t-tests, there's a ten percent chance of making an error.

Between a regression model, or ANOVA, it does not matter. As the mathematics behind each are pretty much equivalent.

What you really want to look for, is the slopes of both models. If the two models have a statistically significant difference between their slopes, then this is indicating an interaction effect.

Two examples of (some, but not all) possible interaction effects:

Carrier A & B have a similar effect on dose-response at 2mmol. But as the dosage approaches 10mmol, Carrier B causes a dose-response that is nearly double that of Carrier A.
Above 5mmol, Carrier B creates a greater dose-response. Below 5mmol Carrier A creates a greater dose response. At 5mmol the dose-response is nearly equivalent.


Do beavers' tails hurt from being dragged? I understand that when beavers walk on land, they drag their tails behind them on the ground. Their tails look quite large and rather heavy, and the ground is often rough - does dragging the tail not cause abrasions and pain for the beaver?

No, it does not, otherwise beavers wouldn't walk with their tails dragging. Here is a picture of the bottom of a beaver's tail:

Found here
and here is a closeup (probably of the top, but they're very similar):

Royalty-free stock photo from Dreamstime
As you can see, the skin looks almost like reptilian scales. It is likely highly-keratinized and is quite thick, as you can see below. Innervation is probably net very close to the surface, like callouses we develop on our hands and feet, so it doesn't hurt to be dragged over sharp surfaces like rocks or thorns. Here is a cross-section of the thick part of the tail close to the body:

Source: Cannundrum blog


Question related to L-arginine biosynthesis With respect to the L-arginine Biosynthesis pathway, the very first reaction converts L-glutamate to N-acetyl L-glutamate.

In the linked reaction scheme, why are only L-glutamate and N-acetyl glutamate considered, and not acetyl-CoA or the coenzyme? Is this because L-glutamate and N-acetyl L-glutamate are the main compounds to be considered? Why are they the main compounds being considered? Are these two compounds (L-glutamate and N-acetyle L-glutamate) the ligands?

The synthesis of N-acetylglutamate is mediated by the enzyme N-acetylglutamate synthase. This enzyme has L-glutamate as its substrate and uses acetyl-coenzyme A as a co-enzyme acetyl donor. Acetylcoenzyme A (Acetyl-CoA) is generally abbreviated in structural formulas, because it is a relatively complex molecule. The only thing of relevance is the acetyl group which is transferred from a thiol group to L-glutamate.

Note that ligands is a term reserved for molecules binding to receptors; substrates is the proper term for intermediates in enzymatic reactions.

N-acetylglutamate synthesis. Source: The Medical Biochemistry page


is there an easy way to remember taxonomy? So I have trouble remembering the order of taxonomy for classification.
i.e domain>kingdom>phylum>class>order>family>genus>species

I can never remember it, is there an good mnemonic to remember them? How do you guys remember it?

Have a look at Wikipedia > List of mnemonics#Biology.

Dear King Philip Came Over For Good Soup
Do Kings Play Chess On Fine Green Silk?
Dumb Kids Prefer Cheese Over Fried Green Spinach
Do Kindly Place Cover On Fresh Green Spring Vegetables
Donald Kills People Cause Other Friends Get Sad

Given the current political situation I would go with the last one but it is up to your personal preferences. You can as well make up your own. Mnemonics are like soups; it is always better when homemade. For example, extending upon the last and inspired by @John's comment, here is a homemade mnemonic

Donald Kidnaps People's Children Causing Outlaw Foreigners Great Suffering

Enjoy the game!


Non-monotonic knock-out effects in prokaryotes Typically, when performing gene-knockout, the experimenters select one gene to remove/replace-with-junk and then see if the prokaryote can still undergo fission. If it continues to reproduce then the gene is labeled as non-essential; if the organism cannot reproduce then the gene is labeled as essential; and some-times (if the organism can reproduce but only for a certain number of generations) the gene is labeled as quasi-essential.

