text:
How many ion channels on average must there be in one µm2 of neuronal membranes?
If the conductance of a single ion channel is 1pS and its capacitance per cm2 is 1uF and the time constant for a human neuron is 1ms
How many ion channels on average must there be in one µm2 of neuronal membranes?
How is it possible to know how many ion channels with only these information? would you be able to explain it?
Thank you

Is this a homework question?

Suggest you check the given units and use those as a hint... https://en.wikipedia.org/wiki/Siemens_(unit) and
https://en.wikipedia.org/wiki/Farad comeback when you have made a slightly bigger effort.

Hi, so I have found the resistance which is = 1/ conductance = 1/110^-12 so resistance = 110^12 ohms per cm^2. (I converted the pS to S). However, I am confused what does it mean by "how many ion channels" do they actually want the number of ion channels, or is there a formula for that, i tried researching a lot but I did not find anything related. Thank you!

I know we have: Resistance, area (um^2), conductance and capacitance but i do not know how to put this information together to find the number of ion channels.

You also have a time constant. That will be key. Look for the relationship between the time constant and the other parameters you have. (note also: you have the conductance of just one channel; you are solving for how many channels you need i.e. how many multiples of that conductance)

does this mean we need to find current?

To notify a user, you should type @ before their name. For e.g. @BryanKrause

OP: I already gave you the hint that you need to use the time constant. Look up equations for the time constant that are in the units of the things you are studying: resistances, capacitances, etc.

I expect your homework was already due, so...
You're supposed to remember what a membrane time constant is. I'll quote from page 12 of my (by now quite old) copy of "Ion channels of excitable membranes", by Hille:

For biological membranes the product, RmCm, of membrane resistance and capacitance is often called the membrane time constant, taum.

Since you know tau and C, your goal is then to determine the membrane resistance. You also need to convert the capacitance to square microns (1e-14F per square micron). In this case: 1ms/1e-14F = 1e11Ohms, or 1e-11S, or 10pS. So on average there are 10 channels per square micron, assuming I didn't make any silly mistakes.


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Don't understand figures in this citizen-science mosquito ID project
The Citizen-based mosquito monitoring system is a Citizen-Science vector tracking project that involves using any of a wide variety of cell phones to capture "sound bites" (sorry!) of mosquitos. These are collected and analyzed in order to gain some insight into the distribution of different species of mosquitos at different times and locations. Attention is paid to ensure the system works with older model phones that are distributed more widely.
While a positive identification of a single insect form a single recording is not likely this way, over time a statistical analysis is expected to give meaningful information. I believe the idea is that similar sounding species are expected to not be in similar places at similar times so often that it muddles the identification too much. This is citizen-science; imperfection is not a deal-breaker.
I was happy to see that there is a BioRvix paper. In fact, I was surprised to see there is such at thing as BioRvix in the first place!
The principle is illustrated in Figure 5, and some of the argument behind species differentiation is illustrated in Figure 7, and screenshots of both are shown below.
I think there is a lot of information densely packed within the figures, and I'd like to understand more of it. In the second figure below, which is Figure 7 in the paper, what does the color scale and color coding represent?
There seems to be some suggestion of time of day as well, but I don't understand exactly how. What about time of year - that should also play a major role.

Some may recognize Manu Prakash as "Foldscope guy".

Thanks for asking about the interesting study. However, you need to clarify your question a little bit. What exactly are you asking? (please update your question with a bolded well-framed, specific question). Right now I htink it's a little too broad. Also, if you could perhaps modify your post a bit so one doesn't need to go to the paper to answer your question (useful for if the link dies later on). This would include better referencing/labeling your photos and perhaps quoting the chunk of statistical text that is most confusing to you). Thanks

@theforestecologist Thanks for your recommendation, and I see what you mean. I will try to dig in and identify what it is that's making it so difficult to understand, and rewrite. This could take as long as 24 hours - should I delete in the mean time, or leave it as is for that long? I'm happy either way.

Thanks @uhoh. You can just leave this post up and update it as soon as you can. Most likely others will see these comments and will wait for you to edit before answering further.

@theforestecologist I've decided to split off the statistics as a separate question - I need more time to read.

In the second figure –
  What does the color scale and color coding represent?

Each color is an individual mosquito species,
arranged the same from top to bottom on all plots.
Here, on the left, all species are gathered on one plot,
with the y-axis now labeled “Species.”

The sounds of many mosquitoes apparently have statistical profiles
similar to each other,
so the individual plots
demonstrate how additional factors help distinguish species
in some such cases.
In the plot for “Time” (C),
the sun and moon merely accompany the species
whose differing circadian habits they illustrate.
It is only a coincidence
that the daytime species is plotted higher.
Just to complete the picture,
here is how these plots mark statistical profiles.

This is a really helpful answer! I'm going to split off the question about the statistical arguments as a separate, new question (it needs considerable effort on my part to define it more narrowly), and edit this question to limit it to the information in the plots. Thanks!

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Number of families in Animal kingdom
I found this question about how many taxonomic families there are. That made me wonder how many are just in the animal kingdom alone. I want to know about families not species. Now the linked question was three years ago, so there should be some new information and numbers. A good answer would preferably include a breakdown of the phyla.

The Integrated Taxonomic Information System (ITIS) is maintained regularly by a consortium of North American governmental agencies, and will give you a list of all the classes, orders, families or genera in any of seven kingdoms they recognize. It might be biased towards North American taxa, but it might be quicker to get a list from then rather than extracting them from Wikipedia.
To help you further, user Rozenn Keribin used an awk script to summarize the number of families per phylum at https://justpaste.it/163c6.
Phylum:  Myxozoa -- 4
Phylum:  Chordata -- 1049
Phylum:  Echinodermata -- 139
Phylum:  Hemichordata -- 7
Phylum:  Xenacoelomorpha -- 9
Phylum:  Chaetognatha -- 9
Phylum:  Arthropoda -- 2504
Phylum:  Kinorhyncha -- 10
Phylum:  Loricifera -- 2
Phylum:  Nematoda -- 192
Phylum:  Nematomorpha -- 3
Phylum:  Onychophora -- 2
Phylum:  Priapulida -- 3
Phylum:  Tardigrada -- 20
Phylum:  Annelida -- 142
Phylum:  Brachiopoda -- 21
Phylum:  Bryozoa -- 133
Phylum:  Kamptozoa -- 5
Phylum:  Mollusca -- 581
Phylum:  Nemertea -- 20
Phylum:  Phoronida -- 0
Phylum:  Sipuncula -- 6
Phylum:  Acanthocephala -- 26
Phylum:  Gastrotricha -- 13
Phylum:  Gnathostomulida -- 12
Phylum:  Micrognathozoa -- 1
Phylum:  Orthonectida -- 2
Phylum:  Platyhelminthes -- 321
Phylum:  Rhombozoa -- 3
Phylum:  Rotifera -- 34
Phylum:  Cnidaria -- 269
Phylum:  Ctenophora -- 19
Phylum:  Placozoa -- 0
Phylum:  Porifera -- 142
Total -- 5703

Wow, that is a MUCH easier to parse source than the ones I knew about or that were given as answers to the previous question! So much easier that I wrote an awk script to do so that provides exactly what OP was asking for. Obviously too long for a comment and I don't want to edit your answer without asking first, here's a link if you want to do so: https://justpaste.it/163c6 (the source you gave would also be a valuable answer to the earlier question the OP referred to)

@RozennKeribin Thanks for the link! I've added it to my answer, but feel free to edit it directly if you'd like!

Your question immediately made me think of the paper "How Many Species Are There on Earth and in the Ocean?", which is about estimating the total number of species based on the rate of discoveries of higher taxa. I imagine writing the paper involved the most thorough investigation of how many taxons there are in any group that you'll find. It's from 2011 so it's not going to include actual new information from the last three years, but given it looks at the rate of discoveries over time you can see the evolution and estimate where things are yourself.
Figure S1 gives the actual plots of number of taxa vs time; from it we can see that Animalia contained a bit over 5000 families (5300 I'd say?) in 2011, with an estimated total number of a bit under 6000 (5700?). So today's number is likely to be within that range.
If you want the actual list per phyla you just need to look at the same sources that were given in the answers to the original question; Wikipedia and the NCBI taxonomy browser (which also links to other resources that might be easier to interpret) have no reason not to be up-to-date.

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Trying to determine Heart Condition? ECG show no P Wave
A young woman was at the gym doing great her normal workout. She would spend 45 minutes on the elliptical and then 15 minutes doing weight training. This was the regular routine for her as she did this almost everyday. One day her normal routine turned upside-down. As she finished her elliptical workout and was making her way to the weight machines, she experienced a rapid heart beat. This washould nothing alarming at first because she had experienced this rapid heart beat before. When it happened previously the rapid heartbeat lasted only 10 or 20 seconds. However, this time was different. She experienced the rapid heart beat, but this time the heart beat did not slow down after 20 seconds. The rapid heart beat continued and she began to feel shortness of bread, some pressure I her chest, as well as feeling light-headed. Scared for what might be happening in general she went home called her husband. Frantically she tried to explain how she was feeling and how scared she was. They went to the E.R during her sTay in the ER her heart rate was constantly monitored. For five hours her heart rate remained between 130 and 150 bpm. After 5 hours her heart rate spontaneously returned to a normal rhythm. She was kept overnight In the ER and attending cardiologist prescribed low-dose beta-blockers She was given a number of different test and the results were: -blood pressure normal - hematocrit normal -cholesterol normal She is 34 mother of two. She is of adequate weight and BMI for her age and height. She has regular wellness checkups every year and has never had high cholesterol or hypertension.

Personal medical questions and health advice are off-topic on Biology. We cannot safely answer questions for your specific situation and you should always consult a doctor for medical advice.

This is something that you need to see your doctor for.  Until then, do whatever the ER doctors told you to do.  When you go, take all records from your ER visit with you.  The ER doctors' diagnosis should be on the discharge paperwork they gave you.


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Are gametes diploid or haploid?
Some sources say that gametes are haploid, some say that they are diploid.
I'm confused.

