Blood antigens and immune response In my textbook, the definition of an antigen is written as follows:

Antigen:  A substance that the body recognises as foreign and that can evoke an immune response

The following image also confused me as it states that, for instance, a person with type A  blood has A-antigens

However, would this statement, and image, not be stating that the antigens found on the surface of our blood cells are foreign? Which would imply that our antibodies attack our own blood which is not what occurs?

Or are the substances found on the surface of blood cells (A or/and B antigens, no antigens) only recognised as antigens when they correspond with the antibodies in the body?

In other words, if I am blood type A, the pink molecules on the surface of my blood are not referred to as antigens as they are not foreign, but the green molecules on the surface of group B blood are referred to as antigens as they are foreign?

The problem is partly the definition of Antigen that you quote. It refers to “the body” leading you to assume it’s a specific body — yours. I'm sure there are better definitions, but just taking this one, I would modify to: “A substance that can be recognised as foreign and evoke an immune response in an organism.”

With this definition, which is actually how antigens are thought of, a particular antigen need not be antigenic in every organism to which it is presented. Those organisms or individuals for which the antigen appears as ‘self’ will not recognize it as foreign as they are ‘tolerant’ to it (e.g. by mechanisms which eliminate the cells capable of producing antibodies against the self antigen). But it is still referred to as an antigen.

So your understanding of the situation is correct, but that of the use of the terminology is not. Even if you belong to blood group A and therefore will not mount an immune response to the pink blobs in the picture when transfused with blood of group A, they are still referred to as antigens as they stimulate an immune response when transfused into a person of blood group B.

If you wished to talk about the fact that the A antigen on blood of type A does not provoke an immune response when transfused to persons with blood group A you could say “The A antigen on red cells is not immunogenic (or even antigenic) when transfused into persons of blood group A”.

Footnote on terminology

Scientific terminology allows us to describe things precisely. As our understanding increases, the terminology may need to evolve to allow us to make distinctions of which we were previously unaware. The word ‘antigen’ was coined in the late 19th century, before anything was known of the structure of antibodies, and was defined in terms of the immune response as that was what was observed. The definition evolved in some quarters to include the idea of binding to an antibody or T-cell (see e.g. Merriam-Webster definition).

However this extended definition raises the problem of the terminology to use if something binds to an antibody but does not provoke an immune response. Thus, the Glossary of the textbook Immunobiology (Janeway et al.) defines antigen as “Any molecule that can bind specifically to an antibody” and uses a different term, ‘immunogen’, for “Any molecule that can elicit an adaptive immune response on injection into a person or animal”. (Which explains my mention of ‘immunogenic’, as opposed to ‘antigenic’, above.)


What is the diet preference of American cockroaches? I found a research article1 on the diet preference of German cockroaches. It reveals that those cockroaches prefer to eat bananas most. I wonder if it is the same for American cockroaches. And also, can American cockroaches survive on wood and water alone?
 1. El-Sharabasy, H.M., Mahmoud, M.F., El-Bahrawy, A.F., El-Badry, Y.S. and El-Kady, G.A., 2014. Food preference of the German cockroach, Blattella germanica (L.)(Dictyoptera: Blattellidae). Cercetări Agronomice în Moldova, 2(158), pp.81-88.

American cockroaches (Periplaneta americana) are omnivorous and opportunistic feeders, and as a result, they eat a large variety of foods. They will eat almost anything.

Favorite foods: They are particularly fond of fermenting foods$^{4,6}$ and also prefer sweets$^2$.

Common foods they eat: plant materials, dead animals, sugar, oil, cheese, beer, tea, soap, leather, bakery products, paper, starch in book bindings, manuscripts, glue, hair, flakes of dried skin, soiled clothing, glossy paper with starch sizing and generally most human or pet moist food or other organic matter $^{1,3,5}$. They have also been observed feeding on dead or wounded cockroaches of their own or other species as well as their own cast-off skins and egg-capsules$^6$.

 According to EOL:

 Some of [their food] items, such as cellulose, can not be digested by normal means. However, like cows and other grazing animals, cockroaches have a symbiotic relationship with a bacteria that allows them to digest such substances.

As a result, they could almost certainly survive on just wood and water.

Citations:

 {1}  Bell, William J. and K.G. Adiyodi. (1981). American Cockroach. Springer. pp. 1, 4. ISBN 978-0-412-16140-7.

 {2} Barbara, K. A. 2014. American cockroach. University of Florida Institute of Food and Agricultural Sciences. Retrieved 11 February 2017. http://entnemdept.ufl.edu/creatures/urban/roaches/American_cockroach.htm .

 {3} Jacobs, Steve. "American Cockroaches". The Pennsylvania State University. Retrieved 11 February 2017. http://ento.psu.edu/extension/factsheets/american-cockroaches .

 {4} Jones, Susan C. 2008. Agricultural and Natural Resources Fact Sheet: American Cockroach (HYG-2096-08). Ohio State University. http://ohioline.osu.edu/hyg-fact/2000/pdf/2096.pdf.

 {5} Milne, L. & M. Milne. 1980. National Audubon Society Field Guide to Insects and Spiders. Knopf, New York, NY. p 393. ISBN: 0-394-50763-0.

{6} Periplaneta americana: Palmetto bug. Encylopedia of Life. Retrieved 11 February 2017. http://eol.org/pages/1076920/hierarchy_entries/51102706/details .


A creature from Mediterranean I have recently encountered this red thing on one of the beaches of east Sardinia. It was pretty close to the coast (around 20 meters) and has sticked to one of my fins.

My question is: how is this creature called? Is it dangerous to have skin contact with it?

This appears to be an anemone, with the pedal disc towards the camera. I can't offer a positive ID, but would hazard a guess at genus Actinia.

Anemones sting, and the stings of anemones range from completely harmless to humans to highly toxic. In the absence of a positive ID, I would avoid poking it.


Stability of the chromosomes of thermophilic bacteria We know thermophiles — generally archaebacteria — can survive high temperature, but their genomic DNA also contains hydrogen-bonded nitrogen bases. Why don't they collapse like ordinary hydrogen bonds?

The stability and replication of the DNA of thermophiles is an interesting problem, for which there does not appear to be a single unequivocal answer. However the way you express this question is unfortunate: the hydrogen bonds in the DNA of thermophiles (which include some eubacteria as well as archea) are the same as those in any other genomic DNA. The question is, rather, why the strands of the DNA do not dissociate. This is not really my area, but as there have been no other answers I shall summarize what I have learned from the literature.

A review that was the starting point for this information is:

D.W. Grogan, Hyperthermophiles and the problem of DNA instability Molecular Microbiology (1998) 28(6), 1043–1049.

One obvious possibility would be that the genomes of thermophiles have a high percentage of GC, as GC base-pairs have three hydrogen bonds, whereas AT base-pairs have only two. However, this is NOT the general case.
It has long been known that the melting temperature (the temperature at which 50% strand-separation has occurred) is increased by increased concentration of cations. It has been suggested that this could be a factor, especially in those thermophiles that are also extreme halophiles.
In eukaryotes genomic DNA is condensed into chromatin by the interaction of the basic histone proteins. These proteins are not found in prokaryotes, but different basic molecules, polyamines, have been observed that are more abundant in thermophilic than mesophilic bacteria. As they have been observed to protect DNA from thermal denaturation in vitro, it has been proposed that they may also perform this function in vivo.
Type I topoisomerases that introduce positive supercoils into DNA (‘reverse gyrases’), occur in hyperthermophiles examined but not in mesophiles, and it was suggested that this could stabilize the DNA. However, the Grogan review presents a body of evidence that casts doubt on whether this is, in fact the case.
In addition to strand-separation, the genomes of thermophiles face the problem of increased damage to their DNA. Although, again, the situation is complex, it appears that they have evolved more extensive and active systems of DNA repair to deal with this.


Are there hybrids that emerge as a new species? We know a couple of hybride (mammal) animals (http://www.rantpets.com/2015/06/03/15-strangest-hybrid-animal-breeds-you-didnt-know-existed/) and perhaps even more and perhaps even insects like the Drosophila.

But are there animals which arise as a new species? And by species I mean animals who can't breed with the species of their parents but can interbreed succesfully with their own species ('brothers' and 'sisters'). Only leaving out pre-mating mechanisms in case they don't get offspring (so that only Post-mating isolating mechanisms counts)

See also: Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?
Have scientists ever produce a new species in laboratory by means of natural selection?

Yes, this is called hybrid speciation.

  Hybrid speciation is a form of speciation wherein hybridization between two different species leads to a new species, reproductively isolated from the parent species

There has been a fair amount of work on hybrid speciation (see here). Hybrid speciation is often thought to be more frequent in plants than animals. In ferns for example, we estimate that 7% of species emerged through hybrid speciation (Otto and Whitton 2000). Typical cases of hybrid speciation include changes in ploidy levels (examples include sunflowers). Hybrid speciation also occurs in animals such as the lonicera fly to cite just an example.


Specific numbers of nucleotides in Okazaki fragments Okazaki fragments are formed during replication of the lagging DNA strand. What determines the length of these fragments?

The length of Okazaki fragments is not necessarily a tight distribution. The lengths are determined by the spacing between adjacent sites where DNA primase has synthesized a short RNA primer on the lagging strand at an active DNA replication fork. In E. coli, as I recall, this occurs on an average of once per 1000 nt.

DNA polymerase holoenzyme then uses that 3'-OH on the RNA primer as a substrate and synthesizes the DNA strand complementary to the Template strand UNTIL it bumps into the next RNA primer.

It is those nicks in the newly synthesized lagging strand, that have a deoxy-3'-OH, and a ribo-5'-phosphate, (that need to be removed and ligated) that mark the boundaries of individual Okazaki fragments.


determining horizontal gene transfer between two genomes? I want to determine if there is horizontal gene transfer between two genomes, in particular I was to use the parametric methods described in wikipedia since I would most likely struggle to understand the phylogenetic methods fully.

