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Resolution of X-ray crystallography
A structure determined by X-ray crystallography has a resolution of 1.5 Å. When I look at the coordinates, I find every backbone C-N distance is 1.32 Å.i.e. Accurately predicted. If resolution is not good why every C-N bond distance is accurately predicted?

The structural model of a protein is obtained using both experimental data and prior knowledge about geometry of macromolecules. As a structural model is refined, interatomic distances are also restrained. So, the C-N distance isn't really predicted. Alternatively, knowledge about this distance is used to construct reasonable model.
In response to the comment below I'll cite Rupp's Biomolecular Crystallography, the most comprehensive book on this subject. Refinement and restraints are covered in Chapter 12, Model building and refinement.

An observation does not have to be an experimental observation
  (measured data) specific to the particular structure, but can be any
  type of general prior knowledge regarding molecular stereochemistry.
  Known stereochemistry can be exploited and implemented in
  macromolecular refinement in the form of geometric constraints and
  restraints. [...]
We know from accurate and precise small molecule and peptide fragment
  structures [...] that bond lengths and bond angles show distinct and
  relatively narrow distributions around their mean positions. [...]
Refinement programs read restraint target values specific for each
  residue and each ligand molecule from restraint library files, which
  are subject to continuous empirical update.

The value given in this book (Table 12-1) for peptide bond C-N is 1.336 Å with variance 0.023 Å.

it's always helpful to include resources for external validation - it may seem silly when the answer is common knowledge in your field, but it is very helpful to those outside of a specific field.

@VanceLAlbaugh: I've added a citation


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Why are victims of Covid19 being wrapped in plastic?
Several articles describe the unique ways Covid-19 patients are being buried.
For example, in this Reuters article about Israel:

These included decontaminating and hermetically wrapping bodies in
  double layers of polyethylene. For Jewish dead, ritual washing of the
  body would be conducted in one of four special stations in the
  country, the document showed.

And this LA Times article about Iran:

Nor are they wrapped in traditional white cloth. They are covered in
  hospital plastic, marking them as victims — both young and old — of
  the coronavirus.

People die from viruses all the time but I've never heard of victims being buried in this way. What is unique about Covid-19 ?

The WHO guidelines for VHF victims (Ebola etc.) do say that they should be buried in body bags, and if those are not available, in plastic sheeting.

If body bags are not available, wrap the body in two
  thickness of cotton cloth and soak with 1:10 bleach
  solution. Then wrap the body in plastic sheeting. Seal the
  wrapping with plastic tape. Spray the body bag as in
  Step 3. Place the body in a coffin if one is available.

Obviously some are treating covid-19 victims with the same amount of caution. I can't tell you at the moment if this is justified or not.

I suppose we might see copper-lined coffins soon.

source: Stack Exchange

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sort: votes


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How to identify genes?
You and me are different at DNA level. My eye color gene is different from yours. So, my DNA is different from yours. How can a scientist identify a certain gene in a chromosome (and its function) if chromosomes are different? How can we talk about "the" human DNA when nobody share the same (except twins)? Please, this is a practical question about how scientists identify genes, not a philosophic one (a question that bother me every time I read about discoveries in genetic)

Humans share about 99.9% of their DNA, see this link (http://biology.stackexchange.com/questions/21699/what-percentage-of-dna-do-people-share/21706#21706), so the phenotypes you referred to are caused by allelic variations i.e. small changes in the genome but the genes are still identifiable as being A or B or a homologue of the two.

First of all: We are not very different on the genetic level - the identity is somewhere around 99.6 to 99.9%. See here for details. If this wouldn't be like this, things like blood transfusions or organ transplants wouldn't work.
To identify genes there are different routes. "In the old days" (meaning before the possibility of massive high throughput sequencing or DNA microarrays), genes were usually discovered when they were connected to a disease which had a noticable phenotype. Researchers then tried to find out which protein or pathway was affected and from there went backwards to identify the genetic region. This way of discovery was relatively slow. An example for this kind of identification is the identification of the Mitf gene which is important for the development of pigmentation.
If you sequence DNA (doesn't matter here if these are complete genomes or only parts of it) you can identify genes based on homology with already known genes. You can also predict the presence of genes in a certain sequence based on regulatory sequences in the region before the gene (the promoter). These sequences are known and also highly conserved, so this gives a good estimate. Predicted genes usually need to be verified experimentally.
What is done today are the so called "genome wide association studies". Here you take a big cohort of people which all share one phenotype (for example blue eye color). Then you take a second group of people which do not show this phenotype and analyse their genomes (usually by sequencing or SNP genotyping). Then you compare the two groups to find the differences. Ideally you can then more or less directly identify a causative mutation which is responsible for the phenotypic difference between the two study groups. This usually needs also to be verified further.

GWAS is what I was looking for.

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Consumption of different type of energy when one is inactive
I'm wonder if there is any study done on this and what are the results?
how much of each type of energy one's body(healthy normal person) uses when inactive(seating down)
I know there are alot of dependencies, but any kind of ball park answer will be great.
ps: when I say type of energy, I mean: fat, carb, protein.

Simple google search gave this ! Good enough to answer your question.

Thank you for this link, but it doesn't provide me with any precise numbers I'm looking for.

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What microscope/magnification would I need to observe P. Acnes bacteria?
I am currently attempting to grow a culture of P. Acnes bacteria.  Right now, my only hope in identifying colonies of the bacteria in the culture is to use a black light to find colonies that glow orange.  I am not sure whether or not this will work since nutrient agar may not provide them with something that helps them produce porphyrins.  It's also entirely possible that another form of bacteria contaminating the culture would produce the same effect.
I would like to entertain the possibility of buying a microscope for this project.  I have never owned a quality microscope(just toy ones in the past), so I don't really know what type of microscope or what magnification I'll need in order to correctly identify and observe the P. Acnes bacteria.
What would be interesting is if I could turn this into a pharmacological project; if I can verify that I have the correct bacteria(to a fair degree of certainty, anyway), I can see how the bacteria reacts to different chemicals and environments.

How a bacterium reacts to different chemicals and environments is often more useful in identification that microscopy. It's also cheaper. You may want to look into some differential/selective media and/or biochemical tests. Or just send it away for 16S sequencing.

I agree with canadianer that chemical tests are generally more useful for identification.  However, morphology does help and some staining techniques can be useful for identification (the Gram stain is the obvious one).  If you are looking for a microscope, look for a nice scope with a 100x oil-immersion objective and a 10x ocular lens (12x would be OK too). Zeiss, Nikon and Olympus are some old names that make good scopes - and there are more.


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Central of Dogma? reverse transcriptase says No
I know what a reverse transcriptase is but I'm not sure why it is suggesting that the central dogma may be wrong -- RNA first then DNA instead of the well-known sequence of DNA -> RNA -> protein

Go to wikipedia and look reverse transcriptase. All your questions will be answered. But to answer your question, reverse transcriptase is an enzyme that uses RNA molecules as a template to make a DNA version of said RNA. ie the flow of information from DNA to RNA is reversed.
The central dogma... is a terrible name. It was an idea state in the 1950s that information flows one way from DNA to RNA to protein. The use of the word dogma is an ill choice to use. Because science does learn new things. And given that DNA was only just discovered in the 1950s....ie the same decade... the word dogma is a bad idea. SHould have waited a few more decades first
Anyhow... the discovery of reverse transcriptase allow information to flow back from RNA to DNA. The discovery of siRNA.. mean RNA can control DNA. The discovery of prions... lead to current work now where pre-existing proteins can be templates for the folding of newly synthesised protein. DNA methylation allows epigenetic inheritance. Ie changes of certain protein levels (say during starvation) in your body can leave inheritable marks on your DNA (which will then affect the behavior of those gene in your children).
The central dogma now (if it still is used) has a lot more lines leading up and down the chain.

You should probably read about the central dogma. Besides its poor naming, all that Crick said (and where he is still right) that no information goes back from the level of protein. Besides that, especially the existence of the reverse transcriptase proves its validity. When you take the wider formulation of it: DNA makes RNA (mRNA) to make proteins, then you see this. You prepare cDNA first, which is then transcribed and translated into proteins. Fits.

I still find the central dogma to be a useful starting place for introductory bio classes. As we go along additional elements are added to build up a more representative model. As a model, I equate it with bohr's atom cartoon- a good place to start.

Chris.... there are such things as RNA dependent RNA polymerases... where information from RNA is copies directly into another RNA molecule with no DNA intermediate. DNA can also be methylated by protein activity.. .changing the expression of the genes or the splice variants that the gene produces... and such changes are inheritable.

[https://biologydirect.biomedcentral.com/articles/10.1186/1745-6150-7-27/comments] This archived comment is informative.


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How can I test a germinating pea seed for the presence of maltose?
I need to do a simple experiment to test whether germinating pea seeds produce maltose for the breakdown of starch into simple sugars.

DNSA colorimetric assay is another popular method to test amylase activity.


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Technical term for water entering a semipermeable membrane?
Would the word happen to be diffuse? I have tried imbibtion but that word is invalid because it isn't specific to osmosis.
Research: http://www.majordifferences.com/2013/12/difference-between-osmosis-and.html#.V9xc4fkrLIU

Why is osmosis not suitable? Do you want a term that can be used to describe osmosis?

This is not imbibition, as water molecules don't get absorbed in the semipermeable membranes commonly found in biological structures like Membrane around cells and cellular organelles (I took this example as you asked it in Biology forum). The water molecules pass through biological membranes via protein channels, that may be an active, secondarily active or passive process. Percolation and permeation are also inappropriate.
If the membrane doesn't hinder a particular solvent it can be said to be permeable to that solvent (e.g. Permeable to water etc.). "Osmosis" is also applicable. As osmosis is only a type of diffusion, you can use the term 'diffusion', but it would be too broad or generalized.