Could you give a source that says gametes are diploid, or that zygotes are haploid? It is hard to tell what it is that's confusing you here; the answer to your question is normally an elementary Google/Wikipedia/biology textbook search away but presumably you're getting contradictory info somewhere, but if we don't know what that info is we can't help.

@ViaLo Can you please edit your question, rephrasing it and improving its wording? I just edited it to add the genetics tag, but I avoided any edit in the question itself because, if I did it, I'd end up substantially changing your own words.

@RozennKeribin despite zygotes never being haploid (since the very definition of haploid), it's possible to find diploid gametes: such gametes are diploid and haploid at the same time.

Well, @ViaLo, I edited the question removing the unnecessary (and confusing) parts, feel free to rollback if you want.

Actually there is some confusion here, and that's quite excusable, because it's extremely common reading that monoploid and haploid are synonyms and have the same meaning. However, they are different terms. According to Hartl and Ruvolo (2012):

The potential confusion arises because of diploid organisms, in which the monoploid chromosome set and the haploid chromosome set are the same.

As we, human beings, are diploid organisms, it's easy to see why haploid and monoploid ended up being considered as synonyms.
However, a more precise terminology would be:

Monoploid: the total number of chromosomes in a single complete set of chromosomes (this does not change whether we are talking about a somatic cell or a gamete).
Haploid: half of the total number of chromosomes in a somatic cell. The haploid chromosome set is the set of chromosomes present in a gamete, irrespective of the chromosome number of the species.

That being said, diploid and haploid are not antonyms nor mutually exclusive terms. A cell can be diploid and haploid at the same time. Let's exemplify this with organisms that perform gametic meiosis:
Human beings have diploid somatic cells, with 46 chromosomes. When a somatic human cell perform meiosis, it produces haploid cells which are monoploid. Human gametes are haploid and monoploid.
In wheat (Triticum aestivum), somatic cells are hexaploid, having 42 chromosomes (that is, 6 full sets of 7 chromosomes). When a wheat cell perform meiosis (producing micro and mega spores, and later on gametes), it produces haploid cells which are triploid. Wheat gametes are haploid and triploid.
The same whay, a tetraploid organism would produce, by meiosis, a cell which is haploid and diploid. Thus, depending on the number of chromosome sets in the somatic cell of a given species, you can say that a gamete is diploid (as stated in this other answer).
In a nutshell, a gamete that was produced by meiosis (there are life cycles where the gamete is not produced meiotically) is always haploid, regardless the number of chromosome sets it has (which will determine if it is monoploid, diploid, triploid, hexaploid etc...).
Sources:

Hartl, D. and Ruvolo, M. (2012). Genetics. 1st ed. Burlingham, Mass.: Jones and Bartlett Learning.
Genetics-notes.wikispaces.com. (2017). genetics-notes - Ploidy. [online] Available at: https://genetics-notes.wikispaces.com/Ploidy [Accessed 1 May 2017].

It depends on the organism in question. (https://en.wikipedia.org/wiki/Polyploid#Examples)
Notice that the gametes carry half number of copies of the normal cells. As such a tetraploid organism will have diploid gametes.

This is a confusing topic when it comes to polyploids. I don't believe the definition for haploid provided in the accepted answer is correct for all species.
Haploid refers to a cell or an organism that has only a single set of chromosomes - my interpretation is that it is only in a diploid organism such as a human that haploid means "half of the total number of chromosomes in a somatic cell", because diploid organisms produce haploid gametes.
A diploid human produces haploid gametes.
A hexaploid produces triploid gametes.
I think the confusion in the accepted answer is that gamete means the same as haploid (which of course is true only for diploids, such as humans). The triploid gametes are not haploid. The definition in my answer supports that, and indeed if you search, other definitions state this also e.g. "Haploid describes a cell that contains a single set of chromosomes".
I should add, to answer the question, that the gametes are diploid for a 4n tetraploid organism - when the gamete is produced 2 of these go to one gamete, and 2 to other (diploid). It may be that the source you read was referring to a tetraploid organism.

Welcome to Biology.SE. (+1) This is much better than the accepted answer, but I saw a few ways to make improvements. In particular, there were couple of statements that could cause confusion. The second of these I deleted since it wasn't necessary to  make your point — while "genome" can be used to refer to the haploid set of chromosomes, it usually means all the chromosomes.

Actually — it appears that we are both wrong and the accepted answer is OK. You can see this in the second sentence of the second link you provided where it says "The term haploid can also refer to the number of chromosomes in egg or sperm cells, which are also called gametes." This unfortunately means that haploid has two meanings that sometimes are in conflict — to be unambiguous we should use monoploid (and it seems to me, completely avoid haploid) ... Would you like to edit your post in light of this information?

Don't get confused by the number of chromosomes. Haploid refers to 1 set of chromosome, diploid refers to 2 set of chromosomes, triploid means 3 set of chromosomes. They don't represent the numbers of chromosome present on a set.
We human beings have 23 chromosomes on a single set. We are diploid organisms and thus all the cells of our body carries two set of chromosomes (thus 23*2=46). Our germ cells however are formed through meiosis cell division and thus they are haploid (23 chromosomes).
So, sperm cell carries 23 chromosome and egg carries 23 chromosome each. When they fuse, zygote is formed and as you can see, zygote carries 23+23=46 chromosomes. Zygote undergoes mitotic cell division and a complete human is formed. So, human zygote definitely is diploid.

Does it mean ONE SET means 23 chromosomes (out of 46).

Yes, one set is 23. one set chromosomes are present in the germ cells like sperm and egg

Gametes must be haploid because they will be combining with another gamete. Sexual reproduction works to increase genetic diversity by having two haploid gametes combine to form a new organism that has a different combination of genes than either of its parents. The new organism has half the chromosomes from its mother and half from its father.
Source from Chromosomes and Meiosis Interactive
For example, in order for humans to reproduce, a sperm cell must fuse with an egg cell, producing a zygote that has a unique set of genetic information. If the gametes were diploid instead of haploid, the resulting organism would have too many chromosomes. By having two haploid gametes fuse together, it is ensured that the new organism will be genetically distinct and still have the correct number of chromosomes that it needs.

Welcome to [biology.se]. It is great that you are contributing to this site by answering questions but please try to read other answers for a given question before answering so that there is no redundancy. Redundant answers are not useful. Perhaps you should add some extra information that is not covered by other answers.

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Should there be separate Ramachandran plots for an amino acid in different contexts?
I understand the nomenclature of the phi and the psi angles of the alpha-Carbon atoms in protein stucture, but I am confused by the Ramachandran plot. Each alpha-Carbon atom (magenta) makes two peptide linkages and has two corresponding neighbouring alpha-Carbons (cyan) and side-chains. I would expect the psi and phi values to depend on the interactions of these side-chains, so I would expect that for a single amino acid one would need a separate graph for every possible combination of neighbouring amino acids.

I am not clear whether this the case. The following graph (1) from Harper, Biochemistry, is for “many non-glycine residues from many proteins”. So, suppose a set of phi and psi is allowed for a right-handed helix (a value or data set taken from the plot) does it mean that it is allowed for any amino acid with any other amino acid? I woud expect an alanine adacent to an alanine to have a different interaction to an alanine adjacent to a bulky amino acid such as isoleucine.

I have also seen plots for specific amino acid and their allowed angles, such as that for proline (2), above. This suggests that the neighbours are not being taken into account. If this is so, why not?

I have edited your question to remove the various erroneous assertions and focus on the key point of interest. The question of whether the plots are for one or several amino acids is trivial — they are for many. The more pertinent question is why there are not different plots for amino acids with different neighbours, or, indeed, whether the different positions represent these different neighbours. This is answered by @VonBeche. (You may think it presumptious to alter your question in this way, but the idea of SE is, as you will be aware, to produce an archive of useful questions and answers.)

@David Oh no! this is absolutely fine. Well, it looks much better now. Thanks :)

The phi and psi dihedrals describe the dihedral on both sides of the c-alpha of a single amino acid, and do not involve any angles of the neighboring amino acid.
The Ramachandran plot is something generated from a set of protein structures, an empirical data set. The top graph represents the dihedrals found for all non-glycine residues in a set of structures. You can filter this for proline only, and you'd get the bottom graph. The top cloud of dihedrals represents those found in beta-sheets, and the bottom cloud those for alpha-helices. Sequence (the amino acid before or after) doesn't really matter that much for what's allowed (although we cannot directly deduce this from the data in those graphs).
If you look a little bit more into the structure of helices and sheets you'll also find out why that's the case. In beta sheets the sidechain of the +1 residue is pointing completely the other way, and also in helices there's little interaction between the sidechains of subsequent residues. Secondary structures are built using the amides, not with the sidechains.

The OP might also find it helpful to look at the diagram in the Wikipedia entry for dihedral angles to see that any alpha carbon atom (with its sidechain) whose dihedral angle one is considering is three atoms away from each of the neighbouring two (note) alpha carbon atoms, and thus the neighbouring residues need not be in close proximity.

I have +1'd your answer, but if the OP accepts my modification of his question, you may wish to modify your answer somewhat. Sorry for the inconvenience, but see my comments to his question.

Some further observations about Ramachandran plots in response to the question:

They were originally calculated. This was done by considering the minimum contact distances shown in the diagram (which is from Wikipedia, but based on that in J. Mol. Biol. (1963) 7, 95–99). The side-chains were not considered, except for the  Cβ of the central residue. In the case of a glycine side-chain that lacks a Cβ, different values are allowed. The original plot had ‘allowed’ regions enclosed by a solid line, with an ‘outer limit’ indicated by a broken line.
The diagram in Fig. 1 in the question, in contrast, is an experimental plot for amino acid residues (other than glycine) in  several proteins. Each point represents the dihedral angles for a single instance of an amino acid. Such plots based on very many amino acids are sometimes used as a check for possible errors in experimental values obtained for new proteins — see review by GJ  Kleywegt.
When plotting experimental values for very many proteins, the points would superimpose, making it impossible to see which regions were most densely populated. That is why in Fig. 2 in the question a coloured contour map is used to represent the density in particular regions. (More elaborate examples may be found.)
On the general plot of the type originally calculated (1) one often sees particular constrained areas marked for chains in which the same Φ/Ψ angles repeat at every position. These are for structures like α-helices, β-sheets etc. (see image below, taken from Wikipedia entry on Ramachandran Plot.)