The two genomes in mind would be Lactococcus lactis and  Lactobacillus helveticus since they are used in the process of cheese making and therefore would be in close enough proximity/environment to argue for tentative events of HGT. (Correct me if I am way off base here in my line of thought...)

Could I just access representative genomes for each from NCBI and calculate/determine the various genomic signatures that are indicative of HGT via the previously mentioned parametric methods(Nucleotide composition, oligonucleotide spectrum, structural features, etc...)?

Or would the genomes need to be rendered and sequenced from a confirmed source where they are both located/habituated to properly argue for HGT?(In which case I believe NCBI does not have this data readily available?)

Since the parametric model is applied to only a single genome to see if there is evidence of recent HGT via a change in the average content in coding regions, it will not tell you from where the HGT came from, just that a HGT likely occurred in an area of the genome. Since you are trying to specifically see if there was a HGT between L. lactis and L. helveticus you would have to run a parametric analysis on both, find a HGT candidate on one of the genomes and then find that sequence as a non-HGT candidate on the other genome and via BLAST.

These papers give a good argument to why to use genome signatures instead of GC content as a parametric method of detecting HGT.

Review from where most of the Wiki figures came from

Genome signature paper

Newer Genome signature paper


If sexuality is genetic, how did asexuality evolve? If sexuality is genetic, then it stands to reason that evolution would strongly favor people who have children. In other words, heterosexuality & bisexuality should be favored, while homosexuality and asexuality should be disfavored and in fact eliminated by evolution. Why hasn't that happened?
I can find plenty of resources via Google for the evolution of homosexuality, such as this one, but not for the evolution of asexuality. Asexuality seems to pose a bigger challenge as well, since the lack of sexual attraction entirely should make it even less likely for asexual people to have children. Some of the explanations for the evolution of homosexuality can conceivably apply to asexuality too (such as "the genes for asexuality do other things"); still, I would like an authoritative paper/reference if there is one.

Update:
See @Bryan Krause comment. Just because something exists (or equally, doesn't exist) does not mean that it was selected for or has any evolutionary relevance. Imputing selection to any particular state of affairs is usually bad reasoning without a lot of evidence.
I didn't do a good job of coming out and saying this in my answer.
My answer is best understood as answering the question: how could asexuality evolve under selection?
It does not at all address the question: DID asexuality evolve under selection (in humans)?
This second question is one for which the answer is probably "no". Without more evidence, we cannot say whether asexuality has any evolutionary/selective relevance at all.
Original answer:
I would suggest looking more into the evolution of social animals for which large proportions of the population is non-reproductive (or sterile). There are many such examples, with insects as the obvious case:

Contrary to widespread belief based on heuristic arguments of genetic relatedness, non-reproductive workers can easily evolve in polyandrous species. The crucial quantity is the functional relationship between a colony’s reproductive rate and the fraction of non-reproductive workers present in that colony.

I would suggest looking more into that paper and citations therein. The question to answer is whether an individual's labor can be more important than their gonads to the continuation of their genes.
As suggested in the wikipedia article on homosexuality that you link to in your own comment, there is a positive effect on female fertility from having homosexual family members ("kin selection"). Granted, what causal mechanism is behind this is likely difficult to sort out.
It's quite plausible that asexuality behaves similarly to homosexuality in this regard. Those authors want it to be a genetic factor driving both sexuality and fertility. But to me it seems a bit more parsimonious to posit that it's good to have more warm adult bodies around to care for/support children.
From a practical perspective, if grandparents with non-functional gonads can help raise kids (i.e. increase effective fertility of kin), why not asexual relatives too?


In what stage of bacterial growth can penicillin inhibit the growth of the cellular wall? The bacterial growth has 3 main stages: lag-phase, log-phase and stationary phase. I was wondering in which one of them penicillin can inhibit the growth of the cellular wall of bacteria and why.
I was thinking that the respons would be lag and log phase, because at these points bacteria multiply the most, while in stationary phase most of the bacteria are in adult form with a well formed bacterial wall already, but I'm not quite sure.

This is a really good question that requires you to appreciate a few different details and to overcome a few implicit assumptions that you might perhaps have.

The bacterial growth stages you refer to only apply to a population of bacteria. Individual cells do not undergo these stages.
Relatedly, bacterial population growth stages are independent of the stage of bacterial cell wall growth.

You can have mature or immature bacteria at any stage of "bacterial growth", with either fully formed walls, or with none. This understanding should answer your question partially.
Here are a few more things to consider, for a more complete understanding:

Penicillins are a class of molecules, of varying efficacy and bioavailability across the body and across different kinds of walls and membranes.
Inhibiting the spread of bacteria can be achieved using two types of antibiotics... bactericidal or bacteriostatic ones. Bactericidal means the bacteria die, while bacteriostatic means their growth is slowed or stopped.
Penicillins are bactericidal agents that exert their mechanism of action by inhibition of bacterial cell wall synthesis and by inducing a bacterial autolytic effect. So even mature bacteria will die off in the later stages of outgrowth. In principle, it does not matter what growth stage the bacteria are at, the bactericidal mechanism will take place regardless.
Pencillins are more effective against Gram-positive bacteria. Gram-negative bacteria have a lipopolysaccharide and protein layer that surrounds the peptidoglygan layer of the cell wall, which acts as a barrier for the penicillin from reach its target (which is responsible for completing the synthesis of peptidoglycans, the structural component of bacterial cell wall). However, penicillin can get into Gram-negative cells, for example through channels called porins.

This is more or less very standard knowledge that is easy to look up. Wikipedia's entry on penicillin is a good place to orient yourself if you already haven't.


What decides whether a lysogenic cycle or a lytic cycle will take place? A virus can either participate in a lysogenic cycle or a lytic cycle. What decides that?

It depends on a few factors, such as how many phages infected the cell, whether or not the cell is in good growth conditions, and so on. If the cell is in stress or has low amounts of nutrients, the lysogenic pathway is typically activated.

The underlying mechanism has to do with a protein cascade involving either the cro or cI protein that is encoded by the virus. The cI protein is a repressor, and it will prevent the lytic genes from being transcribed. By default the virus will transcribe the lytic genes, so they must be repressed for lysogeny to occur. Similarly, cro is also a transcriptional repressor. The two proteins work in opposition to each other. cro binds to an operator, oR3, that is involved in repressing cI, which may prevent cI from being expressed and thus preventing it from repressing lytic genes (however the importance of this is debatable because if you replace oR3, the cell can apparently still lyse).

There are numerous other proteins, such as N and Q, that are involved. The N protein has to be transcribed by the polymerase ‘anti-terminating’, or reading through a termination signal. This will happen more frequently when the protein RNase III is present at high concentrations. The N protein is a lytic regulator. Thus, when there are high amounts of RNase III there will be more N expressed which leads to the lytic cycle. RNase III is not a viral protein. It is a host protein and the host expresses more of it when nutrients are abundant. This is how the virus is able to ‘sense’ if nutrients are high enough to enter the lytic cycle.

The whole system is way more complicated but this is it in a nutshell.

http://www.annualreviews.org/doi/full/10.1146/annurev.genet.39.073003.113656


Do all sea creatures that have scales have to have fins? Do all sea creatures that have scales have to have fins?

Do we know of any sea creatures that have only scales without fins?

I'm especially interested in fish that have scales but no fins.

How about marine reptiles? Sea snakes have a paddle-like tail, so perhaps you would claim that as a fin, but maybe marine iguanas would qualify? And, of course, sea turtles.


Does an old growth forest ecosystem produce more oxygen than it consumes? I would like to consider an old growth forest ecosystem such as a large part of the Amazonian forest. It is common to refer to such beautiful forests as a source of oxygen for the world. For example, the expression Amazon: Lungs of the planet is very common (e.g. this BBC article). I would like to question such an expression.

Questions

My questions are:

Does an old growth forest ecosystem produce more oxygen than it consumes?
Does an old growth forest ecosystem fix more CO$_2$ than it produces?

My Intuition

I understand that such a forest can be an important carbon storage and that if we were to cut the forest down, burn the wood and pour concrete on the soil (to prevent regrowth), then we would definitely release a fair amount of carbon in the atmosphere.

That being said, I am wondering whether, as of today, these forests act as carbon sink or not. It feels to me that while trees accumulate carbon and produce oxygen while growing, this carbon is released when they die and in an old growth forest a tree must die for a new tree to grow. If carbon is being fixed, then it has to go somewhere and I think it is almost by the definition of an old growth forest that there is no more room for more carbon accumulation (competition among trees prevent it). So I would tend to think that calling the Amazonian forest the "lungs of Earth" is very misleading.

Some random WWF article

This WWF article seem to suggest that, contrary to my intuition, the answer to these two questions should be "yes".

Does an old growth forest ecosystem fix more CO2 than it produces?

The intergovernmental panel on climate change summarizes some of the data on carbon flux here. For the amazon similar tropical rain forests, it says:

  Measurements in pristine, seasonal tropical rain forests in Amazonia indicate NEP of approximately 1.0 t C ha-1 yr-1 (Grace et al., 1995a,b) and approximately 2.0 and 5.9 t C ha-1 yr-1 for dense, moist rain forest (Fan et al., 1990; Malhi et al., 1998, 1999).

NEP is net ecosystem production, which, as I understand it, is essentially the total amount of carbon fixed by the ecosystem.

It seems the tropics, and the Amazon, in particular, are important global carbon sinks. This is also discussed in this more recent article in Nature.

This isn't my field, but as far as I understand it, forests are not closed or steady state systems. They do play a role as a sink in the global carbon cycle. I would assume net carbon fixation must come with increased biomass, so I may have just avoided a key part of your question. All the same, I think the point is that, again, even the amazon rain forest is not at steady state.

As far as oxygen is concerned, the report and article don't address it. I suspect this is because there is no documented problem with global oxygen depletion.


Use of beta-2 microglobulin staining to assess frozen tissue sample integrity In a Russian paper I'm reading the authors use staining for beta-2 microglobulin (B2M) to make sure that a variety of frozen tissue samples still express antigens on their surface, so that these samples could be used to assess the activity of an antibody they are researching.

