How can the melting temperature of PCR primers be so far below the extension temperature? Since our primer TM is lower than the extension temperature by design, (and often by a significant amount) shouldn't the primers be released from the template at extension temperatures?

Now, I have done PCR experiments and know they work. I just want to justify what's actually going on molecularly to be at peace. The only thing I can think of is that as the temperature ramps up to the extension temp, the polymerase has already begun adding nucleotides, thus raising the effective TM, preventing dissociation.

Note that 'melting temperature' is actually about POPULATIONS--it's generally the temperature at which 1/2 of all of the millions of copies of 2 things will be stuck together and 1/2 apart. Once stuck, not all primers will leap off the template simultaneously even at much higher temperature... As you indicate, there's nothing to stop the polymerase from starting its work (extending the primer) before the extension temperature.

And, as in another answer, polymerase can add stability to the pairing.


What are the advantages of using interphase cells rather than metaphase cells for gene mapping purposes using FISH? I have been told that interphase cells are better for gene mapping purposes than metaphase cells but don't know why.

In metaphase, chromosomes are at their highest level of condensation. FISH relies on being able to dissociate the two strands of DNA to anneal a sequence-specific probe. So, my guess is that it is technically easier to achieve a good FISH staining in interphase, when chromosomes are much less densely condensed. There might be other reasons I am not aware of (I am not a geneticist).


Brood Parasitism - Parasitism/Ammensalism/Commensalism? Parasitism has the parasite benefitting while the host is harmed. In brood parasitism, the cuckoo lays its eggs in a crow's nest for incubation. How does this harm the host? Why is it not considered ammensalism?
If I see the fact, while laying its eggs, the cuckoo might break some of the crow's eggs, and in this way the crow gets harmed. Parasitism from here fits.
But, as the chicks grow, the cuckoo chicks protect the crow chicks from other birds or predators. Seeing this, yet commensalism fits.
So, if I have to finalise which species interaction brood parasitism comes under, what should I select?
And why is that interaction preferred over the other?

The cuckoo chick hatches earlier and instinctively pushes the host eggs out of the nest. If you view this from the genetic perspective of the crow, it becomes the foster parent of offspring that does not carry its genes. The harm, therefore, is to the host's passing on of genes, rather than to the immediate health or well-being of the individual.

For more information see:

Brood parasite (Wikipedia)
The Ecology of Avian Brood Parasitism (Nature)


Exactly what biochemical factors control the intensity of an allergic reaction? I think have a functional understanding of how an allergic reaction (Type I Hyper Sensitivity) occurs: basically the allergen causes production of antibodies that attach to mast cells and basophils. Later, if the same allergen binds to those antibodies, the cells release histamine and other unpleasant chemicals.

However, it's clear that the degree of allergic reaction varies a lot from person to person. For example, if my wife goes outside all day during peek grass pollen season, she'll end up with a sinus reaction, and not much else. If I go outside for a few minutes, I'll develop that, and if I stay longer, I'll get hives, weepy eyes, and so on.

Clearly I'm more sensitive to grass than my wife, but what exactly causes this? I can imagine a lot of possible factors!

Maybe I have many more antibodies (but why?)
Maybe I absorb more of the allergen per unit time (but why?)
Maybe my mast cells require less allergen to react (but why?)
Maybe my mast cells contain more histamine per cell (but why?)
...

So I guess my question is: What drives the variation in allergic hyper sensitivity responses?

Network of possible factors that contribute to the variability of the immune reaction between individuals is still not well investigated.

Type I hypersensitivity is mediated by IgE antibodies, which means that lymphocytes B after initial contact with antigen undergo oligoclonal selection. Only these with the highest affinity towards the antigen will survive. During this process (see: germinal centre reaction) genomic regions responsible for antigen binding change their sequence in non-deterministic manner. So, each individual has slightly different set of antibodies targeting the same antigen.

Moreover, within the same antigen (allergen), different regions (epitopes) can trigger the immune reaction in different individuals.

Other, more general factors also contribute to the symptoms associated with hypersensitivity reaction. For example: hormones, infections, medications, microflora condition, genetics (eg. major histocompatibility complex) or even psychological status.

Also see:
Article 1
Article 2
Article 3


Structure of biological membranes? Integral membrane proteins have functional asymmetry i.e. they have two different domains of proteins performing different functions. these proteins have Tyr and Trp amino acid residues at the interface between the lipid and water.Because these amino acids have dual nature that their side chains can interact with both extracellular aqueous environment as well as hydrophobic lipid phase and another generalization about amino acid location relative to bilayer is described by "positive inside rule": The positively charged Lys,His, and Arg residues of membrane proteins occur more commonly on the cytoplasmic phase of membranes.My question is that why only positively charged amino acids are faced towards cytoplasm why not negatively charged amino acids or other amino acids are favoured here?

Some thoughts on this. First of all, the positive-inside rule, proposed by Gunnar von Heijne, is an empirical rule based upon observations, not one derived from theoretical considerations, so any explanation is simply an attempt at a rationalisation.

Having said that, here are three of those rationalisations:

the membrane potential is usually negative inside. This will create an electrostatic tendency for basic amino acid side chains to stay inside.
most phospholipid head groups are either neutral or anionic (phosphatidylserine, when the phosphate is included). Again an electrostatic force favouring basic residues inside since to move them out would require overcoming their interaction with the negatively-charged membrane surface
the pK values of the basic side chains (lysine and arginine) are much further from 7 than are those of the acidic side chains, so,  since charged residues must be neutralised to get them through the bilayer, it is more energetically unfavourable to deprotonate basic side chains than it is to protonate acidic ones.


What to do if microarray t-test, ANOVA, SAM and LImma show various selected significant genes? Need advice: how to approach discrepancy in differential microarray gene expression test results: what to do if ANOVA, ttest, SAM and Limma procedures show different results and especially more discrepant when using log transformations and normalization operations?

I wouldn't expect different methods to give the same results. Further, why are you even testing non-normalized datasets, the results of that are completely and utterly useless for any purpose other than showing that normalization is important. In addition, an T-test is a special case of an ANOVA (and of course limma is itself using a moderated T-test, though it's going to have significantly more power than the others), so I have to ask myself exactly what sort of design you're using that it's appropriate to substitute one for the other and still get apparently vastly different results.

In general, I would strongly encourage you to work with a local bioinformatician or statistician for what is presumably your first microarray analysis, particularly if you don't have a strong statistics background.


What is this hopping insect? What species is this jumping insect?

Found in the United Kingdom in summer.

About 1 cm body length + 1 cm feelers.

It looks to be a bush cricket of the Leptophyes genus.  Possibly Leptophyes punctatissima, also known as the speckled bush cricket - not sure if the one in your image is speckled or not.  It is endemic to Europe and can be found in the UK.

Photo source: Wikimedia commons - Leptophyes_punctatissima


Which frequency of UV light damages DNA? I have read that UV light can damage pure DNA (DNA that has been extracted and purified). Is there a particular frequency threshold where this damage occurs or is it more of a gradient where the high frequency, the more damage. I want to understand how much damage light can do at what frequencies.

Not only pure DNA, UV radiations are one of the main causes of skin cancer because they damage cellular DNA in skin cells. Talking about frequency range, two different types of UV radiations damage DNA in two different ways:

UV-A radiation damages DNA in indirect ways. UV-A radiation easily generates free radicals, such as hydroxyl and oxygen radicals, which in trun cause the main damage1. The damage caused by such radicals is mostly single-stranded breaks in DNA. In fact, it has only recently been established that UV-A radiations do damage DNA, while these were originally considered as not (or less) harmful2. UV-A also has immunosuppressize effects on the entire body and is also mutagenic for keratinocytes in skin.

Wavelength range: 315 - 400 nm

Effect: source
UV-B radiation is in fact what causes most damages and deadliest damages to DNA. UV-B radiation directly attacks DNA, it excites atoms of adjacent thymine molecules, which in turn form covalent bonds with each other and lead to formation of thymine dimers. These dimers, because of being bonded side-by-side instead of being bonded to opposite strand base, form a bulge which interrupts structure and function of DNA. Such dimers are removed by a process known as nucleotide excision repair, which involved about 30 diffeeent proteins3, meaning UV-B is more harmful for the body than UV-A. UV-B also causes double-stranded breaks in DNA, which are a major problem for DNA replication and a threat for cell's survival.

Wavelength range: 280 - 315 nm

Effect: source
Other effects of UV radiation on the body include damage to collagen fibers and vitamin-A in the body and accelerated ageing effects 4. Apart from this, UV radiations, because of harmful effects on DNA, are used for sterilization as they destroy microbes' DNA and thus prevent them from replication.

Wavelength range: 10 - 400 nm (complete UV spectrum)

References:

Svobodová AR, Galandáková A, Sianská J, et al. (January 2012). "DNA damage after acute exposure of mice skin to physiological doses of UVB and UVA light"
Halliday GM, Byrne SN, Damian DL (December 2011). "Ultraviolet A radiation: its role in immunosuppression and carcinogenesis"
Bernstein C, Bernstein H, Payne CM, Garewal H (June 2002). "DNA repair/pro-apoptotic dual-role proteins in five major DNA repair pathways: fail-safe protection against carcinogenesis"
Torma, H; Berne, B; Vahlquist, A (1988). "UV irradiation and topical vitamin A modulate retinol esterification in hairless mouse epidermis"


How does it make thermodynamic sense for photosynthesizers to turn CO₂ into O₂? My understanding is that animal metabolism consists of exothermic reactions like

$$\ce{C6H12O6 + 6 O2  ->6 CO2 + 6 H2O + energy}$$

This makes thermodynamic sense to me. Animals need an exothermic reaction to produce the energy we need to move around, etc. However, the other half of the picture, plants and other photosynthesizers producing oxygen, has never made complete sense to me. Are plants consuming $\ce{CO2}$, a "low energy" (I think) substance, and producing higher energy $\ce{O2}$ as a waste product? Is there so much energy available for photosynthesis that plants can afford to waste some of it producing $\ce{O2}$ simply to have enough carbon atoms to store energy via sugars?