Typically, if gene X is essential, and you knock-out both gene X and some other gene Y then the organism still dies; this is an example of monotonic behavior. However, this doesn't always have to be the case, it could be that gene X is essential only in the presence of gene Y (for instance if the two proteins produced are in a delicate feedback loop). Is there examples when knocking out gene X makes the organism nonviable, but knocking out gene X and Y maintains viability? In the most extreme case, is there an example where both gene X and Y are essential, but if both are knocked-out then the organism is still viable? I am primarily interested in simple prokaryotes (an answer for Mycoplasma genitalium or Escherichia coli would be best) but more complicated organisms are preferred over no answer.

Here is an example in which the knockout of a non-essential gene in yeast (Saccharomyces cerevisiae) suppresses the lethal effects of a different knockout.

  Amy L. Kistler and Christine Guthrie (2001) Deletion of MUD2, the yeast homolog of U2AF65, can bypass the requirement for Sub2, an essential spliceosomal ATPase. Genes & Development 15:42-49

The SUB2 gene encodes a protein which is a component of the TREX complex required for nuclear mRNA export. Deletion of the SUB2 gene is lethal. The MUD2 gene encodes a non-essential protein involved in pre-mRNA splicing.

The authors show that -

  "...the essential requirement for the SUB2 ATPase can be bypassed by deletion of the nonessential splicing factor MUD2..."

Detailed information about these (and all other) Saccharomyces cerevisiae genes is freely available at the Saccharomyces Genome Database


What is this tissue? Does anybody recognize this picture and can tell me what organ it came from?

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

Here are some images:

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

And this is one image from the last link:

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


Metabolic efficiency for fats and sugars I am making an exercise for physics students about the first law of thermodynamics, burning heat and evaporation heat. So my idea is to use cycler which runs on fats and sugars where proportion determined by respiration quotient. The amount of evaporated sweats would be determined from inefficiency of using the fuel. Unfortunately I am unable to find efficiency data to form the exercise.

So what are typical efficiencies to run skeletal muscles on either fat or sugar molecules?

EDIT

Assuming respiratory quotient measured at the time of cycling is 0.7 so all energy is obtained from oxidizing fats:
$$ C_{16}H_{32}O_2 + 23 O_2 -> 16CO_2 + 16 H_2O + \Delta G$$
what part of the $\Delta G$ can do mechanical work $A$ or simply what is typical value of efficiency coefficient:
$$\mu = \frac{A}{\Delta G}$$

This is a very complicated question. You need to rephrase your question to be more specific.

Efficiencies of energy utilization from glucose in the presence of O2 (aerobic respiration) are considered to be in the 40% range. Quite good when you consider that an automobile combustion engine is in the 20-25% range.

There is some evidence that betahydroxybutarate (B-OHB) actually provides more available energy for work than does glucose.  See Paper Here.

However, what is often overlooked is the energy needed to generate B-OHB from fat during ketosis, which results in a net loss in efficiency compared to glucose.

One of my favorite blogs is Peter Attia's "The Eating Academy."  He has a Post that goes into this subject somewhat.

I know this isn't a complete answer to your question, but again, you need to be more specific.

Respiration with or without O2.  Efficiencies in generating ATP from source material or only net efficiencies after the ATP -> ADP.


What flower is this blue flower? What flower is this?  All help would be appreciated

Without more detail about the whole plant (including leaves), where it came from, and about whether or not it was spray-painted, watered with dyed water, etc. it would be difficult to ID.

It seems to be in the Asteraceae family, and in the pompon class, as seen in these vender's pictures. (Disclosure: I have no affiliation with the company.)

http://www.fiftyflowers.com/product/Blue-Cushion-Bulk-Flower_10.htm
http://www.fiftyflowers.com/product/Blue-Cremon-Bulk-Flowers_24307.htm
http://www.fiftyflowers.com/product/Electric-Blue-Flowers_10.htm

It is most similar to a blue chrysanthemum.

http://john-hallett.co.uk/2013/04/04/blue-crysanthemum/

Sources:

as listed above for images
http://en.wikipedia.org/wiki/Chrysanthemum (pink image)
http://www.mums.org/chrysanthemum-classes/


What does $g_0$ mean for a centrifuge? I'm about to make some Graphene Oxide and in the paper for Tour's Method it uses a centrifuge to isolate the solution. However it requires $319g_0$. What does this mean, and will a centrifuge with 3300rpm suffice?

https://www.researchgate.net/publication/234084399_Graphene_oxide_for_effective_radionuclide_removal

$g_0$ is the standard gravity.

