text:
does phagocytosis dependent on opsonization?
does phagocytotic activity of macrophages and neutrophils depends on opsonization by IGg (antibody) and C3 complex,if it does, so then why macrophages and neutrophils are categorized in Innate immune defense system (despite the interference of antibody).
and if it is not dependent so why macrophages act as antigen presenting cells to make antibodies, while they lysed it and fragmented it (the pathogen) on it's surface by it's own,so what is the need for it to make antibodies while the innate system can handle it alone?

Well, phagocytosis does not depend on opsonization, but it works better with it because the macrophages can detect the intruders more easily, but the secondary inmune response with IgG depends on the work of the APC cells, so let`s say a bacteria gets in your body for the first time, it can get phagocytated by a macrophage that will after present the parts on his MHC II to start the secondary inmune response.

so what's the benefit of activating acquired immune system while the macrophages  can lys and kill it?


text:
Why would mutation rates increase in a tumour?
This article describes a tumour:

Swanton found that even the primary tumour was surprisingly varied. He found 128 mutations among the various samples, but only a third of these were common to all of them. A quarter of the mutations were “private” ones – unique to a single sample.
The tumour had also split down two evolutionary lines. One area – part of R4 in the picture – had doubled its usual tally of chromosomes and seeded all the secondary tumours in the patient’s chest. The other branch had spawned the rest of the primary tumour. Even though this tumour looks like a single mass, whose cells all descended from a common ancestor, its different parts arehave all  evolved independently of one another.

My understanding is that if non-cancerous cells normally had such a rate of mutation it would be lethal to the cell if not the organism.

What about tumour cells would lead to a higher incidence of mutation?
How are these cells able to survive when non-cancerous cells would perish?

You should read "Hallmarks of cancer: the next generation" by Hanahan and Weinberg - it's a great open access review that covers your question http://www.ncbi.nlm.nih.gov/pubmed/21376230

All cells perhaps have the same likelihood to be affected by some deleterious mutation. When you say "the cancer survives", you do not talk about all the cells in the tumour tissue. Eventually, there may be a few cells that survive and they expand the population.

Cancer cells generally lack the "safety mechanisms" or "check points" that prevent normal cells from replicating, and some of these mechanisms are also involved in ensuring that DNA replication proceeds without serious errors. Inactivating these safety mechanisms lets cancer to cells divide rapidly, but at the same time also causes their genome replication to be "sloppy", introducing various errors.
The P53 protein is probably the most well-known example of such a "safety mechanism". In normal cells, P53 arrests the cell cycle if breakage occurs in the DNA strands; but cancer cells often inactivate P53, and consequently they tend to proceed with DNA replication even if DNA is damaged. A consequence is that DNA is often in a state of disrepair in cancer cells. (A review of P53 here.)
This lack of proper "quality control" can lead to loss of large pieces of the genome, even entire chromosome arms. While it may seem strange that the cells can survive this, keep in mind that the genome encodes information to support the complex working of an entire organism. Loss of a chromosome arm would indeed be lethal to the organism as a whole --- perhaps it would disrupt brain development, or the immune system. But for single cell to survive and develop, most genes are actually not essential, likely because there are so many redundancies. This is frequenly seen in genome-wide RNA interference screens, for example this paper. Remarkably, cells can even lose the entire mitochondrial DNA (which means they cannot even respire anymore!) and still survive.
It is not clear that "non-cancerous cells would perish" if they would similarly lose DNA. They would likely arrest and turn senescent because they detect DNA damage, precisely because of these safety mechanisms --- but that is different. The loss of genes in itself may not be lethal to a normal cell, it's rather that normal cells "choose" not to continue when this happens. But this distinction is probably difficult to test experimentally.

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Fruit Fly Hybrids
I have a food waste bin in which I put fruit scraps. The fruits come from all over the world, mainly Europe though.
I'm in the UK.
I assume the fruit Fly eggs are already in the fruit, in which case they originate in the same country as the fruit.
Are they all the same species? Am I creating Hybrids in my waste bin?

@Remi.b your second statement is incorrect. While D.melanogaster is a genetic model organism, it is only one of hundreds of species in the genus Drosophila. Also your first statement is incomplete. It is the ability to produce fertile offspring that usually classified a species, as hybrids such as ligers or mules are, for the most part, sterile, though there is active controversy to the validity of the reproductive argument for speciation as well,

Probably they are not all the same species, as there are many fruit fly species in the UK and all over the world. It is also probable that you are not creating hybrids, as fruit flies have quite specific mating behaviours that change rapidly sometimes even between strains.
Anyway, you are assuming that the eggs come with the fruit, but that's hardly believable unless you already see larvae when you ate the fruit. Drosophila melanogaster has one of the fastest developments (22h since egg fertilisation, although it can vary with temperature). So, if we take for granted a week span since they were taken out of the country until you bought them (which is very optimistic) you would already see larvae in the fruit. In short, the flies that are thriving in your fruit bin are common flies from the UK.
In case you want to know, the most common flies in the UK according to this article is Drosophila subobscura and obscura, which are pretty similar in development to D. melanogaster.

Excellent thanks very much for your reply. Im amazed that the fruit flies are local species - there are so many in such a short time whenever fruit is left lying around. I guess you've answered that too!

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Why is the brain white?
I have read many articles about how the brain is the most power-hungry organ in any living complex organism, requiring about 70% of it's oxygen supplies in the resting state.
Since the usual medium of oxygen delivery is through respiration, this should mean that a lot of blood is supplied to (and hence present in) the brain.
Why then is the color of the brain almost always white? There is usually a little red tainting on the exterior and that's it, you can see the interior is still white. Should it not be red? Presuming that for a higher surface area to volume ratio, most of the brain cells are in direct contact with the bloodstream.

If I recall correctly, most of the brain cells are not in direct contact with the bloodstream, there is a famous blood-brain barrier that aims to shield most of the brain from the blood. The barrier is that thin, that fat cannot pass through it. Therefore brains can only work on sugar supply.

@CommuSoft - The blood-brain barrier shields of constituents in the blood from the brain. It is formed by tight junctions between the epithelial cells lining the blood vessels in the brain. The only difference with the brain is that these tight junctions are absent elsewhere. Hence, less molecules pass into the brain from the bloodstream than elsewhere. Sugar is imported in every cell with dedicated transporter proteins  - i.e., sugar cannot pass the bloodstream passively anywhere, not in the brain, not in the rest of the body.

The brain is indeed stacked with blood vessels, as shown in a 3D model in Fig. 1.

Fig. 1. 3D-printed model of blood vaculature. Source: Biobots.
The blood supply on the surface of a live brain is readily seen during a craniotomy (Fig. 2.)