Oxygen in photosynthesis does not come from carbon dioxide. It comes from water and this is the step that actually requires light: Photolysis of water.
The proton produced in this process is used to synthesize ATP and NADPH by a chemiosmotic process similar to what happens in mitochondria.
These biochemical pathways are also referred to as Light reactions.

Carbon fixation (or Calvin-Benson Cycle) requires energy (in the from of NADPH) and is therefore dependent on light reactions. The light has no direct role in carbon fixation. Oxygen production also, is not directly coupled to carbon dioxide consumption.


Analogous organs: coevolution or opportunism? The question reads as: "The lens of many vertebrate eyes is a crystallized form of a protein that also functions in digestion as a metabolic enzyme. This shows that

A. Vision and digestion co-evolved

B. Digestion necessarily evolved prior to vision since it is a more basic function

C. Evolution is opportunistic

D. Vision and digestion evolved around the same time"

My approach: Based on the given information it appears the protein might have given rise to analogous organs. I don't feel B has to be true in all cases. C is a good candidate but its meaning isn't clear. I'm not sure about D. To me the answer appears to be A but I would be happy to be have this confirmed.

I think the question you have to answer is a bit badly phrased. Overall, I mainly agree with you, except for point A. Here are my comments for each points:
A
co-evolution is defined for the evolutionary dynamic between two lineages. It is typically not used to talk about two body parts. Consider for example the definition from Understanding evolution:

The term coevolution is used to describe cases where two (or more) species reciprocally affect each other's evolution.

, wikipedia

In biology, coevolution occurs when two or more species reciprocally ("co-") affect each other's evolution.

or dictionnary.com

evolution involving a series of reciprocal changes in two or more noninterbreeding populations that have a close ecological relationship and act as agents of natural selection for each other, as the succession of adaptations of a predator for pursuing and of its prey for fleeing or evading.

I would note that the term coevolution can sometimes be used in its border line case as in this paper for example. It is particularly confusing as the term co-adaptation is sometimes used to talk about the interaction of two phenotypic traits. But stil, I would NOT check A
B
I agree with you! The conclusion is not valid from the premise (which means that it is not necessarily true, so even if the conclusion may be true, it cannot be concluded from the premise)
C
I agree with you! The statement is a bit unclear.
Typically, evolution is opportunistic would mean that throughout evolution history, a lineage may well evolve to reuse an existing gene for another purpose (neofunctionalization for example) which is very likely what happened here.
D
I agree with you! The conclusion is not valid from the premise.
In short
I would check C.


What is the meaning of "within-season variation"? I am reading a paper about phenology and climate change for my assignment and I found this concept "within-season variation", can someone explain it to me? and how it is related to changes over time?

"Within-season variation" may be referring to one of two things (depending on the context):

More commonly: the variation of a variable within a given season (i.e., between months or days within that season).

Öst (1999) demonstrates an example of this use (in the context of breeding season).

Less commonly: the variation of a variable between the same season of different (often consecutive) years. Though this would more often be termed "between years". This is as opposed to "between seasons" which would be be between two different seasons of the same year.


Measuring the density of surface antigens I'm trying to get a sense of the variety of methods used for determining the number of cell surface antigens and receptors. This is notably different from determining the affinity of these surface markers.

Do you mean to count numbers of both antigens and receptors in live cell?

Possible ways:

FRET (unlikely to work)
imaging of receptors with single molecule resolution
western blot to roughly estimate amount of receptors
single cell proteomics techniques (not very suitable)


Mangroves and desalination of sea water I am not an expert but I guess that mangroves (or some other plants that thrive in sea water) perform some kind of desalination to extract fresh water from sea water.

Is this true? If yes, What biological mechanisms are used to remove salt from sea water?

I am interested in any research about biological desalination.

There has been a lot of research in this field which asserts that mangroves desalinate sea water.
Scholander (1968) concludes that this process in mangroves use an ultrafiltration mechanism in the roots of the plant where membranes extract freshwater which is taken up the plant.

 Scholander, P.F., 1968. How mangroves desalinate seawater. Physiologia plantarum, 21(1), pp.251-261.


Why is there now only one Salmonella species? Once upon a time, I chanced upon an old microbiology book that detailed the rather colorful world of enterobacteria. Salmonella in particular stood out, as it seemed there were a lot of species: typhi / typhosa, paratyphi, gallinarum, typhimurium, choleraesuis, and quite a bunch of others that I have now forgotten.

Flipping through a newer book, it now seems that all of these "species" were collated under choleraesuis (and now more recently enterica), with all those species being demoted to "strains" (or maybe I should use the current term of art, "serovar"). Unfortunately, the book didn't give much in the way of explaining about this merger.

So, why is there now only S. enterica? If "S. typhi" is a mere serovar, how come the species name is still used in the literature?

Simply put, old habits die hard; physicians and other medical personnel have grown up with the old species designations so will continue to use them.  This is somewhat the reverse of the case with E. coli, where 80-90% of the genome is variable across strains.

Lin-Hui gives a brief history, where strains identified early were given specific names within Salmonella like typhi, typhimurium, panama, etc.  In 1966 it was proposed to lump serovars together among three species S.
choleraesuis, S. typhosa, and S. kauffmannii.  Shortly thereafter in 1972 with the advent of DNA techniques, it was shown they really should be all piled together.  There is one exception, Salmonella choleraesuis subsp. bongori, separated in 1989.


Hoechst or DAPI for nuclear staining? When is it best to use Hoechst vs. DAPI for nuclear staining? They seem to be very similar on paper. Are there situations where one is clearly preferable?

The Hoechst 33342 dye is similar to DAPI in that both are UV-excited, minor groove-binding, and emit signals proportional to total DNA content. Both are maximally excited around 355 nm and emit around 460 nm.  A UV light source is required, which may harm the cell. However, this is only a risk with Hoechst, as DAPI requires the cells to be fixed and/or permeabilized, which is incompatible with life. DAPI is more stable, but Hoechst is brighter. Both are subject to photo-bleaching after long exposure.

There is another newer DNA dye called DRAQ5 that makes up for all of the issues I mentioned earlier - it is bright, quite photo-stable, can be used in live cell imaging, and its excitation and emission wavelengths are in the far red end of the spectrum, meaning that no UV is needed. I found a good comparison chart at http://www.biostatus.com/product/draq5/live_cell_comparison_chart/ if you're interested. I have no connection to them, by the way, I've just used DRAQ5 a lot in the past.


Can dolphins actually communicate linguistically? Humans use "language." By language, I mean the thing I am using right now to talk to you.

I know dolphins and orcas have very complex communication systems and also seem to process linguistic and gestural commands.

But do they have their own languages? Where is the evidence for or against? If we take two group of dolphins Group A and Group B, would Group A speak one language and Group B speak another?

Dolphins and orcas do have dialects. Of course there are species specific dialects and it has been shown that orcas reared with bottlenose dolphins tend to learn the latter's dialect. Dolphins of the same species also seem to have regional dialects, as mentioned in this BBC post (I personally do not trust in non-research articles much, but nonetheless in this case the article indicates a certain possibility of a phenomenon). However, this page also reports the same finding and this source seems to be much more reliable. There are citations too that are at present inaccessible to me. Both the sources say that bottlenose dolphins from Shannon estuary in Ireland, "speak" different dialect compared to those from Cardigan Bay in Wales.

The actual research work is this:

  Hickey, R. (2005) Comparison of whistle repertoire and characteristics between Cardigan Bay and the Shannon estuary
  populations of Bottlenose dolphins (Tursiops truncatus) with
  implications for passive and active survey techniques. School of
  Biological Sciences, University of Wales, Bangor

Apart from having regional dialects, the cetacean communication also seems to have other features of a "language". I am pasting excerpts from this article which basically reports a study on the acoustic communication or codas in sperm whales. This may apply to dolphins as well.

  Individuals within social units have preferred associates among
  members (Gero et al. 2008), indicating differences in the way an
  individual interacts with other members of its unit. These preferred
  associations among unit members suggest the possibility of an
  individual discrimination system.

  .... most adult animals within a social unit shared the most common coda
  types, with the exception of the mother-calf pair whose repertoires
  were different from those of other unit members and each other. Apart
  from the mother-calf differences, the repertoire similarities of other
  members did not support the hypothesis of individually distinctive
  coda type repertoires. This sharing of coda repertoires suggests that
  they allow group membership recognition, at either the unit or clan
  levels. This hypothesis is further supported by the fact that social
  units seem to form groups preferentially with other units of their own
  clan (Rendell & Whitehead 2003b).


Growth Hormone and diabetes Growth hormone and insulin like growth factors are diabetogenic, so I assume that people with high growth hormone (say due to pituitary tumor) may be at high risk for diabetes.  Has any correlation been established between these two? I know that diabetes is a multifactorial disorder and so only a correlation may be established.

Yes:

  That GH has an effect on glycaemic control is most evident from the abnormal glucose tolerance seen in acromegalics...

acromegaly is defined as abnormal growth of the hands, feet, and face, caused by overproduction of growth hormone by the pituitary gland.

Such an effect has been known for decades, which makes sense given how interrelated the axes are.  Although I think the best evidence is the fact that the side effects of growth hormone therapy says that Some patients have developed diabetes mellitus...


Bug identification - Beetle, grasshopper, moth-like and it also flies Could anyone please help me identify this creature? It can fly and seems to like crawling as well. It has mandibles that are beetle-like.  Approximately 3cm/2inch. Location: KwaZulu Natal, South Africa

That is a mole cricket, Order Orthoptera, family Gryllotalpidae
https://en.wikipedia.org/wiki/Mole_cricket


About the apoptosis mechanisms in a cell The apoptosis mechanisms in a cell are like a type of 'self-destruction mechanism': is this correct?

As with any type of complex system with various necessary functions, if it has a set of self-destruction mechanisms for 'shutting down' the whole system, it would require some sort of 'internal programming' that can somehow 'target' each of the system's necessary functions and 'disrupt' each of them simultaneously or in some 'order'.