You can look up the rpm-equivalent using a nomogram or calculate it yourself.

On some centrifuges you can switch between both. Some vendors provide conversion tables in their centrifuge's manual.


Could a large constrictor kill a small animal? According to this article there was a python whose body circumference was 85cm.  This means its diameter was 27cm.

Would it be possible for this snake to constrict animals that are about the same size as its diameter?  It is hard to imagine it having enough flexibility to constrict a swamp rat, for example, whose size is less than 27cm.  Could it kill such animals by another method, say with its jaws or by crushing them by rolling over them?  Or are such small animals simply off its target list?

Constrictors doesn't have uniform body circumference from head to tail. They coil around the prey accordingly. In your example, if the prey is very small, it just swallows. If its little big, it coils a little bit (check some videos like this) say two turn coil. This will only cover top half feet of constrictor's length which is of lesser diameter than the body.

So basically, they crush the prey and perform a kill. Its not a necessity for any constrictor to use its entire body to coil around a prey. They adjust their coil level to control the prey.


PCR amplification and error propagation Say I have one dsDNA that undergoes normal PCR (where amplification is exponential).  If there is a mistake, say a G is swapped for an A during the 2nd round of replication, what percentage of the final DNA will have the mistake if there are 12 more rounds?

I was talking to my teacher about this today.  I say 33%, my teacher said 12.5%.

Your teacher is indeed correct.

In the first round you would get two identical molecules of the dsDNA.

In the second round you would get 3 identical molecules and one molecular with an A substituted for a G in one of the strands.  ie.

No error (3 of the 4 molecules):

------G-------
------C-------

One mismatch (1 of the 4 molecules):

------A-------
------C-------

So there are a total of 8 strands of DNA after the second round and one of those strands has the mismatch.  1 / 8 = 0.125 = 12.5%

In round 3 you would have 8 dsDNA molecules and only one of those 8 dsDNA molecules would have the mismatch.


Choosing a book to gain general knowledge about biology I will be first year undergraduate at Physics department next year and last year I was at the Medicine faculty. I want do double major in the second year of faculty with Molecular Biology and Genetics. The intersection of biology and physics is my interest. I have two books about biology, first one is What is Life?-Mind and Matter by Erwin Schrödinger and the second one is This is Biology by Ernst Mayr. Which one should I read to acquire general knowledge about Biology?

The books you have

The books you cited won't help you to get a solid and general basic knowledge in biology. I haven't read those books but I think that This is Biology is a book of philosophy of biology written by a biologist and philosopher. What is life is a very influential book written by a physicist who more or less predicted the structure of DNA that was later discovered by Watson and Crick. You won't learn much of biology through these books.

Book Suggestions

This post offers book suggestions for general introductory biology. Here is another post that may also interest you

If you are interested in a specific field of biology, then you may want to ask for book suggestions for this particular field. I think that most biologists that come from a background in physics are in the fields of theoretical evolutionary biology, bioinformatics and biophysics (incl. molecular biophysics).

Here are a bunch of other posts asking for book recommendations that I imagine you may like reading about.

What physics knowledge can be applied to biology of organisms and ecosystems?
Book recommendations for algorithms used in evolutionary biology
Book recommendations for evolutionary models
How to learn biomathematics?
Book recommendation on population/evolutionary genetics?
Introductory literature for synthetic / systems biology?

And eventually you may want to read Value of mathematical models in biology although the post has been closed.

Of course, you might want to read a bunch of wikipedia pages such as Biophysics, Molecular Biophysics, Mathematical and Theoretical Biology, Biostatistics, Computational Biology, Bioinformatics.


Why are bovines different genera if they can interbreed? Why are bovinae a "subfamily", above Genus, when members can interbreed?  Some like the beefalo are fertile, which is the normal defining characteristic of a species. And Genus are groups more distantly related, so by definition they should not be closely related species.

Species are not defined by whether they can interbreed, not even close.