I am not quite sure what you are looking for but maybe the term passive transport will satisfy your needs although it is not specific to water.

Passive Transport is a movement of biochemicals and other atomic or molecular substances across cell membranes without need of energy input. Unlike active transport, it does not require an input of cellular energy because it is instead driven by the tendency of the system to grow in entropy.


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How does glutaraldehyde kill bacteria?
How does glutaraldehyde kill bacteria?
After disinfecting, does it leave the corpses of the bacteria to count?
Does it leave bio-film in tact?

Modifies proteins by reacting at the amino group. Same what formalin does

Gluteraldehyde interacts with amino groups to block the dynamic movements that biology requires.
Yes the corpses of the fixed bacteria can be counted and bio-films will be intact but the bacteria will be fixed in place.
Biofilms that are fixed with gluteraldehyde may shrink when prepared for imaging due to the effects of dehydration.


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Why is a membrane polar on the outside and non-polar in the inside?
Why would the phospholipid bilayer want to be polar on the outside and non-polar in the inside? why would it not want to be the opposite?

why do you think it would be the opposite?

Well, i'm not exactly positive. Both the interior and exterior are aqueous solutions if i'm not mistaken. So why would one be different from the other. Why wouldn't you want the fatty acid chain to be on top?

check out this link and see if that helps...look at the picture of the lipid bilayer and think about what its structure is chemically... https://www.boundless.com/biology/textbooks/boundless-biology-textbook/biological-macromolecules-3/lipids-55/phospholipids-300-11433/

Possible duplicate of http://biology.stackexchange.com/q/9261/3340

Phospholipids in aqueous solution under the proper conditions organize themselves into micelles and other structures - the minimum energy state.  This allows the polar head groups to interact with water in the bulk solution, while the non-polar carbon chains are 'protected' from the polar environment.  Water is attracted to water, and the polar head groups are attracted to water, the non-polar carbon chains are excluded.
You can get inverse micelles in non-polar solvents.

There is a misunderstanding here.  The questioner mentioned "Both the interior and exterior are aqueous solutions", which is absolutely correct.  However it makes evident he was thinking the non-polar part of the membrane molecules are in contact with the interior of the cell, which is wrong.  The non-polar ends of the membrane molecules are entirely inside the membrane, in contact with other non-polar ends of the other layer of the lipid bilayer which forms the membrane.  Both the interior and the exterior are in contact with the polar ends of the molecules.

so the interior and exterior ends are both polar?

Yes, the ends facing the interior and exterior are both polar.  But membranes have two layers, so there are molecular ends in the middle of the membrane, and the ends in there are non-polar (and thus forced away from the aqueous environments of the interior and exterior).


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Genetic Recombination and Mutation
Can genetic recombination yield mutation depending on the new DNA that is incorporated into the genome? I would say yes because when something foreign comes in, the genome is bound to not function properly.

Can you please try to clarify the question? My answer and @canadianer comment underneath shows that the question is a bit unclear.

When you say "new DNA that is incorporated into the genome", it suggests that you misunderstand what genetic recombination. You might to ensure you really understand this concept before going any further.
Mutation rate and recombination rate tend to covary throughout the genome (Lercher and Hurst 2002). So, yes processes leading to recombination events also tend to cause mutational events.

Recombination can be used to insert new DNA into a genome. For example: lambda phage or genetic engineering.

Sure, but that's not what most people think of when using the term genetic recombination and the OP did not comment on that.


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All flowering plants gives fruits. Why does jasmine flower plant not yield fruits?
My question is actually my long term doubt. I have seen most of the flowers turning into fruits. But why not this jasmine flower?

I'm sure they do, unless some genetically modified to hinder fertilisation. Interesting are Banana & sugarcane plants.

They do make berries - they are red to violet. See here.

Flower gives rise to seeds and fruits which are the ways through them the plant distributes the seeds.
Here, one should differentiate botanic term "fruit" and general common meaning of the word "fruit" which are not the same.
Botanic fruit can be subtle, not fleshy and come as a grain or pods.
Jasmine fruits are black berries.


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How is fructose absorbed into the body
I’m finding contradicting methods of   Fructose  transfer to blood
page no 264(10)One of which saYs fructose is absorbed by simple diffusion
And another sources like this say that fructose is absorbed by facilitated diffusion
I Believe that second source is true but still which one is correct ?

Fructose is absorbed by facilitated diffusion in the small intestine by the help of transport molecules GLUT5 or GLUT2.
Sources:

https://en.wikipedia.org/wiki/Fructose
http://diabetes.diabetesjournals.org/content/54/10/3056.long

The source you've mentioned (http://ncert.nic.in/ncerts/l/kebo116.pdf), says that certain monosaccharides, such as glucose, can be absorbed by simple diffusion, but it says nothing specifically about fructose.
In fructose malabsorption, in which the transporter GLUT5 is deficient, fructose absorption can be very decreased, which suggests there is probably no additional absorption of fructose by simple diffusion (PubMed).

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Topic in bioinformatics
I am looking for a presentation topic in bioinformatics. I haven't occupied with this field yet, but I find it really interesting.
It would be nice if the topic would include an algorithm. What source do you suggest to me?

as Joe Haeley suggested you can take a look at alignment algorithms, another algorithm which is quite a lot used is BLAST (https://en.wikipedia.org/wiki/BLAST )

This is not a question about biology.

This question is open-ended, allowing for many possible answers. This is not an appropriate question for SE.

A fairly easy to get to grips with topic, but that digs down to the meat of bioinformatics algorithms, is sequence alignment. Read around Needleman-Wunsch and Smith-Waterman alignment algorithms.
Wikipedia will be a perfectly adequate starting place :) - steal all the references at the bottom of the page!
I don't know how strong you maths ability is, but you'll find quite a few equations while you dig around in the bases of bioinformatics algorithms!

It depends on what you define as introduction. For a start you could always do what Joe Healy suggested and read around to see if it is a field that suits you.
If you want a textbook I found An Introduction to Bioinformatics by Jones and Pevzner to be indeed a great introduction to bioinformatics. It treats you like an absolute beginner and I think you will be able to follow no matter your programming or math abilities.
Now, if you want to get your hands dirty I can't recommend Project Rosalind enough. It introduces you to a variety of (mainly) programming problems while simultaneously teaching you the corresponding biologic concepts.
Phillip Compeau (co-founder of Rosalind) along with Pavel Pevzner have released a textbook of their own: Bioinformatics Algorithms: An Active-Learning Approach, which I admit I haven't read, but it is generally well recieved.
But before all that, I suggest to take a small introduction to Python (if you haven't already) and get familiar with the basic libraries (mainly BioPython). Perl is also a language you would like to consider, but far less beginner-friendly.

Cool I'd heard of Project Euler, but not Project Rosalind


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What is the estimated number of variant surface glycoproteins that trypansomes can express?
In "Vaccination against trypanosomiasis" by Greca and Magez they assert that there are "innumerable" variant surface glycoproteins that the parasite can express. What does innumerable mean here? These proteins presumably have to conform to some sort of structural conditions, so I don't believe it is truly infinite. Is there an estimate of the order of magnitude of the number of these proteins?


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Are there parts of DNA that do not have genes?
A question in my genetics class is "Are the number of genes proportional to the genome size?"
The answer is "no," and is it because the genome is the entirety of all the DNA in an organism, but that there are some segments of DNA that don't have genes on them?  Can someone explain this?  Thank you!

there are many parts of DNA that are not genes - these are things like enhancer sequences or other regulatory coding regions that are not expressed... where have you looked for this answer?

Most the genome is not coding for proteins. Here is a pie chart of what the human genome is made of

As you can see, only 1.5% of the human genome codes for proteins. The term gene is often a bit vaguely defined but if we assume that a gene is all the exons, all the introns and all the regulatory sequences, then 25.5% of the human genome are genes. So, yes many "parts of the genome" do not contain genes.
Now, it is worth highlighting that there is a very high correlation between the genome size and the number of protein-coding genes among lineages. Consider the below graph based on data from NCBI genome reports and styled after Koonin (2011).

There is a high correlation but there are also important outliers. See for example the eukaryotes (green dots) at the bottom right of the graph (probably mainly polyploid plants) that have very big genomes but relatively few protein-coding genes.
So, even though there is a strong correlation, it was quite obvious to me that the answer your teacher was expecting was no, because most of the genome is not coding and despite an existing correlation between genome size and number of genes among lineages there exists species with a very high density of genes and others with a very low density of genes in their genome.

Please add citations/sources for your images.


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Free online image libraries of trachoma
I'm looking for an online source with images of the eye disease trachoma. I'm looking preferably for resources from a credible source that have images from each stage of the disease.

According to wikipedia there are two different way to distinguish stage of the disease. One is from McCallan and one from the World health organisation (WHO). For the second one, on WHO website, you can find their grading card with eyes images. You can download it with also a little description.
Hope it helps.


text:
What type of lizard is this?
The photo was taken in southern Florida.


text:
What is the speed of blood in when flows through the fingertip?
What is the average speed of blood as it flows through the index finger on the right hand?

The answer is going to be highly dependent on the level of the vasculature you are talking: through the largest artery or capillaries you will get different results, and different results in veins as well, and it will depend on many other physiological parameters. You are asking a seemingly specific question but with almost no details, like if I asked "what is the average speed of a person?" Well, do you mean their average max running speed? Their day-averaged velocity including walking, sleeping, driving? Average of all people or just adults? As-is, your question is far too broad.

@BryanKrause I'm asking for use in a heart rate detection application which detects the heart rate based on the user's fingertip pressed against the camera. I'm not knowledgeable about veins and such.

@BryanKrause because of that, which of those blood vessels would directly impact what I'm doing?

Why do you think velocity is important for that?

@BryanKrause my algorithm is slightly different than other ones out there, because it attempts to find the user's blood speed as well. That's why I'm asking.