In other words a self-destruction system in order to be effective would have to be able to 'target' each necessary function in the system. And if a biological system has a mutation or a set of mutations that 'distort' some parts of the system then the self-destruct mechanisms might not be able to 'target' all of the functions.

So maybe the cellular mutation 'automatically' makes it hard or impossible for the self-destruct mechanisms to work. Is this possible??

Not at all. In order to self destruct, you don't need to disable all necessary functions, you just need to disable one. That's why the functions are called "essential". To take a very simple example, in every movie you've seen where the self destruct has been activated, that self destruct mechanism was almost certainly a bomb that blew the ship/installation/planet or whatever up. The self destruct did not go around disabling individual processes, it just activated a bomb and destroyed everything.

Apoptosis is quite similar. While there are many essential processes in a cell whose failure can activate apoptosis, the mechanism of apoptosis itself usually involves the straightforward destruction (lysis) of the cell. Simply put, the cell digests itself, breaking down its various constituent parts and, finally, destroying the cell membrane and breaking up the cell itself. For a summary see this Wikipedia page or here.

Briefly, when apoptosis is triggered, the caspase cascade is initialized which results in the breakdown of various proteins in the cell and, finally, in cell lysis. It really is analogous to setting of the bomb that destroys the facility of the bad guys.


Why doesn't oligodendrocyte produce neurilemma I was searching literature related to neurilemma and oligodendrocyte and came across these lines from WP (Neurilemma)

  Oligodendrocytes do not have neurilemma because excess cytoplasm is directed centrally toward the oligodendrocyte cell body.

I tried tracing more scholarly articles in this  context but I wasn't satisfied.

So my question is: Why doesn't oligodendrocyte produce neurilemma. Any  reference articles would also help.

This statement is made in contrasting oligodendrocytes with Schwann cells. Both of these cell types are glial cells involved in myelination of neurons, but their morphology (shape) is different.

Oligodendrocytes in the CNS "reach out" with extended processes that then envelope axons as a myelin sheath. You could imagine an octopus reaching out arms that then loop around a stick. Like an octopus, they have multiple arms, and each arm can cover a different axon. The nucleus and other cellular machinery is located in the 'head' of the octopus.

Schwann cells in the PNS instead wrap around a single axon. You can think of them more like a fried egg, wrapped around a stick. The egg white is the myelination, the yolk is the nucleus. The outermost wrap is where all the other machinery of the cell is, and this area is called the neurilemma.

The actual presence/absence of the neurilemma isn't that important for the function of myelination, it's just a different shape of the cells.


How does one experimentally obtain a hemoglobin-oxygen dissociation curve? I've always wanted to do comparative eco-physiology studies looking at Hemoglobin-Oxygen affinity of populations in different environments, but I can't find a protocol to experimentally measure the relationship. Does anyone know where I can find a protocol, or know a protocol themselves?

I'm assuming an answer would include what the necessary instrumentation would be, what condition the blood needs to be in (fresh?), if the heme is isolated (and if so, how), and what an appropriate sampling scheme would look like.

There are existing instruments commercially available to measure hemoglobin-oxygen saturation curves. Whole blood or lysed blood can be used; I would expect the instrumentation to come with specific directions for sample preparation because it may depend on the exact equipment.

These devices use a spectrophotometer to measure saturation, taking advantage of the same color difference between arterial and venous blood that is visible to the human eye.

To collect a curve, you start with the sample saturated in room air or oxygen, and the instrument gradually introduces nitrogen to replace the oxygen, while also monitoring oxygen concentrations using a Clarke electrode.

Here is an example paper that uses one of these devices. Their precise methods may or may not be appropriate to your research approach.

References

Head, C. A., Brugnara, C., Martinez-Ruiz, R., Kacmarek, R. M., Bridges, K. R., Kuter, D., ... & Zapol, W. M. (1997). Low concentrations of nitric oxide increase oxygen affinity of sickle erythrocytes in vitro and in vivo. Journal of Clinical Investigation, 100(5), 1193.


Is it possible to express the cistrons from a polycistronic insertion fragment in a single plasmid? I have a insertion fragment that I wish to express from pUC19 in Escherichia coli. The insertion fragment is a sub-section from a larger operon sequence and contains just the last two cistrons from this operon.

I plan to insert this fragment into pUC19 under the control of its single lac promoter. Therefore, there will be two cistrons under the control of a single promoter (which is of course, very similar to how it would be expressed in the WT operon).

In my mind, expressing both the cistrons under the control of the single pUC19 lac promoter should allow both genes to be translated; once the mRNA is transcribed, both cistrons have their respective Ribosome Binding Sites upstream of their ORFs, and should be translated.

My question is, has anyone ever had experience expressing poly-cistronic fragments from plasmids using just a single promoter for the entire fragment? I cannot see any glaring issues with this in theory, but I thought i'd ask before I went ahead. Ultimately, I'd rather express both cistrons from a single plasmid, rather than express each cistron on a separate plasmid.

Cheers!
Izaak

If I understand correctly, you are seeking option for polycistronic expression. Have you considered using T2A or P2A sequences? These come from virus and essentially break polypeptide into two parts, so-called self-cleaving peptide T2A. Real mechanism of its work is that ribosome stalls on the sequence and unable to create peptide bond, effectively re-starting translation with next after T2A amino acid.

Of course, you lose independent control over expression, both products will be expressed at same level (but degradation might be different).

So, you should consider creating construct that looks something like that:

lac:gene1-T2A-gene2-stop

Thing is that a) it might not work in E.coli and b) it might not be necessary, because primary purpose of T2A is equal expression level of two polypeptides. And, if your 2 genes are big, for bacteria it is easier to handle two separate plasmids, rather than one but much larger.


Are bacterial RNA polymerases distributed evenly throughout the cell or localized? Bacterial cells aren't internally compartmentalized with membranes (like eukaryotes). This naturally leads to an image of a homogeneous interior, but bacterial cytoplasm isn't homogeneous. Case in point, the DNA is localized in the nucleoid. If the cell goes through the trouble of putting all its DNA in one spot, having RNA polymerases everywhere would be pretty wasteful (even counterproductive). So, is the more intuitive image of bacteria, with RNAPols everywhere, right? Or are they localized? If so, how?

If species matters, lets primarily talk E. coli.

In E. coli most RNA polymerase molecules are bound to DNA, and those that aren't are within easy reach of the DNA.

According to Larry Moran

  A typical E. coli cell contains about 5000 molecules of RNA polymerase. When the cells are growing rapidly, 2500 molecules will be bound to genes in transcription complexes. Another 1250 will be in initiation complexes of various sorts and most of the remaining RNA polymerase molecules (1200) will be bound to DNA non-specifically. Only a small number (~50) will be free in the cytoplasm.

The numbers that he quotes for number of molecules of polymerase and proportion that are engaged in transcription are in reasonable agreement with values available at Bionumbers. So it seems that most RNA polymerase molecules will be located in the nucleoid; any molecules that are free in the cytoplasm are within easy reach of finding a DNA binding site since a typical protein can diffuse across an entire E. coli cell in 10 ms. (Bionumbers)


Why do oranges in the US have a small separate part? Why do oranges in the US have a small separate detachable part at the tip which is separate from the other pods? It looks like a tiny orange itself and has a long fiber attached to it.

This is specific to navel oranges, which have a conjoined twin fruit.

This blog gives an account of this.


Are there any multi-cellular organisms out there that do not sleep? Looking around I see animals - ants, bees, birds, lizards, roaches all the way up to humans appear during a part of the day and not other parts. I would guess there is a sleep/recovery cycle involved.

Is there any multi-cellular organism with a nervous system, on record, that works without sleep/rest?

Well, you may want to re-state your question. There are numerous multi-cellular organisms without a nervous system. So you could say that they never sleep: sponges, plants, mushrooms.

This paper on the evolution of sleep concludes:

  A phylogenetic evaluation of sleep demonstrates that all
  mammals, birds, and reptiles engage in sleep, and evidence
  for sleep in amphibians, ﬁshes, and invertebrates is strong if
  not certain.

So it seems that once you have a nervous system, you also have some rest periods. However, it may not be clear if the rest periods are dictated by the lifestyle (e.g. nocturnal foraging) or by a requirement to "recharge" the nervous system.


If a bacterium had a protein on its surface that humans also have, would it cause an autoimmune disease? Suppose that a bacterium happened to have a protein on its surface. This protein can also be found in the human body. If this bacterium were to then infect a human with an otherwise normal immune system, would his/her immune system attack the person's body, in addition to the bacterium?

The reason I'm asking this is because I have read a book about how, supposedly, the Soviet Union created a bacterium that did just that: they modified Yersinia Pestis to produce myelin which, supposedly, caused multiple sclerosis. The book's author claims that this really happened, but I am skeptical of that claim.

It's believed that many autoimmune cases are triggered by what you describe - pathogens or opportunist bacteria and viruses that contain proteins similar to human proteins.For example:

Autoimmunity to hypocretin and molecular mimicry to flu in type 1 narcolepsy
Translocation of a gut pathobiont drives autoimmunity in mice and humans
Autoantigen cross-reactive environmental antigen can trigger multiple sclerosis-like disease

However, it's important to understand that although these cross-reacting proteins may be required in the process of autoimmunity, they aren't sufficient to cause autoimmunity alone (or else everyone would have autoimmunity all the time). Autoimmunity needs to have a whole bunch of steps, including several pieces of genetic susceptibility and environmental conditions, before the specific trigger will cause a problem (and it's likely that once the many other conditions are satisfied, there are multiple potential triggers that can set up the final cascade).


What does chromosome CHR_Un, CHR_MT in the ftp site of NCBI mean? I am not a biologist. But need some genetic data. So I searched internet and reached NCBI's website. I came to know from the FAQ page that I can the complete genome data of organisms from ftp://ftp.ncbi.nih.gov/genomes/. So I went to the FTP site and opened the homosapien section ftp://ftp.ncbi.nih.gov/genomes/H_sapiens/. I found folders CHR_1 to CHR_22, CHR_MT,CHR_Un, CHR_X and CHR_Y.