The authors write that "since virtually each cell expresses B2M on its surface, this assay ensures that other antigens have remained on the surface of the examined cells as well".

Is there a special term for this kind of check? Is this anti-B2M staining a routine procedure, and are there papers dedicated to this procedure? I haven't found relevant papers.

I'd say it is not common practice to look for B2M, although I guess there will be heavy users would would disagree.

Without seeing the paper I cannot be sure, but I guess they are using B2M as a housekeeping gene, that is, a molecule whose presence and quantity is largely unregulated in living cells, and which is commonly used in labs as reference. Biological samples vary greatly in their content. It is hard to tell if a molecule is made or destroyed in response to a treatment, by merely measuring, and finding more or less of it. But if the ratio between the aforementioned molecule to an unregulated molecule goes up, you can be more sure it responded to the treatment. That is called an internal control. You may be familiar with "normalization to actin" or to GAPDH in immunoblot and qRT-PCR.

The use you are describing is diverging from the typical use of housekeeping genes in a lab, and not optimal for what they were trying to show. Since it's there in pretty much any tissue measured by immunoblot, B2M is expected to be present in any tissue assayed by microscopy. If a tissue slide lacks B2M, it is likely spoilt. But if it has B2M, it doesn't make it 100% certain that other, scarcer, more unstable molecules have been preserved as well. It would be ideal if they looked for the specific molecule they were studying; but if many of their samples were supposedly devoid of the latter, they had to replace the ideal with something more practical.

Note that I am using "molecule" in an ambiguous manner. With antigens in the referenced paper, it's obvious B2M is used as a reference protein. But housekeeping genes, including B2M, are also used as internal control for mRNA measurements ("gene expression").


What are the factors on which protein-protein interaction depend? Does protein-protein interaction only happens when one of them is basic and the other acidic? Do protein interactions also depend on the protein structure? Are there more factors?

It depends both on structure and charge. Binding sites of proteins are essentially formed by amino acids placed in a particular conformations such that it will match the binding site of their counterpart protein or substrate. This is commonly referred to as the lock and key model of protein binding. This is similar to how two puzzle pieces fit together, the pieces are exactly the same shape at the point at which the puzzle pieces connect. At a protein binding site amino acids are clustered together to form the matching shape to the appropriate binding partner. This however is not just dictated by 'physical shape' of each amino acid but also their charges. This is important because negatively charged amino acids will repel other negatively charged amino acids, and attract to positive amino acids, thereby modulating the exact 'shape' of the protein binding site.


Recommended reading to quickly get up to speed on infectious diseases I am in the beginning stages of a capstone project for my master's in Data Science. For various reasons, I have landed on the subject of Clostridium difficile infection. My background is in Computer Science, Mathematics, and Statistics, but biology is way outside of my wheelhouse. While most of my project will focus on the statistical modelling aspect, I would like to be able to speak intelligently on the subject itself and be able to read through journal articles without getting tripped up on some of the terminology.

I'm not trying to cut corners, but I'm on a tight timeline (about 4 months). What resources - books, references, online courses - would you recommend to bootstrap me into the field of infectious diseases?

Since I didn't get an answer, I'll mention what I did.

My goal was to understand a particular disease well enough to talk intelligently about it while focusing mostly on the statistics. So learning Epidemiology from the ground up wouldn't have been practical in the 4-5 months I had.

I started with a high level patient-oriented book, C. diff in 30 Minutes. That gave me a general understanding of the disease. Then I began reading academic articles. Not only were these useful for citations in my paper, but it also helped expand my understanding. I would notice common terms that kept popping up. Gram-positive, rod shaped, anaerobic, endospore-forming is intimidating at first, but each of these modifiers can be googled individually to build an understanding.

Finally, it was necessary to know how much I needed to know. I began reading about the hypervirulent strain, ribotype 027 with its binary toxin yadda yadda. None of that was actually important for my paper because that level of detail wasn't in the data.

So while knowing the general landscape was important, knowing each and every detail, for my purposes, wasn't.


How is Glyceraldehyde 3-phosphate converted into glucose? In the light-independent reaction of photosynthesis, one of the products is glyceraldehyde 3-phosphate, and the Wikipedia page on the light-independent reactions states that 6 of these can be used to form glucose.  However, the Wikipedia article on gluconeogenesis does not mention this, and the Wikibooks article on gluconeogenesis only mentions the molecule glycerinaldehyde 3-phosphate (which I'm not sure if it's a typo, because I can't find any information on glycerinaldehyde).

So how does G3P actually become glucose (and is there a good reason this information is not available on those Wikipedia pages, plus the page on G3P)?

Advice to students of biochemistry

This site is concerned with biology, not with biological entries in Wikipedia. Wikipedia is a voluntary effort to which anyone may contribute, and is full of errors and omissions. It’s structure means that it is focussed on individual small topics, rather than presenting an integrated account of various areas of science. The student who wishes a balanced integrated account of a topic that has been subjected to editorial review should consult a text book. Those whose resources do not permit this should try searching on NCBI Bookshelf, which provides free on-line search-only access to old editions of texts. For biochemistry, Berg et al. is recommended.

The generation of glucose from triose produced in the dark reaction is well understood

The answer to the question can be found in e.g. Berg et al. 20.1.3:

  The 3-phosphoglycerate product of rubisco is next converted into three forms of hexose phosphate: glucose 1-phosphate, glucose 6-phosphate, and fructose 6-phosphate... The steps in this conversion (Figure 20.9) are like those of the gluconeogenic pathway (Section 16.3.1), except that glyceraldehyde 3-phosphate dehydrogenase in chloroplasts, which generates glyceraldehyde 3-phosphate (GAP), is specific for NADPH rather than NADH. Alternatively, the glyceraldehyde 3-phosphate can be transported to the cytosol for glucose synthesis.

Berg et al. Fig. 20.9

The Section 16.3.1 referred to is a general treatment of gluconeogenesis, which is the same in all organisms or cells that possess the enzymes to catalyse its unique steps. (Some cells may not have — or need to have — the initial steps from pyruvate. In fact, Fig. 20.9 shows the steps to G 6-P — the only step missing is the phosphatase step that generates glucose.) There is therefore no reason to expect an account specific for plants.


Positive control for microorganisms I'm planning to test the antimicrobial activity of endophytic fungi (their secondary metabolites) against Gram-positive bacteria, Gram-negative bacteria, and one fungus (Candida).

I was wondering what could be a suitable positive control for them? One kind of control each for the Gram (-), Gram (+), and the fungus? If yes, what kind? Or is there one kind of substance that would work against them all?

Streptomycin or penicillin/streptomycin, and potentially amphotericin B. If you need a penicillin-free alternative, gentamycin is a good option.

I think streptomycin is a good candidate with a broad enough spectrum to target Gram positive, negative and yeasts. You can buy from Thermo Fisher a 1000X penicillin/streptomycin cocktail that you simply add at 1X to your medium, and the spectrum is broader. Due to penicillin allergy, you may need to find an alternative. Gibco markets gentamycin in 10mg/mL and 50mg/mL formats, but I think with gentamycin you definitely want to add amphotericin B. Use the same cocktail across all three types of control.

You can even go as far as to test your antibiotic cocktail in advance, in triplicate on your strains of interest, to ensure you have a valid positive control.

I find these compounds to be quite common and so there are other anti-fungals you could use, but I can't attest to their efficacy.


How does electroporation mediated recombination work? For yeast and other organisms, DNA can be readily taken up into the cell naturally or through membrane disruption. What does applying a voltage to cells do exactly that allows more recombination to occur?

Electroporation is a fairly common way to introduce exogenous nucleic acids into cells. Its name essentially describes the process - an electric voltage potential is applied across a biological membrane, eventually leading to the production of conducting hydrophilic pores. The image below is from the Wikipedia page linked above, showing non-conducting (upper) hydrophobic and conducting (lower) hydrophilic pores. Depending on the voltage, membrane composition, and other factors, these pores can eventually "heal" and close back up, or join together and lead to the rupture of the cell.

Electroporation is used in the lab as a method of transfecting or transporting nucleic acids (usually DNA) into cells, to make them express genes they otherwise wouldn't, or to otherwise alter the genetic machinery. The transfected DNA can either remain in its own structure (such as a plasmid), or be incorporated (recombined) into the host genome, similar to what happens during a retrovirus infection. Whether or not this happens is dependent on the structure and sequence of the construct being introduced, not the method of introduction.

So, in reference to your question, electroporation doesn't do anything that directly allows more recombination to occur - all it is is a method of transportation. However, electroporation may allow for certain constructs to be introduced into the host more efficiently, or for a larger quantity of them to be introduced, leading to a greater transformation efficiency. Some cells, especially primary cells like neurons, for example, may only be transfected with any sort of efficiency with electroporation. However, electroporation can also have its down sides, as it can be rather stressful to the cells, and if the voltages and timing aren't properly adjusted can lead to high levels of cell death.


Coordinates of amino acids in a protein sequence In PDB format, the coordinates of each of the atoms are available. Are the coordinates for the amino acids available separately? As in say a protein sequence consisting of a chain of amino acids MKL... Where would I get the coordinates of M and K and L separately? Is there any method by which the coordinates of the amino acids can be calculated? I don't want the coordinates of the atoms, I want the absolute coordinate of each of the amino acid in a protein sequence as a whole...

If what you are after are the structural co-ordinates of particular  amino acids crystalized individually (i.e. considered as small molecules independently of any role in proteins), then you should find them along with other small molecules in the Cambridge Structural Database.


Is it possible to distinguish between coding and template strands from the sequence? Let’s say you have the following DNA sequence fragment:

5’-ACCAGTACTTCGT-3’
3’-TGGTCATGAAGCA-5’

Is there any way to determine which strand is the template strand and which is the coding strand for RNA synthesis solely from the above information?