I see - interesting approach, but I just don't see any meaningful interpretation of the blood speed in that context, because it will vary greatly, even within individual vessels. You can't use the speed to estimate volume per time because the vasculature does not maintain a constant diameter; in fact, changes in vessel diameter are the major contributors to changes in flow volume.

@BryanKrause I'm not actually using this speed value to estimate the volume; rather, I've already built an algorithm that can do that, and I'm merely looking for an average blood speed value I can use to compare to see if my algorithm is accurate.

How do you plan to convert speed (distance/time) to volume/time?

This reference gives about 10-20cm/s in the major arteries and 5 cm/s in the major veins of the index finger in 5 male subjects, though there was a lot of variation.
The answer is going to be highly dependent on the level of the vasculature you are talking: through the largest artery or capillaries you will get different results, and different results in veins as well, and it will depend on many other physiological parameters.
Because it will vary greatly, even within individual vessels, you can't use the speed to estimate volume per time because the vasculature does not maintain a constant diameter; in fact, changes in vessel diameter are the major contributors to changes in flow volume.


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Snake with orange spots found in South Florida
I found this snake near my doorstep. What species is it?

Although there's an answer with what looks like a very plausible ID, it would probably be helpful to give more information, such as the approximate size of the snake, what it was doing when you found it and so no.

corn snake.

Looks very much like a red rat snake (Pantherophis guttatus). Nonvenomous, and wonderful.

First I thought that the coloration was off, but an image search showed a big variation and some of them looked exactly like the picture in the question.


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Function of Co-enzymes
Is the function of a co-enzyme to make a reaction run quicker? If catalysts speed up reactions, and enzymes are catalysts, and co-enzymes make enzymes work better, does that mean the co-enzymes just make reactions quicker?

Where coenzymes are used, they are generally required for catalysis.

What research have you done to answer this question for yourself? Have you googled for "coenzyme"? This site expects posters to demonstrate that they have put in some effort themselves.

@David I think the biggest problem with the question is that it is unclear. We need to know what enzyme/co-enzyme OP is asking about before google even enters the fray. Either way, I think the question needs to be developed further.


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Standard graph - Determining sizes of restriction fragments

I have marked out Lane M and gotten a roughly straight line, it then says that I am supposed to estimate the length of lane H and R. I am not sure what they are asking. I am still supposed to measure the distance migrated and then just plot it next to lane M on the graph or am I using lane M in order to actually plot the rest of the lanes, is it that by having both the length and fragment size of lane M, that I should be able to look at the fragment size and by using lane M be able to tell how far the DNA has migrated?

could you rotate the picture 90 degrees counterclockwise?

PLEASE DO NOT POST TEXT AS IMAGES. Copy and paste the text into your question. Images are not searchable, and can not be interpreted by screen readers for those with visual impairments. Use the [edit] link to modify your question. See this for more information.

The lane marked 'M' contains molecular weight markers of known sizes (in this case we are not using the actual MW of each double-stranded DNA fragment, instead we are using the length of each dsDNA fragment, measured in either base pairs (bp) of kilobases (kb)).

Plot the size of the MW standards on the log axis of the semi-log paper, and plot the distance that each fragment migrated through the gel on the other axis (the linear axis). Depending on the electrophoresis conditions you should be able to connect these points in a smooth line with a negative slope. At higher MW the line's slope will curve and get steeper.
Measure the distance that each band in lane 'H' migrated through the gel. Take those distances, and see where the fall on your standard curve that you plotted at Step. 1. You should be able to place the distance on the x-axis and read off the corresponding dsDNA fragment size on the Y-axis.
Repeat Step 2 using the distances that you measured for the fragments in lane R to find out the approximate sizes of those dsDNA fragments as well.


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When is a DNA sequence a gene?
I am a newbie is DNA sequencing and BioInformatics. I am writing a school project that determines whether a DNA sequence is a gene or not using a Machine Learning Algorithm, Hidden Markov Model. After understanding the the algorithm, I now want to know when we can say this particular DNA sequence is a gene. Any help or pointers would be appreciated. Thanks

This question is too broad. From the [help/dont-ask]: Your questions should be reasonably scoped. If you can imagine an entire book that answers your question, you’re asking too much. Entire books have been written on HMMs and other algorithms for finding genes, depending on the exact situation. Please [edit] your question and narrow it down to one particular circumstance.

We can devide algorithms for protein-coding genes in eukaryotes in two main categories:

Extrinsic, these algorithms rely on the comparison with external data sources,  such as comparing genomes
Intrinsic, I suggest you are more interested in this one when you acctualy want to predict gene coding regions on your own (If I'm wrong I will further explain extrinsic methods). The intristic methods are based on ab into predictions.

I will continue on Intrinsic methods, so what can we use to identify coding genes in the sequence. Ofcourse we need to know the charasticts of those coding regions:
Most of the time we see CpG Islands(regions of a higher than expected occurrence of CpG dinucleotides over a patricular region).

About 70% of human promoters have a high CpG content (Wiki)

Those CpG islands are important for the regulation of gene expresion.

the basics of a coding sequence are the promotor, introns and exons.
you are probably familiar with the fact that a mRNA has to be spliced in order to cut the introns (non coding regions) out, this is done by the splicesome wich recognizes special sites where it can cut, So you can search for these sites in your DNA sequence.  I will summarize some points about the coding regions here:

CpG Island near the promotor
splice sites for splicesomes
Start and stop codons (I hope you are familiar with these)

There are more things to consider but I would to suggest to look at the algorithms of these programs: GENSCAN, FgeneSH, GeneMark, Xpound and to read this atricle which is about identifying the protein-coding regions

This is in general not a totally solved problem. How difficult it is will depend a lot on the exact nature of your problem. For instance:
1) Are you working in a eukaryotic organism, or in a prokaryote? Most bacteria lack introns - this makes finding genes much easier, you can just look for start codons followed by regions with no stop codons - open reading frames or ORFs
2) Are you using other data sources as well? RNA data, e.g. mRNA sequences, make it much easier to find genes. Comparing to other organisms also helps a lot.
3)Do you only want coding genes, or are you interested in noncoding RNAs as well? Finding these is much more difficult. Finding very small coding genes is also very hard.

You are right his question is quite unclear

Sorry if my question is not clear. I really have no idea about how wide the subject in question is. I am a student just trying to implement the HMM algorithm to find whether a DNA sequence is a gene or not. I have successfully been able to determine if its from a CpG island or not. So was confused whether if a DNA sequence is from CpG Island then its a gene.


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Potentials between endolymph/cytoplasm and endolymph/perilymph
I am studying for an exam and there is something I can't seem to understand. My textbook says that the endolymph contains 150mM potassium, 2mM Na+ and 130mM Cl-. The perilymph contains 5mM potassium, 140mM Na+ and 110mM Cl-. "Thus" the electric potential between perilymph and endolymph is +80mV (endolymph being positive).
I can see that there are chemical gradients but why is the endolymph so much more positively charged than the perilymph?

I've already asked this question before and it was closed as a "homework question", which I would need to give suggestions on myself.
However, I seriously don't know what to suggest because I do not have the faintest idea how the endolymph can be +80mV as compared to perilymph, although the listed ions suggest that the surplus of positive charges is higher in the perilymph. I would love to make suggestions but I honestly don't have a clue.

Thank you in advance!


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Evolution, What would the first plants have been like?
I am curious what the first plants are thought to have been like, what they may have evolved from, and how much earlier (or later) than animals they are thought to have moved to land, if they even started in water like animal-life?

You can have a look on tolweb.org to see what the most basal branches in plants look like and what the sister branch of plants look like. You will find the plants (archeoplastidae) here on this website

You can have a look to the most basal branches and you may get a pretty good idea of what those early plants looked like.
What we call plants is what we call plantae or Archaeplastida in Latin. This clade contains the red algae and the green algae. Within the green algae are the land plants. In the land plants are the embryophyta which contain all what you think of when talking about plants. Below are a bunch of pictures so that you can get an idea of what the basal branches look like.
(Basal Plantae) Red algae

(Basal Green Algae) Green Algae

(Basal embryophyta) Green Algae > Embryophyta > Hornworts

(Basal embryophyta) Green Algae > Embryophyta > Mosses

You can explore the tree of life by yourself by going on tolweb.org. You can try to find the apple tree, the ladybug of the human by clicking on the links. It is fun and it is good to learn a bit how the tree of life looks like.

A pair of comments: 1. fossil record must much more illustrative for multicellular forms. 2. simplest and basalmost red algae are unicellular.


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To which SCOP Class corresponds the following secondary structure?
I need to classify this protein into one of the SCOP class (all $\alpha$, all $\beta$, $\alpha +\beta$, $\alpha/\beta$, or small protein).

I'm having difficulties understanding the difference between $\alpha +\beta$ and $\alpha/\beta$. I would have said, that it belongs to the group $\alpha/\beta$, due to the fact that presents an alternated combination of $\alpha$-helices and $\beta$-sheets, where the $\beta$-sheets are mainly parallel, but I do not know if I'm understanding the concept right.
Has anyone a tip to identify the differences quicker?


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Genomic control explanation
I am following the original genomic control article -
http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.167.8448&rep=rep1&type=pdf
What's the role of $p_i$ in the article? It says that $p_i$ denotes the frequency of $A_i$ allele in population. Is it derived from Hardy-Weinberg equilibrium?
I would like to know how I should calculate $p_1$ for a specific data set.