My doubt is this : Normally there are only 23 pair chromosomes right? 1 to 22 pairs OK. XY make another pair. Then what are MT and Un ?

And the folder which I am looking is a genome of male right?

chr_MT: List of variations that map to the mitochondria

chr_Multi.txt.gz: List of variations that map to multiple chromosomes

chr_UN: List of mapped variations that are on unplaced chromosomes

see here for more information.

This is the reference genome for human, as far as I know there is no discrimination for it into male/female.


Why don't moles repair their DNA? Cells have mechanism to repair damaged DNA. So why don't the cells in moles (the spots), repair themselves and the moles dissappear?

DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome. However it is yet to be linked closely to mammalian moles.
Information here, states:

"Moles are overgrowths of skin cells called melanocytes, but the genetic factors involved in their development are not well understood."

The BRAF gene is one of the most well-studied genes involved with benign moles, if a mutation arises in this gene - there may be a production of an altered protein that causes melanocytes (melanin-producing cells located in the bottom layer of the skin's epidermis) to aggregate into moles.
I cannot answer why DNA repair does not occur. Maybe the cell cannot identify the mutation, maybe the cell cannot corrects the damage, or maybe it is also from environmental factors. This is an active area of research, but receives far less attention compared to cancer or heart disease.


Why is the inside of a cell negatively charged So my teacher asked: "$[K^+]_i$ (k+ on the inside) is about forty times higher than $[K^+]_o$ (k- on the outside). With so many more positively charged potassium ions inside versus outside, why isn’t the interior of the cell positively charged compared to the exterior?"

My Thoughts: I am assuming that there must be enough negative charges inside the cell from other things like chlorine or ATP and proteins that the net coulombs on the inside is lower than the net coulombs on the outside. Does this seem like the correct answer? I am hesitant to use this because so far my teacher has only talked about potentials and not charges. I completely understand that the potential is negative, but potential and charge are two different things.

Edit: posted exact question from teacher as opposed to original summary of question

Net Potential on a cell surface is always measured in comparison to the extracellular media...so it is a relative parameter. So inside of the cell membrane is negative implies that there is more negative charges inside or more positive changes outside compared to the respective opposite side of the membrane. As we do not deal with the "absolute potential" we need not calculate the values of them.

K+ concentration is more inside the cell compared to outside...but there are other ions in and outside cells...e.g. Na+, Ca+,  proteins, Cl- etc...all of them together determine the potential difference across cell membrane.


Puffball mushroom species ID? Found this mushroom today. It's a kind of puffball mushroom and I think pestle puffball but I hope someone can confirm that/point me to other likely species.

It was in Central Eastern Sweden (Uppsala) in a pine and birch forest. Autumn has been quite dry so the season may be a bit delayed. They were in bunches of 2-5 mushrooms, they are about 1-4cm across the ball and the stem is quite fat plus about 1-3cm long. They are white through the middle.

Given what you've said in the comments, and how much more common they are, I'm going with my first gut reaction of Lycoperdon perlatum.  The big give away for me was that you said there was a good taste.  L. Perlatum has a rich nutty flavor (my wife grows them), but Handkea excipuliformis (pestle puffballs) don't have much taste if any.  They are seriously notably bland.  H. excipuliformis can take on the flavor of what ever you cook them with, so if you cooked in a nut oil or with nuts, then you would have given the flavor that way.

Not that I support taste as a primary means of id...  In this case most of the puffballs are edible so you were in a low risk situation.  I just don't want to start a wave of fungus ID's that include taste info!


Can an Ichthyologist identify this Canadian freshwater fish? This will be very simple for a lot of you! But I been getting mixed answers about his catch. Is this a chinook salmon or brown spotted trout? Caught in Angus, Ontario, Canada. (Hwy 90 Bridge)

I appreciate the help!

Judging from the curved caudal (tail) fin, which is more square in brown trout, this appears to be a chinook salmon. The mouth also appears to be black whereas in brown trout the mouth is white.

Sources: Michigan Department of Natural Resources


Do local field potentials (LFP) create waves on the surfaces of nerve cells? Are waves created by the LFP on the surfaces of neurons cell bodies? Since the cells have a resting potential, do these waves create harmonic oscillation of the membranes at particular frequencies?

Are there studies available that look at electrical potential waves on the cell surfaces? I think that membranes should be sensitive to the LFP since they maintain a charge.

A LFP can be measured at any point in space and is just the sum of all the fields generated by nearby charges.  Conventionally, it's assumed to be some distance from a cluster of neurons, but you technically could measure the LFP near the external surface of a neuron (but that would bias your signal towards the reading of that one neuron).

LFP's are relatively weak, but have some small influence on the neighboring cells:

Modeling the coupling of single neuron activity to local field potentials


Does the repellence of an insecticide affect its efficacy (measured in insect mortality)? I am currently working on assessing the efficacy of a suspected insecticide on a particular species of insect. I happen to be looking into any repellence caused by the substance. I test for both effects at the same time by putting that insect in a no-choice bioassay. To be specific, my assay set-up consists of a petri dish, and the test article treated with the test substance is placed on one side of the petri dish. Insect species X is introduced into the petri dish, and every 24 hours, I get to count and remove the dead ones. All these are repeated for different concentrations of the test substance.
What I found is that mortality (proportion of insect X killed) initially increases with concentration, but then decreases after a particular concentration. I also found that repellence increases with the concentration of the test substance. So, what exactly is happening here? Is the repellence of the test substance having an effect on the mortality, such that repellence is causing a decrease in mortality?

You have a good hypothesis: the decrease in mortality is mediated by an increase in repellence. It sounds like you have a measurement of increased repellence, and it's a plausible mechanism (if an insect isn't near an insecticide, it can't be killed by that insecticide). Now you should test it.

If you are measuring repellence using a different assay (e.g., a choice assay, where the insect can enter a chamber with the insecticide vs. one without), than you could use as the denominator insects that enter the chamber with the insecticide. Compare mortality of insects that enter the chamber with insecticide changes with increasing concentrations in this assay with the mortality in your no choice assay.


How do you express and detect GLP-1 receptors? I am currently working with a peptide which is an analogue for glp-1, but during invitro studies am not able to detect for the presence of GLP1- receptors.
The cell line used is Min-6. How do I detect it?

The question is slightly unclear since it fails to clarify whether the GPL-1 receptor is endogenous or is over-expressed. Also does the GLP-1 belong the same species that Min-6 originates from or it belongs to a different species? Those are important points since if the receptor is endogenous then the main problem is sensitivity of the detection method, which can be difficult sometimes to detect an endogenous protein relative to an over-expressed one. Also if the GPL-1 belongs to a different species, which you are trying to over express in Min-6 it might not work since the cellular machinery might not support its production (tho unlikely) or its transport to the cell surface, which I have had this problem before. It could be that for the particular expression levels you have in those cells, if the GLP-1 is over expressed or if its non-endogenous, it causes toxicity and kills the cells that are expressing it hence why you do not see any GLP-1 expression (e.g due to excessive receptor activation). Also could you clarify what you mean by "analogue for glp-1"? does this mean it is not exactly GPL-1 or its a homologue or orthologue, which you are trying to detect using a GLP-1 specific antibody? that might again be a problem if the GLP-1 Ab you are using detects a region of the receptor, which is not conserved in its homologues.

In terms of solutions as pointed in the comments, the best way to go about this is to use a polyclonal Ab, which is raised against a large section of the peptide in question, allowing you a better chance of its detection. If that did not work, you might have to resort to GLP-1 mRNA detection using RT-PCR or qPCR, which you would need to design primers for based on you GPL-1 sequence which you can get help with here.


Do insects' muscles become stronger with exercise? I am curious to know if insect muscles become stronger with exercise, because I have seen many insects get tired out, but I have never seen one get stronger. They always seem to become permanently weakened from excessive exercise. Do they get stronger like people do?

There are instances of insect muscle growth in response to increased use. The flight muscles of the tsetse fly (Glossina morsitans) have been observed to grow at a faster rate when subjected to enforced exercise (Anderson and Finlayson, 1976). Also larger mandibular adductor muscles (which power the feeding apparatus), and associated head capsule have been noted for caterpillars and grasshoppers feeding on particularly hard grasses (Bernays, 1986). However these examples occur immediately post-eclosion (i.e. after emergence as adults), and during immature stages respectively. Insect muscle typically grows during larval/nymphal (immature) stages, and often for a brief period at the start of adulthood - known as the teneral period. During immature stages, insects typically have a flexible membrane to allow for tissue growth and expansion, this can also be the case during the teneral period, before the inflexible exoskeleton has fully hardened. However at full maturity, insect growth is limited by the rigidity of their exoskeleton.

As far as excessive exercise is concerned, that some insects may be weakened permanently may be more to do with the fact that their life strategy is different to ours. Due to the vast number of offspring per adult, and subsequent low survival chance of any given individual, there could be an evolutionary advantage for individuals pushing themselves to possibly deadly extremes. This could lead to many deaths, whilst retaining a viable population and thus accelerate the emergence of a population of fitter individuals.

References

Anderson, M. & Finlayson, L.H., 1976. The effect of exercise on the growth of mitochondria and myofibrils in the flight muscles of the tsetse fly, Glossina morsitans. Journal of Morphology, 150(2), pp.321-326.
Bernays, E.A., 1986. Diet-Induced Head Allometry among Foliage-Chewing Insects and its Importance for Graminivores. Science, 231(4737), pp.495-497.


What prevents platelets from clotting regular blood vessels? Platelets clump together to initiate clotting, but, why don't platelets clot within healthy tissue and cause heart attacks all the time?