Fig. 2. Surface of the brain. Source: The Sterile Eye.
When freshly prepared, the interior of the brain appears pink, indicative of the presence of blood (Fig. 3):

Fig. 3. Coronal sections of a non-fixated brain. Source: Documenting Reality.
Mostly, images of the brain are taken after fixation of the brain. The fixation process includes removal of the blood in the brain and the fixative pales the color of the tissue markedly. Fixation results in the more familiar pale-appearing pictures of the brain as shown in Fig. 4.

Fig. 4. Coronal section through a fixated brain. Source: Wikimedia.
Also note that the blood supply mainly targets the areas where the cell bodies are located, i.e., the gray matter. The white matter is pretty much devoid of blood supply and mainly consists of heavily myelinated, fatty tissue supporting axonal fiber tracts (Fig. 5).

Fig. 5. Arterial innervation of the brain. Source: Human Physiology Academy.

Nicely illustrated answer :) +1

Nice answer. Can you also add a note on blood-brain barrier and the role of CSF as a medium of metabolite exchange?

@WYSIWYG - the blood-brain-barrier is not really of relevance for oxygen exchange. And since the question is on oxygen, and not on metabolites, I deliberately left CSF out of the answer.

@AliceD Fine enough. I have seen some sources say that CSF "stores" oxygen.

@WYSIWYG - I didn't know that, but I'd rather not overcomplicate the answer. Thanks for the appreciation and the comments!

A person can be alive and awake with his skull open and brain exposed like that? o.O

@Abdul Not only can be, it's necessary for them to be, for most forms of brain surgery. Feedback from speaking with the patient is vital to allow the surgeon to find and identify the right bits to cut/prod/etc.

@MatthewNajmon that's gotta be worrisome as the patient as you feel pressure to give very accurate feedback, and try to be as least subjective as possible. It's like during an eye exam, it's not too big of a deal when you choose the wrong lense, when the optometrist asks you which lense allows you to see clearer, and you can't really tell


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Are genes uniformly dispersed throughout the genome?
I think that telomeres and centromeres are regions with a very low gene content (= regions that contain few genes). To the exception of telomeres and centromeres, are genes uniformly distributed throughout the genome or do they tend to clump together or to scatter as much as they can? Do genes tend to clumped or avoid specific regions such as regions with low mutation rate or low recombination rate?

No they are not. High gene density is correlated with GC content. Most genes are found in GC rich isochores, which are not distributed uniformly (as can be seen on any karyotype). It is also shown through direct sequence analysis (gene density shown in red, GC content in green):

Venter et al. go on to say:

This inhomogeneity, the net result of millions of years of mammalian gene duplication, has been described as the “desertification” of the vertebrate genome. Why are there clustered regions of high and low gene density, and are these accidents of history or driven by selection and evolution?

Desertification refers to this 1985 article by Ohno:

The net consequence of hundreds of millions of years of continuous gene duplication is the desertification of the euchromatic region of modern vertebrates; the average distance between still functioning gene loci becoming progressively longer.

This would seem to suggest that these deserts are the result of gene duplication and subsequent degeneration into pseudogenes, though this is surely not the only cause. I'm not sure that your last question or those posed by Venter et al. have an answer as of yet. This more recent paper offers some interesting ideas (references removed for brevity):

More than 20 years ago, Ohno (1985) postulated the desertification of the euchromatic region of the higher vertebrates’ genomes owing to continuous gene duplication events followed by degeneration of newly emerged gene copies in their evolutionary history. Only with the first release of the complete sequence of the human genome in 2001 was Ohno’s prediction of the existence of such deserts confirmed. Another mechanism to generate imbalance of gene deserts between chromosomes might be large intra-chromosomal duplications, from which some mammalian-specific gene deserts appear to have evolved. However, the functional or evolutionary significance of gene deserts is not yet fully understood. At first glance, gene deserts seem to be devoid of biologic functions because of their lack of protein-coding DNA. Despite this, some gene deserts have been shown to contain important regulatory and sometimes ultraconserved regions for neighboring genes that function over large distances. In addition, the observation of stable gene deserts with homologous flanking genes (often transcription factors), which are maintained for long evolutionary durations, as well as the existence of numerous conserved nongenic sequences in mammalian genomes suggest that gene deserts are not just genomic junkyards but instead might be of functional significance. However, some gene deserts can be deleted without noticeable phenotypic effects. Thus, it remains unclear whether the uneven accumulation of gene deserts in eutherian chromosomes, which appears to be the strongest causal agent for the observed relative lack of a NG/LC relation in the genomes of placental mammals, is simply a byproduct of their genome evolution and possibly the long-term decrease in population-size, as would be suggested by the enrichment of gene deserts along the evolutionary lineage leading to mammals. Upcoming detailed reconstructions of ancestral vertebrate genomes will help clarify these points.
Alternatively, this particular architectural feature of eutherian genomes might be linked to some of their morphologic, physiologic, neurologic, and cognitive evolutionary innovations, possibly by regulating genes with essential functions in development. It has recently been hypothesized that regulatory elements in gene deserts function in the regulation of core vertebrate genes. Furthermore, approximately 20% of conserved noncoding elements are eutherian-specific. Thus, the uneven distribution of gene deserts could itself be caused by an underlying pattern of uneven distribution of some core genes in placental genomes. This hypothesis should be tested in the future.


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Cis-AB phenotype verification
I know that my blood type is AB. I wanted to know if I am cis-AB since cis-AB seems to have a different approach in blood transfusion.
Is there a lab test that can verify is a person is under cis-AB blood group phenotype?

First,do you have any probe that your type is AB chimera transferase? I discovered it because my mother is type AB and my brother type O. I have 2 sisters and my self cis-AB (my younger sister and me rh-). If you carried a cis-AB allele and another allele was  B1, surely you got A and B type compatible, but if you carried an A1 or O1 allele, surely you got O type compatible or worse luck. For example, I have a very rare multi-blood genotypes (rh D- C-G-, K1-, M+N-S+s+ and another unknown antigen). Actually, it doesn't matter if you are cis or trans AB phenotype, the most important thing is to know if another 34 blood groups and 200 minor groups and 600 blood antigenes have a rare combination that makes blood incompatibily or autologous like Bombay phenotype or autotransfusion like me.
If you want to be sure about your genotype, you must make dna test with SNPs of 10 cis-AB alleles


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Is the sun's damage to skin sufficient to warrant protection anytime the average person goes outside or just for extended periods?
According to the American Academy of Dermatology website,

Everyone needs sunscreen
Sunscreen should be used every day if you will be outside. The sun emits harmful ultraviolet (UV) rays year round.
Even on cloudy days, up to 80% of the sun’s harmful UV rays can penetrate your skin.