I have not read the article but in general the allele frequency is pretty much the easiest statistics to compute from population genetics data.
The allele frequency $p_i$ of the allele $A_i$ is the relative frequency of this allele $A_i$ in the population. In other words, it is the counts of haplotypes having the allele $A_i$ divided by the total number of haplotypes. For the specific case of diploid organisms, this frequency is the count of allele $A_i$ divided by twice the number of individuals.
Consider for example the following data, where we have two alleles in the population, $A$ and $B$. Each individual is denoted by its two haplotypes separated by '|'. For example individual A|B is heterozygous.
A|B A|A A|A A|A B|B A|B A|B A|A A|A A|A A|A A|B A|A A|B
In this population there are $7$ Bs over 14 individuals. That makes a allele frequency for B of $\frac{7}{28} = \frac{1}{4}$.
Of course, if you have genotype frequencies, you could - making a number of assumptions - calculate the allele frequency using Hardy-Weinberg but typically from empirical data, you don't need to go through that.
More information about Hardy-Weinberg rule at the post Solving Hardy Weinberg problems.


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Corrupted chromosome will be in any cell of body if zygote was corrupted?
For example, zygote had abnormal number of chromosome (45, 47, 48 etc) or corrupted chromosome. And fetus was born. Then it means that in any cell of newborn's body there will be the same not normal or corrupted amount of chromosome?

The terms 'corrupted chromosome' and 'corrupted zygote' are very unusual and quite loaded. Mutations occur all the time (of the order of 1-10 mutations per individual per generation in humans, Drake et al. 1998) and it is unclear how big a mutation needs to be so that you talk about "corruption".
But in any case, yes, the egg will copy itself via mitosis to create the whole body. As such any mutation (whether a small substitution or a chromosomal duplication) present in the egg will be transmitted to all the daughter cells and will therefore be found in the entire body. Note that many of the changes in chromosome numbers lead to unviable zygotes and the baby never develop fully.
Note that during mitosis, sister chromatids are being separated and therefore the number of chromosome copy should not matter much in the general case.

The answer of @Remi.b is true in general case. Still, we can consider at least two mechanisms which will lead to fetus mosaicism.
First one is a mitotic recombination. It is a rare process of recombination in a somatic cell which can result in unequal genotypes in daughter cells. Therefore, if one chromosome of zygote possesses some minute mutation it is possible that after first division only one of daughter cells will have got a mutation. In such case, about half of fetus's cells will be mutation free.
The second possible process is a back mutation. They are such mutations that restore genotype to a state of the wild type. According to this paper, such mutations are not so rare in human cells. As a result, the fetus will consist of both mutated and wild type cells.
It is important to say that such mechanisms are quite rare and will work only for small mutations (i think only for point mutations).


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What tree has three balls
I have seen this tree in Spain and Portugal. Its leaves and bark bring to mind the American Sycamore or London Plane Tree, but not exactly. Also, it has three spherical fruits, an arrangement I am unfamiliar with. Like an idiot, I left my tree identification book at home and the Internet has failed to satisfy my curiosity in this matter. Any help would be appreciated.

As you noticed this is definitely tree from Platanus order.

The London plane which is Platanus acerifolia, which is more casual is actually a hybrid of two platanus. Those two names are Platanus occidentalis and Platanus orientalis.

Frankly, I think the one of what are you looking for is that Platanus orientalis. See it on a picture of seeds taken from Wikipedia.

What a useful and interesting answer! Thank you. Additionally, the links you included made for fascinating reading. I am charmed even more by these magnificent trees.


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What enzymes I shall use for preparing single cell suspension from cardiac tissue for flow cytometry?
Can anyone suggest which enzymes I shall use for preparing single cell suspension from cardiac tissue. I will be looking at both cell surface and intracellular antigens involving cardiomyocytes and fibroblasts.


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How long do Ziehl-Neelsen stained samples keep?
I have acquired TB slides from my city's health center that are supposedly acid-fast bacteria (AFB) positive. However, when I took a look at it, I see basically no carbol fuchsin stains.
They were individually neatly folded in paper. When I opened them, the stains were slightly wet with immersion oil, facing down. So far, so good (page 6). I've been later informed that these samples were prepared Q1 2019. Based on my research, the staining solutions themselves last up to 12 months (page 33). I can't find any data on how long a stained sample would keep though.
Do they decolorize over time? I expected the AFB to be bright, or at least slightly pink, but I see no such thing. I do see bacilli, though all of them are nearly transparent/methylene blue in color.

Here are some sample images. The first 2 are how I expected AFB to look like, while the next 2 are what I captured (and I think should contain AFB). The last pic is a 10um/div calibration slide for reference.

This TB study might help you: external page
Briefly, they used 6 to 19 months old samples of mostly bad quality (due to their age). The last sentence of the quote below sounds promising though.

The 12,543 sputum smears stored at the national TB reference
laboratory for 6 to 19 months were stored at room temperature in a
wooden slide box without a cover slip. Most of them had lost their
stain reflecting the counterstaining with methylene blue. Restaining
of 436 doubtful slides by ZN gave disappointing results throughout [...]
After a 6 to 19 months storage of ZN stained sputum smears in a
non-air conditioned atmosphere, the bright red color of eggs due to
carbolfuchsin had virtually disappeared. [...] In such case, the ZN restaining of sputum smears allows to rediscover AFB that were discolored.

When I did this the last time, we used fresh and few months old samples which looked similar to the first of your images. Just have a look at the paper, I guess.


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How do mesosomes respire?
So how can mesosomes (found in prokaryotes only) participate in cellular respiration, if a prokaryotic cell doesn't have mitochondria?


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Mysterious spherical mass of feathers (Reddit)
Original posting from Reddit
I am posting this here in the hopes that an ornithologist might be able to shed some light on this unusual finding.  Locality is Boise, Idaho.
This appears to be a roughly spherical mass approximately 6 cm diameter, most of which comprises tightly packed feathers with a central core of dermal tissue.  The mass has been parasitized by maggots.
I speculate that this is some kind of tumor, which detached from the afflicted organism, and the decaying tissue attracted flies after detachment.  But that's just a guess.  If anyone has seen such a phenomenon before, please feel free to enlighten me!
Note, I am not the individual who found this object.  I am merely relaying the question to this forum.

This is a flap of feathered skin from a Mallard, birds do not shed their skin. The bird in question is likely dead or at the very least, severely injured.
The skin and curved feathers has curled up around itself into a "ball". As it's flattened/separated you can see there is reddish skin with some tissue on it the maggots have gathered on. The feathers here are relatively small and curved and the pattern is SPOT ON for the breast/belly feathers of a Mallard.
While it's not really obvious in the photo of the Mallard below, it is very common for them to have that little bit of pale edging on the dark reddish-brown feathers, as seen in the first photo.

Photo by Jo Garbutt (Flickr: https://flic.kr/p/jVbHwP )


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Up to date, extensive documentary about dinosaurs?
I just finished reading the Wikipedia page about dinosaurs, and I very much enjoyed it. I knew that much of what I learned in the 80's as a child is (and was) incorrect, and now that I am a parent, I am excited to finally make some time to learn about this stuff.
It seems that a lot is known about ecosystems, socialization, and interactions between different species, herd behavior, and other interesting things.
Before I start reading books, I want to watch a good documentary.  A quick google search turned up some suggested documentaries, but in general they seem to be either old or focused on a particular dinosaur, and not on the era in particular.  All are short.
I watched the 10 hour documentary "The Life of Mammals" by David Attenborough a few years ago, and developed a much better understanding of how we as humans evolved, and how we are related to other mammals. I'd love it if there was something as extensive about Triassic/Jurassic/Cretaceous era dinosaurs. Is there something recent, extensive, and mostly correct?

Doesn't have to be in English either

David Attenborough I stay away from. Since his Aquatic Ape hypothesis. Do read books - and until you do check out the work of a much more modern and better educated evolutionary biologist, Neil Shubin, who discovered Tiktaalik and wrote the Your Inner Fish book. There's a three-part documentary, Your Inner Fish - Monkey - Reptile. http://video.pbs.org/program/your-inner-fish/ Now that's a serious documentary by a scientist. The dinosaur documentaries are usually for kids, and are usually very wrong.

Try Planet Dinosaur (2011) or Dinosaur Revolution (2011). Neither is as good as the original Walking with Dinosaurs trilogy, but both are relatively informative and entertaining at the same time.


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Do humans perceive temperature or heat-flux? (or both?)
The general understanding is that when I touch an object, I perceive its (relative) temperature.
A metal object at room temperature, however, will often feel cool to the touch.
This leads me to believe that the skin senses heat flux in addition to, or instead of temperature.
(The metal conducts heat well, and therefore creates a greater flux when touched than a more insulative material.)
I am unfamiliar with the chemical process by which temperature or flux is converted into meaningful signals.
Do humans perceive temperature or heat-flux? (or both?)

related to: http://biology.stackexchange.com/questions/27535/why-do-we-experience-temperatures-below-37-degrees-celsius-as-hot/27541#27541

check my answer now - I have written in greater detail

I am not really convinced by the arguments in support of flux perception; I'll also think about it but here is a point that you (and @CRags) can also think about: If our body could really perceive flux then it can anticipate the final temperature before it actually reaches. In differential control mechanisms, this is used to regulate the levels of any feature in advance (See PID controllers). I haven't heard of differential control of thermoregulation or any biological process, yet. Though I agree that one can perceive flux with conscious effort.

@WYSIWYG But the final temperature is already fixed (the set point) which the body is trying to maintain?

@CRags It is better if we discuss this on chat

It is really easy to show we sense heat flux, just hand someone two materials that are drastically different thermal conductors but are the exact same temprature (room temprature) and the person will tell you the better conductor feels colder.