Platelets activate when the exposed collagen (which is normally present below the endothelium) at the wound site binds to the platelets, forming a plug. Other factors are also secreted which aid in stronger binding. A signaling cascade is triggered which then makes platelets release proteins called integrins, which help for tighter binding of platelets at the site. Activated platelets also release many stored compounds from their granules which initiate further signaling cascades to form a clot.
In a healthy tissue, there is no exposed collagen. Ergo, No clotting.


What happens to Km when enzyme concentration is *very* high? Let Km be an empirical measurement of a certain enzyme with concentration [E]. Theoretically, this value is constant and shouldn't vary when [E] goes up or down. Now let [E']=10*Km. Under this concentration of enzyme, it's clear that if [S]=Km, V0 cannot be 1/2*Vmax (as there's only enough substrate to saturate 1/10-th of the enzyme molecules). What's happening here, and how does this relate to the derivation of the Michaelis-Menten equation?

Michaelis-Menten is often challenging for students because of the importance of the conditions that must exist in order for the model to hold. Walking through the derivation and the relevance of the assumptions can be helpful. Berg's Biochemistry is available via NCBI, and the section on Michaelis-Menten kinetics does a good job here, illustrating the following points:
Assumption 1:  The rates of all the relevant reactions are linear.
This assumption is what allows us to write down the equations the derivation starts with. We look at each separate reaction, and say that the rate of that reaction is equal to some rate constant times the concentration of each thing on the left side. From the equation $E + S \rightleftharpoons ES \rightarrow E + P$, we get the following

$E + S \rightarrow ES$

$Rate = k_1[E][S]$

$ES \rightarrow E + S$

$Rate = k_{-1}[ES]$

$ES \rightarrow E + P$

$Rate = k_2[ES]$

This assumption (the rate is linear) only matches the experimental evidence early on in the reaction, while most of the substrate is free $[S]$ (rather than bound up in $ES$).  Remember this. It will come into play when we evaluate assumption 3.
Assumption 2: The $ES \rightarrow E + P$ reaction is irreversible
In order for us to combine the above rate equations to derive the Michaelis-Menten equation, the only source of ES should be from $E + S \rightarrow ES$. We can't have any measurable $E + P \rightarrow ES$. Experimentally, for enzymes that follow Michaelis Menten kinetics, this is true when $[E]$ and $[P]$ are small relative to [ES]. So here we have our first requirement that $[E]$ be small. Biochemical reactions tend to not involve very high changes in free energy. The in situ free energy of ATP hydrolysis is the high end for a reaction in the cell, and that releases about $50kJ mol^{-1}$. We're not talking about combustion here. So in fact, these reactions are often reversible at appreciable levels of $[E]$ and $[P]$
Assumption 3: ES formation and breakdown is at steady state
This assumption is often described in a confusing way, i.e. the entire reaction ($E + S \rightarrow E + P$) is at steady state. Lets drill down to what we're actually talking about. In order to derive the MM equation. We need the rate of formation of $ES$ to equal the rate of breakdown of $ES$, that is, for $\frac{d[ES]}{dt} = 0$. That is steady state. Let's say that in words: the change in $[ES]$ needs to be zero. We only achieve steady state at an early point in the reaction (remember, we need most of the substrate to be free $[S]$ for assumption 1 to hold), if $[S]$ is substantially greater than $[E]$. $E$ needs to be saturated with $S$ while $S$ is still mostly in the free form. This is the key combination of assumptions that the situation you described violates.
Once we meet the three assumptions above, we can write down the following equality:
$k_1[E][S] = (k_{-1} + k_2)[ES]$
This equation says that the rate of formation of $ES$ (the rate from equation 1 at the top) is equal to the combined rate of the breakdown of $ES$, either into $E + S$ or $E + P$ (equations 2 and 3 at the top). Once we have this equality, we can derive the Michaelis-Menten equation: $V_o = V_{max} \frac{[S]}{[S] + K_m}$, where $K_m = \frac{k_{-1} + k_2}{k_1}$. Again, see Biochemistry to walk through this.


Why do we get scars? Feeling the hardened tissue of a scar on my head I wondered what the purpose of that scarring is, such skin scars are pretty harmless but from what I understand internal scarring can cause major problems if internal organs get damaged.

An extreme example I vaguely remember is the scarring following nerve damage, the new scar tissue can't transmit signals and so the nerve stops functioning properly.

Why does scarring occur when it seems so detrimental, why don't we rebuild the old tissue?

Scars are fibrous tissue that is left after an injury. The body does its best to fix a body part after an injury and scars are their best attempt at doing so. It would be pleasant to think we could have Wolverine type of healing capacities but we don't and the best we can do are those scars.

The ability to completely regenerate the damaged tissue depends upon the specific tissue. Also, some species are better of than others at regenerating their tissues. Such differences relate to the concept of cellular specialization.

For more information you should have a look at the wikipedia articles

Wikipedia > scars
Wikipedia > Regeneration
Wikipedia > cellular specialization

and the Biology.SE posts

Can a lizard shed a regrown tail again?
Can the regeneration mechanism of lizards be used in humans?


How does the flow of ions along voltage-gated channels lead to nerve conduction along axons? Let's say the axon lies along the x axis, and voltage-gated sodium channels lie parallel to the y axis. When a channel is opened, sodium ions will flow along the y direction into the cellular fluid. My question is, how does this flow of ions in the y direction cause a flow of electric current in an entirely different direction (i.e., the x direction along the axon)?

Both layman and technical explanation would be appreciated.

The flow of current during action potential generation is perpendicular to the axon length. The channels that transmit ions in neurons are often voltage-gated. Voltage-gated Na+ channels (VGSCs) open when the membrane depolarizes. So when excitatory neurotranmitters (e.g., glutamate) open up channels (e.g., AMPA receptors) in the dendritic region, anions (e.g., Na+) flow in. The ensuing membrane depolarization opens up VGSCs in the axon hillock, that subsequently opens VGSCs adjacently in the axon, that opens up VGSCs a little further up in the axon etc etc. Hence, while the flow of Na+ is perpendicular to the axonal membrane, the net effect is a wave of VGSCs opening up along the axon length. With some delay, voltage-gated K+ channels open that allow K+ to flow in, repolarizing the membrane, preparing the neuron for another action potential (fig. 1).

Fig. 1. Action potential mediated by step wise activation of voltage-gated ion channels. Source: Human Medical Physiology

Hence, although neuronal ion fluxes and networks can be modeled by electric currents flowing in electronic circuitry (Fig. 2), nerve conduction is not anything like it. Current flow in electronic circuits is a flow of electrons. In action potentials in neurons it is ions that carry the transported charge.

.
Fig. 2. Hodgkin & Huxley's axon model. The power sources are the electric gradients of Na+, K+ and a leak current source. The conductances are represented by those same ions. The cell membrane is modeled by a capacitor. Source: Bonabi et al. (2014)

Reference
- Bonabi et al., Front Neurosci (2014)


How does the brain's energy consumption depend on mental activity? What is the impact of mental activity on the energy consumption of the human brain?

I am most interested in intellectually demanding tasks (e.g., chess matches, solving a puzzle, taking a difficult exam) versus tasks with a similar posture but less demanding (e.g., reading a newspaper, watching TV).

I heard that energy consumption stays remarkably constant regardless of the mental activity (and energy consumption can be explained by elevated heart rate due to stress). However, it seems to contradict techniques such as fMRI, where the change in metabolism is measured (unless the relative change is really small).

The energy consumption doesn't vary that much between resting and performing tasks, as discussed in a review by Marcus Raichle and Mark A. Mintun:

In the average adult human, the brain represents approximately 2% of
the total body weight but approximately 20% of the energy consumed
(Clark & Sokoloff 1999), 10 times that predicted by its weight alone.
Relative to this high rate of ongoing or “basal” metabolism (usually
measured while resting quietly awake with eyes closed), the amount
dedicated to task-evoked regional imaging signals is remarkably small.
The regional increases in absolute blood flow associated with imaging
signals as measured with PET are rarely more than 5%–10% of the
resting blood flow of the brain. These are modest modulations in
ongoing circulatory activity that rarely affect the overall rate of
brain blood flow during even the most arousing perceptual and vigorous
motor activity (Fox et al. 1987, Friston et al. 1990, Lennox 1931,
Madsen et al. 1995, Roland et al. 1987, Sokoloff et al. 1955).
[...]
From knowledge of these relationships, one can estimate that if blood flow and glucose utilization increase by 10%, but oxygen consumption does not, the local energy consumption increase owing to a typical task-related response could be as little as 1%. It becomes clear, then, that the brain continuously expends a considerable amount of energy even in the absence of a particular task (i.e., when a subject is awake and at rest).

Techniques like fMRI measure relatively small differences, their existence does not contradict the claim that the energy consumption of the brain doesn't change a lot between the resting state and performing an activity.

1. Raichle ME, Mintun MA. BRAIN WORK AND BRAIN IMAGING. Annual Review of Neuroscience 2006 Jul;29(1):449-476.


Does orgasm cause a dopamine crash? There's some theory around that orgasm will cause a dopamine surge and drop, and that this can lead to a period of low mood or depression. A come down.

Is this true, does orgasm have a negative psychological consequence ?

To answer your last question, I very much doubt it's true in general. It does have unplesant effects in some people though. Form a popsci account

  He [a psychoanalyst] was puzzled about a 24-year-old man whom he viewed as psychiatrically healthy except for intense depression that lasted for several hours after sex. [...] Could it be that some patients have particularly strong rebound activity in the amygdala after orgasm that makes them feel bad?

And this post-coital dysphoria can happen to women too, for which there is some prevalence data:

  Forty‐six percent of respondents reported experiencing PCD symptoms at least once in their lifetime with 5.1% experiencing PCD symptoms a few times within the past 4 weeks.

"No sex before game day" was a tenet in some sports psychology/physiology corners, but more recent research failed to find significant differences of sex acts on mental performance... at least in (healthy) athletes. A 2016 review notes

  Despite the major differences found in the recovery phase, where higher values of HR [heart rate] were found 2 h after sexual intercourse, no significant differences were found in workload achieved and in mental concentration of the athletes.