The reason Fig. 1 of the question excludes glycine is that its lack of Cβ means it can occur in regions such as Lα, from which most (but not all) larger amino acids are excluded. Likewise, the plot for the imino acid, proline, is different from the other amino acids because of the constraints imposed by the proline ring.
Small, non-repeating hydrogen-bonded structural motifs in proteins may also impose constraints on allowed dihedral angles at certain positions in the motif. Such motifs may exert other constraints which influence the amino acids at particular positions.  One might possibly regard this as an influence of amino acid side-chain on allowed dihedral angles, although it is perhaps better to regard it as an influence of amino acids on the occurance of the motif as a whole.


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Has aloe vera been proven to help heal burned skin areas?
I don't like buying into "natural remedy" type things without seeing scientific proof behind them. There's an almost universal belief that aloe vera helps to heal burned skin, and whether that includes assisting in cell regrowth, preventing inflamation, or something else, I haven't bedn able to find any real scientific evidence.
Can anyone cite legitimate scientific evidence that aloe vera has any helpful effect for burned skin? If so, how does it work?

No, there is no reliable proof of its effectiveness (if I remember correctly, one decent study found delayed healing.) And I actually like "natural remedies", which is why I look for supporting studies. But you might cite a source and ask on Skeptics.SE.

A quick Google Scholar search gave me this paper which is a list of abstract of research that suggests it helps with would healing, inflammation and burn wounds


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Is it possible to have a mechanism to use carbon dioxide as a source of oxygen in human body?
Is it possible to seperate O2 from CO2 and use it for energy In Human? Why Plants and not Humans can do it?

It's possible, though complicated, and I believe is done on the ISS.  I'm not really up on the exact method, but searching NASA web sites should provide info.  The problem is that it takes energy to do the separation, as explained in the answer below.

Most energy in humans is generated by reducing O2 to water and CO2, using something like sugar or fat. Converting CO2 into oxygen would require energy, not generate it.
Plants do have mechanisms to convert CO2 into oxygen, but they use light as an extra energy input to push this energy-costing process.


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Help identify these (two) fishes - Netherlands
Yesterday my kids caught these two fish. I tried to figure out what kind of fish (species and name, to tell my kids a bit more about them) they are but I was not successful. Today we made a trip to a nearby sea-life exhibition which exhibits native sea animals but I couldn't find similar fishes there :-)
They were caught in Callantsoog (north-western Netherlands) in salt water in shallow water next to a breakwater wall at low tide.
This is the first fish. To me it looks like some kind of catfish.

It is approx. 10 cm long.
This is the second fish. To me it looks like some kind of eel.

It is approx. 20 / 25cm long.

It's possible the first species is a juvenile cod. Check out this identification guide for fish in the Wadden Sea

"Identify these two fish"

The second fish looks like a rock gunnel (or Butterfish; Pholis gunnellus).

This is an eel-like fish found in the intertidal and subtidal zones of the North Atlantic.
Interestingly, the rock gunnel is capable of remaining above the waterline at low tide and breathing air.
According to Campbell (1984):

Fully grown adults can reach 30 cm in length. A long dorsal fin spans the body from just behind the head, supported by soft spiny rays. Its anal fin begins roughly midway along the body. The head is rather small with its lower jaw protruding and mouth turned upwards. Coloration is highly variable, ranging from hues of yellow-green to brown to crimson. A row of 9-13 dark spots, each surrounded by a pale ring, lines the dorsal fin

Sources:
1 Campbell, A.C. 1984. The Country Life Guide to the Seashore and Shallow Seas of Britain and Europe. Country Life Books. ISBN 0-600-34396-0


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Examples of chromosome fusions
One of the best "smoking gun" pieces of evidence of humans' close relation to chimpanzees, gorillas and orangutans is that human chromosome 2 is a fusion of two primate chromosomes, with a double telomere in the middle and a centromere on each side. This fusion, which occurred some time after our MRCA with chimpanzees, was an accident with no evolutionary importance, but it happens to provide extra support for our common ancestry with other African apes. In theory, such fusions could be so commonplace that they can be used to infer much of the family tree of life on their own. I'm sure they're nowhere near that common, but this got me thinking: are there any other examples of species with chromosome fusions (or splittings?) that betray their closest relatives?

Related: https://www.quora.com/Is-there-any-evidence-of-chromosome-fusion-in-any-other-species

See https://www.physicsforums.com/threads/chromosome-fusion.312786/
for answers and several points of discussion on what are called Robertsonian translocations. https://en.wikipedia.org/wiki/Robertsonian_translocation

My question concerned intraspecific cases (a topic of your link 1), not variation in humans (viz. your link 2). I'm glad for both as I learned much about the effects of translocation besides "it needn't matter because loci can line up in a way that lets meiosis work", which explains why natural selection tolerated the fusion in us but was the previous limit of my knowledge. The RT case reveals how acrocentric chromosomes can introduce complications.

You can go to ensembl.org and look up synteny between closely related organisms, like rats and mice.  Below is one example: rat chromsome 1 is made up of all of mouse chromosome 7 and 19, plus parts of 17, 10, and a smidge of 13
https://uswest.ensembl.org/Rattus_norvegicus/Location/Synteny?db=core&r=1%3A126594509-126694509&otherspecies=Mus_musculus


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Why social animals attack odd members of their own group?
Some social animals are known for attacking odd members of their own group, for example, chicken:

If you have a large group of one type of chicken, they will usually gang up on the one or two others that do not look like they do. They recognize color differences the most and will beat up on the odd chickens in a group.

Of course the same behavior is most commonly observed in humans, where any difference can be a reason for aggressiveness.
Why this behavior developed and still exists and how it is called?

The same article also states that "being kept in too small of an area can also create aggressive situations in chickens of the same breed". This happens with many other animals, including humans. Perhaps the behavior you relate happened in an isolated area? In this case, kin selection theory predicts that the first attacked individuals will be those that do not look like relatives.

@Rodrigo, as I understand it, space constraints just increase aggressiveness, not cause it.

I couldnt find specific terms for aggression more than territorial disputes, hyerarchy disputes, persecution, xenophobia. It doesn't seem to have been studied as a general phenomenon. I found something about malawi fish attacking individuals of the same color. Wild chickens don't differ much genetically, and a persecuted albino/mutant can normally leave the flock. to the chickens, the mutant perhaps looks unwholesome and they are trying to chase it away, except it can't escape. Reasons why are very interesting and hyper complex and take several pages to list.

@comprehensible, can you at least provide a summary of these reasons, so I would know what to search for?

In ethology, aggression is part of what we call agonistic behavior. Yes, space constraints increase aggressiveness. Hens do attack each other in order to establish an hierarchy (the pecking order). Maybe the conditions in which the observations of your source were done help to explain what was going on. I think it may be a mix of territoriality, kin selection and restricted space.

Persecution is not a term often used in zoology, compared for example to the notion of social exclusion and hierarchy disputes/social animal hierarchy. That is because humans incarcerate animals which would otherwise flee to safe distance from the group if they are attacked. Wild Mammals, birds, fish, other animals with free movement can normally get safe distance from an aggressive group in order to be safe from persecution.
Fish and insects/island animals sometimes have restricted ranges, and "social exclusion of a mutant" - studies are difficult to find and perhaps won't give masses of information to know why it happens, for categorization and prevalence of different reasons.
I found only one research on social aggression based on appearance:Aggressive biases towards similarly coloured males in Lake Malawi.
Useful related terms for further research for your question are i.e.:

"social exclusion mutants traits aggression"
"social exclusion zoology"
"social exclusion injury zoology"
"social exclusion zoology mutation"
"hyerarchy disputes appearance zoology"

It's an interesting notion for research that you have found, for which a lot can be written, because it gives a complex range of potential reasons for the given behaviour: warding off a contagious individual, warding off a tribe from far away that could displace the current group, inability for the brain to average the mutant's appearance to associate with it, habituation of species to a type of social companion since their birth (i.e. birds sometimes think they are humans)
And so a research requires a broad understanding of juvenile establishment of appearance recognition of other individuals of the group, i.e. where humans search for an average appearance compared to the social group, and chimps recognize close relatives and mate with the most distant, chickens can adopt humans... and animal behaviour towards an ill individual, it's difficult and takes a while to gather actual sci documents for.
When you have found all the closest related research, the given write up would be very fascinating!!! i hope you can search the given topics and give a summary of some previous examples of vaguely related research.

Thanks, I appreciate your answer. I've upvoted it, but I'll leave the question open for everyone to contribute, if you don't mind.


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Anyone know what this bug is? (Southern California)
I found it in Southern California on the fringes of the Mojave Desert. They seem to have nests similar to ant hills but don't look like any ant I've ever seen. They seem to have shown up within the past week or so and have their nests near some big red ants (Camponotus castaneus I believe) though the ants don't seem to be eating them. They are around the same size as the little black ants (Monomorium minimum), but unlike ants they seem to get blown around by the wind. There were hundreds of them around and had several apparent nests. They were also climbing all over a wood fence nearby. I was able to get a picture, hopefully it is clear enough to make out the bug in. You can see a few of them on the gray rock.

The only thing I could think they might be is some kind of termite or something. Are they harmful, and if so, how would I deal with them?

They seem to be true bugs (Heteroptera) nymphs, they have long antennae, an oval shaped abdomen and the wings are not fully developed yet.


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Is the affinity of an enzyme or transporter for its substrate or solute influenced by the amino acids at the binding site?
The affinity of an enzyme or a protein transporter indicates the strenght of the binding of substrate/solute. An enzyme with higher affinity binds its substrate more strongly than a counterpart with a lower affinity. Is affinity always a function of the protein structure of enzyme? If the same enzyme in two different species had different affinities for substrate, would that indicate that there were differences in amino acids at the binding sites of the enzyme in the two species?