Short answer
Humans sense temperature differences.
Background
(Including edits based upon comments)
Because the question is "Do humans perceive temperature or heat-flux?", I will answer the answer from a psychophysical perspective, i.e., by dealing with sensory awareness.
Just as with many other sensory systems, temperature sensors in the human body adapt to ambient stimuli (i.e., constant absolute stimulus levels). In other words, after being exposed for a while to a certain temperature, one looses the perception of temperature per se (assuming temperatures are within comfortable limits of course, otherwise general discomfort will arise such as shivering or sweating etc.).
Therefore, temperature sensing in humans is not absolute, but differential, and occurs when differences occur relative to the baseline.
Holmes and Wood (1968) mention in their Introduction the following, and I quote:

...three variables of thermal stimulation [...] affect the sensitivity of human subjects to warm and cool stimuli. These are (1) the temperature to which the skin has been adapted, (2) the area of skin over which the thermal energy is applied, and (3) the rate at which the temperature of the skin is changed.

Variables (1) and (3) clearly emphasize the differential nature of temperature perception in humans. Variable (2) is a general psychophysical phenomenon, and basically shows that when a stimulus is sufficiently large, temperature differences will be more easily felt, while when the skin surface being stimulated is excessively small (say a needle with a small temperature difference is pressed against the skin) certain temperature differences may not be felt any longer.
With regard to your question on metal and whether heat-flux can be sensed: a metal surface will feel cool only when it is lower in temperature than your body. Suppose now you touch a metal object at room temperature, i.e. lower than your body temperature. In that case, as you already indicate, it will draw away heat quickly from your skin by conduction, creating a 'heat-flux' if you like. The extraction of heat thereby elicits a powerful stimulus, because a large temperature difference creeps into your skin as heat is drawn away from your skin and underlying tissues. As such, and contrary to other answers given elsewhere, I explicitly say yes, 'heat-flux' can be sensed as it per definition generates a temperature difference. This in contrast to touching insulators like wood or plastic, which will quickly adopt the temperature of the skin very locally where you touch it. However, as has been pointed out by others - this does not mean that temperature is measured by heat-flux sensors per se. In contrast, temperature is measured by temperature sensors that detect temperature differences (differential stimuli) between skin and external media. Because a temperature change is also a differential stimulus, it will also be detected, and hence 'heat-flux' will therefore be detected as well.
Reference
Holmes & Wood, Perception & Psychophysics 1968; 3:81-4

"I say yes, heat-flux is definitely sensed as it per definition generates a temperature difference." I disagree with this statement. The temperature difference causes heat flux and not vice versa. Heat flux is dependent on the nature of the material and this may differ for skin types. But ultimately thermal equilibrium is reached.

I can understand the point on adaptation that you raise but temperature ultimately affects metabolism. Adaptation has a limit. For pain sensations the responses can be heightened if the tissue is already sensitized. Temperature difference is sensed but this doesnt mean that the response will be the same as long as the difference is the same. The operations of temperature sensor is non-linear. Nothing in biology is linear.

Your first comment: (1) no, nothing needs to be fixed - when equilibrium is reached, you don't feel temperature differences, that's the whole point. (2) Heat flux is definitely dependent on the material, see my answer last paragraph. With regard to your second comment: (3) Adaptation has of course limits. Everything has. I am talking physiological conditions. (4) Of course pain increases on top of an already existing pain. It is a difference! (5) Many sensory systems are non linear! I have never mentioned linearity. Don't put words in my mouth. I don't see any points in your two comments.

when you say that absolute temperature doesn't matter as long as the temperature difference is the same means: f(T₁-T₂)=f(T₁)-f(T₂) which denotes linearity. I am saying that this is not true. The function does not behave the same at all points as long as temperature difference is the same

I have never mentioned linearity. Adaptation is what I explained and I support that to the fullest. I have never said sensations are identical across the dynamic range. Again, don't put words in my mouth.

I believe this answer is most correct of the three submitted.
The disagreement over the phrase, "heat-flux is definitely sensed as it per definition generates a temperature difference" seems to be largely a case of semantics.
Temperature difference will cause heat flux, but flux will always be accompanied by a temperature difference. The key is that the temperature of the skin will decrease over time, not that the skin and surface were different temperatures to start with.

SYSIWYG's answer added valuable information on the chemical sensing, which seems to be absolute in some regards, but this is mitigated perceptually by the effects of habituation. (C Rags makes good points about the body's drive to achieve homeostasis, but I feel this only impacts conscious perception minimally in normal operating conditions.) Thanks everyone!

@ChrisStronks Check my answer below

@th3ophilos - This is most definitely a heated and fluxed discussion here :) The best questions generate discussions. Hence - my compliments to your excellent question! Thanks for your careful analysis of the answers. Most definitely WYSIWYG has added important points about the definition of heat flux (which was indeed a source of confusion). He excels in bringing terminology down to its core. However, his answer was at the physics and protein level (bottom-up), while I have chosen a top-down answer, which is a choice one has to make given the question and/or based on ones expertise.

This is the modified answer in response to the discussion:
Facts:

There are warmth and cold receptors in the body at two places: The Peripheral receptors and the Central Receptors
The peripheral receptors are present in skin and the central receptors in the body core at multiple sites the notable site being the hypothalamus
The Temperature receptors have two patterns of firing - The tonic response (sustained firing rate due to steady rise and maintainance in temperature over long time) and the phasic response (also called dynamic response - response to short changes in the temperature)
The Warmth receptors fire maximally at 44 - 46 degrees celcius. The firing stops almost completely at about 48-49 degrees celcius beyond which there is no effective thermoregulation
The Cold receptors fire maximally ar 20 - 35 degrees celcius.

What is measured?

The peripheral receptors sense the temperature of skin.
The central receptors measure the core body temperature.

Only the temperature is measured as WYSIWYG mentions.
However the frequency of stimulus (How frequently the nerves fire - this depends on the temperature range in which the respective receptors fire) and the two types of receptors present on the skin allows the brain to interpret the flux. So Chris Stronks is correct in telling the heat flux is perceived.
Mechanism of feeling cold:
When you touch a cold object the heat is lost through conduction and radiation through the portion of skin that is in contact with the object. The cold will cause vasoconstriction of that part of skin - This means that the temperature of that part of skin rapidly equilibriates with that of the object. As there is rapid cooling (assuming that the object is cold) the rate of firing of the warmth receptors decrease and the rate of firing of the cold receptors increase. This allows the brain to interpret that the skin is losing heat (the flux).
The radiation part of heat loss is more appreciated when you pass a uncurtained window during the winter - the temperature difference is so great that very high loss of heat occurs through radiation that you shiver. You have to note that during these instances there is no decrease in the core body temperature. The actual decrease in core body heat needs a long exposure to such conditions. In the scenarios detailed above the heat loss is primarily from skin which reflects the ambient conditions (very quickly). Thus the peripheral receptors effect Anticipatory Control which is effectively measuring the flux of heat through skin.
The opposite occurs when you suddenly stand beneath the sun coming from a cold room - the radiant temperature of the sun being so great will cause the skin temperature to rapidly rise causing the body to feel very hot (though the core body temperature has not changed much).
Interesting details that may increase your understanding (though not directly related to the question):
The heat control effected through sensing the change in the skin temperature is called Anticipatory Control. In this the brain "anticipates" what is going to happen - for example a sudden cold draught - and will respond to it - reponds by increasing the heat production (shivering).
The heat control effected through sensing the core body temperature is Negative Feedback Control. In this the brain responds to increase in the core body temperature and takes steps to remedy this (the response will bring the temperature back to the set point).

For more see:Boron & Boulpaep Textbook of Medical Physiology, 2nd Edition, Chapter 59.

I disagree. There is no way to perceive heat flux.

@WYSIWYG I did not say our body measures heat flux. I said our body is concerned about heat flux (loss or gain).

I think this is the correct answer, but you should point out that receptors measure temperature rather than heat flux. However, the main process that causes body temperature to increase/decrease is heat flux.

@CRags I would say that the body is finally only concerned about its temperature because the metabolism will get affected. The flux is an effect of how effectively the environment transfers heat to the body. The body just responds to the heat and not explicitly to its rate - Mathematically it is $f(T)$ and not $f(\frac{dT}{dt})$.

@WYSIWYG: I agree with your last comment which is basically what I was trying to say.

@ChrisStronks The beneficial point was raised by CRags. Not me.

@WYSIWYG Check out my answer

@CRags I totally agree that firing rates are affected by temperature difference and ranges. I also agree that flux can be deduced with conscious effort but is not measured which I mentioned in the comments. What we basically have is like a water level sensor- we can deduce the flow rate but all the control systems (except differential control, the example of which I have not seen in biological systems) are regulated by one parameter i.e the level. Same is with temperature. I still don't buy the "flux" argument.

@WYSIWYG I am saying that the flux is deduced by the brain. I clearly pointed out that flux is not measured and only temperature is measured. But coupling the fact  that the skin temperature rapidly equilibrates with the ambient temperature and the rate of firing of the temperature receptors, the flux is perceived and the response is effected

@CRags - Nice answer !! I +1d already :)

I still feel that this statement, "However the frequency of stimulus ... and the two types of receptors present on the skin allows the brain to interpret the flux" is incorrect.
These stimuli allow us to perceive a delta in temperature. Given that we do not have any perceived area metric, we cannot (it seems to me) call it flux.

It seems to me that Anticipatory Control attempts to guess at a flux value over the surface of the body, and uses the internal temperature changes to confirm its modifications. (If the core is slowly dropping, the guessed flux must be low.)

So I'd say Humans sense changes in temperature (which would be absolute, but are modified by our body's adaptation to a specific environment), while our subconscious uses the same information to guess at flux and compensate.
(Sorry for the multiple comments, I keep accidentally posting them with the return key and then timing out the editing period.)