I also saw this video a while ago.
The two of these make it sound like we should be wearing sunscreen even if I step outside to get my mail.
Is the sun's damage to skin sufficient to warrant protection anytime I go outside or just for extended periods? What is the general criteria this kind of organization uses to determine what is "sufficiently" damaging to warrant sunscreen protection?

There are dermatologists who advocate for never exposing the skin to direct sunlight.  The interview I saw had terrific looking skin. The increase of UV content of sunlight over the past few decades makes this seem like a better idea now than previously.  Clothing, hats, gloves and parasols may be recommended in these cases because of the chemicals in sunblock.

Interesting. As an aside though, specific opinions are part of the problem. I don't know what the criteria are by which they are making these recommendations. Doctors are not infallible. I need to know the metric they are making these recommendations based on so I can decide for myself who is being rational and who is just saying stuff.

It is very much dependent on skin type.

@WYSIWYG What specific properties do you have in mind?

@StanShunpike A simple parameter is melanin content. Dark skin contains higher concentration of melanin which helps protecting the skin against UV. I have seen many people who are constantly exposed to sunlight but do not suffer from skin cancer or even sunburns.

Probably as important, the incidence of skin cancer is up over the past 30 years because of 1) the idea that getting a tan is healthy 2) the intensity of sunlight hitting the earth's surface is going up. An increase in melanoma has been documented.  http://www.who.int/uv/faq/skincancer/en/index1.html  http://www.skincancer.org/skin-cancer-information/skin-cancer-facts

@shigeta thanks for that comment. Very interesting. I never thought of it like that

related: Radiation and “Safe Dose”

Because the website you link speaks of cancer, they probably go by the rule that a single exposure and even a single photon of UV may be sufficient to cause that one mutation in that one skin cell that will eventually lead to cancer.
In the end, they are right, because mutagens (UV, cigarettes, radiation) do not follow typical toxicological rules. There is no threshold dose of UV that does not cause cancer, as even a single short exposure may do the trick. Obviously, multiple exposures and longer exposures increase the chance. This, as opposed to toxic substances that generally feature a threshold dose. Below this threshold dose they are considered harmless.

Let's suppose a person gets cancer from a small does of radiation. This person could just be an outlier, in which case we simple must accept that that person just has bad luck. But is there a general trend --- a statistical threshold --- of radiation exposure? For example, I walk to class which takes about 5 minutes. Am I supposed to put sunscreen on for that walk? Do I need to put it on if I take a bus downtown? Knowing the statistical threshold of sufficiently "safe" sun exposure to determine if it warrants all those precautions is what I am asking about.

'sufficiently safe' is opinion-based. Obviously, the linked website adheres zero-tolerance policy. As I say above, there is no safe threshold. It's a gradual thing.

There should be objective measures I would think. Rates of skin deterioration. Risk of cancer. These are objective measures. What one considers safe is subjective. Am I thinking about this question the wrong way? Just asking. I haven't really asked a question like this before.

@StanShunpike - And I normally don't answer these kind of questions :) +1 for the question btw. It's a good one.

AFAIK, other than acute radiation sickness (where someone gets a massive dose of radiation within a short period of time) there is no way to tell. When we talk about radiation damage, usually we end up using metrics equivalent to "x dose will increase your chances of cancer within y years."

Since your questions seems to be motivated by personal health protection, consider an alternate view, which is that not only is the sun's damage to the skin not "sufficient to warrant protection anytime I go outside or just for extended periods", but that lack of sufficient unblocked exposure to the sun may be, overall, even more harmful--not only for the risk of various cancers, but for a large number of serious diseases.
Dr. Michael Holick is a Professor of Medicine, Physiology and Biophysics at Boston University School of Medicine, and has researched vitamin D--which is produced by our skin when exposed to the sun's UVB radiation--and its critical role in health for over 30 years. In addition to his book, The Vitamin D Solution and an entertaining and informative (and at times, zany) lecture, he recently (Jul 24, 2015) wrote about this in The Washington Post. For example:

the risks associated with sensible sun exposure have been exaggerated
  by well-meaning health authorities, and the measures to guard against
  them often have nothing to do with the sun’s occasionally malignant
  effects. Contrary to the paranoia generated by years of messaging, the
  sun is not our enemy. It’s safe to step back outside — and, please, go
  easy on the sunscreen.

The book and lecture provide much more detail, but the main points are that 1) vitamin D, a hormone, is critical to many bodily functions, 2) that lack of it in a majority of people in many countries is a "pandemic" related to many important diseases, 3) that the current United States 400 IU/day guidelines are too low, 4) that it is easily produced by sufficient exposure to unblocked mid-day summer sun, and, importantly, 5) that there may be additional "photoproducts" (other molecules our skin manufactures in response to UVB rays) that we may find are similarly important to cellular processes and so he prefers sun exposure to taking supplements. In regards to diseases that are related to vitamin D deficiency, he writes:

A lack of vitamin D is associated with increased risk for Type 1 and 2
  diabetes, multiple sclerosis, rheumatoid arthritis, Crohn’s disease,
  cardiovascular disease, stroke, depression, Alzheimer’s disease,
  schizophrenia, colon and breast cancer, influenza and tuberculosis....Of the 30 leading causes of deaths in the
  United States in 2010, 19 were linked to low vitamin D status.

He does not deny that one needs to limit exposure to the sun reasonably, and recommends sun block for the face and basically exposing arms and legs something like 10-20 minutes at a time, several times a week, from 10am--3pm (when UV-B is sufficiently strong, else one only gets UV-A, which does nothing for vitamin D but is linked to skin damage), though exact "dosing" will be dependent on latitude, skin color, time of year, and perhaps other factors (which he covers in the book).


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How to get Population Genotype Frequency from 1000 genomes Perl API
Posted a similar question on Biostars but got no response. Not sure if I'm allowed to link to it? Basically I want to pull genotype frequency data for a population group (such as CEU) instead of allele frequency data, via the Perl API for 1000 genomes. I have tabix and perl API installed. This is for 100,000+ SNPs so the solution should hopefully not involve manually downloading genotype and calculating the frequency manually in a for-loop. My understanding also is no solution exists in BioMart (according to the Biostars answer).
Following the instructions here, I can see how to get specific genotypes for all individuals as a list.
Eg: Input -> Some snp, CEU... Output -> G/G 0.87, G/A 0.13 (frequency of some snp for CEU population).
I need to do this for 100,000+ SNPs, so I imagine manually pulling all genotypes for each SNP and calculating the frequency manually in a loop would not be practical.

Please add a link to the data repository and show a dummy example of the data format. Questions about a specific programming language are considered off-topic. So you should edit the question to make it "Language-neutral", focussing only on the methodology rather than the actual script.

Hi, I think Perl is the only way to access the 1000 genomes data genotype frequency, according to this post: https://www.biostars.org/p/153923/#153929 Unfortunately I got no further answer there on how to actually do this.