I don't know about your specific example (perhaps look for triplets that code start codons?), but machine learning has been used to predict promoters from sequence information (from promoter regions, you get downstream initiation of transcription of DNA to RNA). You would probably need more sequence to predict a promoter with more certainty. Cites: https://en.m.wikipedia.org/wiki/Promoter_(genetics) and https://academic.oup.com/bioinformatics/article-abstract/35/16/2730/5270663


Is saturation of olfactory cells able to create a feeling of another odour when it stops? I'm looking for at least one scientific study about how odours could impact human olfactory system and create some phenomenon that could be loosely compared to retina remanence.

As an example, with standard eyes, when you look at a cyan area for a long time and then look at a white paper, the paper looks yellow for a while (see some fun experiments here). This seems to be called an afterimage.

In the type of study I'm looking for, if it exists, the olfactory cells would be involved instead of the retina.

Being exposed to a strong odour for some time would make the subject smell an other odour (a complementary odour?) when the strong odour disappear even if nothing casts this new "complementary" odour to the nose. We could call this an "afterodour" or a "complementary ordour".

Yes, there is something like an "odor afterimage", at least in rodents. This is the paper:

http://www.pnas.org/content/110/35/E3340.abstract

But have in mind that this phenomenon is quite different from visual afterimages. First, it doesn't depend strictly on "adaptation", because adaptation is a property of the sensory organ, not of the brain. Second, besides all the qualia questions, it doesn't seems to create different olfactory sensations, or a "complementary odour" as you said. One of the reasons for this lack of "complementary odour" is that the complexity of olfactory receptors (simply put, the number of different receptors and their activity) is way higher than that of visual receptors, so, it's not a simply matter of receiving more impulses from the non-adapting receptors than from the adapting ones, as in vision.


Why are there not effective pharmaceutical treatments to prevent weight gain? Hunger is caused by signals from the brain, so is there a way to suppress the signal of hunger in the same way we suppress the signal of pain with painkillers?

If people felt less hungry, they would eat less and find it easier to lose weight, so why aren't there pharmaceutical hunger suppressants yet?

The two main factors are:

Hunger is more complex to treat than pain (more pathways, more potential targets), and I would argue against your suggestion that we are good at treating pain: despite the term "painkiller" we aren't great at blocking pain except for with local anesthetics that block all nervous activity (lidocaine for example). For systemic pain relief, there are lots of long-term efficacy issues with either opiates or NSAIDs, and that isn't even taking into account:
Side effects. Amphetamines are great for suppressing appetite. They also mess with the cardiovascular system, are habit-forming, and cause psychological issues. "Fen-phen" is a famous example of an anti-obesity drug that had major side effects leading to massive lawsuits. A more recent supplement, Ephedra, had many of the same problems and was banned by the US FDA for those reasons.

There are some drugs that are used to treat obesity, but many of these have come into regulatory issues with side effects and are only used in special cases like in diabetics or as an absolute last resort.


Water sample preservation I am taking my students to collect water samples from different bodies of water. These bodies of water include the local river, a park pond, and water accumulation from recent rain. Once we gather the samples students will be analyzing the samples under standard light microscopes. I was wondering what is the best way to preserve any life that may be found in the samples in case there is no immediate opportunity to analyze the samples under the microscopes? Is there a specific time frame to analyze the samples before they have to be replaced? Also if they are kept in a bottle/jar does the container have to be unsealed or with perforations to allow air flow? Thank you.

Depending on what you are trying to look at, for zooplankton you can take water samples and filter them through a 100-200um mesh and store them in glass or plastic bottles. For my research we used mason jars that were cleaned thoroughly. After filtering just submerge the biomass in 70-90% ethanol and they can be stored in a fridge for quite some time.

If you want to look at phytoplankton, you can look into using Lugols Solution for preserving your samples. The nice thing about using lugols is that it will stain the phytoplankton as well. Your best bet for these is to store in amber bottles and keep in cool dark place. Here is a decent guide on how to collect the samples and prep the solution.


How do mutations with very little fitness benefit get fixed? I have one little issue with evolutionary theory that I have not been able to understand.
Suppose genetic mutations happen from generation to generation. Nevertheless, from one generation to the next the mutation will present very small changes (I don't suppose a giraffe's neck would grow 10cm). If this were the case, then the advantages one gains from this mutation would be very small. So shouldn't it be the case that the mutation in the case of the giraffe and every other mutation for that matter present very very little advantage so shouldn't transmission of genes at this stage be random? If this were the case I don't see how natural selection could take place?

In the long run (over hundreds or even millions of generations), small statistical advantages are bound to accumulate.

Even if a mutation gives only a +1% average reproductive advantage, it is still above chance and therefore this mutation is more likely to spread through the population.
(If you can code, I have found it to be an interesting exercise to write scripts that simulate generations of evolution.)

It is also not necessarily true that effects of mutations have to be small. Single mutations can be deadly, they can change colors, create large morphological changes, and so on. It just happens to be the case that most mutations that have large effects are deleterious, and therefore won't generally spread for long throughout the population. But some mutations will be beneficial and therefore have improved odds of being passed on.


What's the recommended maximum passage number for mammalian cells (NCI-H441)? Is there a generally accepted maximum number of times you should split and reseed mammalian culture cells before restarting cultures from new stock?

This is a very good question and it highlights a very frequent misconception about cell culture and it is using the passage numbers as an indication of how well a cell is behaving. Although this can be a good barometer but it is misleading. Passaging can stress the cells if performed very frequently, although again that depends on how fast the cells are dividing.

You should not think of passage (and cell culture in general) in terms of the procedure itself but in terms of population doubling (PD) which can be calculated using the formula provided here (http://www.sciencellonline.com/site/techsupport.php). I personally use [Log10(harvesting cell No/seeding cell No)/Log10(2)]. This should allow you to characterise your cellular behaviour between every passage and allows you to draw a cumulative PD graph. Once the cumulative PD versus time becomes non-linear, then you would know that the cells have changed behaviour and it might be best to use a fresh stock.

The main advantage of this method is that you are not relying on guess work and deal with solid numbers and allows you to predict when you should expect to start a fresh batch for passage. Although passage numbers can do the same job if you assume per passage, the cells have done a certain PD but this is more of a guess work and you can not track how well your cells are doing at a given time point. For example one of the main problems with using a passage as a measure is that you can passage the cells at 98% confluence to a fresh flask and although that counts as a passage but it is pretty uninformative in terms of cell behaviour and gives you no solid numbers and you can do this many many times and although you would have done high number of passages but your cells would appear ok. Although such an exercise is pointless and will probably stress the cells but it is just to make the point that passage numbers are not necessarily a very informative and quantifiable measure of how well the cells are doing or behaving hence PD and cumulative PD should be used. Another advantage is that since you are dealing with actual cell numbers, if you changed your cell culture flask size from lets say T-75 to T-25, you don't have to be worried about changes to your frequency of passage or having to make further guess work on how that has effected your cell behaviour.

My main advice is that you should keep you frequency of passage the same at least in the beginning (although keep an eye on the cell density as you don't perhaps want to let cells to be too over-confluent or unconfluent when passaging, depending on your specific methodology and what has been established in your lab), but count your seeding and harvesting density (cell No) and calculate the PD and cumulative PD and draw a cumulative PD vs time graph and monitor the behaviour of cells. This should give you a good indication of you cellular behaviour under the conditions you are working with them since guidelines are just that, guides and they can never substitute experimental characterisation of your cells under your conditions and handling method!


How are long time periods measured in biological systems? Biological systems are pretty good at measuring fairly long times, for example, menstrual cycles (month), or puberty (years). Counting days or years seems to be implausible, and chemical concentration also seems implausible. What are the physiological processes that are involved in keeping track of such long periods? Is it just a long sequence of finite state changes?

I understand there are environmental correlates such as seasonal changes and relative position of celestial objects to measure the relative time, but regardless of these external cues, I suspect that a pretty good internal clock for longer time scale could exist. For example, the time to menopause can actually be thought of as a counting mechanism of a shorter clock which is the menstrual cycle. But, how does the body know when to stop growing? I cannot think of biological processes with such long time constants that is stable.

The short answer is: we do not know exactly, although we do have some insights.

I will take the example of puberty.

Although a clear definition of puberty is lacking, it is quite clear that it corresponds to a period where gonadal function starts.

This, in turn, is derived from the activation of the gonadotropin system, which consists of two main cell types:

a small number of neurons located in the preoptic area of the hypothalamus (a nucleus at the base of the brain) called the GnRH neurons. GnRH is the Gonadotropin-releasing hormone, a small peptide that stimulates the production of gonadotropins from the pituitary.
the gonadotrophs, a specialised group of cells in the pituitary (a gland located underneath the brain) which produce two hormones, called luteinizing hormone (LH) and follicle-stimulating hormone (FSH) which stimulate the gonads to produce various hormones, such as estrogen.

In mammals, the secretion of GnRH, and thus LH/FSH varies during the course of the menstrual/estral cycle. This cyclicity lasts several days (4-5 days in rodents, ~1 month in humans) and entrains the cyclical secretion of estradiol (E2) from the gonads.

Note that this is a sort of self-sustaining cycle, as cyclic levels of E2 will then allow for cyclic GnRH secretion and so on.

But, back to your question: how does the GnRH/LH/E2 system "wake up" at puberty?

The exact mechanism is still unknown, but recent work has found an important mediator, called kisspeptin, that is produced from two population of neurons in the hypothalamus, called the kisspeptin neurons.

Kisspeptin has been shown to be a very potent activator of GnRH neurons and work in the mouse has shown that these neurons appear at the time of puberty, their number increasing dramatically between 25 and 31 days (puberty is at around 30 days in mice).

Postnatal Development of Kisspeptin Neurons in Mouse Hypothalamus; Sexual Dimorphism and Projections to Gonadotropin-Releasing Hormone Neurons  - Clarkson and Herbison - Endocrinology, 2006

Similar work exist in the monkey:
Increased hypothalamic GPR54 signaling: A potential mechanism for initiation of puberty in primates - Shahab et al. - PNAS, 2005

In humans mutations in either kisspeptin, or its cognate receptor GPR54 results in disturbances of pubertal maturation because of underactivation of the system (hypogonadotropic hypogonadism) or hyperactivation (precocious puberty).