Yes thats basically it. You can also view the chat room conversation between Chris, WYSIWYG and me which is linked in the comments for more details. @th3ophilos

Flux is defined as amount of heat transferred per unit area per unit time.
Our body does not perceive heat flux. It perceives temperature and tries to adjust heat exchange mechanisms until thermal homeostasis is achieved (in all warm blooded animals). This is a feedback controlled process.
If it were to measure heat flux then the body cannot sense if it is at 47⁰C and the environment is at 60⁰C or if it is at 37⁰C and the environment is at 50⁰C. The heat sensors in our body have evolved to function at 37⁰C. Their conformation changes with increase/decrease in temperature thereby opening or closing the ion channels. The conformation is a function of temperature. If you put that channel in 45⁰C and try to measure a temperature higher that that then it wont work in the same way.
Body function and metabolism are sensitive to absolute temperature. Also see this post.
So while temperature sensing is absolutely necessary even for cold-blooded animals, plants and other organisms, there is no mechanism to measure heat flux. You can just measure the effect of heat not the flow of heat. For e.g. you cannot say if a body is cooling more rapidly than the other just by perceiving it for a short duration. It is possible to consciously calculate heat flux but it is neither measured nor (afaik) is fed in as a parameter to any control systems that regulate body temperature.

I've got two examples that I can't really bring in line with that: First, why then do we feel such a difference between, for example, 10°C cold water and air? Second, what about the density of the surrounding medium? I was once told that you would still freeze in the thermosphere (up to 2000°C) because of its low density.

@Hav0k heat perception is different from the density problem that you are talking about. It is because of the relationship between boiling/melting points and pressure. State transition is dependent on not just temperature but pressure too. Now heat essentially needs molecules for its effect. There cannot be a hot vacuum. Temperature is a measure of the heat (so it is not possible that something is 2000⁰C and not hot)

@Hav0k Regarding your first question. It is like asking why does polyester feel different from wool. The perception of a material is not solely because of its temperature. For perceiving temperature the heat signal has to be relayed to the thermoreceptor neurons. This will depend only on the thermal conductance of your skin; not of the material that you are touching. Moreover this just affects sensitivity.

@ChrisStronks Can you explain how. I cannot see the reason. Imagine two bodies are cooling by dissipating heat with different rates. You get to touch both of them at a point when they have the same temperature. How will you tell which one is cooling faster unless you make another measurement.

I disagree strongly with some of your statements. Most of all your last sentence "...you cannot say if a body is cooling more rapidly than the other just by perceiving it for a short duration" is nothing less than exactly the opposite of how sensing in general works. Moreover, your answer has a tendency to explain things teleologically, like 'why would the body need data on temperature differences?'. This may often work in evolution, but in physiogical mechanisms it can easily put you on an incorrect mindset

i added another critique in my comment. To your question - Yes, indeed, when you touch something an infinitesimally short of time, then yes, of course no temperature difference is felt. Likewise, if a digital sensor has a sample rate of 1 kHz and you sense 1 ms, then of course, no difference can be registered regardless of how sensitive it is to temperature differences as there is just one sample to be analyzed... This then should be added very explicitly to your answer and not in a generalized way as it is an exception to the rule

@ChrisStronks A thermometer measures temperature. But it can be used to measure heat transfer rates. This is not the equivalent to thermometer measures heat transfer rate.

@ChrisStronks Shall we debate about this in the chat

authors: محمدمهدی سعیدی نیا


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Are there any eusocial swarms which act prosocially?
My layman’s observations of eusocial colonies (like ants) is that while individual ants are extremely cooperative, different swarms in aggregate tend to act aggressively towards other swarms. Are there organisms where entire swarms will collaborate or otherwise act prosocially with other swarms?

Closely related ant colonies do this. E.g fire ant colonies in Australia don’t attack each other.

Are you using swarm interchangeably with colony? There are ant megacolonies.

Argentine ants.
https://en.wikipedia.org/wiki/Argentine_ant

Global "mega-colony":   The absence of aggression within Argentine ant
colonies was first reported in 1913 by Newell & Barber, who noted
“…there is no apparent antagonism between separate colonies of its own
kind”. [8] Later studies showed that these “supercolonies” extend
across hundreds or thousands of kilometers in different parts of the
introduced range, first reported in California in 2000,[9] then in
Europe in 2002,[10] Japan in 2009,[11] and Australia in 2010.[12]
Several subsequent studies used genetic, behavioral, and chemical
analyses to show that introduced supercolonies on separate continents
actually represent a single global supercolony.[11][13]
The researchers stated that the "enormous extent of this population is
paralleled only by human society", and had probably been spread and
maintained by human travel.

This is true only in the introduced range.  I read that in Argentina, this ant species is like any other and different colonies compete.  A mutation led to the strain of ant that has colonized the world because of its cooperativity.
I was interested to read in the comment by @Polypipe Wrangler that fire ants from different colonies in Australia do not fight each other.  Different fire ant colonies definitely fight each other in Florida.


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Is the leading strand consistent in the same chromosome with multiple replication forks?
If a chromosome has multiple origins or replication, do those origins necessarily pick the same DNA strand as leading and the same one as lagging, or can they be of opposite orientations, sending replication forks in opposite directions and therefore picking different leading vs lagging strands?

Replication proceeds in both directions from a single origin of replication, so the same strand acts as both the leading or lagging strand for the two different replication forks.


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Why are there "Old World" and "New World" families?
I've been reading on biological classification of the animal kingdom and have come across the New World and Old World terms a few times when they are applied to ranks (family, as much as I could find). Some examples of what I mean:

Old World porcupine vs. New World porcupine.
Old World rats and mice vs. New World rats and mice.
Old World vulture vs. New World vulture.

Old World X and New World X are usually not considered closely related. I assume this is because (at least partially) they evolved separately long enough to be distinct, if they were even related (at a non-trivial level) to begin with.
Is this naming scheme only thanks to convergent evolution? Researchers found families (or species etc.) in the new world that look like families in the old world and called them New World X, which prompted the other to be Old World X? I understand that a good deal of this classification was done in the 19th century when diagnosis tools were limited and conventions varied.

Yes, I think this is exactly right in the three cases you mention, convergent evolution noticed by the humans who were doing the naming. There are other cases (Remi.b mentions simians) where the "Old World" and "New World" versions are sister clades that became geographically isolated from each other.

So in some cases they weren't related and converged to look similar, and in some cases they were related and differ due to geographic isolation?

Yes, that's correct.

Lineage split due to continent drift
Due to continental drift, at some point a lineage was split into two, the afro-eurasian lineage and the american lineage. It is then common to refer to the  american lineage as the new world lineage and to the afro-eurasian lineage as the old world lineage.
Origin of the terms "New World" and "Old World"
In case you are unfamiliar with the origin of the terms "New World" and "Old World" and why for example "New World" is associated to the americas you should have a look at wiki > New World. In short, the americas was termed "New World" by europeans during the "age of dicovery". Geographers at that time (16th century) thought of the world as being limited to Africa, Europe and Asia (the old world) but suddenly europeans discovered the americas, a new world to add on their map.
New World Monkeys vs Old World Monkeys
Such nomenclature is typically used for monkeys. There are New World Monkeys (Platyrrhini) and Old World Monkeys (Cercopithecoidea). Homo sapiens for example is an Old World Monkey. Prehensile tail is a famous adaptation among New World monkeys that is absent among the Old World Monkeys.
Evolutionary consequences for these terms
These terms therefore do not result from convergent evolution or any other fancy evolutionary process. The terms refers to a specific split between lineages due to continent drift, where one (set of) lineage is found in the americas and the other is found in afro-eurasia. In the above case of monkeys, Platyrrhini and Cercopithecoidea refers to monophyletic lineages.

I don't think this is correct. The examples cited by OP are not sister clades.


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Is it inevitable that antibiotics will become useless in the future due to bacteria immunities?
Antibiotics are developed in an ever smaller amount due to the difficulties of discovering new ones. Bacteria, on the other hand, keep "finding" more ways to render antibiotics ineffective, and they are doing it faster than new antibiotics come to market. It seems that by a simple qualitative assessment at some point in the future all antibiotics will be ineffective.
However, there are 2 things I could think of that can suggest otherwise:

Antibiotics which were rendered ineffective long ago can be reintroduced since it's possible that the bacteria mutated away from their defense mechanism. This would allow for cyclic reintroduction provided we have enough types of antibiotics to sustain the cycle.
Antibiotics which bacteria can't defend against.

Are any of the above 2 possible futures? Can it be (at least theoretically) proven that antibiotics in point 2 can exist? Are there any other methods to "win the antibiotics war against bacteria" (assuming we are losing it as I assessed)?

http://mobile.the-scientist.com/article/37629/giving-antibiotic-cycling-another-shot

@canadianer Thanks. The sentence "as soon as the drug that is stopped cycles back on, the resistance comes right back" confuses me as it implies some long term memory of the system. If we cycle A-B-A then it's understandable, but I assume we would cycle A-B-C-D-E-A, and by the time we reach E do the bacteria still "remember" how they adapted to A in first place and can use that to adapt faster than they did in the first place?


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Low cost cell free expression system
I am a graduate student looking to incorporate some protein engineering into my training. I have been reading a lot about E coli lysate based systems, but they still require 3rd party additives like amino acids etc.. ($$$).  I need this to be ultra cheap as this will be a side show until I can show something for my efforts. I prefer a cell free workflow because of the quick turnaround from template to protein and ease of purification. My backup plan is just to add a tag at the end of my constructs but I would prefer to avoid this.
Any suggestions would be much appreciated.
Thanks

There is nothing like a cheap cell free translation system if you buy it, as these systems needed a lot of optimization in the development (I once worked for a company who developed such systems). If you want it cheap, go for a tagged protein where the tag can be cleaved.

What kind of scale do you need? If you need some milligrams that might already rule out cell-free expression completely. Afaik cell-free expression systems are only used where normal expression is really not an option (to incorporate non-natural amino acids, when no purification is possible, for small peptides perhaps, radiolabels, that sort of stuff).