Can you add a link to the actual repository? You may be able to simply download the entire data (from here perhaps) and parse for the desired data. Moreover, the API mentioned in your link would allow you to customize the data that you want to download. You may have to do it one by one using a loop.

I'm new to 1000 genomes so not sure how to access the data directly, I've just been following the perl API tutorial for homo sapiens as per the link. That link you provided seems helpful but it looks like I'll need to manually iterate through the hundreds of genomes and calculate the frequency in the loop as you suggest, rather than there being an actual functional call like there is for allele frequency? I think if that's the case I'll just stick with the HapMap genotype frequency data.

You don't have to manually do it. Get the VCF or GVF file.  A small script will parse the desired co-ordinates in a few minutes (or less than that).

At the very bottom of the Ensembl link you provided it explicitly suggests using their mailing list if you have further questions. That might be more productive then hoping someone in Biology SE has experience with the API.

If you want population specific allele frequencies you have three options: * For a single variant you can look at the population genetics page for a variant in our browser. This gives you piecharts and a table for a single site. * For a genomic region you can use our allele frequency calculator tool which gives a set of allele frequencies for selected populations * If you would like sub population allele frequences for a whole file, you are best to use the vcftools command line tool.
This is done using a combination of two vcftools commands called vcf-subset and fill-an-ac
An example command set using files from our phase 1 release would look like
grep CEU integrated_call_samples.20101123.ALL.panel | cut -f1 > CEU.samples.list
vcf-subset -c CEU.samples.list ALL.chr13.integrated_phase1_v3.20101123.snps_indels_svs.genotypes.vcf.gz | fill-an-ac |
    bgzip -c > CEU.chr13.phase1.vcf.gz
Once you have this file you can calculate your frequency by dividing AN (allele number) by AC (allele count)
Please note that some early VCF files from the main project used LD information and other variables to help estimate the allele frequency. This means in these files the AF does not always equal AC/AN. In the phase 1 and phase 3 releases, AC/AN should always match the allele frequency quoted.

Another possibility is to use glactools. I will show this by using data from the 1000 genomes.
First, we download the chromosome names and length for the reference:
 wget ftp://ftp.1000genomes.ebi.ac.uk/vol1/ftp/technical/reference/human_g1k_v37.fasta.fai

We then require information on the panels from the VCF file:
  wget https://personal.broadinstitute.org/armartin/ginger/integrated_call_samples_v3.20130502.ALL.panel.txt

 grep -v ^sample integrated_call_samples_v3.20130502.ALL.panel.txt  | cut -f 1,3  > panel.txt

You can run the following to transform VCF into allele counts format (ACF):
 tabix -h ftp://ftp.1000genomes.ebi.ac.uk/vol1/ftp/release/20130502/ALL.chr2.phase3_shapeit2_mvncall_integrated_v5a.20130502.genotypes.vcf.gz 2:136486829-136653337  |glactools vcfm2acf --onlyGT --fai human_g1k_v37.fasta.fai  -  |glactools meld -f panel.txt -  | glactools view -h -

This will print the allele counts:
#chr    coord   REF,ALT root    anc AFR AMR EAS EUR SAS
2   136486850   G,T 0,0:0   0,0:0   1322,0:0    694,0:0 1008,0:0    1006,0:0    974,4:0
2   136486967   C,T 0,0:0   0,0:0   1321,1:0    694,0:0 1007,1:0    1006,0:0    978,0:0
2   136487007   C,T 0,0:0   0,0:0   1322,0:0    694,0:0 1007,1:0    1006,0:0    978,0:0
2   136487181   C,T 0,0:0   0,0:0   1322,0:0    693,1:0 1008,0:0    1005,1:0    978,0:0
2   136487214   G,A 0,0:0   0,0:0   1321,1:0    694,0:0 1008,0:0    1006,0:0    978,0:0
2   136487246   G,A 0,0:0   0,0:0   1282,40:0   693,1:0 1008,0:0    1006,0:0    978,0:0
2   136487336   G,T 0,0:0   0,0:0   1322,0:0    694,0:0 1008,0:0    1006,0:0    977,1:0
2   136487417   G,A 0,0:0   0,0:0   1321,1:0    693,1:0 1008,0:0    1006,0:0    978,0:0
2   136487504   A,C 0,0:0   0,0:0   1316,6:0    694,0:0 1008,0:0    1006,0:0    978,0:0

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text:
Is the PCT of the nephrons of the kidneys of marine vertebrates to minimize the natural tendency for exosmosis?
For marine vertebrates, the concentration of salts outside their body (in the water, that is) is more than that inside their body. So, there is a natural tendency for exosmosis to occur.
To minimise this natural tendency for exosmosis to occur, these vertebrates would need to retain more salts inside their body.
I understand that the Proximal Convoluted Tubule (PCT) of the nephrons of the kidneys is involved in selective reabsorption of salts. So, making the PCT more coiled would increase the surface area of absorption, thus increasing the absorption, and therefore retention of salts in the body.
So, my question is: is the PCT of the nephrons of the kidneys of marine vertebrates more coiled than that of terrestrial vertebrates?

What kind of marine animals are you interested in? Have a look at this post.

I've modified the question to be more specific.

Plus.. During osmosis, salts are not lost.. It is the water that is lost. The marine animals have to conserve water, not salts. You can see that other link. It is quite related to your question but is not about the kidney organization.

First off, I agree with @WYSIWYG - marine life has adapted to conserve water, not electrolytes. Osmosis in sea water draws water from the body and hence their problem is to keep the water in, not the salts.
Osmoregulation in marine mammals is accomplished mainly via differences in hormonal regulation of the kidneys. The histology and morphology of the kidneys are different, but the adaptations have more to do with adaptations to diving/pressure than anything else. Instead, most marine mammals take care not to drink too much sea water and obtain their water from metabolism and foods (Ortiz, 2001).
Reference
- Ortiz, J Exp Biol (2001); 204: 1831-44


text:
Cause-and-effect questions about growth and development of plant
I need to solve some cause-and-effect problems. The problems are related to growth and development of plant. "Growth and Development" chapter is the first chapter in third level of high school (senior high school).
Show your answer with "Is the statement true?", "Is the reason true?" and "Are the statement and reason have cause-and-effect relationship?"
Problem 1

Anthurium should be sprayed with cytokinin hormone to prevent from wither easily.
Reason
Cytokinin hormone promotes/stimulates the growth of axillary buds that will produce lateral branching.

Problem 2

The stem of Avena sativa with the coleoptile is being cut, couldn't elongate.
Reason
Phytohormone that used for growing is only available at the end/peak of coleoptile.