I wouldn't say "can bind with more substrate" I would say "binds substrate more strongly" - the answers to your other two questions are yes - affinity is a function of the structure of the enzyme (as well as the shape/structure of the ligand), and yes a difference in affinities in two species indicates there is a difference in amino acids that affects the binding site. Note that it wouldn't necessarily have to be directly at the binding site, just as long as it affects the shape of the binding site.

Km can most easily be understood as the concentration of ligand that results in half saturation of its target. https://arxiv.org/pdf/1305.5533.pdf

I have edited your question to remove the erroneous description of affinity, corrected in the comment and tightened the wording. I have changed the title to reflect the actual question. I have removed reference to Km because 1) transporters are not enzymes and do not have Kms 2) Km is a parameter that is interpreted in terms of affinity, which may only partially be correct. However as your question is about affinity there is no reason to muddy it with mention of Km. Apologies to @WYSIWYG, but this seems the only way to produce a good question worthy of an answer.

@David It depends on how narrowly you define "enzyme", but transporters can indeed be treated identically to enzymes, where the reaction is converting "substance inside" to "substance outside" (or vice versa) rather than making/breaking chemical bonds. Transporters will show the same saturation kinetics as enzymes, and will have kinetic descriptions which have a term equivalent to Km. (Whether you actually call it "Km" is another question.) -- That said, the mention of Km was unnecessary to the question, and I have no issue with its removal.

@RM — That same point struck me after writing. But transporters was an odd choice. I'd have thought general ligand binding as for membrane receptors and proteins such as heamoglobin should be included, in which case you would be talking about Kd, I imagine.

@David - Thanks for bringing Kd up. I agree with what you and RM have said above. Yes, transporters show the same saturation kinetics as enzymes. e.g. - an organism can be exposed for short term with metal and its influx can be studied at different concentrations and this data can be fitted into MM equation to get Km and Vmax. Important caveat is that these Km and Vmax are blended values from several transporters. I have read that -Log of Km can be called Log Kd (dissociation constant). Higher the log Kd, stronger the binding. Would you be able to shed some light on this relationship? Thanks

In a reaction which follows a saturation kinetics, KM is basically the concentration of substrate/ligand at which the rate of the reaction is half of the maximum rate (or the binding sites are half saturated).
The biophysical meaning of KM would depend on the underlying model. For example, in the equilibrium approximation of Michaelis-Menten model, KM is same as dissociation constant (of enzyme and substrate). In the Briggs-Haldane model (quasi steady state approximation), it is slightly complex: KM = (kr + kcat)/kf.
Overall, the thumb rule is that lower the KM faster will the reaction saturate.

Is affinity always a function of the protein structure of enzyme? If
  someone study same enzyme in two different species and observe that
  the enzyme has different affinities in two species, then does it
  indicate that there might by slight difference in key amino-acid
  component at the binding sites of the enzyme between these two
  species?

Almost every property of the protein (not just affinity towards a ligand) is because of its chemical composition and structure. Although they are directly involved in binding, the amino acids at binding site are not the sole contributors to the affinity. The other amino acids that are critical for the overall structure of the protein are also important in preserving the function.

I will add to the answer by @WYSIWYG by turning your question round: “If you changed the amino acids at the binding site, would this affect the affinity of a protein for a ligand*?”
The answer to this is yes, and for an enzyme you can change the substrate specificity entirely, as one can discover from reading this review by Wilson and Agard.
However one should also be aware that changing residues at parts of a protein outside the ligand-binding site can also affect the affinity of binding — see, for example, this paper by Oue et al.
[*This makes the question more general to include other proteins that bind ligands such as membrane receptors and transport proteins such as heamoglobin.]


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Denaturation of protein

Exposure of native protein to heat leads to partial denaturation of the protein due to breaking of-
a. S-S bonds
b. H-bonds
c. Hydrophobic interactions
d. Peptide bonds

After a bit of surface googling I understand peptide bonds are not broken in the process of denaturation and di-sulphide bonds are not broken either (by heat) but by reducers like $\beta$- Mercaptoethanol. These reducers are added in experiments to ensure that the bonds which contribute largely to the tertiary structure are broken.
So either H-bonds or hydrophobic interactions are affected. I cannot make out which one would be the most affected/first one to be affected since the question says partial denaturation, meaning, it was not heated for long.

If you think about the boiling of water, I'm sure you can understand that heat breaks hydrogen bonds. Next consider that the hydrophobic effect is driven entropically and so, by the equation $\Delta G=\Delta H-T\Delta S$, its strength increases with temperature (to a point). See here and here for further explanation. Also, this paper for a more empirical view.

So as the temp. increases the hydrophobic interactions become stronger /are favoured until it is high enough to be disturbed. In the latter is it due to high KE that the hydrophobes are unable to maintain their interaction(closeness)?

@Tytoalba Thanks, I'll add the link (and some others) to the answer. I don't like some of their wording, but overall it's pretty intuitive. I think the first link should answer your question in the comment.

Protein found in a biological system with a unique three-dimensional
  structure and biological activity is called a native protein. When a
  protein in its native form, is subjected to physical change like change
  in temperature or chemical change like change in pH, the hydrogen
  bonds are disturbed. Due to this, globules unfold and helix get uncoiled
  and protein loses its biological activity. This is called denaturation of protein. During denaturation secondary and tertiary structures are destroyed but
  1º structure remains intact. The coagulation of egg white on boiling is
  a common example of denaturation. Another example is curdling of
  milk which is caused due to the formation of lactic acid by the bacteria
  present in milk.

According to the above paragraph, denaturation occurs due to disruption of hydrogen bonds. The answer should be option (B). Note that the energy of hydrogen bonds are 3 - 10kcal/mol. Therefore, hydrogen bonds can be broken and formed easily. You can imagine the process of replication, transcription, etc. where H-bonds are broken and formed easily.
NCERT XII CHEMISTRY (PART II) Chp.Biomolecules 14.2.4 Pg. 141 of that PDF, but in actual book Pg. 416

Thank you :) for putting an effort at writing an answer.

It is my first answer on this site and you are welcome.


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16s rRNA Sequencing From Gut Microbiome (stool)
Do I extract RNA or DNA from gut microbiome (stool samples) if want to do 16s rRNA sequencing?

Genomic DNA, see Illumina's own protocol.

More correctly: you are sequencing 16s rDNA, the gene coding for the 16S rRNA.

Well, it depends on what you want to know. If you want to find who is there, then DNA, if you want to know who is there and their functionality, then RNA. Though if you have a lot of samples and limited budget, 16S rRNA is a cheap reliable option.

In general, you extract DNA, then PCR out the 16rRNA coding regions and finally sequence them.
Here some links
http://press.igsb.anl.gov/earthmicrobiome/protocols-and-standards/16s/
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0068739
https://support.illumina.com/content/dam/illumina-marketing/documents/products/other/16s-metagenomics-faq-1270-2014-003.pdf


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Examples of enzymes working in reverse?
I have always been taught that enzymes can catalyze both the forward and reverse reaction, and will increase the reaction rate in both directions. I understand that the thermodynamics of the reaction are not altered by the enzyme, but I have yet to find a good answer / example for an enzyme that actually does this. (E.g. can a nuclease join DNA together if the products are in excess? Can a protease form a peptide bond?) I am having difficulty finding a resource online that actually justifies this claim without just saying "Yes enzymes work both ways."

you are having trouble becasue it is only technically true. In practice becasue of energy profiles, inhibitors, and a few other factors many reactions will never be reversed or cannot be reversed in conditions that the enzyme will survive. This may help http://bip.cnrs-mrs.fr/bip10/stellen.htm

Remember that these chemical reactions have some equilibrium. This can be pushed to to the right side of the reaction by having an excess of educts - then the reaction goes completely in this direction. If it is the other way, the reaction can be reversed...

Enzymes alter the rate of a reaction by lowering activation energy; they have no effect on the reaction equilibrium ($\ce{K_{eq}}$). Since $\ce{K_{eq}=\frac{k_f}{k_r}}$ and $\ce{K_{eq}}$ is constant, an increase in forward rate ($\ce{k_f}$) requires a corresponding increase in the reverse rate ($\ce{k_r}$). Intuitively it may help to think that the same effect an enzyme has on lowering the energy of the transition state in the forward direction should also be present in the reverse direction. Whether or not the reaction actually proceeds in reverse depends on the free energy difference between the reactants and products and their concentrations (among other things). See this answer for a great explanation.
Because their reactions are in equilibrium ($\Delta G\approx0,\ce{K_{eq}\approx1}$), many enzymes in the glycolytic pathway also catalyze the reverse reaction in gluconeogenesis.

[image source]

What about the ATP synthase? https://en.wikipedia.org/wiki/ATP_synthase it uses proton flow to generate ATP but it can also burn ATP to generate proton flow.

Like other enzymes, the activity of F1FO ATP synthase is reversible.
  Large-enough quantities of ATP cause it to create a transmembrane
  proton gradient, this is used by fermenting bacteria that do not have
  an electron transport chain, but rather hydrolyze ATP to make a proton
  gradient, which they use to drive flagella and the transport of
  nutrients into the cell.
In respiring bacteria under physiological conditions, ATP synthase, in
  general, runs in the opposite direction, creating ATP while using the
  proton motive force created by the electron transport chain as a
  source of energy. The overall process of creating energy in this
  fashion is termed oxidative phosphorylation. The same process takes
  place in the mitochondria, where ATP synthase is located in the inner
  mitochondrial membrane and the F1-part projects into mitochondrial
  matrix. The consumption of ATP by ATP-synthase pumps proton cations
  into the matrix.

Examples of enzymes working in reverse?

Except three enzymes of Glycolysis (Hexokinase, PFK-I and Pyruvate kinase) all catalyse reversible reactions.
As these enzymes catalyse the backward reactions too they are part of Gluconeogenesis pathway.
(A comparison between the two pathways)

Beat me to the example!

At first I felt it was a coincidence. :)

I forgot to upvote. This seems like the most salient example.

You mention nucleases and proteases, but if you turn these processes around and think about the actual nucleic acid or protein synthesis reactions an interesting point emerges:

These synthetic processes involve the production of pyrophosphate — not
  orthophosphate — from ATP (etc.).