So, now the question is shifted: why do kisspeptin neurons show up only at puberty? We don't know for sure, but it looks like increased levels of E2 could be important for this.

Again, we get into a self-sustaining cycle. Growth of the body generates an increase in E2 production (possibly due to increased volume of the gonads?), which, when over a certain level permits the development of kisspeptin neurons, which will then stimulate the GnRH neurons, resulting in increased LH and E2. We then have more E2 and this makes kisspeptin neuron grow even more etc etc.

From: Postnatal development of an estradiol-kisspeptin positive feedback mechanism implicated in puberty onset. - Clarkson et al. - Endocrinology, 2009


Wouldn't a non-poisonous variety of a mutant plant be at selective advantage? I don't know much of evolutionary biology, but when someone asked, this seemed very much plausible to me.

Say there's a mutant plant, that produces much lesser toxin than its usual counterparts (same species). Then, wouldn't this plant be at a selective advantage over the others, since the predators (here, herbivores) wouldn't consume it assuming it to be poisonous. But sowly, as these mutants increase in number, the herbivores too realize and start feasting on them. Again selecting out ones with more toxin. Ultimately reaching some kind of equilibrium (?)

Is this phenomenon(?) called something? Is it similar to the selection that occurs in the  sickle cell trait? Are there real examples with plants with toxins showing this?

Your question is very sensible; we would indeed expect this kind of negative frequency-dependent selection: i.e., if toxin-producing plants are common, non-toxin-producing plants should gain an advantage because they don't pay the costs of producing toxins but they do (or may) gain an advantage from herbivore deterrence. (Conversely, if toxin-producing plants are rare, they could gain an individual-level benefit by being the only ones in the population to deter herbivores.)
As of 2007, however, it seems that the empirical evidence for this phenomenon was pretty weak. In the following, "resistant genotypes" means genotypes that have some kind of anti-herbivore trait (typically production of secondary compounds that deter herbivory) [emphasis added]:

... Only a few studies have examined the role of frequency-dependent selection on plant defenses against herbivory (i.e., Berenbaum & Zangerl 1998, Roy 1998, Siemens & Roy 2005). ...  No study has manipulated the frequency of resistant/tolerant host genotypes explicitly to examine if the evolution of plant defensive strategies is subject to frequency-dependent selection. However, some studies tested some of the predictions of the frequency-dependence selection hypothesis (Berenbaum & Zangerl 1998, Roy 1998).
The study by Berenbaum and Zangerl (1998) found that in Pastinaca sativa, the range of variation in the level of a resistance component (coumarin) against its consumer Depressaria pastinacella did not change from 1873 to present, suggesting a cyclical dynamic promoted by frequency-dependent selection. In a reciprocal transplant experiment Roy (1998) did not find evidence that common hosts are eaten more and have lower fitness than rare hosts.  In a recent paper, Siemens and Roy (2005) evaluated the following: (a) if the amount of damage experienced by the most common host genotype was higher than that expected by its frequency, and the amount of damage experienced by the most rare host genotypes was lower than that expected by its frequency (assortative damage hypothesis); (b) if the most common host
genotype had higher levels of damage and lower average fitness compared with the more rare host genotypes; and (c) if the amount of damage correlated positively with the frequency of the most common host genotype. ... Unfortunately, their results provide little support for the hypothesis of frequency-dependent selection acting on plant defenses against herbivory.
... Although two studies have explored the potential for
frequency-dependent selection on plant resistance, no study has yet
examined this possibility on plant tolerance. Before
frequency-dependent selection can be put aside as an explanation of
the maintenance of variation on tolerance and resistance, explicit
experimental tests of the hypothesis are required.

(I haven't followed up the more recent literature to see if there is more recent evidence ...)
There is a related phenomenon that's much better documented: toxin-producing bacteria produce antibiotics to kill other bacteria of their own and other species, to minimize competition for resources. In "rock-paper-scissors" systems (2), cheaters (bacteria that are resistant to toxin but don't produce it themselves) invade toxin producers; then non-resistant bacteria invade the cheaters (because there's no toxin being produced any more); then toxin producers reinvade (because nobody's resistant any more, so there is once again an advantage to producing toxin).
I would say that the connection between this type of frequency-dependent selection and the selection that maintains polymorphism for the sickle-cell allele is loose. Sickle-cell is usually cited as an example of heterozygote advantage. It is loosely speaking a form of negative frequency-dependent selection at the level of alleles rather than genotypes; a gamete carrying a sickle-cell allele is more likely to end up in a heterozygote (and thus gain an advantage via malaria resistance) when it's rare and more likely to end up in a homozygote (and lose fitness due to sickle-cell disease) when it's common. It's also theoretically possible (although I haven't seen it discussed, and I would guess that it's not very important in practice) that increasing frequency of sickle-cell heterozygotes could also feed back at the population level to reduce the incidence of malaria, lower the advantage of resistance, and hence generate a more analogous form of negative frequency dependent selection.

Núñez-Farfán et al. "The Evolution of Resistance and Tolerance to Herbivores", Annual Review of Ecology, Evolution, and Systematics, Vol. 38 (2007), pp. 541-566 http://www.jstor.org/stable/30033871
Kirkup and Riley, "Antibiotic-mediated antagonism leads to a bacterial game of rock–paper–scissors in vivo", Nature 428, 412-414 (25 March 2004) .


Identification for a bird in the middle of the tree In the central city of Dobrich Bulgaria, I was following a Great spotted woodpecker in a tree and suddenly I found this other bird on the same tree.

The context of the picture is:

Country: Bulgaria
City: Dobrich, Center urban area
Period: mid August (2016)

I think this is a specimen of Silvia Curruca, can anybody confirm this?

Yes, Lesser whitethroat indeed. Grey head with contrasting white throat and brown body, small bill (the similar Orphean warbler has a much bigger bill).


What does dominant generation mean In my texbook it is written that for non- vascular seedless plants the dominant generation  is the gametophyte as the gametophyte generation is larger and longer lived.
Is the criteria for dominant generation?-( Which generation the plant spends most of its life in?)

According to "Wile, Dr. Jay L. Exploring Creation With Biology. Apologia Educational Ministries, Inc. 1998" and reported here,

  In alternation of generations, the dominant generation is the generation that occupies the largest portion of the life cycle

I guess that it has to be understood in terms of "time". I am not quite sure though if it has to be understood in terms of generation time of life span. Intuitively, I would say that generation time would make much more sense. Therefore, I'd say that, the dominant generation is the generation which have the longest mean generation time (=mean time from the birth to reproduction).

As @Shigeta said in the comments: For example, in Homo sapiens, the dominant generation is the diploid phase (sporophyte, you and me) and the non-dominant generation is the haploid phase  (gametophyte, sperm/ovule).


Can someone identify this jellyfish? Recently, I saw this video but I couldn't find out if it's CGI or if it's an actual jellyfish. If it's real, what explains its beautiful bioluminescence pattern? And could the output from the ROV thrusters rip it apart (in the video description it says so)?
Photo:

Location: off the East coast of Africa.
Size: unknown, but it can be compared to the objects in the surroundings.
Additional info: footage taken in 2013.

The video you linked to, and from which you got the still shot. is real.  There are  hundreds of such videos now that Underwater Remotely Operated Vehicles (ROV) are more commonplace.

...could the output from the ROV thrusters rip it apart(?)

A working class ROV needed for deep ocean floor exploration can be the size of an SUV. There's no reason to believe its thrusters can't generate the shear forces needed to (sadly) tear a delicate jelly apart.

...I couldn't find out if it's CGI or if it's an actual jellyfish.

Although not a jellyfish, it is similar in being delicate; it's a ctenophore or comb jelly. The refraction/bioluminescence pattern is common in ctenophores.

And what dazzling colors these creatures display! The cilia of the ctenophores refract light in iridescent waves. Certain species are even capable of producing light, like fireflies of the sea!

For more information and videos, this short Youtube video might help. Or for a written explanation, this article, Introduction to Ctenophora  (https://ucmp.berkeley.edu/cnidaria/ctenophora.html) is good.


Factors on which one compound transforming to another compound depend Considering the Metabolic Pathway:
http://www.genome.jp/kegg-bin/show_module?M00166
Consider the reaction R01523(the very first reaction). How is it possible to know that the compound  C00199(D-Ribulose 5-phosphate) will get transformed to C01182(D-Ribulose 1,5-bisphosphate)? What are the factors on which this transformation depends?One factor I know is structure but how does structure effect this transformation? Does two similar structured compound means that one of the compound can get transformed to the other one?

From my answer on chemistry:

After looking at the website I found the reaction is based off of an enzyme called: phosphoribulokinase. In biological systems many reactions occur under the auspice of enzymes or proteins. These are incredibly large molecules made of an extremely long chain of amino acids which are a set of 26 or so small molecules that can 'hook' into the chain structure of a protein. Each amino acid has different properties and thus experiences different forces pulling it towards and away from other amino acids on the chain. What this means is the whole chain folds up into an extremely complex structure. For a protein to allow a reaction to occur it has a small region that the reacting molecule can hook into. There are then sets of atoms and molecules that act as scaffolds that allow atoms in the reacting molecule to be moved without the need for nearly as much energy as would be required without the scaffold. Now this is how it changes structure. Now whilst the protein can just as easily allow the molecule produced to be converted back to the original, this may be less energetically favourable which brings us to equilibrium chemistry involving dynamic forward and backward reactions. What makes this more complicated is that proteins often have separate 'hooks' for molecules to disable them. That is if a lot of substance A is around then the protein will be disabled and no longer convert B into A until more A is consumed and thus stops inhibiting the protein.


What roles do cyclooxygenase, lipoxygenase, and epoxygenase have in signal transduction? Besides oxidizing fatty acids to form prostglandins, leukotrienes, and epoxides, what other roles do cyclooxygenase, lipoxygenase, and epoxygenase have in signal transduction?

I just took a quick look.

These classes of enzymes are important to a family of lipid based molecules which perform intra and intercellular signalling with a lot of medical importance.