My attempts to those problems are here:
Problem 1
What I know about cytokinin is when you soak the green leaves in the water with cytokinin, the green color will stay longer than without any soaking. I don't have any idea about the effect of cytokinin to flowers. I think I need to dig more knowledge about the hormone.
I'm not sure with the reason too. Quick searching in Google Cytokinin and Wikipedia gives this:

... This promotes shoot growth, and restricts lateral branching.

The problem is my textbook clearly said that the cytokinin promotes the producing of lateral branching.
Because I couldn't prove the statement and reason, I couldn't give their relationship.
Problem 2
I think even the coleoptile is being cut, the flower must not easy to die. The phytohormone must be related with auxine hormone or other thing.
Because I couldn't prove the statement and reason, I couldn't give their relationship.
Any idea or answer is appreciated!
Feel free to edit my grammar. English is not my native language, but I could understand your post in English.


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Difference between Category, Rank and Taxon
Is there any differences between the terms Category, Rank and Taxon or they all are same?
I remember an explanation which goes on like this:
Category and Rank are the same and are the categories of taxonomic heirarchy whereas taxons are the organisms present in those.
Is this correct?

Maybe adding some example context would help answer. Anyway, a taxon is not an organism, but rather any level and grouping one can distinguiah, the last smallest one being a species (a group of individuals). Of the other two, no idea to be honest.

A taxon (plural taxa) is any taxonomic unit. For example, the class Mammalia is a taxon which includes all mammalian species. Similarly, a species is a taxon, Panthera tigris being the tiger. This taxon contains lower taxa, which are sub-species, such as Panthera tigris tigris (Bengal tiger) or Panthera tigris sumatrae (Sumatran tiger).
Rank is simply the level of a taxon in the taxonomic heirarchy. For example, the taxa Mammalia and Aves both have the same rank since they are both classes. Panthera tigris sumatrae is of a lower rank than Panthera tigris because the former is a sub-species and the latter a species. Use of the term rank is only truly meaningful when comparing two taxa.
Taxonomic category is usually – for better or worse – used interchangeably with the term taxonomic rank. A Dictionary of Biology (6 ed.) certainly indicates that the terms rank and category are equivalent. The major taxonomic categories are domain, kingdom, phylum, class, order, family, genus, and species. A category can contain one or more taxa.
Another example, to summarize:

Carnivora is a taxon, which contains many species including Vulpes
vulpes (red fox)
Carnivora is in the category of order
Carnivora (order) is a higher rank than Vulpes vulpes (species)

Welcome to Bio. Great answer, but adding a reference or two would be appreciated.

I am not sure if Reptilia is considered a taxon. It is most definitely not a clade.

@WYSIWYG Yes, it was a bad example - I've changed it

@HarryVervet Please correct me if I am wrong -- you said "the taxa Mammalia and Aves both have the same rank since they are both classes"... which would that imply that class is the name of their shared rank, and thus kingdom, phylum, etc refer to taxonomy ranks, and are not taxons themselves


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When does DIFFUSION occur and not OSMOSIS, and the otherwise?
For example, I do know that red blood cells have both the Na+/Cl- co-transporter and Aquaporin (water channel) that allows both Na/Cl and water molecules to pass through. But why in biology textbooks they imply that osmosis occurs instead of the diffusion of Na/Cl molecules, though red blood cells have the channels for them, too? (that leads into crenation or lysis of the cells)
NOT ion PUMPS, but ion CHANNELS (those that don't require energy). The Na+/Cl- co-transporter works along with the gradient (not against!).
If an RBC is to put in a hypertonic solution, why wouldn't it absorb the excess NaCl using this channel instead of letting the water out?
I do know in the case when we put cells in a hypertonic/hypotonic glucose solution, osmosis will occur instead because the cells need insulin to allow glucose in (via GLUT4).
But when does exactly osmosis occurs instead of diffusion?

But when does exactly osmosis occurs instead of diffusion?

These processes are not mutually exclusive. Both can happen simultaneously. Their rates depend on different parameters such as permeability of the membrane towards water and the solutes. A semi-permeable membrane has different permeability for different molecules. There are cases when one of these two processes may happen but not the other (again, a function of the parameters):
Osmosis+/Diffusion-
When there are no solute transporters expressed in the membrane of the concerned cell. For e.g. RBCs do not express the Sodium-Chloride symporter. It is expressed in the distal convoluted tubule of the nephron.
Osmosis-/Diffusion+
When the osmolarity of the cytosol is same as that of the ECF and the cell expresses ion channels. The action potential in a neuron would be an example of this phenomenon.

I think you could address more specifically why some cells lyse in hypotonic solutions when they contain substrate channels. I think the answer is that in most cells the various channels are gated, but I have no idea what "RBC" is.


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Interaction study of oligomeric proteins
I'm dealing with two different protein(say, protein_a and protein_b) which stays in an interacting-oligomeric form in biological system.
I have so far successfully been able to purify both the proteins using IMAC(Ni-NTA) protocol.
Further TEM analysis of the purified protein is showing the presence of oligomeric form(for each of them separately) in the purified sample.
But, how can I be able to detect or show how the oligomers of protein_a and protein_b is interacting to produce a much larger macromolecular entity ? And how can I be able to quantify that interaction ?
Any ideas regarding this issue would be highly appreciated.

Are the oligomers of a defined size? Gel filtration chromatography or native PAGE could show an interaction and give an apparent Mr of the complex.

Previous data regarding oligomer size shows that protein_a forms ~600kd oligomer(using analytical ultra centrifugation), however protein_b's oligomer size not yet known. So, I'm not sure whether native PAGE could resolve such big mw. @canadianer

Though I've never tried, there are native PAGE systems capable of resolving proteins upwards of 10000 kDa


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Does alcohol really do more damage to the body of a child compared to an adult?
Beside the fact that children and teens (people under the age of 18 year) usually have less body weight than the average adult, is there a   biologically fundamental difference between the damage done to their bodies compared to an adult when drinking alcohol?
I often read that their organs are still developing and thus alcohol will do more damage, but has this actually been proven?

As is stated in this article by Hiller-Sturmhöfel and Swartzwelder from the National Institute on Alcohol Abuse and Alcoholism, there are ethical issues surrounding research on human subjects that preclude direct testing, however studies in model mammals and observational studies do find that "adolescence is a unique stage of brain development which is particularly sensitive to the disrupting effects of alcohol."
A research review by Tapert, Caldwell, and Burke, also finds that studies support the conclusions that alcohol use by adolescents and young adults has a negative effect on cognitive abilities.
Hope that begins to provide you with an answer to your question.

Is the cognitive damage by alcohol uniquely restricted in "the stage of brain development"? What if the fetus is in its embryo phase without neural system developed yet?