(In the case of nucleic acid synthesis this should be obvious; in the case of protein synthesis I am refering to the aminoacyl-tRNA synthetase ‘amino acid activation’ reaction which drives peptide bond formation.)
Why pyrophosphate? The answer commonly given is that this is to prevent the reversal of the reaction. The generation of pyrophosphate achieves this because it is rapidly degraded to orthophosophate by pyrophosphatases in the cell. (See discussion of DNA polymerization in Berg et al.)
If this argument is accepted, it paradoxically illustrates the potential reversibility of the synthetic reactions.


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In (human) zygote cell differentiation, do we know how the cells coordinating the process know their current position?
I've seen this question asked in a mature person -- e.g. lip cells will create more lip cells -- but how about in the developing zygote.   I've seen neighboring cells help determine the type of the new cell. Do we know how they know where they are located, and how many cells of a certain type have already been made, making "lips" complete, or teeth, etc.  So in summary:
1) how do the cells in the growing zygote know "where they are", assuming they need to, to determine what cells to build where for the body?
2) how do the cells know, when the cells of that type building a bone or lips or teeth, etc, are done, since obviously many participate in the process. ?

Can't put up a detailed answer right now, but this link might help for you and anyone else who wants to answer. http://www.popsci.com/body-electrician-whos-rewiring-bodies

This answer may interest you.

There's a protein called Bicoid in fruit flies (see https://en.wikipedia.org/wiki/Bicoid_%28gene%29) that determines the head/tail axis. I remember from biology class that there's a similar protein that determines the up/down axis as well, although I forget its name.
There's almost certainly something similar in humans.


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Why Hfr cells are called high frequency recombination cells?
I understand that Hfr cells are formed when fragment of bacterial plasmid integrates itself in another bacteria's (host) genome through homologous recombination but my question is why do we call these cells as "high frequency recombination cells". Where is the term high frequency coming from?

According to Luca Cavalli-Sforza, the scientist who coined the acronym Hfr:

Recombination as observed at the beginning had a very low frequency. It stopped being rare when I found a mutant strain which I called Hfr for “high frequency of recombination.” I found it accidentally in 1949 while I was selecting mutations resistant to nitrogen mustard and radiation. The first two resistant mutants, which had undergone a rather heavy treatment in the process of selecting for resistance to nitrogen mustard, proved to be exceptional in their mating behavior. One was Hfr and it showed immediately its remarkable mating ability, which was higher than that of normal crosses by a factor of 1000 or more. I repeated the experiment two more times before believing it. The other mutation, as I later proved, was an F- (self-sterile) mutation of an F+
  (fertile) strain. (emphases mine)

Source: Forty Years Ago in GENETICS: The Unorthodox Mating Behavior of Bacteria


text:
Clonal and subclonal mutations in cancer
Likely this will sound as a silly question, but I don't know whom to ask. Ok, here it goes.
McGranahan et al link found that tumors with high clonal antigen load are more likely to respond to the immune checkpoint blockage.
Bozic et al link (at the same time) proposed a probabilistic model to determine the number of clonal and subclonal mutations. They found that fast growing cancer types (where growth is cell division over cell death) are more likely to generate a higher number of subclonal mutations.
Knowing that melanoma and NSCLC are fast growing cancer types, these results seem to contradict each other. We know that they are fast and we know that both melanoma and NSCLC are cancer types where immunotherapy is most effective.
Plus, probabilistically how likely it is for a certain cancer lesions to have lots of shared mutations? A totally genetically homogeneous lesion with no branches with a very high number of mutations.
Or (much more likely) I'm missing something.

Your question is not fully clear. Are you interested in knowing what is the rate of mutation in different cancer types? If so, here is a good starting point https://www.nature.com/nature/journal/v502/n7471/full/nature12634.html

@alec_djinn rather than the rate of mutations, how mutations are distributed in a single lesion.

That depend on the cancer type. Most of the mutations are randomly distributed but some tend to cluster. Check the paper I have linked before. The question is maybe too broad, have a look here http://www.nature.com/tcga/

@alec_djinn (1/2) I will read it, thanks.
But that's the thing, the first paper states that higher number of clonal mutations (present in all cancer cells) rather than subclonal (present in a subgroup of cancer cells) is more favorable for the treatment. The second paper states that fast growing cancer types are more likely to develop subclonal mutations rather than clonal.

@alec_djinn (2/2) Melanoma (for example) is a fast growing cancer, which should develop more subclonal mutations (following the model of the second paper) and should have worse outcome for the treatment (following the results of the first paper). But it's the one showing the best outcome.

I will read the paper you cited and try to answer. In general however, there are some common mutations present in different cancers, like TP53 or BRCA mutations. These mutations are often the "founder" mutations, i.e. they occur at the beginning, so all the other generations will have it as well. If you have a therapy targeting those mutations then the majority of the cancer cells should be sensible to it.

However, fast growing cancers have a higher chance of accumulating new mutations that may confer RESISTANCE to the therapy to a few subclonal population. This will end up in a relapse since the few resistant cells will grow over time and the nasty cycle continues.

@alec_djinn Yes that's what I knew for traditional chemo or targeted treatment. Immunotherapy however targets the immune system. Fast growing highly mutated cancers become more likely to cause immune response via their higher neoantigen load. Now this hypothesis perfectly fits with what we know: indeed we see immunotherapy to work better for melanoma or NSCLC rather than, say, prostate. That's why I cannot fit the first paper into the story.

I have read the papers and I can see you point. But again, in the second paper the authors use data from colorectal cancer. I would not generalize their findings assuming they are valid for other cancer types.

@alec_djinn thank you for the time spent reading the two papers, not everybody is willing to do it ;-) I also thought the the discrepancy could be given by the cancer type, but formula (6) where they estimate the number of clonal mutations seems to be dependent only on the growth rate. Which is the point of my question. I get that they tested only for CRC, but it fits so well that I'm wondering what's the probability that the model does not work for other cancer types. I guess very low.

They don't really contradict each other; the clonality of neoantigens adds an extra layer over the overall mutational load ; but overall mutational load (and consequently overall neoantigen burden, because mutations in a fixed sequence context generate neoantigens at a certain rate) by themselves are also predictive.
Tumours with a high neoantigen burden tend to generally respond better anyway (See Snyder et al, NEJM , Rizvi et al, Science and Van Allen et al, Science) and also the fact that mismatch repair deficient cancers generally tend to respond.
So if you take high neoantigen tumours already (both lung and melanomas have extremely high mutation burdens), and then stratify them based on neoantigen clonality , you tend to further stratify patients by response associating with checkpoint blockade.
The whole point of McGranahan et al was to point out that it is possible to raise immune responses that target all the cells in a tumour, and that the ability to do this may dictate survival in general and checkpoint blockade response in particular, but only when antigen presentation and immune infiltration are intact. McGranahan et al note that clonal neoantigens do nothing in Lung squamous cancers because of depleted CD8 infiltration and MHC class I expression and there is other work (See http://www.pnas.org/content/113/48/E7759.abstract )
As for this bit

Plus, probabilistically how likely it is for a certain cancer lesions
  to have lots of shared mutations? A totally genetically homogeneous
  lesion with no branches with a very high number of mutations.

That is quite complicated to answer; but as a general rule it is worth remembering that,  as the number of divisions and the number of mutations (and ergo prospective subclones) increases, for tumours to stay clonal it requires extremely strong selective sweeps so that at any given time a very small number of clones tends to predominate, and at least in untreated/pre-treatment tumours, there is the tendency for a lot of them to show effectively neutral patterns of evolution ( http://www.nature.com/ng/journal/v48/n3/abs/ng.3489.html )


text:
Pelleting bacterial cells using centrifugation and getting proteins in the supernatant
Do significant amount of proteins from cells find their way in supernatant during pelleting? If the answer is yes then I see two ways in which protein can be in the supernatant
.
1) Through lysis during pelleting
2) Through leakage of protein from cells during pelleting
if significant amount of lysis occur during pelleting then obviously protein will be there in the supernatant due to lysis alone. However, If most cells (like 98%-99%) remain intact  then only by leakage significant amount of protein can be in the supernatant. Both way can also contribute. Which is the case?

I don't have an answer, but secreted proteins will be in the supernatant.

@canadianer I know. But here I am interested in the protein that are inside the cell and are forced outside so to speak by the process of pelleting.

Have you actually seen intracellular proteins in the supernatant after centrifugation that weren't there before?

@canadianer No. Someone suggested that possibility.


text:
Bone fracture cause
I had bone fracture twice in the same arm. So I had first bone fracture in right forearm with 45 degree break on two bones, after 3 months of that fracture while I was climbing a slope I fell and I  used my two hands extended to stop kissing ground, I got hairline fracture in upper arm in middle on right arm again. Why left arm did not get fracture while right arm did, was it due to muscle loss I had incurred during first fracture or my bone became weaker in right arm after first fracture?

Its not off topic question is if muscles weakness happens or bone weakness happens after fracture in limb

the issue is the question is still medically liable, rewrite it to be less about your personal event and more about bone weakness due to fracture in general and it should be fine.


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Are there medical imaging devices to look inside artery?
Are there medical imaging devices to look inside artery? If yes, what is there sensitivity i.e. smallest object they can detect?

Smallest object really depends on the size of the vessel and type of object. i.e., it is much easier to detect a small object that occludes a vessel than one that does not; it is much easier to detect a small, dense object with IVUS than one that is similar in density to the artery wall; it can be easier to detect an object on the inner lumen of a vessel rather than deep in the adventitia, etc.


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Why must gene entrapping constructs be integrated into introns and not exons?
Homework Question:
In enhancer trapping, reporter transgenes are integrated randomly into the fly genome and their expression identifies enhancers and thereby genes expressed in particular patterns. In mice, a similar technique for gene identification is employed called “gene trapping.” In gene trapping, an exon encoding a reporter protein such as GFP (see below) is integrated into random locations in ES cell chromosomes (when DNA constructs are introduced into mouse ES cells, most recombination events are into random sites; homologous recombination is relatively rare). ES cell lines with randomly integrated transgenes are used to generate mice.