Epoxygenases can create epoxides of arachidonic acid,  which can modulate cell proliferation.  Arachidonic acid is a well known second messenger in many tissues in the cell, so these enzymes clearly would affect many signalling pathways.

Cyclooxygenases (COX) enzymes are such important mediators of inflammation signalling that they are the primary targets of aspirin and other Non steroidal anti-inflammatory drugs.

Lipoxygenases oxygenate compounds such as prostaglandins which are downstream from aranchidonic acid (as does COX).


Searching for comprehensive textbook I am extremely interested in science in general and in particular biology. Due to a different choice of career-path I probably will not be learning any more biology anytime soon.

So I would love to get my hands on a comprehensive textbook biology which hopefully will enable a goal in lifelong learning of biology.

What are some good recommendations? I looked up biology textbooks on Google and found candidates such as Campbell Biology by Reece and Biology by Brooker. But as there are so many of them, I have no clue which one to get.

So, biologists of stackexchange, can you help me out?

Try Campbell biology.....it covers almost all the topics under biology in a lucid way...also the book has packed quite a volume of info in it ranging from a beginner level to a fairly advanced level....excellent book also in matters of presentation & writing style so that one won't feel bored....

Pros:

Genetics ( both classical and modern)
Ecology (including ethology)
Evolutionary biology
Animal classification
Immunology

Cons:

Biochemistry ( it somewhat feels short)
Plant anatomy ( not adequately covered)
Plant classification ( same as above)

& the rest of the chapters are like animal physiology etc. they are mixed...like some
principles they have gone thoroughly...some others not...but it's acceptable as they have to cover everything in one book...

But of course it's my personal opinion...so before considering it I would rather recommend downloading the book in pdf format & have a look at it yourself...but I feel you won't be disappointed....


Would tattoos be considered a phenotype? I'm trying to understand how broad the definition of "phenotype" is. If someone gets a tattoo, would that tattoo be considered part of their phenotype?

Broadly speaking it most likely is. The exact meaning of phenotype has changed quite a lot over the years. There isn't a clear distinction between what should or should not be included in the definition, and reasonable people can disagree on sound arguments.
Phenotypes were defined by Johanssen in 1911. His definition was "All “types” of organisms, distinguishable by direct inspection or only by finer methods of measuring or description, may be characterized as “phenotypes.”". So in his definition a phenotype is a class of individuals that share a common observable property. Take Mendel's experiment: short and long peas are 2 phenotypes. From heredity we can infer multiple genotypes. An identical phenotype (tall) can result from 2 different genotypes (tall-tall, or short-tall). That is why the distinction is important, because truly understanding genetics will require not only to understand the genetic makeup of individuals (we have more or less solved that), but more importantly how the genes are expressed into a phenotype. Keep in mind all of this was speculated long before we actually found out what genes were. Ironically, Johannsen thought it was an idle pursuit: "The question of chromosomes as the presumed “bearers of hereditary qualities” seems to be an idle one. I am not able to see any reason for localizing “the factors of heredity” (i.e., the genotypical constitution) in the nuclei.".
At the time, genes were really thought to produce strict discrete categories of individuals that were slightly smoothed out through random individual variations. Over time it became obvious that Mendelian traits were more the exception than the rule and that trying to classify individuals in discrete categories was not really helpful. So over time phenotype became to used for traits instead of individual. That's the way I hear people use it today at least (i.e. we would call "being tall" a phenotype of peas, and not "all peas that are tall").
So the modern definition of a phenotype is the observable characteristics of an organism, anatomical, physiological or behavioral. The first 2 points are easily accepted and uncontroversial. But there is debate about what exactly should be included in "behavior". I'm going to ignore behavior for now.
An important point, and I think this is where there is disagreement between Remi.b and me, is that a phenotype must have a genetics basis. I realize this is not explicitly mentioned in any definition, but that is very much the way people mean it. And if not, the definition is totally meaningless. Take the example of a monkey missing a finger congenitally. This is a phenotype, it is due to its genes. If the monkey is missing a finger due to a fight, this is not a phenotype because genes have nothing to do with it (again, ignoring behavior for now).
So, in my opinion, what would not be a phenotype is something that you could conclusively prove to have no genetics basis whatsoever. That's an extremely (impossible) hard case to make. But in retrospect I was perhaps to quick to include behavior in the definition, and this is due to my own biases as a behavioral neuroscientist.
I think this is the narrow definition of phenotype and I don't think anyone would disagree up to that point. You might notice that there has been no mention of evolution so far. It is because genetics and evolution have been developed independently, and even though everybody was quite aware they must be 2 sides of the same coin evolution is not directly relevant to the genotype/phenotype distinction.
This is when the definition of phenotype started to be extended beyond purely physical traits (people included behavior in phenotype but they mostly meant things like gait that require a behaving animal to measure, but it is not behavioral in the broad sense). I see 2 reasons for that change, and R Dawkins was largely involved in popularizing these ideas. First as genetics and evolution started to be integrated together, it became obvious that genes must be selected through evolution, and that phenotype must reflect something related to fitness. W. D. Hamilton did important work on the topic and his ideas were popularized in the "The Selfish Gene" from Dawkins. The second idea is the ethological "revolution" from Tinbergen and Lorenz. Until then animals were seen as automatons (following Descartes) that behave the way they do because of simple conditioning. Ethologists showed that complicated behaviors such as courtship or altruism are instinctive, and therefore must have a genetic basis (Hamilton also worked on altruism a lot). A new generation of scientists pushed things even further with people like E. O. Wilson who studied the social life of insects, J. M. Smith who showed that individually detrimental behaviors can be optimal at the scale of a population etc.
At this point it became clear that the definition of a phenotype was too narrow, because behaviors are (at least partly) related to genes and therefore must have been shaped by evolution. This is the idea put forward by Dawkins in his second book "The extended Phenotype" where he explicitly makes the case that the definition of phenotype should be enlarged to include behaviors such as courtship, nest-making and the like (Dawkins was a student of Tinbergen so it's not entirely surprising he is biased to like animal behavior). Although these 2 books became very popular and widely read in the general public, they were actually meant mostly for biologists. Note that the extension of the definition of phenotypes shifts the focus from pure genetics to evolutionary theory as the rational for extending phenotypes is that more stuff than pure physiology contribute to fitness. That's not entirely relevant to the genotype/phenotype distinction but there is a great interview of Smith by Dawkins where he discusses a lot the history of genetics, evolutionary theory, and the socio-political debates behind it (link below).
So today some behaviors are widely, and I think uncontroversially, thought to have a genetic basis and therefore should be considered a phenotype. This is the second part of the disagreement between Remi.b and me (which derives from the first). If phenotypes must have a genetic basis, then how do you know that a behavior has a genetic basis or not? The gold standard is to show heritability of the trait in a twin-study. If the trait co-occur more in identical twins than fraternal twins, and/or in identical twins raised separately than expected from chance, then you know with confidence that this trait is partly genetically determined. Most famously, for example, this is known to be true for sexual orientation. So I am not saying that a phenotype can only be inherited. Obviously a random mutation is a phenotype but has not been inherited. But to show that a behavior is genetically determined I don't know how you can do that without showing heritability (but I'm not a geneticist so maybe there are other ways). Siddhartha Mukherjee's The Gene is a very good summary of the state of the art in that area.
So where does that leave us concerning phenotypes and tattoos? Well if you agree that behaviors should be considered phenotypes, such as courtship, nest-making in birds, aggressive displays in monkeys... Then I see no reason not to include tattoos in it. Any criterion you apply to "animals" should apply equally to humans. Some birds decorate their nests with flowers as part of courtship. The question left is whether it has a genetics basis or not, and I think you are very likely to find that getting tattooed would co-occur more than expected from chance in twins. Of course the tattoo is not genetically determined. It's probably something like open-mindedness, but a tattoo is observable and open-mindedness is not. This definition of phenotypes means that you can more or less already include quite a lot of things in it. So I can see why someone would disagree with extending the definition of phenotype beyond pure physiology. But clearly phenotypes must be linked to genetics otherwise the definition is purely meaningless.
Johannsen W. The Genotype Conception of Heredity. The American Naturalist 1911;45:129-159.
Dawkins, R. (2016). The selfish gene. Oxford university press.
Dawkins, R. (1982). The extended phenotype (Vol. 8). Oxford: Oxford University Press.
Tinbergen, N. (1951). The study of instinct.
Lorenz, K. (2013). The foundations of ethology. Springer Science & Business Media.
Smith, J. M. (1982). Evolution and the Theory of Games. Cambridge university press.
Wilson, E. O. (2000). Sociobiology: The new synthesis. Harvard University Press.
Siddharta, M. (2016). The gene: An intimate history. Scribner, New York, 9-9.
https://www.youtube.com/watch?v=0b0Nm_L3TKg&list=PLVV0r6CmEsFzJSvAc4MBuUP_GrjO1lLHp


Why to choose a grammar from a lot of grammars that can describe structure of proteins? Why do we choose a grammar from a lot of grammars that can describe structure of proteins? Usually, there are a lot of (maybe infinite) grammars that can describe one language. Why do we choose a specific one? Especially the language of proteins of gene just has finite sentences or words.

I did not understand your question completely but this is what I guess you want to know:

Why genetic code evolved to be what it is ?
How the sequence of the protein coded by a mRNA give rise to a particular structure ?

Answer to first question cant be definitive. The textbook explanation for why a 3-letter code exists is because a 2-letter code cannot describe all the 22 amino acids, with all its permutations. But then comes another question: why only 22 amino acids. I can't even speculate the answer to this question; the simple amino acids are fine but for an example why lysine and not a similar amino acid with a shorter side chain - no idea.

So, given 22 amino acids, a 3-letter code and 4 nucleotides, the multiple codons for an amino acid are similar in sequence (usually the first two bases are conserved in accordance with the wobble hypothesis. The last base usually doesnt base pair strongly with the tRNA and is of minimal importance).