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How does drug-induced photosensitivity work?
Some drugs (tetracyclines, for instance) can cause photosensitivity reactions—that is, some patients become extremely sensitive to the sun, developing rashes or inflammation after spending time in bright sunlight. Sources I've read describe this as an immune reaction similar to an allergy, but I've also heard that antihistamines are generally ineffective at treating such reactions.
So my question is, what are the biological processes behind this reaction, and how does it differ from a normal skin allergy that could be treated by antihistamines?

Drug induced photosensitivity (DIP) refers to the development of a cutaneous disease in response to the drug chemical in combination with light. Only the drug or light alone cannot cause the reaction and both are required to be present together. The underlying pathophysiology is important clinically to identify the type of cutaneous manifestation the drug-light combo has caused. There are majorly two types of reactions, phototoxic and photoallergic reactions.
Also, the kind of light required depends on the kind of drug and the the wavelength at which it gets photoexcited. Although UV-B is a mojor cause of sunburn, the wavelength required for DIP for most drugs falls in the UV-A part of the spectrum.
Phototoxic reaction
Phototoxic damage refers to the direct damage the photoactivated drug can cause to the tissue. Light leads to excitation of electrons and as they return, they can lead to formation of reactive oxygen species which damage the cell membranes and DNA. This tissue damage leads to activation of proinflammatory cell signal transduction pathways and leads to inflammation in the area. Clinically, it looks like an exaggerated sun burn.
Photoallergic reaction
This is similar to the same old hapten story. A drug which is otherwise non-antigenic turns antigenic after a photoreaction. Most probably, the reaction should have caused the modified drug to bind to cutaneous proteins leading to cell mediated immune reaction. This T-cell mediated inflammatory response usually has an eczematous morphology if the photoallergen is applied topically or the characteristics of a drug eruption if the photoallergen is administered systemically
It is important to differentiate the kind of reaction, a drug would cause.For example, the tetracyclines that you mention are phototoxic but not photoallergic. Photoallergic reactions have far lesser incidence than phototoxic ones.
Coming to the other part of your question, on the treatment, most important is to educate your patient for appropriate photoprotection. If severe, the drug could be withdrawn and switched to a safer one. Treatment includes topical corticosteroids to bring down the inflammation in either reactions. Oral antihistaminics are reported to have limited advantage. Why this is so,I'm afraid, I do not know. Hence your question remains partly answered.
Reference: http://emedicine.medscape.com/article/1049648-treatment

Thanks for the detailed answer. I admit I'm not familiar with some of the terms in your answer but it has shed a lot of light on the topic. It stops just shy of stating why oral antihistamines are not effective, but perhaps that aspect has not been studied thoroughly.


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Cut strand of hair longevity?
Quick and useless question : what can be the longevity of a cut strand of hair, assuming we kept it in (good) normal conditions ? Any idea ?

"assuming we kept it in (good) normal conditions" - your definition of normal matters.I recently read that some of the dead from Herculaneum had intact hair. That was more than 2000 years ago. And that's far from the oldest hair specimens.

Fossilised hair can last over 200,000 years. http://www.telegraph.co.uk/news/earth/environment/archaeology/5299352/200000-year-old-human-hair-found-in-dung.html

In order to keep the hair from decomposing, my first assumption is you'd need it in an environment that inhibits decomposers, e.g. dry. We can see in the mummification process that hair may be preserved for hundreds of years. Hair is also composed largely of keratin, however, and in my own search of the literature: (1) we need microbial (bacteria, fungi) keratinases to decompose the keratin in hair [source], and (2) this process is slow. There's a really old article here, from the abstract:

Keratin, prepared from horn meal, was added to moist field and garden soil and allowed to decompose in the laboratory. The keratin was found to undergo a decomposition resulting in a slow, but steady accumulation of ammonia and nitrate. 35–40 per cent, of its nitrogen was transformed into nitrate after 120 days.

More recent numbers to shed light on a rate of degradation for keratin are either obscure, or untested. This is more so for hair specifically as I couldn't find much more.


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How did people's liking of ceremonies evolve?
Habitual group activities are prevalent across many animal species, particularly in mammals, especially in primates.
However, I do not see any evolutionary benefit of this. 'Ceremonies' take time, and in many cases seem to exert more energy than they reap. Note at this point I am not talking about hunting groups, but rather about group activities that serve a purely social purpose (mourning is a  good example of this and is present in elephants, chimpanzees, bonobos, and probably more). This costs significant amounts of resources, time, and energy which apparently could be better spent hunting, foraging, traveling, mating, or grazing.
I'm interested in finding a timeline, and explanation, of why and how this phenomenon of higher social rituals (perhaps using mourning as an example) evolved throughout the mammalian kingdom.
A cursory google revealed nothing about how this 'liking' of interaction evolved.

I'm voting to close this question as off-topic because this is an anthropological question.

We'll need an accurate definition of rituals in order to answer this question. For the moment it is too broad. Do you restrict rituals to social traditions? Do you include personal habits and obsessive behaviour in rituals? You posted several links (without much explanation), you should probably report what you read so far, that would help.

Questions about the evolution of human behaviour are on-topic to my opinion.

@AliceD The question is about evolution, and as far as I know, evolution falls firmly within the realm of biology. Perhaps it would be better on a anthropology Stack Exchange, but one does not exist.

@Remi.b Okay, I re-wrote the question. Do you have any ideas to further improve it?

Thank you the question is much improved this way, I retracted my close vote. Note however, that the question is not so much about evolutionary genetics but fall within the field of "evolution of traditions/culture", or more broadly speaking "evolution of memes" also called "memetics", which is a field that has been created by biologists but in its current state is in between biology, sociology and philosophy. I think the question is on-topic but will appreciate to see what the others say. Might be a bit broad also...we'll see.

the question in it's present form does not have a biological perspective, the user thinks it is, but it's really more of a question of how did our cultures take the shape that they have today. What you can ask is why is our behaviour different from that of other animals, and how has it come to be so...

@KoustavPal What do you mean it doesn't have a biological perspective? Is there not some evolutionary advantage to ceremonies? Is that not biological?

no the evolution of ceremonies themselves have no biology, but neural development does, I'm not making myself clear. Ceremonies are our inventions, for instance mammalian males are generally polygamous, traditionally that has been so, in came the church and instituted monogamy, then in 19th century a few mistresses on the side were fine, and in the 20th century feminism started to pick up the pace and again we reverted to monogamy. So where is the evolutionary part of ceremonies. I will also point this out, the basal character of humans have not changed.

you would still prefer to sleep inside a closed space facing the point of entrance, why do you think that is?

@KoustavPal This is very far away from any biology particularly if you start talking about specific rituals from your own culture. For example, weddings in western culture have changed dramatically over the last century as media & adverts changed the concepts of a wedding. These are not biological evolutionary timescales.
Bird models are often used to study social dynamics, and primate studies often turn up habitual social group activities. Starting there might narrow down your question. Elephants have been observed mourning their dead too.