And, yeah, I know sex doesn't necessarily mean orgasm, but it seems close enough to mention.


What is the significance in an alpha-helix being right-handed or left-handed? Why is that often when alpha-helices are discussed, it is also mentioned their direction - right-handed (clockwise) or left-handed (anti-clockwise)?

I have heard that left-handed alpha-helices are usually less stable, but I'm sure there is more to it than that?

Some experimental and modelling observations suggests, folding energy for right handed in more favorable. You can find more detailed answer to this question here.


Why do retroviruses go through a DNA stage to replicate their RNA genome? Why do retroviruses (e.g.HIV) convert their RNA genome to DNA (using reverse transcriptase) and then transcribe it back into viral RNA (and translate that into viral proteins). Surely to replicate their genome it would be simpler to use RNA-dependent RNA polymerases as RNA viruses like Measles Virus do.

Interpreting the question

Initially I interpreted the question as little more than “Why one type of virus rather than another?” (dsDNA. ssDNA, ssRNA [+ve v. –ve] etc.), and this (which would be unanswerable) was the way @Taimur seems to have understood it. And I also felt that the poster’s reference to ‘complexity’ reflected more his familiarity with other viruses than any real appreciation of what is complex in a molecular manner.

However I now think I misunderstood the question because of not appreciating the erroneous assumption on which I believe it is based. If I am correct, it could be rephrased in the following manner to make that assumption clear:

  “If the only purpose of integrating a DNA copy of the retroviral RNA
  into the host genome is to replicate the RNA in the virion, why is an
  RNA-dependent RNA polymerase not used as in other RNA viruses?"

Answer

  This stage of the retroviral life cycle in which a DNA copy is
  integrated into the host genome is not an incidental stage in a
  mechanism to replicate the virion RNA — it is the key element of the
  modus operandi or strategy of existence of the virus.

Explanation

As explained in the first paragraph of the Wikipedia article on retroviruses, once integrated into the host genome it can persist there:

  “The host cell then treats the viral DNA as part of its own genome,
  translating and transcribing the viral genes along with the cell's own
  genes…”

One way of thinking of this is as a strategy the virus adopts for ‘hiding’ until circumstances are suitable for it to produce more infectious progeny. One might even regard the form that is integrated into the host DNA as the viral genome — rather than the form that is encapsulated by lipid and protein into virus particles.

This sort of lifestyle is similar in some ways to that of certain DNA bacteriophages that can produce either lytic or lysogenic infections. Such persistence of viral genomes in the host is also seen in some eukaryotic DNA viruses like herpes simplex virus, in which an individual may have what is called a latent infection, which produces occurrences of cold sores (in the case of HSV1) throughout the lifetime of the individual as the virus is activated from time to time by various stimuli.


Why don't we keep evolving until we are super-human? Humans (homo sapiens) have been on the earth for thousands of generations, and we have kept evolving throughout that time. Why don't we just keep evolving so that, let's say, we live for an average of 300 years? Or why don't we evolve so that we don't need to sleep?

This could also apply to many other species.

Welcome to Biology.SE!

There are a many misunderstanding of what evolutionary processes are in your post and it is therefore quite hard to answer (hence the current two close votes I guess). You might want to read some introductory textbook on evolutionary biology or other online resources such as the "understanding evolution" project.

The most obvious misunderstanding is that evolution is NOT some kind of forever "improvement" process in a static environment. Evolution is something else! But I can't make a good overview of evolutionary processes in just one post.

  [why don't we live on] average of 300 years?

You may want to read about this post concerning the evolution of aging but it would probably be slightly too advanced but you would probably still get something out of the answers.

  Why don't we just keep evolving [..]?

Humans, definitely keep evolving. Nothing have stopped. We evolved as we have always and it won't stop until we get extinct! This post may for example help you to understand that evolution keep occurring today in humans.

When you say Humans (homo sapiens) have been on the earth for thousands of generations it sounds a bit like human have came to existence some time ago and have evolved since. It is a terribly misleading point of view, one of the reason is that one cannot date the existence of the first humans without making a very arbitrary decision about what a human is. A more correct way of looking at life on earth is that everything have come to existence about 3.5 billions years ago and everything have kept evolving since. Any single living thing on earth have been evolving for the exact same amount of time. Humans have evolved for 3.5 billions (even if we don't call earlier forms as humans) and unicellular algea have evolved for 3.5 billions years (even if we don't call earlier forms as algea).

Hope that helped!


How much shorter is the short arm of a chromosome? And why? I keep reading that the p arm is shorter than the q arm. But I cannot find an explanation of how much shorter nor an explanation for the difference.

It varies from chromosome to chromosome and from species to species. In some cases, both arms are roughly the same length. In some cases, one arm is so short that it is almost inexistant. For chromosomes with equal length arms, of course the terms p and q do not apply.


How do we know that mild forms of rabies are nonexistent? Wikipedia's rabies article says: "Death usually occurs 2 to 10 days after first symptoms. Survival is almost unknown once symptoms have presented, even with the administration of proper and intensive care."

I am wondering why we exclude the possibility of bite victims developing a mild form of rabies, in the same way that influenza can be mild or asymptomatic depending on the individual and the season. I noticed that rabies vaccines use an inactivated (killed) virus, while influenza vaccines can be attenuated, for example cold-adapted, so that a live virus may be used causing minimal symptoms. Clearly, for these vaccines to work, influenza infection must be able to proceed without symptoms. Similarly, the bubonic plague bacillus Yersinia pestis is endemic in many regions and presumably spread through asymptomatic carriers. Rabies vaccines are made from viruses whose infectivity upon intracranial injection is titrated according to a method of serial dilutions, suggesting that a harmless live vaccine would also be feasible at some level of dilution (barring, perhaps, the infeasibility of intracranial administration of such a vaccine).

What evidence do we have to suggest that rabies is different from influenza or plague, i.e. that it is not possible to have an infectious case of rabies with no or with mild symptoms?

There are many people worldwide who are exposed to rabies and don't die (they get treatment), but there are very few of these cases where people don't die after rabies has entered the central nervous system, and even fewer who didn't receive post exposure prophylaxis before the virus reached the central nervous system. Rabies isn't as rare as many would like to believe, unfortunately, with approximately 15 million exposures and 59,000 deaths a year, so data is available.

"Once symptoms have presented" in the Wikipedia article should probably be edited to "once central nervous system symptoms have presented". As discussed in this review rabies entry to the central nervous system is typically the "point of no return". One of the main challenges of rabies is that the virus hides from the immune system inside cells, making its way from muscle to peripheral nerves to the central nervous system before the immune system can mount a response. Once in the central nervous system, it has special protection from immune surveillance. The goal of post exposure prophylaxis is to allow the body to generate an immune response clear the virus before it gets to the central nervous system.

Generally, we say that central nervous system rabies is almost uniformly fatal without treatment because that is what has been observed and reported. *I'm not aware of any published epidemiologic survey looking for anti rabies antibody in healthy non-immunized adults. I know it's not very satisfying, but I would strongly suspect that someone has done a seroepidemiologic study and not published these results, since they're exactly what physicians have been taught since before Hippocrates: a dog bite followed by the characteristic illness leads (almost inevitably) to death. Other illnesses, on the other hand are observed to produce an antibody response in individuals' with mild disease. It is possible that there are unknown cases of mild non-encephalitic rabies that are self limited, but given the 150 years of intense study, I don't think it is likely there is a major aspect of the disease's natural history that hasn't been observed and reported.

Re: your idea about dilution of the vaccine suggesting you could dilute the virus, I think you may have a misconception about what that method actually involves. A killed virus vaccine cannot replicate, and so cannot cause rabies (though some forms of rabies vaccines used in the developing world have fairly high rates of nasty side effects).

Pasteur's risky rabies vaccine trial in 1885 may have involved a live vaccine, but he was notorious for incomplete documentation on his methods. It was essentially, a specimen of air dried rabbit spinal cord that didn't cause rabies in dogs. Here, his method was reported as drying spinal cord segments for longer and longer periods of time until the specimen did not produce rabies in dogs. This isn't a method that "dilutes the virus", but rather a method that attenuates the virus, making it less virulent. Pasteur didn't have methods for detecting what exactly that meant, other than that it didn't cause rabies, but did prevent the animal (or human child) from developing rabies after exposure to a virulent sample.

You can read more about rabies in Murray Medical Microbiology, Ch. 60

*Please see the link in @iayork's comment for a very interesting example of rabies serology in members of two communities in the Peruvian Amazon.


Which proteins are most sensitive to electric fields? Many Proteins have ionic charges that can attract each other (e.g. Formation of salt bridges) or repel each other. On the other Hand, Proteins are mostly immersed in water that screens most of the Electric charges of the proteins. The reason is that water is a dielectric, the H2O-molecules can be polarized easily. So the Electrostatic Forces are reduced in aqueous solution.

Now I am asking which Proteins can be easily affected when applying an Electric field? That means which Proteins will Change their conformation substantially even when weak Electric fields are applied?

Can some proteins immersed in water also be dependent on external Electric fields?

There are various proteins sensitive to changes in electric field. More precisely, they are activated by changes in voltage (surrounding the protein), and immersed in water, as all cells are mainly composed of an aqueous solution. You are correct that most charges in the side chains of the proteins' amino acids are 'masked' by the dipole character of water molecules, but the electrochemical potential of the cell is primarily due to ions, and not to the interaction between side chains in a protein. However, it is important to note that within these proteins sensitive to changes in the electrochemical field, there are domains that contain charged aminoacids (i.e. not covered by water), very important to be able to 'sense' the changes in voltages.

You can check out some of the voltage-sensitive ion channels, which participate in different cellular pathways, including the generation and transmission of the action potential in neurons:

Wikipedia has a good entry about them.


Is the prostate problem unique to humans? In human males the urethra goes through the prostate rather than around it, which tends to create problems for older men as the prostate enlarges. Is this only a human problem or do other animals, primates in particular, have the same problem?