@VonBeche Really small quantities in terms of amounts and say 100AA in terms of size. I would use this platform to try and engineer protein linker. I read that you can turn around a protein quickly and I will fail a LOT. I would want to take advantage of non-natural amino acids for smFRET to get a feel for the dynamic motion.

It sounds like you want to try a lot of new things at once (although I don't know which techniques you have up and running). Also, keep in mind that building good linkers shouldn't be that hard and therefore they are scientifically not that interesting. I'd expect that a standard linker would work. If it doesn't work, scale up to a few more. Because the usual lack of secondary structure in a linker usually there's not that much to engineer. If you really want to, just try a standard one vs polyproline or something like that.

@VonBeche I was hoping to make a disordered linker that can pass information between domains bound at each end. So I am looking for something more sophisticated than just a polyG peptide sequence.

Could you post an example in nature or someone that did something similar previously? It sounds very interesting, but I don't understand how that would work.

@VonBeche This is sort of what I am looking to do [The Hsp70 interdomain linker is a dynamic switch that enables allosteric communication between two structured domains. J. Biol. Chem. 292, 14765–14774 (2017)].


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Could an action potential produce few or more neurotransmitters based on the stimulus received?
I reckon that if you would be able to widen the AP width, it would produce more neurotransmitters in that larger time interval. Is that correct? Or does the neuron have a standard amount of neurotransmitters it releases in order to pass the signal post-synaptically?
(bonus: could it NOT result in neurotransmitter release, or does the definition of an AP include the release of neurotransmitters?)

Short answer

Widening of the action potential increases neurotransmitter release;
Generally, an action potential results in the release of about one vesicle of  neurotranmitters;
An action potential does not have to lead to neurotransmitter release - the chance being anywhere between 9 - 100%, depending on the synapse under investigation.

Background
Neurotransmitters are released in packets, called neurotransmitter vesicles:

Source: Science blogs
Vesicles are released via a mechanism involving Ca2+. When an action potential reaches the synaptic terminal, voltage-gated Ca2+ channels open, which leads to Ca2+ influx. The increased Ca2+ in the terminal leads to release of vesicles.
A study by Sabatini & Regehr (1997) showed that widening of the presynaptic action potential in rat cerebellar cells resulted in enhanced Ca2+ influx, which in turn greatly enhanced neurotranmitter release.
According to a study in rat hippocampal cells it was shown that, on average, a single action potential releases approximately 0.5% of the vesicle pool from the presynaptic terminal. The presynaptic vesicle pool was estimated to be 100 - 200 vesicles, which hence added up to 0.5 - 1 vesicle released per action potential (Ryan & Smith, 1995).
An earlier study of Rosenmund et al. (1993) confirms these findings in hippocampal neurons, and investigated the variability between different synapses in greater detail. They found that the chance that a single action potential released neurotranmitters was 9 - 54%. They reasoned that larger synaptic terminals, or terminals triggered by long-term potentiation have a higher chance of releasing neurotransmitter. Moreover, such terminals with enhanced release probability may also have a higher chance of releasing multiple vesicles per action potential. They predicted that 54% of release events from such enhanced terminals may release multiple vesicles per action potentials, whereas just 9% of normal terminals may do this.

References
- Rosenmund et al. Science 1993; 262: 754-6
- Ryan & Smith, Neuron 1995; 14: 983-9
- Sabatini & Regehr, J Neurosci 1997; 17: 3425-35

Neurons encode the "largness" of the stimulus in firing frequency. Neurotransmitters are stored in vesicules near the end of the axon. It has been shown that neurotransmitter release follows Poisson-distribution and that usually a single "packet" (quantum) is released - this is known as quantal release. Although the actual number of molecules in a single vesicle vary a bit, and ocasionally multiple vesicles may be emptied, it is accepted that for a single AP a neuron releases a single vesicle.
These two pages can give you more info and details:
http://neuroscience.uth.tmc.edu/s1/chapter04.html
http://neuroscience.uth.tmc.edu/s1/chapter05.html
Also this link provides introductionary info on the topic
A great image from :http://onlinelibrary.wiley.com/doi/10.1113/jphysiol.2006.123224/full

+1 for your answer. In an article (Ryan and Smith) I cited it was said that neuromuscular junctions released relatively small percentages of vesicles. Perhaps an interesting read?

I rather focused on the quantal nature of the release than actual release frequency, because in my opinion that is what the OP is interested in. I do not doubt that neurotransmitters are not necessarily released but when they are released it is done in a quantal manner. Also the graph shows that most of the time no release event occured that corresponds to what you've described.


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Why is there no cure for Dandruff?
It looks like a simple problem, affecting almost half of the population at the post-pubertal age and of any gender and ethnicity [wikipedia]. What is so complex about finding a cure? Also, if you know some of the most effective treatments, they're welcome.

http://curebird.com/condition/search?keys=dandruff

Dandruff is dead scalp, i.e. skin. Your skin everywhere is constantly renewing itself. Everwhere else in your body, dead skin gets scraped off on e.g. clothes, things you touch etc. so you don't notice it - dandruff gets caught in your hair and thus you do notice it. Dandruff is not a condition, it's a consequence of natural healthy skin turnover. If you aimed to prevent it from forming, you would interrupt a natural process and most likely also incur some sort of damage. Thus, the best way is to get rid of it periodically once it has formed - i.e. wash your hair ;)

Ok this seems like a natural cause, but Dandruff has other causes such as Seborrheic dermatitis, psoriasis.. The results are similar (dry skin flakes) and they have nothing to do with washing. Some literature state fungi like Malassezia furfur as a cause, but it doesn't seem to be clear evidence for a permanent cure

For dandruff caused mainly from dry scalp, I imagine that there is a delicate balance between moisturizing the scalp and getting oily hair. In my uninformed opinion, this is what shampoos like Head and Shoulders attempt to do.
Taking a more general look at skin health, growing research suggests that the right compilation of microbiota dictates lots of skin health issues. Just like your bowel has an endless supply of mutualistic bacteria, so does your skin. Disruption to this ecosystem (whether genetic, by way of a pathogen, or environmental) could have various negative effects. Dandruff, I imagine, is one of them. It is unfortunately very difficult to understand what a healthy ecosystem looks like, as every person is different both in genetic and environmental factors. This is part of the reason why other dermatological conditions like acne are difficult to treat.
You may be interested in research done through the Human Microbiome Project. Additionally, this article includes some discussion of the fungi mentioned above in the comments and postulates the role of microbiota in determining their success.


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What kind of a microscope do I need to see cell organelles?
I would like to study cells and looking for a microscope that would allow me to see:

groups of cells
individual cell
cells organelles

I would like to target insects and mammal tissue.
I would be very grateful for info in magnification ranges that I need and maybe some popular models of microscopes.
Is there a difference between digital and non-digital microscopes for that purpose?

groups of cells

A normal light microscope. 4x-20x magnification

individual cell

Lo resolution: Light microscope with 40x magnification.
High resolution: Confocal microscope with 40-100x magnification.

cell organelles

Low resolution: Confocal microscope with >=60x magnification.
Note: some organelles are easier to visualize while others are difficult. With confocal you can manage to see almost all of them with low resolution i.e you will be able to detect their location and distribution but wont be able view their fine structure.
To view the structure of organelles you would definitely need an Electron Microscope.

Is there a difference between digital and non-digital microscopes for that purpose?

If you are not too much into the optics of it then I guess it wont matter. I prefer if it has an analog mode along with a digital mode. Image acquisition is anyways digital.
Popular models: Leica, Zeiss and Olympus are popular brands. You select the model as per your requirements.

Is 40x magnification enough to see if a bacteria is dead or alive?

@user46147 you cannot, that easily. Also depends on the type of bacteria. You would need some kind of stain/fluorescence marker to differentiate viable cells from dead cells.


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Gibson assembly using NeBuilder
I am supposed to construct a plasmid that contains features from two other plasmids.
My strategy is to generate three fragments form the two other plasmids. I was encouraged to try Gibson assembly, so I went to NeBuilder entered my sequences and got I list of primers with overhangs and ordered them… But now I am I bit unsure about the linearization of the backbone and insert into that fragment.
In NeBuilder you can choose "by sequence position" in for the insert in the backbone the description reads “Entering the sequence positions of the bases immediately flanking the insert site. Primers for inverse PCR terminating at these endpoints will be calculated automatically”.
Does anyone have experience using NeBuilder? i am completely unfamiliar with inverse PCR ?
also my regular software package Geneious is unable to comprehend the two primers for the inverse PCR reaction


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Can solitary animals show extroverts traits?
So far as it is known there are solitary animals and social animals.
Does introversion exist among nonhuman primates? says that there are introverts among social animals:

Recent studies have identified extraversion/introversion in great apes, including chimpanzees, gorillas and orangutans. Chimps exhibiting greater solitary and reserved behaviors are considered more introverted, whereas those that are more playful and interactive fall on the extraverted side of the spectrum. Extraversion/introversion behaviors, such as sociability, have also been identified in species of monkeys.

Are there extroverts among solitary animals? I mean those who seek union with others although the vast majority of animals of their species are solitary?

I don't think it makes sense to talk about extraversion/introversion in anything but social animals; those are also quite anthropomorphized terms (though I have no problem applying them to other primates).

So solitariness vs sociality in animals is a little more complex than we usually give it credit for. For example, even in species previously thought to be largely solitary except for mating, sustained observation and tracking often shows that previously assumed to be solitary individuals actually do interact and sometimes develop lasting social relationships with conspecifics, just not at times when people are observing them. This is a particularly common finding in nocturnal animals among males who are assumed to be solitary, such as buck deer who turn out to be more social than does--just primarily at night!
That Wikipedia article you cited for 'solitary animal' is actually pretty shitty when you get down to it; the list of "solitary animals" include several generic terms for animals that include common species known to have variable social systems depending on region, such as badgers, moose, jaguars, cheetahs (in whom males, often brothers usually form lasting social relationships), red fox, and devils, who actually encounter each other quite frequently over kills and scavenging sites. (Citations are listed in this Collabedit file, because Stack Exchange is yelling at me for trying to provide actual links.)
In that context, I don't think many people have done behavioral syndrome/"animal personality" work on sociality, because it's not a particularly good thing to measure--you're really measuring something more like 'aggression threshold.' People have done work on species like social spiders where sociality varies significantly between individuals, however.