@KoustavPal I'm not asking how ceremonies evolved, as like you said, that would be cultural. I'm asking how the liking of ceremonies in general evolved. Given that this liking has existed for a very long time and is observed in other species, this seems genetic and biological.

@GoodGravy You might want to see the response I gave to KoustavPal.

Now I understand. You frame the question with in a very cultural-centric way. I'll try and suggest an edit.

@Kyth'Py1k I have made some major edits to the question so feel free to roll back, but I think the question is back on topic. It still remains vague. If you can better define a "ceremony" or restrict it to mourning, then it will probably be specific enough to re-open.

@GoodGravy You made a good edit. I'm not sure how to make it less vague without taking away from the meaning of the question. I could try to narrow the question down to a specific ceremony, for example burials, but this would only give an answer to one small part of the question. I'll do this if you do not have any better ideas, though.

@GoodGravy Okay, I asked a new, more specific, question.

Perhaps customs (and culture as a whole) arises to some extent as a result of relationships between individuals of the same species. For example, I think a good example of a custom is how elephants bury their dead. This does not benefit the surviving elephants in any noticeable way, and is a "waste" of energy and time. If customs do arise because of a group dynamic, then there is clear evidence supporting that social behavior in higher organisms (chimpanzees, dolphins, etc.) does increase fitness.
However, this speculation is based upon the idea that customs are a natural result of social interaction. As to why these customs arise, perhaps it is because it enforces the group dynamic over the participating individuals.

I don't think elephants bury their dead, it's just that they appear to hesitate to move on from a dead elephant. Happy to be proven wrong!

"...They then began to throw leaves and dirt over the body and broke off tree branches to cover her." I stand corrected!


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How is Glycophorin A and straphylococcal related to Escherichia coli and what does readily purified mean in this context?
I am reviewing the paper "Glycophorin A Dimerization Is Driven by Specific Interactions between Transmembrane Alpha-Helices."  There is a statement in the abstract which I don't understand:
"The transmembrane alpha-helical domain of interest is fused to the C-terminus of staphylococcal nuclease.  The resulting chimera can be expressed at high levels in Escherichia coli and is readily purified."
As I understand it, this describes that an alpha-helix within Glycophorin A is fused to straphylococcal nuclease?  Then, how does Escherichia coli come into the discussion and what is meant by being readily purified?

Basically, they engineered a vector which, when transfected to E. coli, produces transcripts of -and thus proteins to- a fusion gene which produces these transmembrane α helices conjugated to the staphylococcal nuclease. In other words, the E. coli are just factories for producing proteins:

Expression, Extraction, and Purification of SN/GpA - For high
  levels of SN/GpA production, pT7SN/GpA was transformed into E.
  coli MGT7 (kindly provided by D. LeMaster), containing the plasmid
  pLYS-S.

And the reasoning therein was proposed in the discussion,

We report here the use of a chimeric protein to show that
  the presence of just the transmembrane domain of GpA, fused
  to a normally monomeric soluble protein, is sufficient to
  mediate the dimerization of this artificial membrane protein
  -in SDS

What they mean by readily purified is that the protein can be extracted relatively easily, and in the experimental method they explain some commonplace methods of purification:

One-step purification of milligram quantities of SN/GpA from the
  extract could be achieved by reversed-phase HPLC utilizing an acetonitrile/isopropyl
  alcohol/water gradient on a semipreparative Vydac
  C4 column. Alternatively, purification of larger quantities was
  achieved using two rounds of cation-exchange chromatography...
...The chimera SN/GpA131, but not truncated forms, could alterNaCl,
  50 mM Tris-HC1, 5 mM EDTA, 1 mM PMSF, 0.025% NaNa,
  natively be extracted by sonication of the pellet after cell lysis in 1 M
  pH 7.9, containing no detergent. This extraction was of similar
  efficiency to that with Lubrol, and was utilized in the preparation of
  material for generation of transmembrane peptide by trypsin treatment.


text:
Do mutations come in pairs?
As DNA is organized in a double-helix, a change in one strand must be accompanied by a corresponding change in the other strand. Let's say an original sequence CATCAT mutates into CATGAT. The other strand must change from GTAGTA to GTACTA - or, more precisely, as the other strand is read in the opposite direction, from ATGATG to ATCATG, possibly in a completely different gene. Has the effect of this pairing of mutations been explored mathematically?

Welcome to Biology! What exactly do you mean with Has the effect [...] been explored mathematically? Mathematically implies you wish a theoretical analysis of the occurrence of mutated base pairs? Or do you want to know if indeed mutations are characterized by changed base pairs?

If a mutation has to be accompanied by a second mutation, only loosely related (by an accident of being on a strand exactly opposite the first mutation), it should affect a frequency of survival, or of a beneficial change. We should not consider a single mutation in isolation.

Note that DNA repair mechanisms catch odd bases. A mutation is per definition a change in base pair. Further, only 1 strand serves a basis for transcription. The other one does not. This question is quite unclear to me and I vote for closure until refined.

If a mutation occurs in one strand and is missed by repair mechanisms, it will be copied to the new complementary strand during replication. You'll end up with one double helix with the mutation and one without. That said, I also don't understand your question.

@AliceD This is a technicality, but rarely you will find two genes that overlap on complementary strands and so both strands serve as a transcription template at that locus.

@canadianer - we might have to take this to chat, but I always thought the complementary DNA strand was the template and the other coding strand just acts as a backbone. So the coding DNA strand carries the code, but does not act as the template during mRNA transcription. If that makes sense...

@AliceD You're absolutely correct, I was just referring to cases of overlapping genes, like this. So both strands at that locus act as a template for transcription. One of my previous professors claimed that essentially every part of the genome is transcribed at some point, which seems to be at least partially validated by papers like this.

While the question of mathematics makes no sense. The intention of the question is clear. What would happen if the DNA repair like nucleotide excision repair has failed to repair the DNA? I think the answer is that the mutated base will be replicated among with its new base-pair.


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Unsure why Synechococcus moves at angle in cuvette
I'd really appreciate your help. I'm working with Synechococcus. In my experiment, I have Synechococcus in a solution of milli-Q water. I illuminated it with a focused white light through a pinhole and observed it using a CCD camera. The Synechococcus flows downward, which I think is due to gravity. But, in time, the Synechococcus flows downwards at an angle. Is this due to heat convection? If it is heat convection, it's strange that it sometimes stops flowing. The only visible motion seems to be Brownian motion.
Thank you your help!


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How much does the nutritional value of insects depend on what they're fed?
Insects are often touted as being the food of the future due to their nutritional value and small amount of resources required to raise them. However, how dependent is the nutritional value of an insect on what they are consuming. How many vitamins and amino acids are they able to synthesize?