Dogs get benign prostatic hypertrophy, so, yes, other animals (in fact most old male dogs, so that would mean a whole lot of other animals) do get BPH.

  The most common conditions affecting the canine prostate include benign prostatic hyperplasia, prostatitis, prostatic cysts, and prostatic neoplasia.

However, you're almost correct.

  [T]here is no risk for prostate cancer in any other aging mammal except the dog.

Though this article addresses cancer, the same appears to be true for BPH.

The prostate and breast appeared at the same time with the origin of mammals (possibly as long as 195 million years ago). While all male mammals have a prostate, seminal vesicles only appear in  primarily herbivorous species with the exception of man. The human male has seminal vesicles and consumes meat. Thus, it has been postulated to be a dietary cause. Bonobos, on the other hand, exist primarily on a high fruit and vegetable diet. They don't get BPH.

It isn't known what dogs ate before domestication (were there 'dogs' before domestication?) But it's postulated that ~10-15,000 years ago, humans (and their newly domesticated partners, dogs) dramatically altered their diets, breeding animals for food.

Why haven't we evolved a solution? Well, on the one hand, if BPH is only 15K years old, that's only a fraction of a blink in the human evolutionary scale of things, so not enough time to "evolve" a way around it (maybe reroute the urethra?)

On the other hand, we have. We've evolved medications and surgery for treatment of prostatic hypertrophy.

Similarities of prostate and breast cancer: Evolution, diet, and estrogens
New concepts in tissue specificity for prostate cancer and benign prostatic hyperplasia


Can a small polypeptide fold over itself and have a tertiary structure? What I want to know is if polypeptides (those which are not considered as proteins) can also "exhibit" a tertiary structure.

Your instinct is valid, there are other molecules which can be defined as having tertiary structure.

The most common example is RNA, which can fold into a vast array of conformations. These can be part of ribonucleoprotein complexes like telomerases, spliceosomes, or ribosomes or they can function on their own like tRNAs and many ribozymes such as RNase P. An example of a common tertiary structural motif in RNA is the pseudoknot; a haripin loop in which some of the bases in the loop have base paired to another portion of the RNA molecule.

It is also possible for DNA to possess tertiary structure, though the term is used less often when referring to DNA. Usually DNA tertiary structure describes topological structures formed by supercoiling, protein scaffolding, etc. However, DNA can also form cruciform motifs similar to RNA hairpin loops (though it is less common). If multiple cruciform motifs and other structures were to interact in three dimensions, this could be another form of DNA tertiary structure.

You may also be interested in DNA origami, in which 3D building blocks made from DNA are assembled in desired ways by using sequence complementarity (generally).

I think that polysaccharides and oligosaccharides are also sometimes referred to as having tertiary structures, but I don't know as much about those. I encourage you to look into pectin, amylopectin, branched oligosaccharides, etc in the context of tertiary structures.


More general term than "adaptation" The Wikipedia article about adaptation states:

  Adaptation differs from flexibility, acclimatization, and learning.

What is a more general term than adaptation? For example, is there an umbrella term for adaptation and learning (and optionally other phenomena)?

Edit: Some examples of possible definitions of terms that I'm looking for:

mechanisms that change/improve fitness over time [over lifetime (learning) or generations (adaptation)] by matching the environment
how the phenotype changes [over lifetime (learning) or over generations (adaptation)] to match the environment
properties of anything that is alive that change [for example in the gene pool (adaptation) or in the brain (learning)] to improve chances of survival

Adjustment = a small alteration or movement made to achieve a desired fit, appearance, or result; the process of adapting or becoming used to a new situation (Google Dictionary).

Adjustment is a very general term; it doesn't mean anything specific in biology or other sciences and it can cover all the terms you've mentioned: adaptation, acclimatization and even learning.

If you check in Thesaurus.com, you can see that synonyms for adjustment include acclimation, acclimatization, modification and improvement, and that one of the synonyms for adaptation is adjustment.


Definition of synaptic strength The canonical definition of action potentials found in textbooks states that action potentials are all alike in shape.
From techniques such as spike sorting which are used to attribute electrophysiological recordings to individual cells, we know, however, that shapes and amplitudes of action potentials vary.
Synaptic strength is defined as the average amplitude of postsynaptic potential evoked following a presynaptic action potential.
Given that the incoming action potentials might differ for different synapses (and for instance lead to more or less vesicles being released), how can we hence have a uniform definition of synaptic strength?

Synaptic strength is defined as the average amplitude of postsynaptic potential evoked following a presynaptic action potential.

This is a correct definition. Synaptic strength is a fairly abstracted measure. It can be influenced by both presynaptic (for example: number of vesicles/concentration of neurotransmitter per vesicle) and postsynaptic effects (for example: receptor number and composition). So yes, changes presynaptically such as the character of an action potential can influence synaptic strength, but that isn't a problem: we still represent this as part of the synaptic strength if it affects the average postsynaptic potential.
Biologically, action potential amplitude in the axon does not really matter much for synaptic release, but local conditions in the presynaptic terminal that influence calcium influx do. The section on presynaptic inhibition in the answer here may help a bit.


What are the clotting factors' effect on avascular necrosis development? Do clotting factors tpa and pai-1 lead to degenerative osteoarthritis in the same way that lupus anticoagulant and prothrombin might? Is one of these pathways particularly detrimental during formation of osteoarthritis or avascular necrosis (if these factors are inhibited or modified in some way)?

First of all we should distinguish between the physiological clotting factors that are parts of the normal clotting pathways, and those that might affect clotting pathways but are not observed under healthy conditions.

TPA (tissue plasminogen activation), PAI-1 (plasminogen activator inhibitor) and prothrombin are normal clotting factors that are essential for blood clotting. Any deficiency (congenital or acquired) might cause certain pathologic conditions, including the osteoarthritis and avascular bone necrosis.

Lupus anticoagulant, however, is an antibody against cell membrane that is common for Lupus. This antibody can intervene into the process of clotting and increase the prothrombine time (the common lab method to test blood clotting properties), hence the name "anticoagulant". But this effect is just a sort of "side-effect" of this antibody, that leads to certain symptoms in case of auto-immune attack against different target organs.

So, after this introduction I can rephrase your first question as: "Does the deficiency of clotting factors TPA and PAI-1 lead to degenerative arthritis in the same way that lupus anticoagulant and prothrombin deficiency might?"

The part of the answer is already in this question: yes, the deficiency of these factors might and under certain conditions, leads to the development of osteoarhritis and avascular necrosis.

I must confess, I found no evidence whether the underlying mechanism is different or not. Papers just prove that these factors are discovered in the affected joins, and see the correlation in mice models between the factors and the articifially induced arthritis. But I found no study which would try to address the mechanisms of these actions or to show, whether these are different.


Difference between Bioscience and Lifescience Are bioscience and lifescience the same things? I am a little bit confused about it. If not, then what is the difference between the two?

I agree with the comments and largely see them as the same thing, and many dictionaries would probably agree with this. However, in practical use (from my experience) Life science is used somewhat more broadly (everything from ecology and agricultural science to genomics and biochemisty), while Bioscience is more often applied to "whiter" lab-based biology and more technical applications (biotechnology, genetics, etc.). Personally, I would feel comfortable to label my research as life science but a bit more uneasy with bioscience. However, the terms are so vague that I wouldn't pass judgement on the content of research just based on these labels.


Natural examples of XOR functions at the cellular level We can often think of cells as a sort of circuit on macromolecules, and can show that they can accurately and robustly implement functions like $\text{MAJ}(x_1,...,x_n)$ (return $1$ if more than half of $x_1,...,x_n$ is $1$ and $0$ otherwise) under natural conditions (Cardell & Csikász-Nagy, 2012).
Not all functions are created equal. $\text{XOR}(x,y)$ is a boolean function that is $1$ if exactly one of $x$ or $y$ is $1$ and $0$ otherwise (i.e, if $x = y$). It is often generalized to a multi-input function parity (or odd) as $\text{ODD}(x_1,...,x_n)$ which returns $1$ if an odd number of $x_1,...,x_n$ is $1$. Notice that this is superficially similar to $\text{MAJ}$ but is doing its counting in base 2, which one would expect to be easier for say finite state machines.
However, in some ways, this sensitivity makes the function much more difficult to the point that Valiant (2009) writes:

[Parity] appears to be biologically unnatural. That is exactly the prediction of our theory, which asserts that evolution cannot be based on the evolvability of [the class of functions parity belongs to]

Synthetic biologists used to agree to some extent, with Tamsir et al. (2011) writing that the closely related XNOR (i.e. $\text{XNOR}(x,y) = 1 - \text{XOR}(x,y)$) is empirically impossible to implement. However, they were proven wrong when Bonnet et al. (2012) implemented XNOR among many other amplifying gates by exploiting the structure and process of transcription. Unfortunately, this is an example from synthetic biology, and I really want to learn ones (if any) that occur naturally.
Are there any examples of XOR or related gates implemented (without human engineering) at the cellular level? Are there any naturally occurring molecular pathways that compute something similar to parity? (i.e. something similar to the majority result, but for a more 'sensitive' function) I am primarily interested in empirical demonstrations, but I would be satisfied with theoretical examples that are appealing to biologists (i.e. not something purely comp. sci. like P-systems or something).

References
Bonnet J, Yin P, Ortiz ME, Subsoontorn P, & Endy D (2013). Amplifying Genetic Logic Gates. Science, 340(6132): 599-603. PMID: 23539178
Cardelli L, & Csikász-Nagy A (2012). The cell cycle switch computes approximate majority. Scientific Reports, 2: 656. PMID: 22977731
Tamsir, A., Tabor, J. J., & Voigt, C. A. (2011). Robust multicellular computing using genetically encoded NOR gates and chemical wires. Nature, 469(7329), 212-215.
Valiant, L.G. (2009) Evolvability. Journal of the ACM, 56(1): 3-22.

When I think about your question of natural examples of XOR, it pushes me to think about what type of natural environments (i.e., evolutionary pressures) would lead to the selection of an XOR equivalent.