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Can a human increase cold resistance through some practice?

Can cold showers, moderate underdressing in cold weather increase your cold resistance?
What is responsible for cold tolerance? It's physiology/psychology or it's genetic thing?

By increasing cold resistance I mean feeling more comfortable/survive in low temperature environment comparing to state before practice(cold showers, underdressing, etc).

Purely my own experience, but certainly.  Just spend time in a cold (or hot) environment (without the frequent changes induced by central heating or A/C) and your body will adapt.

A tropical person is much worse adapted to cold by habituation. they did measurements of people in cold baths and tropical people fared worse. Some chinese schools send their children to play in shorts in the snow to make them more resistant. people who endure very cold conditions are able to adapt to them very well, some people who live in the extreme north can jog an hour bare foot in cold conditions and not get frostbite. So, yes they can increase by habituation.

comprehensible: See the Canadian temperature scale https://www.backyardchickens.com/threads/official-canadian-temperature-conversion-chart-joke.35915/

The advanced Tibetan Buddhist meditational practice known as g Tum-mo (heat) yoga allows control of aspects of body temperature.
Physiological measurements on practitioners are described in the paper Benson et al. (1982) Body temperature changes during the practice of g Tum-mo yoga. Nature 295: 234-236

Since meditative practices are associated with changes that are consistent with decreased activity of the sympathetic nervous system it is conceivable that measurable body temperature changes accompany advanced meditative states. With the help of H.H. the Dalai Lama, we have investigated such a possibility on three practitioners of the advanced Tibetan Buddhist meditational practice known as g Tum-mo (heat) yoga living in Upper Dharamsala, India. We report here that in a study performed there in February 1981, we found that these subjects exhibited the capacity to increase the temperature of their fingers and toes by as much as 8.3 °C.

In this paper the authors report measurements made on three subjects. The Figure shown below is the data for the third of these. The authors describe these results as follows:

His finger temperature rose 3.15 °C while toe temperature  increased 8.3 °C (Fig. lc). There were no other large changes in skin temperature. Rectal temperature was unchanged…The most likely mechanism to account for the increase in finger and toe temperature is vasodilation.

If you wish to try this for yourself, here is a description of the practice as quoted in the paper:

g Tum-mo yoga is a form of meditation which allegedly allows its practitioners to alter body temperature. Previously, only subjective descriptions of this phenomenon existed: "The neophytes sit on the ground, cross-legged and naked. Sheets are dipped in icy water, each man wraps himself in one of them and must dry it on his body. As soon as the sheet has become dry, it is again dipped in the water and placed on the novice's body to be dried as before. The operation goes on in that way until daybreak. Then he who has dried the largest number of sheets is declared the winner of the competition".


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Are there animals who do things just for pleasure like humans?
In a debate my father said that only humans do things that are not directly linked to survival(painting, playing musical instruments, singing etc). He said that this is because we are "special" and not like other animals on the planet.
I said that this is only because we have much more developed brain than other animals. But now I'm also interested in one question.
Are there animals who do similar things(not exactly same, of course) not for mating/survival but just because they like it?

Isn't there an argument to be made that art is simply a form of sexual display? (Although I'm not making it!)

Dolphins and some whales blow toroidal vortices: https://www.youtube.com/results?search_query=dolphin+toroidal+vortices

Why does my dog bring me a stick (tennis ball, Frisbee, &c), and keep poking me in the knee with it, or toss it at me and bark, until I relent and throw it for him to chase and bring back?

@jamesqf - Can it possibly be that, like humans, they want to have some purpose? My Border Collies think their purpose is to herd tennis balls, and they definitely want to work. My new dog just wants to play with squeeky things. I don't know what's up with that. I've had border collies for too long.

@anongoodnurse: And work (or at least certain sorts of work) isn't a pleasure?  And my border collie/Aussie mix loves to chase tennis balls, but won't bring them back.  She just lies there with the ball between her paws, grinning.  Now if that isn't pleasure, I don't know what is :-)

@jamesqf - Absolutely it's a pleasure. BC/Aussi: "No take ball! Just throw!"

@anongoodnurse: Though in her case, I think it's more like "Well, I chased the ball over here, now it's your turn to walk over and get it.  Fair's fair!"

Show your Dad this video of a Panda playing in the snow. It seems obvious to me that she is sliding down the hill just for the fun of it. https://www.nbcwashington.com/news/local/giant-panda-family-tumbles-around-in-snow-at-smithsonians-national-zoo/2556848/?amp&fbclid=IwAR20D6QAMTHaqRZnuo39GtWx6DZaO6Xi70xNUeHcG18rkwmiGuZVoN3CmQM

I see that Gerardo has said effectively what I was going to: animals don't do things because they have reasoned out that these things will help them survive; they engage in behaviors because these behaviors lead to reward circuitry response and animals who find general categories of behavior rewarding have tended to survive better. Sometimes behaviors that are not directly related to survival trigger the same circuitry.
(P.S.: this is exactly what is happening in humans, too.)
Masturbation is one example, as above; so are animals that 'adopt' either conspecific or heterospecific juveniles who don't belong to them, which is not uncommon in many species. (Barn cats in particular do this often; aside from all the cute Youtube pictures of cats who think ducklings are kittens, it's very common for queens with kittens about the same age to co-nurse them.) You can argue that sociality and taking pleasure in altruistic activities with no immediate personal benefit is a survival adaptation, but that's not a calculation the animal is consciously making at the time.
Animals often have strong aesthetic preferences, especially for conspecifics; female and male animals often prefer traits that don't have anything obvious to do with survival in potential mates, and there is an entire discipline of sexual selection in biology devoted to teasing out why. It's worth noting, however, that in many species it turns out that females have preferences that vary widely for a number of traits, and that female preferences do not always line up to male reality...
Outside of naturalistic social behavior, numerous examples of elephants and chimpanzees creating drawings or paintings in their enclosures without any conscious reinforcement from their keepers have proved interesting reading. There are also examples of animals who keep "pets", including the famous case of Koko the gorilla and her pet kittens. You may find this article, with descriptions and citations of several animals who may or may not be engaging "art" for its own sake, to be a useful read.

Thanks for reply, it's very interesting. Where can I find free researches(can only read abstract in last link) about animals who do art "without any conscious reinforcement from their keepers"?

I'd check ResearchGate or #icanhazpdf on Twitter.

Arguably, yes.  There numerous species of non-human animals which have been observed to masturbate wikipedia.  Non-human animals will frequently choose less-healthy foods over healthy foods.  (Offer a cat a raw fish and a can of tuna, most of them will choose the canned tuna every trial even though a diet of only canned tuna would be disastrous due to the high salt content.)
Arguably, these are just instinctive behaviors firing outside the ideal circumstances, but that plus endorphins or species-specific analogues may be as good a definition of acting purely for pleasure as any.


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Pros/cons: linear vs. circular DNA
Why did Eukaryotes evolve to have linear DNA and not circular like Prokaryotes? What are the pros and/or cons?

Some prokaryotes have linear DNA too..

This question has been asked before: Is there an advantage to linear chromosomes?
Firstly, I should state that the generalisation that ALL prokaryotes have circular genomes is incorrect. A growing number of prokaryotes have been discovered which have linear chromosomes, such as Borrelia burgdorferi ,which causes Lyme disease, members of the Streptomyces family and Agrobacterium tumafaciens, which has both a circular and a linear chromosome.
Anyway, on to the question being asked:
Generally, my feeling is that large circular chromosomes would have much greater supercoiling and related torsional problems, making it difficult to unwind them for transcription, replication or repair. This limitation on physical size limits the amount of genetic information that can be carried in a single chromosome, thereby limiting complexity of the organism.
You could increase the number of circular chromosomes to compensate for their lack of size, but again, you end up having a physical limitation (size of the nucleus or size of the cell for anuclear organisms) on how many chromosomes you can pack into the cell.
Linear chromosomes are just a more efficient shape when it comes to larger sizes.
=====================
Here are a few good references to dig further, if you're interested:

A new beginning with new ends: linearisation of circular chromosomes during bacterial evolution. Pubmed: http://www.ncbi.nlm.nih.gov/pubmed/10802162
Why do we have linear chromosomes? A matter of Adam and Eve. Pubmed: http://www.ncbi.nlm.nih.gov/pubmed/10422538 -- Proposes that meiosis was the driver for linear chromosomes.

I concur with your argument but it would be great if you can add some references.

Added, as requested.
Here's a really interesting experiment where they linearised the normally circular E. coli genome and studied the cells: http://www.ncbi.nlm.nih.gov/pubmed/?term=PMC1796773


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DNA replacement: new species
This is a hypothetical question
What would happen if the DNA of a prokaryote was replaced with the one of a prokaryote of another species, would the cell structures change and adapt to the new DNA and would the cell survive?
(Would the result be similar if we did the same with two eukaryotic zygotes of different species?)

Such genome transplantation was performed between two Mycoplasma species in Craig Venter institute Genome transplantation in bacteria: changing one species to another. They found that the donor genome completely changes the recipient cell to accept the identity of the original donor cell.
Note of caution: the above experiment was conducted between two highly similar species, and as of yet it is unclear what is going to happen if the exchange is performed between two distantly related bacteria species.
As for eukaryotes -- the transplants may be not viable at all, because naked DNA is going to lack epigenetic information (histone modifications, DNA methylation) that is preset during gametogenesis.