Where in the genome must a gene trapping construct integrate in order for ES cells to express GFP?
Answer:

My Question:
Why can't the construct simply be knocked into the coding DNA sequence of the mouse genome? Why does it have to be integrated into an intron?

I don't know that they must integrate into an intron. It seems perfectly reasonable that they could also integrate into an exon, as long as the reporter is in-frame. There is obviously an element of chance in that, and so the advantage of integration within an intron is that splicing will ensure that the reporter is translated correctly. Intragenic regions are also more abundant in the genome and so insertion is more likely. They discuss the advantage of this design in the original paper:
Gossler A, Joyner AL, Rossant J, Skarnes WC. 1989. Mouse embryonic stem cells and reporter constructs to detect developmentally regulated genes. Science 244:463-465.

...ES cells permit selection for rare-occurring integration events, which allowed us... to design and use a "gene trap" vector. The vector contains the lacZ gene, lacking a promoter and translation initiation signal, inserted in frame into the homeobox exon of the En-2 gene such that a splice acceptor is placed at the 5' end of lacZ. Integration of the construct into introns of genes in the correct orientation should create a spliced lacZ fusion transcript and a functional fusion protein when the reading frame is maintained. Evidence for this came from experiments in which a construct lacking the 5' En-2 splice acceptor yielded 12-fold fewer lacZ-expressing transformants than the construct carrying the splice acceptor.

Exonal insertions by gene traps have been reported:
Song G, Li Q, Long Y, Gu Q, Hackett PB, Cui Z. 2012. Effective Gene Trapping Mediated by Sleeping Beauty Transposon. PLS One 7.

Insertion of a trapping cassette into an exon or an intron of transcriptional active loci can generate a fusion transcript that contains the upstream exon and the reporter/selectable marker.
...
Eighteen transposition events were obtained from distinct cell colonies. Blasting the human genome in the NCBI and ENSEMBL database... indicated that seventeen of them landed in an intron and one of them integrated in an exon at active genomic loci. These data are in consistence with the fact that exons and introns comprise 1.5% and 24% of human genome, respectively.

See here for further reading.


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Basic behaviour patterns of animals for a modeling project?
I am working on a project (a tool) for my GIS class that models natural habitat of an animal based on landcovers, distance to the nearest watersource and distance from developed area in Kansas, USA. I need these numerical values for at least a couple of animal species (larger herbivores that can occur in Kansas) so the user can enter these values and visualize the natural habitat.
Now, I know it is very difficult to determine such values (and modeling natural habitat is much much more complex than this) but these values don't need to be very accurate as it aims at showing the capabilities of the GIS software rather then producing real-world output (again, its a school project).
I've contacted a professor at the Department of Biology but she only provided me with tons of over-detailed information and links to scientific research which are of no use for me.
For example: a deer goes to drink water twice a day and doesn't move more than 10 miles a day -> it is most likely to occur within 5 miles from a water source. I know it is a crude simplification but it really doesn't matter in this case.
Is there a source of such information?

I am pretty confident you won't find a source that has the data you want in a nice table format - you will have to extract the information from scientific literature gathered for other purposes. I'd suggest searches on scholar.google.com for specific species you want to track, and pairing that species with some other terms of interest. For example, "white tailed deer GPS" might turn up some papers relevant to you (I tried this search and several seem applicable). Like you say, you don't need precise data, but you can make some estimates from these types of sources.

Also note: it seems like there is a lot of GIS work with white tailed deer in particular, so you can even just search for "white tailed deer GIS" and maybe add in other keywords that are relevant to you like "water." I'd also suggest you go back over the work provided by the professor you talked to: I very much doubt she was steering you wrong, probably the information she provided is very useful, you just need to apply some search strategies within that information to extract what you need. That is an essential skill to have and probably more important than 95% of your coursework.

You might be better off looking for gps tracking data and pulling the relevant information out of it.

\You are not going to find a lot of what you are looking for, generalizations like that are not often published together. As Bryan mentioned you need to search the sources you have in detail, statements like that are not going to be prominent but will be dispersed as minor details in many many studies. You will have to compile them. worse these will rarely be consistent animals change behavior depending on the conditions. You will also have to become very familiar with the terminology involved.

This kind of study is what you are looking for, https://academic.oup.com/jmammal/article/96/2/279/900871/Purposeful-wanderings-mate-search-strategies-of

Thanks a lot to both of you, Bryan and John! This is definitely going to help. And I am sure the professor provided me with very useful information it's just way too complex considering what I am looking for & how much time I have.


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What voltage damages a neuron or a group of neurons?
Neurons are stimulated for research and therapy purposes. How much voltage (current, duration, etc) can a neuron or a group of neurons, in humans, take without being damaged?

There are way too many factors involved to give you a simple number, and "damage" is also a very non-specific term. Also, when you write "voltage (current, duration, etc)" it makes it sound like you don't know what terms like voltage and current mean: for example, current is not a type/part of voltage, so you might want to start there first.

i know current and voltage are different but related quantities.  for damage,all three or any one of the three parameters may be enough;that is why i included all. also, yes,damage is subjective,so be it. if you know anything about any type of damage,write about it. are there so many types of damage that it cannot be summarized here? even then, some major ones can be mentioned.

also,another way to think about it is how much is known to be safe.

It probably mostly depends on how you stimulate them, when we probe the ulnar nerve in practical classes with a stimulator on the skin, then 20V seems about fine. Most students will handle 20V 100 ms pulses, but some will flinch.
If you have a neuron connected directly to an electrode (in a dish), then you will get decent responses from 50-100mV square voltage steps. Individual cells will respond after 10-40 mV (depending on cell type), much more than 150-300 mV will probably be problematic (and not physiological) for single cells.
It sounds like you need to read some early electrophys, start with the squid giant axon, then Neher and Sudhof were the gods for the start of my PhD.


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Does mechanical shock kill animals?
I heard that loss of blood kills shot animals, a lot. But a few times, I heard that mechanical shock kills animals. For example in this video (starts to play at the right spot; relevant from 14:35 to 15:03).
That loss of blood kills an animal seems pretty obvious as the brain can't function without being supplied oxygen and it can't be supplied oxygen if there is no blood to carry the oxygen.
If the mechanical shock is applied to the head, it also seems somewhat reasonable. I guess it could be that the shock destroys vessels in the brain. But other than for a headshot: Is there a biological reason why an animal couldn't continue to live after experiencing mechanical shock due to being hit by a small projectile (being hit by a truck which is able to accelerate the entire animal doesn't count)?

@canadianer Yeah, moving. Of course, you can move a car slow enough so it's true. If you move a car slow enough, its kin. energy is equal to that of a flying fruit fly. Example: The mass of the bullet an AK 47 fires is 7.9 g = 0.0079 kg. Its muzzle velocity is 715 m/s. A car typically has a mass of at least 1000 kg, so let's take that. The kinetic energy of that bullet is equal to the kinetic energy of the car when the car moves at sqrt(0.0079 kg * (715 m/s)^2 / (1000 kg)) = 2 m/s. You don't die when hit by a car moving at 2 m/s. Alternatively, you could walk against a car with 2 m/s.

Yeah I pressed the square root button instead of the square button in my rough calculation. I'd better just stick to biology…

With a small projectile you will always get some sort of shearing forces: the tissues directly impacted will accelerate faster than adjacent tissues, and so on. This can cause tearing of many tissues, including blood vessels, but other tissues as well.
In the context of the brain, the effects of traumatic brain injury are a constant area of research, for example see here.

But is that shock sufficient for killing a reasonably-sized (deer, wolf, human) or big (giraffe, elephant, hippo) animal? Is it what actually kills an animal when a hunter shot it? As stated in the question, the effects of hitting the heat aren't in particular interest for this. Typically, less fragile parts of an animal's body are hit. You probably could die if someone threw a rock at you hard enough and hit your head but you wouldn't die if that rock hit your stomach or thigh.

Usually hunters are aiming for vulnerable organs like the heart. If a hunter hits a deer in the gut, it will probably die later from blood loss or much later from infection. If your side-view mirror clips a deer in the head as you drive by, you might cause enough concussive force to cause death even without vascular trauma, though both would be a factor.

But if the hunter doesn't hit a vital part (e.g. hits the deer's thigh), can the shock kill a deer or will it just really ruin its day and handicap it?

I can't think of any reason, besides the possibility for blood loss, eventual infection, or a secondary cause due to impaired mobility, that a gunshot to a deer's thigh would kill it.


text:
How would you model the evolution of two genotypes across generations?
Say you have a genotype A that produces x offspring and another genotype B that produces y offspring, where x>y.  These x offspring are of genotype A but with modest differences in fitness due to mutation and these y offspring are of genotype B but with modest differences in fitness due to mutation.  How would you model how many offspring these x offspring can themselves produce and how many offspring these y offspring can themselves produce as a function of the quantity their original parents produced?
Obviously, you could say that each descendant of genotype A produces x and each descendant of genotype B produces y, but that would unrealistically benefit genotype A, since realistically, one of B’s offspring could have a chance to be fitter than A’s by developing a favorable mutation or one of A’s offspring could have a chance to be less fit than B’s by developing an unfavorable mutation.
You could say that each descendant of genotype A and B produce (x+y)/2, but this would not be fair to genotype A, since it is fitter, so its offspring would probably be fitter than B’s offspring.
You could use the breeder’s equation and say that each of A’s offspring produce xh+m(1-h), where h is the heritability of fitness and m is the population mean, and that each of B’s offspring produce yh+m(1-h).  But this is also unfair to genotype B because all of its offspring are less fit than all of A’s offspring, since x>y.  So, what’s a way of modeling how resultant mutations might occur, such that B has a chance of producing some offspring that are fitter than A’s offspring?

A few questions: 1) you seem to be conflating fitness and number of offspring. How sure are you that this is a good idea, if only on a conceptual level? 2) "m" is population mean of what, fitness=number of offspring? Does this mean "m" changes as the makeup of the population changes, or is it just the mean of "x" and "y"? 3) if "h" is nil then A's offspring produce "x" offspring and if it's 1 they produce "m"; shouldn't it be the other way around?