In fact, there is no objective, scientific standard for what defines species, or genera, at all. What is a species is determined by little more than the "feels" of the individual naming it, or the committee approving it.

And the same is true of the entire rest of taxonomic structure. It's not really science, it's just a way of organizing ideas that got popular, and in fact is under constant assault now by somewhat more scientific things like genetic testing. The hierarchy of the taxonomic system changes pretty much daily, and has no official structure or definition at all. Even the number of kingdoms is entirely up in the air.

Getting back to the specifics here, since there is no objective, scientific standard for what is a species or genus, it's no surprise that separate ones can interbreed.

And it's not like bovines are the only ones. There are many other intergeneric hybrids possible, like sheep and goats, wheat and rye, camels and llama, house cats and servals, marine and land iguanas, et cetera.

Perhaps someday there will be objective definitions to establish a truly scientific taxonomy. But for the moment, it's just whatever people in positions of power feel makes sense, at any given moment.

List of Intergeneric hybrids


Technologies that rely on evolution It's possible that this is offtopic here; if so, please let me know.

I'm wondering what technologies exist that rely on evolution being a correct model; I'd like to be able to offer examples of that to people who find it to be "just a theory". As an example, I can point out lots of technologies for which our models of electromagnetism have to be correct to an immense accuracy for them to work - computers, any electrical wiring, electrical motors, light bulbs, electrical ovens, etc. etc.

The best I could find as examples of technologies that require our models of evolution to be fundamentally correct are things like pharmaceutics that work against germs that have developed a resistance against other pharmaceutics.

What are some good examples of technologies that require our models of evolution to be fundamentally correct for those technologies to work?

Evolution is not the type of theory that is mainly directed towards technological applications, as opposed to many physical theories. It is a principle to understand living systems, from the simplest to the most complex. So it mainly gives understanding, not 'solutions' to particular problems.

That being said, evolutionary principles can be applied to many 'practical' problems.

For one, all of the technologies that rely on sequence alignment and phylogenetic inference use models of substitution based on evolutionary principles, in which you have hypotheses based on the probability that some evolutionary changes occur (these changes can be at the nucleotide level or at the organismal level), and then you infer which hypotheses are the most plausible given the evolutionary and ecological context of the problem. A 'practical' side of this, for instance, would be to infer the evolutionary trajectory of the COVID-19 epidemic, or the study of the geographic spread of the virus given the sequences of the virus at different locations/time. A lot of modern molecular biology is based on a comparison of sequences.

Another 'application' is that of designing enzymes or other molecules, that have a desired function or feature. In fact, a recent Nobel prize was awarded to Frances Arnold for harnessing the power of evolution in her research on molecular design.

Some other applications besides the ones people have mentioned in the comments above are medical applications. It is well known that cancer lineages evolve, so the principles from evolution can be used to better treat cancer progression, for instance by adjusting the evolutionary outcomes of a particular treatment (you can read a fascinating example here). In fact, the understanding of cancer itself, besides therapeutic interventions, has used evolutionary principles for some years now (see a nice example of evolutionary dynamics in metastases here).

I also want to mention an important example from microbiology. It is a pressing issue of public health the fact that no novel antibiotics have been developed in the last few years, and that the existing ones are less and less effective given to the evolution of antibiotic resistance. What if we could make "evolution-proof" antibiotics? That's a fascinating question that some people are starting to explore, for instance by combining classical antibiotic treatments with phage therapy or molecules different than the traditional antibiotics (a cool paper here).

Finally, I want to mention that these applications of evolutionary principles do not "rely" on evolution being "fundamentally correct". Evolution is a process for which we have a lot of evidence, so at this point (and for a long time) evolution is an uncontroversial fact to the scientific community. This is similar, for instance, to the fact that we have lots of evidence for the phenomenon of gravity; so what scientists are doing at the moment is figuring out the mechanisms by which evolutionary processes occur (just as physicists are looking for gravitons). Another addendum is that evolution seems to be an open-ended process. This means that many of the mechanisms we can find in evolution will be, to a high degree, statistical in nature, because there are just so many possibilities that we cannot account for all possible outcomes. This is a fundamental difference to many theories in, say, physics, where there are clear "solutions" to a problem (in the form of an equation, for instance). I say this because people keep coming up with examples that "disprove" evolution, but they just don't consider that evolution is a statistical process, which allows for "outliers". In fact, the outliers are quite informative for evolutionary theory, not at all undesirable (consider for instance the origins of life, or the emergence of consciousness, these are unique 'events' for which we have no mechanism to explain why did they emerge).