The answer to second question is somewhat straightforward. The sequence can give rise to infinitely many structures but in a given environment (consisting of the solvent, other solutes etc), the sequence adopts a particular structure in accordance with the free energy minimization principle. There is a possibility that given an environment a protein can have two different optimal structures and can switch between these two structures.


What is the common diet of food-related IBS patients? Besides most patients being lactose intolerant, what other intolerances do they face? I am currently writing a paper on irritable bowel syndrome, and I was wondering what the common diet of a patient with food-related IBS consists of. I've already begun discussing the pathogenesis of the disorder, but I want to start making a connection between food and IBS. I understand that most patients tend to be lactose intolerant, but I am also interested to see if there are any other common intolerances associated with IBS.

IBS stands for Irritable Bowel Syndrome. The IBS symptoms include belly pain, diarrhea, bloating and constipation. Different persons have an intolerance to different food items. You can know what's causing trouble in you by taking a test at http://intolerancelab.co.uk/intolerance-2.

The most common diets that you can prefer to get rid of IBS symptoms are:

High Fiber Diets can help prevent constipation.
For some people, high fiber diet is intolerant. They should switch to a low fiber diet.
You should prefer a gluten-free diet.
Have a low-fat diet and get rid of a number of health problems.

Some food items that can cause food intolerance are:

Dairy products
Soy products
Fructose
Wheat
Gluten


Can you identify this (possibly waterstoring) plant? My son brought home a sapling, and after 4 years in a pot it is now about 30 cm or a foot high (from the "ground" to the top of the "stem"). It doesn't need a lot of water and can go weeks without being watered, in fact it seems to me as if it is storing water in the thicker upper part of its stem. When I water it "too much", new leaves start to grow. There are tiny "blossoms" along the stem, and every now and then small, dark brown, spherical seeds about 2 mm in diameter pop out from the "blossom" and are thrown across the room as far as a meter (about a yard) or two.

What plant is this?

I believe that it is not native to my European home but some kind of decorative plant imported and sold through a florist or imported privately, but I'm not sure.

It is an Euphorbia leuconeura (Madagascar Jewel), which is native to Madagaskar. The leaves and the thick (waterstoring) stem with a narrow base is very typical.

The plant is cool in the sense that it easily produces seeds (also as potted) which it can shoot away from the plant. I've had it myself and you can sometimes hear seeds hitting the window or floor. Even if it is easy to grow and to reproduce it is actually considered threatened in its native habitat (IUCN Red-listed as Vulnerable) due to habitat loss

The flowers are very small and found directly on the stem, see below:

(picture from Wikipedia)


On which date did the official name change of Lactobacillus sanfranciscensis change? When did the change of official name from Lactobacillus sanfrancisco to Lactobacillus sanfranciscensis happen? An answer ((to the exact day OR within a few days) AND the name of the conference at which it happened) would be appreciated.

Lactobacillus sanfranciscensis first shows up in pubmed in Gänzle et al. (1998). They reference Trüper and De'Clari (1997) for the name Lactobacillus sanfranciscensis. The latter say:

  As none of them makes sense in the nominative apposition construction,
  we hereby correct these names to forms that are in agreement with Rule
  12c as follows.

  ...

  Lactobacillus sanfrancisco ("the city San Francisco") is corrected to Lactobacillus sanfranciscensis (adjective: "from San Francisco").

That issue of Int J Syst Bacteriol was published 1 July 1997, so I guess that's your date.

References

Gänzle M G, M Ehmann, and W P Hammes. 1998. Modeling of growth of Lactobacillus sanfranciscensis and Candida milleri in response to process parameters of sourdough fermentation. Appl Environ Microbiol 64(7):2616–2623.

Trüper H G, De'Clari L. 1997. Taxonomic note: necessary correction of specific epithets formed as substantives (nouns) "in apposition." Int J Syst Bacteriol 47:908–909.


How to correctly preserve organic matter with ethylene and polyethylene glycol? I am trying to preserve and dye flowers, especially roses. Let me walk you through the process I am trying to optimize:

1) Soaking flowers in 96%-ethanol for a day to dehydrate them. This step removes a lot of the color from the petals - red roses for example become faint pink. The flower itself becomes brittle to the touch, since almost all water is removed.

2) Putting the dehydrated flower into a mix of 96%-ethanol, polyethylene glycol 400 and reactive dye which is used in textile industry. I am still experimenting with the ration of ethanol:PEG. Soaking duration is a couple of days. In theory, the PEG gets into the cells of the petals - this preserves the petals and gives them most of their flexibility back.

3) Removing the flower from the mix and rinsing it for a minute in 96%-ethanol. This should remove the excessive PEG on the surface of the petals. Otherwise it looks glossy and stays sticky.

My problem begins at step 1): If I remove a flower from the dehydrating ethanol-bath, the petals turn opaque in a weird way. Some connected areas of a petal start to change their appearance abruptly (some sort of bursting, cracking, rupturing)! This starts some seconds after removing the petal from the ethanol and after a couple of minutes, almost all of the petal has turned opaque. Usually the outer edges of the petals don't turn opaque. I am not sure about this, but could it be, that the ethanol somehow destroys the cells of the petals? Is this a behaviour that is to be expected or am I doing something wrong? I think I would benefit a lot if I could understand where this abrupt change of quality comes from.

it doesn't matter, if I remove the flower after step 1, 2 or 3, the result is always this abruptly turning opaque behaviour.

Since my goal is to dye them to look nice and pretty, I need to find the mistake I am making. I was hoping you experts could help me.

You find two pics of already dyed petals attached.

(I wouldn't mind if they stay all transparent. In that case the petals should not turn opaque. But I also wouldn't mind if they become opaque - but on 100% of their surface. Also at the outer edges. This actually may be better - I think it looks nice this way.)

I find that using mixture of PEG 400 and Ethanol 2:1 reduce the transparency. You also need to bake the pental in microwave 360w for 15 seconds. Still some small transparency but acceptable.


Does fat on our heart come from the fat that we eat? If we eat fat:

Does the fat go into heart, arteries and fat cells.

OR

Is the fat digested, following which our body creates fat that goes into heart, arteries and fat cells.

Which one is right?

Fat is, in molecular terms, triacylglcerol. In order to be absorbed in the small intestine triacylglycerol molecules are broken down by lipases into fatty acids and monoacylglycerols. Once these have got across the enterocyte membrane they are reassembled into triacylglycerols and packed up into a special class of lipoprotein particle, a chylomicron, which enters the bloodstream via the lymphatic system.

The triacylglycerols in the chylomicrons are then able to be passed around through the system of lipoproteins (LDL, VLDL etc.) and pretty much can end up anywhere, including fat cells (adipocytes) or they can be metabolised as fuel molecules

So, because of that initial digestive step I would say that a single intact dietary fat molecule cannot end up as a body component directly, but complete metabolism of the components of the fat molecule is not necessary for these to contribute to body fat.


E. coli bioreactor or E. coli fermenter? I have a Requirements Specification in Russian for a "Fermenter" that would be used for "E. coli cultivation". This E. coli strain would be used to make a generically-engineered drug. The "fermenter" would consist of two "reactors" of 200 and 2000 liters, linked by a "pipeline system for transferring the half-finished product between them".

Would the whole thing be called a "Bioreactor" or "Fermenter", or are the two terms interchangeable here?

I don't think that there is a clear division between bioreactor and fermenter and the terms are often used interchangeably, but they do carry a difference in connotation (and marketing). The term "bioreactor" implies complexity, research driven, and/or maximal cell growth. Bioreactors are more state of the art and are used primarily for studying microorganisms or producing difficult to grow cells or for peak production of cells- while the term "fermenter" implies production of a substance besides or other than just the cells and might have the connotation of utility.  Fermenters also carry a historical connotation of brewing beer, wine, and other fermented food stuffs or materials. Also, it's important to bear in mind that bioreactors are used for fermenting, because bioreacting is not a real word.

If you just need a simple design for producing the bacteria or a bacterial product, then the term fermenter might be more appropriate. If you need computer control, or if you are using it to investigate/research growth and/or production parameters then you could call such vessels bioreactors without the risk of looking foolish. I think the best way to describe the difference is probably by example, but instead, I tried to itemize some of the distinguishing details, as follows:

Fermentors commonly have all or some the following elements: Agitator (of simple design), pH meter, temperature control (jacketed vessels are common), pipes for transferring nutrients, water, etc., and a sampling port (maybe). It may be made out of wood or clay, but if it is made from steel, plastic, glass, or other modern materials, that certainly wouldn't disqualify the term fermenter, but I would probably not call an oak barrel or a clay pot a bioreactor.

Bioreactors generally have the same things as fermenters, but bioreactors also usually have some or all of the following additional elements: oxygen probe, air or oxygen pump(s) and diffuser(s), other gas ports, additional ports/pipes for pH monitoring and control (often a programmable computer controlled pump is used for multiple solutions), electrolyte balance, radial or axial impellors- which operate at hundreds or thousand of RPMs, a vapor condensor (maybe), spectophotometer (for cell density measurements), nutrient processing data, and any variety of data measurement and/or recording is the often the point of interest, or when growth of tricky or finicky cells is necessary (especially like hybridomas, phytoplankton, or perhaps generally eukaryotic cell culturing). Also, there are different kinds of bioreactors like wave bioreactors (often in bioreactor bags on shaker tables instead of having an impellor).

In general, sterility is more important for bioreactors whereas many fermenters (or fermentation products, like yoghurt) can kind of take care of themselves, or a certain "cleanliness" will work. In both cases, steam sterilization is common. Again, the division is a bit blurry, and the terms might be used interchangeably by some people, like a jacket (light) versus a coat (heavy).

So, for your specific example, it would definitely be a fermentation system (not a bioreaction system), but regarding whether to call the vessels bioreactors or fermenters is more of an opinion, I'm afraid; but personally, I would probably say the fermentation system has two fermenters, since the idea is to produce a product and it sounds like they may be simple vessels. However, if the system has on-the-fly computational checks and balances, then I might be tempted to call the vessels bioreactors (if dazzle demands it).