You seem to ignore the variation you postulated within your populations. It all depends on that; for example if the 2nd-gen fitnesses are normally distributed with a mean of the parent gen fitness, then "but what about B's offspring that are fitter than A's" doesn't necessarily matter, since B's less-fit offspring would be less fit than A's least fit, and A's fitter offspring would be fitter than B's fittest (i.e it will come down to the mean, which is x and y). And if the distributions between the two are different then all bets are off. Surely this needs to be in the model somewhere.

(for example you said each descendant of A producing x and each descendant of B producing y unfairly benefits A, but if the variation in fitness is that half the offspring produce "parent fitness + z" and half produce "parent fitness - z", then do the calculation you'll find it's equal to if each descendant of A produced x and each descendant of B produced y).

Thank you for the questions.  1)  My understanding of fitness is that it has a number of definitions depending on context and I think my usage of the term is okay.  Fitness covaries with the ability to produce offspring.  2)  Yes, m is population mean of fitness (or number of offspring).  m should change as the makeup of the population changes.  I am not suggesting I should use heritability in this way though.  Just gave an example of what I'm trying to get at.  3)  You're right.  I apologize.  Will edit it.

A's fittest offspring wouldn't necessarily be fitter than B's fittest.  It would just be more likely.  B's less fit offspring would not necessarily be less fit than A's less fit (especially since A would have more offspring).  And yes, that would also be unfair to B because it wouldn't give B the possibility of having more grandoffspring or greatgrandoffspring like some kind of random process would.

"A's fittest offspring wouldn't necessarily be fitter than B's fittest. It would just be more likely." But that assertion depends 100% on how your fitness varies from parent to offspring. That variation must follow an equation (a probabilistic one if needed); if you've decided what it is then it should be in the model. If you haven't decided what it is then you need to decide, because that equation will determine your results more than anything. I already gave an example of one (clearly not what you have in mind) that would give results contradictory to what you seem to expect.

What I'm asking is what is a good way of representing this?  That is, what is fair to both A and B?  Have you seen anything in the theoretical literature that models something like this?  You gave a good example, but in that example, B would have no shot of having more grandoffspring.  I haven't seen in which offspring fitness varies as a function of a parent's fitness.  The assumption commonly made is that the fitnesses of all offspring are equal, which is unrealistic.

Sorry, I hadn't seen (or had forgotten by the time I wrote my later comments) that "what equation would allow B to have fitter offspring than A" is basically your question. I'll put the rest in an answer.

Allows B to have fitter offspring than A in a realistic way.  Obviously, A would be more likely to have fitter offspring, but B would have an opportunity.  How has/can this be represented?  Thank you.  I look forward to your answer.

So, what’s a way of modeling how resultant mutations might occur, such that B has a chance of producing some offspring that are fitter than A’s offspring?

Here's one possible solution that fits your criteria. You could have something like this (with "d" being the distance between "x" and "y", i.e. d=x-y and "n" being the n-th offspring, so it varies between 1 and x for A and 1 and y for B) :
A: n -> x + r(n), where r(n) is a random number between x-d and x+d
B: n -> y + r(n), where r(n) is a random number between y-d and y+d
(I write r(n) not because r is a function n, but because a different number is drawn for each n. I also didn't specify r's distribution, that would also need to be decided when making an actual model)
This is your situation where some offspring of B have a chance of being fitter than offspring of A, and the least-fit offspring of B can even be fitter than the fittest offspring of A. I think it fits your criteria and thus answers your question. The sum of the grandoffspring is basically the basic x or y squared (that you would get if each offspring had the same fitness as their parent) + the sum of all the "r"s.

OK thank you for the effort you made.  Can I upvote your answer but not give it a check because I would like to leave the question open for other ways of modeling this (perhaps ways people have seen in the literature)?  Can there be multiple "accepted" answers in a thread?


text:
Does vegetable oil allow methane to pass through?
I'm doing an experiment investigating how temperature affects the rate of methanogenesis. I'm using a peat sample that will be kept in a conical flask connected to a gas syringe with a layer of Janus Green B administered (to indicate if aerobic conditions are present) and vegetable oil (to prevent air entry and to allow carbon dioxide to pass through). There are two main concerns I have about my experimental design at the moment. Firstly will methane also pass through the vegetable oil and secondly one of the pathways of methanogenesis (Carbon Dioxide + Hydrogen → Methane + Water) uses Carbon Dioxide as a reactant, so I'm worried that some of the carbon dioxide produced by the decomposition of acetic acid will be used in the other pathway and not arrive at the gas syringe. Does anybody have any suggestions about making my methanogenesis experiment feasible?

Welcome to Biology.SE! This question might be a better fit for chemistry.SE


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What are homologous chromosomes?
I've read that homologous chromosomes are composed of one maternal chromosome and one paternal chromosome.

I want to confirm if this image is for one set of homologous chromosomes:

They have the same size, length, loci and same genes but are not identical.
They have different DNA sequences, so contain different alleles.

Still, I'm confused if it should be one maternal chromatid and one paternal chromatid.

I thought, homologous chromosomes are supposed to be one maternal and one paternal chromosome?

Can someone kindly explain if chromosomes are duplicated as to one paternal and one maternal chromosome or not??

Now is this image a homologous chromosome duplicated? So there are two sets of homologous chromosomes?

A similar question from January.

Wow thank you for the simple way of explaining it.
I got it clearer now.

Part of the problem is that chromosome is a slippery word. Really it should refer to a single DNA molecule, but since chromosomes came before DNA this sometimes gets a little loose.
This explanation refers to the five Figures in your question as 1-5 from the top.
Figure 1 A pair of homologous chromosomes from a diploid cell  drawn to illustrate their relationship in terms of genes, alleles, centromeres etc. This doesn't really correspond to any biological event. Colour coding is to emphasise that they originated from different parents. I suppose this is what you see in a karyotype.
Figure  2 An homologous pair again, different colours again, but they aren't closely side by side. When each one replicates we end up with pairs of sister chromatids joined at the centromere. These are four homologous chromosomes. At mitosis each of the pairs of sister chromatids will be pulled apart with one chromosome going to each daughter cell. So the daughter cell will end up with a pair of homologous chromosomes, one maternal, one paternal.
Figure 3 is very similar to Figure 2, nothing to add really.
Figure 4 is similar to the right hand half of Figure 2 except that the chromatids are shown not joined at the centromeres. This image is being used to show that recombination can take place between chromatids. This would be during meiosis, but the pairs of sisters would actually  be joined at the centromeres
Figure 5 Up to now the images have been designed to illustrate one chromosome either individually, as an homologous pair or as a pair of sister chromatids. But of course most organisms have more than one chromosome. Leaving aside the X and Y chromosomes your cells have 22 pairs of homologous chromosomes or 44 individual chromosomes. When these replicate the cell  will have 88 chromatids, forming 44 pairs of sisters, corresponding to  22 homologous sets of four.

Nice to see you around here again!

Thanks!  I was getting obsessed so needed time in rehab.

Ha! I think I could use that too.


text:
Identify this spider from Bangladesh
Location: Jahangirnagar university, Savar, Bangladesh

EDIT: Here is the video from which image is taken

It  is a jumping spider. Could be Genus Epocilla sp. .
Jumping spiders have their posterior lateral eyes placed high up the cephalothorax and the rest three pairs in a typical arrangement as observed in your specimen.

An image of Epocilla sp. from Wikipedia.
Your specimen more closely resembles the E. calcarata .

Epocilla calcarata? http://farm2.static.flickr.com/1265/1229102333_2d73378d43.jpg

I can't assure. Not an Arachnologist myself, I think an expert can shade some light.

Accurate Spider identification to species level is done by viewing the tiny structures of their anatomy under a microscope examining the spider’s reproductive organs. To find out which family your spider belongs to comes with experience. Helpful in identification are the eyes of the spider and they are not visible in this photograph. How many does it have? How are they arranged? How does each eye’s size compare to those around it? Here is a helpful link to some rules for identification. Good luck!!
http://www.spiders.us/articles/identification/#spider-location

Here is a video. https://youtu.be/52lSx_yl45A

Welcome to Biology.SE. Your answer seems more like a comment and does not fit our standards for good answers (see here and take the tour) - this is not a common discussion forum, so if you cannot answer the question, you should not give an answer. As is, your answer is very likely to be down-voted or deleted. Please edit you question if you want to make a suggestion regarding the id of the spider or delete it if you do not have a suggestion. Thank you!


text:
Kinetics of allosteric regulation
I have found a diagram similar to the following one in my biology textbook. The diagram describes allosteric regulation.

However, I do not quite understand why the maximum reaction rate $V_{max}$ is still reached, even though I thought this is only possible for a competitive inhibition.
I think that the diagram should look something like this where the maximum reaction rate is not reached.

Is there simply an error in the diagram or have I misunderstood something here?

My textbook states clearly that $V_{max}$ remains the same in a case of competitive inhibition but is is lower in case of non-competitive inhibition under which, according to my textbook, you can count allosteric inhibition. Also I see diagrams like this everywhere where $V_{max}$ is lower for a non-competitive inhibition

Your text-book is incorrect in saying that allosteric inhibition is not competitive. I do not know what your text book actually says (and do not care). The curves usually show the negative effector not reaching the maximum rate because a very high concentration would be needed to achieve this (and in any case the curves only reach this at infinite concentration). I have added my own answer to the question I cited (as I had been meaning to do for a while because of the confusion these terms cause). Look at my diagram carefully and you will see why allosteric negative effectors are competitive.

To clarify. The diagram in your textbook is probably correct, if idealized, but I cannot be sure as I presume you have redrawn in it from the spelling mistake "inhibtor".

Ok, so after watching this video on Khan Academy and reading your answer to the other question, I got it clear that allosteric inhibition can be competitive. So in the diagram in my textbook I have a competitive allosteric inhibition, right?

Yes, I have redrawn it, but took caution to have it be exactly the same. I apparently messed up the spelling, though, sorry.