When we implemented a synthetic XOR by "double flipping" one transcription terminator as a type of gene expression "check valve" it was the case that I did not know of any natural examples of flipping terminators, whereas I know of several examples of nature flipping promoters.

Why do we have plenty of natural examples of flipping promoters but (unknown to me at least) as yet no charismatic examples of naturally flipping terminators?

Perhaps we haven't been looking in the right environments to find them?

E.g., for a terminator to exist in nature, there needs to be something that must  be expressed upstream of the terminator, and also something that should not be expressed downstream of the terminator.  Since there are plenty of terminators there must plenty of examples of nature selecting for terminators.  My favorite example is the "Tø" terminator in phage T7 that is just downstream of the major capsid gene (highly expressed) but just upstream of a minor particle protein (weakly expressed).

But now reason thru what would need to be true in order to select for terminator flipping.  I'd need all the requirements of a static terminator (above), and then another such pairing of selective requirements under different environmental circumstances for additional gene products encoded in the opposite direction on the complementary strand of DNA. Phew!

I'm not saying that it is impossible to imagine such a complicated coupling of selection requirements emerging in nature, but it definitely seems a much more improbable aggregation of selective pressures to co-mingle all within a single genetic loci.

I'm still nevertheless very curious and would be grateful to learn of any natural examples.  -DE


Do organisms use detergents to fight off viruses? Common advice against contracting bacteria or viruses is to wash your hands because soap dissolves the viruses' shell. Does any organism exploit this effect to protect against infection, e.g. by having detergents in their mucous membrane? If not, why not?

To answer your question, consider why soap is effective against bacteria and viruses.  The chemistry of detergents allows them to interrupt the lipid layer that surrounds cells and some viruses.  Viral envelopes, in particular, tend to be composed of host-derived phospholipids and proteins.  So, if an organism were to synthesize a detergent to fight off a pathogen, that detergent would pose a threat to the producing organism, as well.

Edit - most air-breathing animals produce a pulmonary surfactant in their alveolar cells, though the purpose of these molecules is lung function and cell size regulation, not immunity.


Biologically, does life and death matter? (Sorry that I'm on mobile, so I can't make a good formated question (no links). I will add them later. Just can't resist the urge to ask)

In the recent hot question about whether mitochondrial is alive or dead (it's technically dead), the top answers don't only explain whether it is dead or not, but also further explain why it doesn't matter: they just do what they need to do. This provokes me a question:

Q: Biologically, do life and death matter? Is the functionality of something the only thing that life cares?

We human are scare of death. Because of that, we tend to apply that idea into everything we can observe, even if it's meaningless. But why is death scary? Isn't it because when you die, you stop function anymore? So ultimately, isn't what we really mean when discussing whether something is dead or not the functionality of that?

Not only that, "there is no consensus regarding the answer to the question as to when does life begin". If we approach this in a different way: the time when an individual function begins to work, will there be a consensus? I mean, just don't think if an organism is alive or not, just think that how much functions of it have started to work.

If we are the combination of the numerous of selfish genes, would "humanity" be a collection of functions?

We human are scare of death. Because of that, we tend to apply that idea into everything we can observe, even if it's meaningless. But why is death scary? Isn't it because when you die, you stop function anymore?

Fear of death is hard-wired into our nervous systems. A thirsty wildebeest will approach crocodile-infested water very, very reluctantly. The wildebeest isn't thinking about the selfish gene or the loss of his function in the world; he's hardwired to be afraid of the situation. The same is true for any prey animal: fawn, rabbit, gazelle, mouse. The difference (maybe; simplifying for convenience) is that we are rational, and like all of our primitive fears (e.g., of the dark, when there really were sharp-toothed predators with better night vision than ourselves), we try to rationalize them. We also rationalize our existence.

  Is the functionality of something the only thing that life cares?

Nature is red in tooth and claw. If you want to anthropomorphize Nature, then sure, we matter (we're destroying the earth at unprecedented speeds). If you believe in a spirit, we matter. But if you believe in none of it, the only purpose we serve is to propagate ourselves, and when the last of our species is gone, Nature will not care a whit. Just as it doesn't care that dinosaurs, wooly mammoths, passenger pigeons, tasmanian tigers or baiji river dolphin are gone.

It can be argued that in the grand scheme of things (and here I'm speaking of the entire Universe), biological life doesn't matter at all.


How is mankind important to nature? Like mosquito eggs are important for fish, what’s our role in balancing the life on earth or its ecosystem.
Please suggest if this question doesn't fit in this community.
I am a mechanical engineer with interest in knowing biology and biochemistry.

The classical division of humans and animals has always been self-centered and artificial. Humans are animals, competing with other organisms under exactly the same rules. Evolution involves trade-offs, strategies, and adaptation. Humans have been set on a path to use their brains to compete, rather than claws. But the concepts are the same. It happens that this is a very effective strategy, such that humans now dominate virtually every ecosystem on Earth, to the point that some are now calling the age we live in as the "Anthropocene". Humans are the apex predator. We now have no natural enemies, however as vectors of disease, mosquitos control our populations more than any other animal.


Are the seeds in a single capsicum fruit genetically identical? Hopefully not a too-basic question for the venue. I'm a chile pepper growing hobbyist and have spent some time searching around and reading up on pepper (angiosperm) reproduction, but I'm not getting a clear picture of the details.

It seems like flowers have multiple ovules and it seems like one pollen-grain landing on the stigma leads to fertilization of a single ovule. And it seems like that process produces a single seed.

But that fertilization also prompts fruit growth and flower death and capsicum fruits have many seeds, never just one (that I've ever seen).

So, does each seed have a potentially different father? Or are the multiple seeds generated through a reproductive/cloning process that I'm not seeing written about? Or something else?

No, the seeds are not genetically identical.  Each seed come from the fertilization of an ovum with a sperm from a separate pollen grain.  Since each pollen grain can come from a different plant, the seeds will generally differ from one another.
Additionally, even ova from a single plant will not usually be genetically identical to one another.  This is because the process that creates the ova (meiosis) shuffles the genes of the parent plant on then places only half into the ovum.  The same kind of shuffling goes on in the creation of pollen grains.
In the chili pepper genus (Capsicum), plants are predominantly self-pollinating. This means the majority of the pollen for the seeds in a fruit will come from the very same plant.  This generally reduces the amount of variation seen in the offspring compared to complete cross-plant pollination. Some cross-pollination can nevertheless occur if there are other varieties in the neighborhood.  The fruit will not show the effects of the new genetic combinations present in its seed, but only a plant grown from the seed will make the differences evident.


Microarray probe and target In a microarray, which one is called a target and which one is the probe? the one that is added later , is that the probe or the one present in the slots of the microarray, that is the probe?
(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if the question seems to silly, forgive me)

In an RNA microarray, a hybridization event between a probe and target sequence would indicate a presence of the transcript within the sample. The probes are oligonucleotide sequences found on the microarray chip. The target sequences are representative of the entire transcriptome. The targets are found within your biological sample and have gone through many rounds of amplification in addition to labeling with fluorescent dyes. The fluorescently labeled target when bound to the probe can then be detected using a scanning laser.


Critical discussion: Gene expression and systems biology allows us to understand the control of complex traits I'm having a bit of trouble tackling this question. Any help on what I should write about or the points I should mention would be much appreciated. I keep seeing articles about eQTL and QTL are these relevant as well?

Turns to be too long for a comment.

If you are looking for explanation of the title/question, than it is following (roughly).

If we get information about gene expression from all different cell types, and extract also interactions between those genes (if a gets higher then b gets lower), this will allow studying multigene traits. E.g., life quality, height, mental disabilities, cardiovascular risks etc. Thing is that for most health problems that stem from single gene variation we already know named gene, or can easily find it out.

More complex issues are often hidden in statistics, links are not so clear. So, for example, autism is described by genetic variations (so far) only in less than 30% of cases or so. In other cases there is no genetic predisposition or strong evidence. Mainly that is so because many genes interact to produce final trait or illness. Looking with microscope one gene at a time will not provide information about it.

You should look into multi-gene traits, maybe pick your favourite illness (e.g. autism) and see how it is hereditary (tip: not fully). Whole-genome sequencing is important tool in tracing such issues because it gives wide overview and a lot of genetic information about patient.


Vibrio vulnificus from liquid soap At some point between 2002 and 2006 I attended a departmental seminar in the UK on Vibrio infections, and particularly on the (then relatively unheard of) V. vulnificus, which causes necrotizing wound infections and septicemia when it enters open wounds. The speaker discussed two case studies: the first was of a case (possibly a cluster of cases) in a garage, I think in Australia, where the workers repeatedly topped up a liquid soap dispenser from a big bottle rather than replacing the bottle, and it had at some point become contaminated with V. vulnificus, which had survived in the soap, and infected an individual who went to wash their hands because they cut themselves.

The second case, which I only mention because it was part of the same talk and I have a suspicion the seminar speaker (whose name I can't remember) might have written papers on both, was about the rise in V. vulnificus cases in the Middle East (Israel, I think) which arose from a new trend for fish markets offering live fish in tanks at market rather than transporting them for a few hours on ice before sale (which was previously killing the bacteria, which occurred fairly ubiquitously in Israeli fish farms due to the high water table and high groundwater salinity).

This was a great seminar with two great stories that illustrate the ecology of Vibrios and I'd love to have sources for either, but particularly the first one. However, I can find no mention of either in the literature. Can anyone help?

The Isreali outbreak (associated with changes in fish marketing) was reported in Lancet a few times. It was particularly important for identifying biogroup 3. I hope that might be helpful, but I'm not sure it will be. Since it was an important epidemic, I wouldn't be surprised if it was discussed in a visiting lecture by someone who wasn't part of the Isreal Vibrio study group.

I'm not aware of a soap dispenser case for V. vulnificus, but soap dispensers have been implicated in the transmission of other pathogens. Could it have been some other halophilic bacteria, possibly another Vibrio?