Also, the smaller (200 L) vessel could be called an inoculation vessel without any connotations.


What is 'independent assortment'? What is the definition of 'independent assortment'. I tried researching this term but came back with two results:

alleles assort themselves independently of different alleles
the alignment of homologous chromosomes is random along the metaphase plate; resulting in the daughter cell inheriting either maternal or paternal chromosome based on 50:50

Which is the correct term?

The term was pioneered by Mendel, who had no knowledge of chromosomes, so definition 1 would perhaps be the best answer. However, we now know that definition 1 arises from definition 2 (chromosomes are inherited independently of each other) and from the fact that chromosomes recombine (cross-over).

That said, independent assortment does not apply to linked genes, which tend to be inherited together. That is, they are not independently assorted.


Can you still contract a disease after being vaccinated and be able to spread it? I assume I know the answer to this already but wanted to confirm before I respond to someone that appears to be arguing that vaccines don't make you immune (they only stop your symptoms?) - but you remain infectious?:

She also doesn’t realise that if a vaccine works like she believes then the vaccinated would have less symptoms which in result offers more chance of spreading it. literally how covid spreads so fast now. “no or mild symptoms“ to most. Thats the sole reason it spreads so fast. So technically getting vaccinated is more dangerous in spreading disease than someone that gets sick and stays at home.

Edit: This question is about vaccines in a more general scope as that was the discussion at hand, but if anything it would be more closely targeted at COVID-19, which I'm aware there is currently no vaccine for.
My understanding of vaccines in general is that they don't technically make you "immune", but they make you immune to the effects of the virus, because your body will already know how to beat it.
But in saying that, my assumption has also been that because you have somewhat of a immunity to it then if you get "infected" with the disease you aren't contagious to others.
Additionally, I assume getting "infected" with the disease and being protected against it's effects is different to being asymptomatic - both have no symptoms, but you are still truly infected with it if asymptomatic and can still pass it to others, it's just not affecting your body enough to give you symptoms.
Just thinking now, but if your body knows how to fight it off already, then maybe you are truly immune to it - just because it enters your body doesn't mean it infects you right? Your body knows how to fight it off before it does. Like, an attacker can enter your grounds and knock at the door, but your guards know how to fight them off before they enter the area of your grounds where they 'cause the trouble'.
...but on the case you CAN get infected with it, but it doesn't present any symptoms, are you still contagious to others?
Additionally, I'm not talking bout virus shredding here from getting a vaccine, I know all about that.
One would think the proof is in the pudding in that many diseases have all but been eradicated from the world because of some vaccines, but I argue with myself that if vaccines don't make you immune then perhaps these diseases have only largely seemingly been eradicated because most everyone has been vaccinated (with vaccination preventing you from the effects only, not getting infected?) - thus only appearing on the surface they have been eradicated, but they are still around, but just don't pose a health risk to those that are vaccinated?
So, primary question is, what is meant exactly by "immunity", can you still contract the disease and if so would you still be contagious to others?

I tried to break down your question into smaller parts and answer them individually:
Q. What is immunity?
A. Simply put, immunity is the ability to react to an infectious agent and stop it from causing disease.
Q. Do vaccines make you immune to infectious diseases?
A. Yes, by definition. If it doesn't make you immune, it's not a vaccine.
Q. Can we get disease even after being vaccinated?
A. Yes, because no vaccine is 100% efficacious. For example, the MMR vaccine has about 97% efficacy in preventing measles.
Q. Do vaccines prevent infection?
A. It depends on how the vaccine works. Some vaccines enable the immune system to actually reduce survival and multiplication of the infectious agent. The polio vaccine is an example$^1$. It leads to generation of antibodies that neutralise the virus$^2$.
Other vaccines prevent disease (or reduce its severity) but do not prevent infection. The diphtheria toxoid is a good example of this$^3$, because the antibodies generated by vaccination neutralise the toxin while leaving the bacterium unscathed. (I believe all toxoids behave like this.)
Q. Can we spread infection even after getting vaccinated?
A. Yes. This is easy to see for those vaccines (like diphtheria, mentioned above) that prevent disease but not infection.
Vaccinated individuals can spread infection with the other, multiplication-stopping kind of vaccines too. Again, this happens because no vaccine is 100% efficacious. Note that chances of spread are reduced (as compared to the unvaccinated scenario), even if they are not zero. For instance, see the work of Seward et al$^4$ on breakthrough varicella.
Q. The big question: is getting vaccinated more dangerous than not getting vaccinated?
A. Sorry, but this is not the place to discuss it. It requires a careful look at the risks and benefits of vaccination, not just for the individual but also for the community at large. That would be a discussion more appropriate for Medical Sciences Stack Exchange.
To summarise: yes, we can catch a disease and spread it even after being vaccinated. The chances of this happening vary with the kind of vaccine.

Journal articles cited

Howe HA. Am J Public Health Nations Health. 1957 Jul;47(7):871–5. https://doi.org/10.2105/ajph.47.7.871
Faden H, Modlin JF, Thoms ML, et al. J Infect Dis. 1990 Dec 1;162(6):1291–7. https://doi.org/10.1093/infdis/162.6.1291
Miller LW, Older JJ, Drake J, et al. Am J Dis Child. 1972 Mar;123(3):197–9. https://doi.org/10.1001/archpedi.1972.02110090067004
Seward JF, Zhang JX, Maupin TJ, et al. JAMA. 2004 Aug 11;292(6):704–8. https://doi.org/10.1001/jama.292.6.704

Suggested reading

https://www.who.int/health-topics/vaccines-and-immunization
https://www.ncbi.nlm.nih.gov/books/NBK27131/


Is genetic drift necessarily deleterious? I read that genetic drift is random variation in the relative allele frequencies of a population.

This question however seems to pin genetic drift down to increasing deleterious allele frequencies. Is the answer to this question correct? I don't think that increase of a deleterious allele necessarily indicates that genetic drift is operating; it suggests genetic drift, because one would think that such alleles should decrease in frequency rather than increase, but random chance in a large population can also increase the frequency of deleterious alleles.

Drift is a random element of evolution from one generation to the next, it is equally likely to spread a deleterious mutation as a beneficial one.

The reason the answer is D is because selection should remove a deleterious allele, while drift makes no distinction, and is therefore the only scenario where drift is expected to be a reasonable answer. However, it is possible for drift to contribute to all of those scenarios.


How complete is the information in DNA? Everyone talks about how DNA is the "molecule of life" and "the set of instructions for building you." How complete are the instructions, really, though? To make the question concrete, say I were to remove all of the DNA from a bacterium and replace it with the nuclear DNA from a eukaryote, would the cell (and it's daughters) be able to transition into the same sort of eukaryote as the DNA source? Granted, the lack of mitochondria would be a huge hindrance, but assume we could add some when the bacteria swelled up to a large enough size to accomodate them inside of it. Are there other barriers to this process?

I know that adding any single gene for producing a protein would function as expected when added to a bacterium, but would the lack of a nucleus and organelles prove fatal, or does the nuclear DNA have the information needed to build them up using only the machinery available in a bacterium?

What about an archaea? Or going the other direction - remove the nucleus from a eukaryote, add bacterial DNA, does the cell and its daughters survive to become bacteria?

This is a good question, because the answer to the overall question (is the information in DNA complete - yes) is not the same as the one to the more specific ones (would a cell survive if the DNA was swapped with that of another life form - no). Let me elaborate:

The information in the DNA of in any given organisms (except for a virus) IS complete. This means that the DNA has 'code' for all the molecules required to build and sustain this organism.

However, the DNA of an organism alone (or placed inside an unnatural environment like a completely different cell) is not sufficient to actually make or build that organism. The reason for this is that, while the DNA has all the necessary code, without the correct machinery to actually read that code nothing can or will happen. Eukaryotes and bacteria are so vastly different (which is to be expected after millions of years of evolution for both), basically all the different machineries are not compatible anymore: transcription binding sites are different, gene structure (exons/introns vs. operons) is different, Ribosomes are different, ... [btw this also means that just putting the gene of an eukaryote into a bacterium doesn't work, researchers have to modify it accordingly to work].
Even between different eukaryotes (and probably some bacteria but I'm not sure about that) exchanging the nuclear DNA would not produce viable cells (or at least not ones that could grow into an organism), since again the transcription machinery would not match up sufficiently.


Can this image be the result of a Western Blot? I am currently researching image manipulation in the life sciences and stumbled upon a Western Blot looking very similar to the image below.

For creating the image I have cut out the blot using the Fuzzy Select Tool of GIMP and then greatly adjusted the local contrast of the blot as well as the background. By using the Fuzzy Select Tool some pixels of the original background are also captured. That is why the blot shown has a brighter background around the edges. I normally would not expect to see bright edges around a blot.

While I know how Western Blots look when they are captured with a digital camera, I do not know about techniques like Chemiluminescent Blotting (I am an undergraduate student in Computer Science). Maybe there is a blotting technique that results in an image like the one i created.

Is it possible to get a Western Blot result like this without inappropriate modification of the image?

I do not think that a publication quality blot should have such an artifact, but I was able to find something similar by purposely over blotting (not the same as over exposing) a gel.  If you use too much primary, secondary, or developing reagent, you can get your HRP signal to "burn in" a membrane where you get a distinct "negative band."

By negative band I mean a region that is more clear/white than background. This happens mostly when you have way too much secondary antibody.  Normally when this happens, the CENTER of the band burns in first so you would see a white center with dark edges.  And that's only when you are imaging the membrane as it is burning in.  Often the whole band is white.

After going through the westerns of grad-student who is working with me, I found this image:

It came with the clear notation that it was burned in and disregarded (said student was learning how to do Westerns at the time).  It's a GAPDH blot for those that care.  When this does happen, it's obvious because you can then see the band with your naked eye on the membrane.  Again this would be a reason to not publish the blot.

The image could have non-maliciously been edit via compression, screens, filters, etc as mentioned by others in the comments.  This is the only way I can think of to experimentally have a similar image.  Ether way I don't think the image should be reported as is.