Easy to make typos in figures. As for your question, I would never use the "term competitive allosteric inhibition" for the reasons I give in my answer. Don't learn terms by rote to parrot back to someone. Think about what is happening and describe it clearly.

Yeah, you are right, but in general I'm right with saying that allosteric inhibition can be a form of non-competitive inhibition but it does not have to be and could also be a form of competitive inhibition, right?

So in conclusion, allosteric inhibition can be both competitive and non-competitive. Right?

Wrong. As far as the other answers to the question go, and in terms of the kinetics and my diagram, I cannot see how there could be a negative allosteric effector that acted in a non-competitive manner.


text:
Is human blood useful as food?
Lacking other resources, could a healthy adult slit his wrist to feed a starving child with his blood? Would it be nutritional and would a starving dehydrated child eat it?

Interesting... but hopingly just a hypothetical situation? Seems platelets (coagulating blood corpuscle) and immunoglobulins may cause problem.

High amount of minerals ( iron for example) could show their toxic effects.

Yes, blood is nutritious, and whether a child would drink it is up to the child. It's not exactly palatable in large quantities; it's warm, and coagulation renders it gooey relatively quickly. It should help in dehydration (the degree depending on the cause of dehydration) because it's isotonic. The Maasai drink blood from their cattle instead of slaughtering them for meat. All that being said, the adult, if not pretty careful, will not be able to care for the child, and they'll both die.

@AlwaysConfused do human enterocytes have receptors also for other classes of Ig, than for IgA? Do you believe that the number of Ab resorbed this way could cause a life threatening problem?
Also, Ig are quite stable molecules, but wouldn't most of the platelet compounds get digested in stomach?
Just a note: in our culture (middle-east europe) it's common to eat pre-cooked blood from swine and it's considered quite nutritious and delicious meal. (pre-cooking however means that most of the mentioned proteins are probably already denatured )


text:
Why do people with type O blood have anti-A and anti-B antibodies?
People with type O blood have anti-A and anti-B antibodies, even without receiving a transfusion. Why?

I'm supposing that you're asking why O-type individuals have anti-A and anti-B antibodies without having had any transfusion, because if they had the antigens in their blood they would not produce antibodies (the molecule would be recognised as self). Anyway, I believe you want to improve your question a bit.

On a second thought, I should simply delete my answer: your question's title is kind of understandable, but your question's body makes no sense! Maybe the person who upvoted it may shed a light on this.

@GerardoFurtado — Take the bull by the horns and rewrite the question to fit your answer, otherwise the whole thing is meaningless and is likely to be shot down as such. Are you sure the question has not already been asked?

@David The problem is that, despite the title being somehow meaningful, the body of the question makes no sense. I'm afraid of, by editing it, turning it into something different from OP's intent (whatever it is). Well, I'll try, OP can roll it back anyway if he/she doesn't like the edit.

Similar to https://biology.stackexchange.com/a/5724/1320

even though @GerardoFurtado 's answer is very interesting, i think it fails to explain why there are the antibodies there in the first place. so if that was your question, i posted my answer to it!

To understand what's happening here, let's have a look at the actual ABH (or ABO) antigens:

As you can see, they are not very big molecules: quite the opposite, they are relatively small globosides.
That being said, how is it possible a type O individual producing anti-A and anti-B antibodies without having any contact with the antigens? And that is the same as asking "how is it possible that a type A individual produced anti-B antibodies without having any contact with the antigen?"
The answer is: there was contact with the antigens, even without a blood transfusion.
According to Laura Dean (Blood Groups and Red Cell Antigens, chapter 5):

ABO antibodies in the serum are formed naturally. Their production is stimulated when the immune system encounters the "missing" ABO blood group antigens in foods or in micro-organisms. This happens at an early age because sugars that are identical to, or very similar to, the ABO blood group antigens are found throughout nature.

Thus, from an early age, we have contact with the antigens, coming from food or bacteria in our digestive system. As we get in contacts with antigens A and B, this is what happens:

People with type A blood: they will produce anti-B antibodies.
People with type B blood: they will produce anti-A antibodies.
People with type O blood: they will produce anti-A and anti-B antibodies.
People with type AB blood: they won't produce antibodies (regarding A and B antigens).

Source: Dean, L. (2005). Blood groups and red cell antigens. 1st ed. Bethesda, Md.: NCBI.

Antibody-producing cells (B lymphocytes) generate antibodies through a gene recombination process, that allows a virtually infinite number of antibodies to different antigens to be created, including against self-antigens (https://en.wikipedia.org/wiki/V(D)J_recombination).
A process of maturation, if working correctly, allows for those cells producing antibodies that strongly bind to self-antigens to be suppressed or eliminated, preventing autoimmune attacks (https://en.wikipedia.org/wiki/Immune_tolerance). In this process, specialized cells present a myriad of self-antigens to the maturing lymphocytes, signalizing them to undergo apoptosis or become regulatory cells if they bind to them. Organisms with the A antigen will present it to maturing lymphocytes and thus create tolerance to it, not having cells producing A-antigen binding antibodies; but they don't have the B antigen, so their lymphocytes won't be selected over it, and they will have cells producing B-antigen binding antibodies, which, if such antigen is introduced into the body, will mount an immune response against it.
Likewise, someone with an O type blood won't have both the A and B antigens, and so cells producing antibodies that bind to them will be allowed to mature, and they will have anti-A and anti-B antibodies circulating in the blood.
In conclusion, we can and do have antibodies for more antigens than we will ever encounter, and we have then before ever encountering them. If we do encounter them, then the cells that produce those antibodies will multiply and the number of those antibodies will greatly grow. Typically, we only don't have antibodies for self-antigens.


text:
Which Geologic time scale is the most accurate?
I kindly ask to show me some pictures that is a generally accurate geologic time scale.
In google, a lot of geo time scales are different.
On what i have searched there are 2 major eons which are
I.Precambrian eon
 1. Archean eon
 2. Hadean eon
 3. Proterozoic eon
II.Phanerozoic eon

Palezoic
Mesozoic

3.Cenozoic
But along with it Precrambiann is further divided to proterozoic eon, archaaen eon and hadeon eon are ERAS of but it clearly says its an EON.
And how about in Phanerozoic eon?
Kindly please clarify the following. Thank you!!

I don;t quite understand your question. The only question mark in your post is "And how about in Phanerozoic eon?" which question is rather vague. Are you asking for the subdivision of the Phanerozoic eon? It would not match with the title. Are you asking "What is the difference between an eon and an era?"?

According to these Wikipedia pages - https://en.wikipedia.org/wiki/Geologic_time_scale#Table_of_geologic_time, https://en.wikipedia.org/wiki/Precambrian - the Precambrian is a "supereon" not an "eon".

According to these Wikipedia pages - https://en.wikipedia.org/wiki/Geologic_time_scale#Table_of_geologic_time, https://en.wikipedia.org/wiki/Precambrian - the Precambrian is a "supereon" not an "eon".
The ICS International Chronostratigraphic Chart, ambiguously, puts "Eonothem/Eon" over both the "Precambrian" column and the "Hadean - Archean - Proterozoic" column, with the next column over being "Erathem/Era", which corresponds to what's in the other periods.
It seems clear that 1) the Hadean, Archean and Proterozoic are considered "Eons" like the Phanerozoic is (with their sub-divisions all being called "Eras"), 2) the Precambrian is a larger period of time that encompasses the Hadea, Archean and Proterozoic, and 3) there might be some disagreement as to how to name the period of time the Precambrian is; Wikipedia says "Supereon", which makes sense, but the ICS chart doesn't include that word and seems happy to have it share the name "Eon" with its immediate subdivisions. But the name is just a name, the more important things are how the different periods relate to each other, which is covered by 1) and 2).


text:
When to decide that two similar sequences are different genes or not?
Working on RNA-Seq data directed me to ask this question. In RNA-Seq jobs, after de novo assembly we have lots of transcripts with different rates of similarity (0 to almost 100 percent) that we sometimes don't know their loci.
So regardless of locus, on what reasons we differentiate two or more sequences?
How can we differentiate alleles of a gene from paralogous genes?
I hope my question is clear enough.


text:
Why gout attacks mostly big toe?

A gout attack typically causes pain, swelling, redness, and warmth (inflammation) in a single joint, most often the big toe.

What makes big toe more susceptible for gout?
Also I was said that it mostly occurs in right big toe, if this is correct then what could be the reason for its right sidedness?

Source : http://www.webmd.com/arthritis/gouty-big-toe

That link doesn't say anything about the right side being more often affected.

it was told in my class by the lecturer.

Then I think you should drop the part about the right toe. Without a peer reviewed source, I don't think it's relevant.

Edited the title. the part about right toe is now subordinate.

The question has been explored in great depth in the cited paper. Have a look.
Roddy E. Revisiting the pathogenesis of podagra: why does gout target the foot?. Journal of foot and ankle research. 2011 May 13;4(1):13.
Summary:

Nucleation factors: The site of Gout depends on where the Monosodium Urate (MSU) crystals are likely to form. This process of nucleation depends on a variety of factors. One is temperature, its solubility decreases with temperature and hence the fingers and the toes are more likely sites of MSU precipitation. Further, trauma and pH also affect the nucleation. Repeatedly stubbing a toe makes the first metatarsophalangeal joint (MTPJ) specifically vulnerable.
Cartilage damage and Osteoarthritis(OA).OA sites are correlated with those of higher MSU deposition and cartilage damage (for reasons and evidence, refer to the cited paper). Hence, factors which make MTPJ more susceptible to OA can increase the predilection for MSU deposition. These include "increased concentrations of chondroitin sulfate, degradation of protein-polysaccharide complexes, and epitaxial MSU crystal nucleation and growth on cartilage fragments"

The right sided predilection might be because most people are right-handed, and they might be more likely to injure or stub their right toe.

Is it true that it also attacks mostly right side?

See the edit @JM97

could you answer this: https://biology.stackexchange.com/questions/58779/why-are-sutural-bones-more-common-in-lambdoid-suture  ?

@JM97 I went through the question. I couldn't find a satisfactory resolution of the query, only peripheral hints and such. Will post, in case no one does.