Please help me identify this jelly fish I've seen these jellyfish in thailand and was wondering what species they were. All I know is that there are lot in the Chonburi area and they sting in not deadly but hurts.

Images for the jellyfish

Thanks for the help!

It looks like a Rhizostomae, or crown jellyfish, but it's hard to tell. The  article here does mention that it's edible though and it's found in Thailand so I'm pretty happy with that guess.

More specifically, it looks similar to the jellyfish asked about here, which was eventually classified as a Lobonemoides, perhaps Lobonemoides robusta


How do ribosomes interpret stop codons as selenocysteine and pyrrolysine? How does the protein synthesising machinery determine that UGA and UAG in mRNA should be decoded as selenocysteine and pyrrolysine, respectively, in certain circumstances, rather than as stop codons?

Summary
Reassignment of an UGA codon as a selenocysteine codon is thought to involve the interaction of obligatory secondary structure elements called selenocysteine insertion sequences (SECIS) with the dedicated translation elongation factor that presents a unique tRNA aminoacylated with selenocysteine to the ribosome. However the location of these elements and their specificity differ between prokaryotes and eukaryotes. Less is known about the less common reassignment of UAG to pyrrolysine, but some organisms may employ similar mechanisms to those involving selenocysteine, whereas others may almost completely avoid the use of UAG as a termination codon.
Preliminary — Presentation of selenocysteine to the ribosome
Although the question specifically relates to the translation of erstwhile termination codons, it is worth mentioning how selenocysteine (Sec) is presented to the ribosome.
     In most species a specific tRNA — tRNASec — is aminoacylated with serine catalysed the standard seryl-tRNA synthetase. The Ser-tRNASec is then converted to Sec-tRNASec — in Escherichia coli, by the product of the SelA gene.
    Whereas all other charged elongator tRNA species are brought to the A-site of the ribosome by the same elongation factor (EF-Tu in prokaryotes, EF-1 in eukaryotes), there is a specific elongation factor for binding Sec-tRNASec.
Reprogramming UGA codon as a selenocysteine codon
The reprogramming of UGA as a selenocysteine codon requires a stem–loop secondary structure — the SECIS — in both prokaryotes and eukaryotes. However there are differences in how these operate. Quoting from a Nature News and Views piece written in 2007:

In bacteria there is a site-specific recoding signal embedded in mRNA that flags a nearby UGA codon as encoding selenocysteine rather than stop (Fig.b). In other organisms, ranging from worms to mammals, a recoding signal located outside the coding part of the mRNA (Fig.c) signifies that all UGA codons in its mRNA specify selenocysteine (one essential human mRNA has ten UGAs).

The mode of action  of the SECIS elements is envisaged as interaction with the Sec-tRNASec-specific elongation factor, as in this illustration from Ch 13 of Molecular Biology by Clark et al.:

A shortcoming of this cartoon, is that it fails to show that in prokaryotes the SECIS element encompasses the UGA codon. This is important as it may indicate that  termination factors are prevented access to the UGA by secondary structure, which the Sec-specific elongation factor is able to unwind. (In eukaryotes there may UGA codons may also be made inaccessible by local secondary structure.)

However sequence context effects have also been suggested.
Pyrrolysine
The situation for pyrrolysine (see, for example, Ambrogelly et al. (2007)) differs from that for selenocysteine in that it is synthesised before it is charged to a specific tRNAPyl in a reaction catalysed by a specific pyrrolysyl-tRNA synthetase. The reassignment of UAG to pyrrolysine was thought to involve a change (or almost complete change) in the genetic code of certain archaea in which it is found, with UAG not or rarely being used as a termination codon. However, according to the Nature News and Views article aleady cited, this is not the case for other organisms, in which I am unaware of the mechanism of reassignment.