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Spider Identification Illinois
I noticed a really huge, beautiful web on my porch last week, and tonight, I discovered its resident. I'm thinking it's an Araneus diadematus (Cross Orbweaver), but I was hoping for some confirmation.
Can anyone confirm this or offer a better suggestion?

I would agree this is some species in the Araneidae. Do you have a picture of the spider's belly? Or a better picture of the spider's web? Thanks.

This is very likely an araneid (or Orb-weaver spider) in the family Araneidae.
Without further evidence, it's hard to narrow down to a species.
One possibility:
Neoscona crucifera (Hentz orbweaver, spotted orbweaver or barn spider)

 Source: Will Cook 2001

 Source: Wikipedia

Description:

Relatively variable in color (and sometimes pattern), but is usually rusty-red or golden orange color.

This site suggests females are reddish-brown to brown and males are lighter brown with the sides of the carapace nearly black.

Dorsal abdomen is brown and hairy; abdomen underside = black, with two white spots
The epithet crucifera refers to the cross-like pattern on their back
Legs have alternating light and dark brown bands.

Size: females = 9.5-19 mm long; males = somewhat smaller
Web: very large (up to 0.61 m diameter) and often on buildings and other man-made structures
Range: Eastern/Central USA + Mexico

According to Will Cook,

Several other species of Neoscona are confusingly similar...Other species usually have a bolder pattern.

We can rule out Neoscona domiciliorum because Illinois is west of its range and the colroation is different. [Source].

@Dan Do you remember if the spider had dots on the underside of the abdomen?


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Decomposition Rate of A Body In A Wet Environment
I have a photo of a decomposing dog which is in a water logged environment. My peers and I are debating how long that body has been decomposing. They are saying it is at least a year old. I however think it's much more recent (1-3 months).
My understanding is that when a body is put into a wet environment either partially submerged or fully it speeds up the decomposition process provided the water is not lacking oxygen such as if it was deep on the ocean floor.
The carcass has its skull fully decomposed, which I think is due to the bacteria rich water having more access to surface area through the various orifices and also the skull having much less flesh than the rest of the body.
The torso looks for the most part intact, and I don't see any bloating from gas buildup (not sure when and how long such a feature would be present), and there appears to be a pink area which could be muscle.
Would these features be typical of a recent death in this type of environment or am I overlooking some other important processes that could be speeding up or slowing down the decomposition?
Photo (image unboxed in case graphic for some viewers)

Bugs, scavengers, microbes, time, the environment... a lot of factors at play in decomposition, for example: Forensic entomological decomposition.

Could you clarify the question a little? Are you trying to find out how long ago this dog died, or are you after a recognised method for estimating the "age" of a corpse in this specific type of wet environment?

I'm suggesting that this question as off-topic because I find it unclear what the user is asking and I'm not sure forensic methods are on topic.

@rg255 How is forensics not related to biology? There is a whole area of forensics that involves biology see: https://en.wikipedia.org/wiki/Forensic_biology

I'm not sure that the photo alone is enough information to give a precise answer. I'm voting to close for "unclear question" reason, but I enjoy the idea of forensic puzzles for biologists to solve!

It depends on the temperature of the environment as well. In the heat of summer and in a watery environment, I can verify through unfortunate personal reference that stuff can decompose very quickly. I honestly didn't look at the image, but judging by your description it can't have been there a year. There would be nothing left. Hungry bacteria and decomposers would have left nothing but bones by then. I would say your guess is more on target.

Can you please add some references to your answer?

Unfortunately in my case it's simple experience living in a rural/wooded area :/ Occasionally we have to do cleanup.


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Explanation about cytogenetic notation
What is the correct meaning of cytogenetic notation "inv(4)(p13q22)" ?

Inversions at chromosome 4, at the p arm 13 is inverted AND at q
arm 22 is inverted

OR

Inversions at chromosome 4, the p13 is
Swapped with q22

Do you have a source

Those are the break points of the inversion. So chromosome 4 was cut at p13 and q22 and the fragment was reinserted in the reverse direction, giving a pericentric inversion.

So the explanation number 1 is the correct !!!!

@d.putto Actually neither really sound correct to me.


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How can a chromosome translocation in somatic cells lead to disease?
Looking at this picture...

(source: nih.gov)
...I get the impression that the part of chromosome is attached to other chromosome, but it is not mutated. When we assume that all genes in the translocated part are intact and can still make mRNA, my question is:
How can a chromosome translocation in somatic cells lead to abnormality or disease?

The concept of "in somatic cell" that you recently added to the post is a little unclear to me, probably just because I am not aware of any particular example. Can you cite an example of an abnormality/disease that you are interested in?

https://en.wikipedia.org/wiki/Chromosomal_translocation#Role_in_disease

Thank you. I think what you mean by "in the somatic cell" is actually "for the balanced carrier". I tried to expand on my current answer. Let me know if that make more sense now.

You can't assume that all genes remain intact. What if the translocation break occurs inside a gene and inactivated it? And what if that gene is a tumour suppressor.

In the Down syndrom typically, the translocation does not induce (usually; see later) any disease. We call someone carrying the translocation a "balanced carrier". The problem arises after, at the moment of segregation.
When balanced carriers reproduce
Consider someone who has a translocation as you showed. You showed only one chromosome of each types (1N), below are the 2 chromosomes (2N). On the below image, the person with the translocation is assumed to be mating with someone who does not have the translocation.

The balance carrier is usually healthy. As a consequence of this translocation a kid has probability 1/4 to be "normal", 1/4 to have the translocation (and therefore to eventually have offspring with trisomy/monosomy) and a probability 1/2 to have trisomy/monosomy.
Balanced carrier
Citing from wikipedia:

Most balanced translocation carriers are healthy and do not have any symptoms. But about 6% of them have a range of symptoms that may include autism, intellectual disability, or congenital anomalies. A gene disrupted or disregulated at the breakpoint of the translocation carrier is likely the cause of these symptoms.

Indeed, even a balanced carrier can be affected by the translocation. Gene regulation network is often quite complex and separating a gene from its regulatory region can eventually have important impact. It is also possible that the break point occurred in the middle of a gene (or a regulatory sequence).
I think that one cannot say much more about why a balanced carrier can be sick in a general form. We'll need to go case by case and ask specifically what are the genes and regulatory processes involved in the disease. However, it is easy to conceptualize that moving genes around can affect the genetic network and the expression of genes.

Thanks for this fantastic explanation. This make complete sense in case of Meiosis but my original question was intend to chromosomal translocation in somatic cells. If you can add some detail about somatic cells chromosomal translocation  I will accept it as answer.

Let us know if you feel like the updated answer (based on you updated question) does not answer your question?

You have made an incorrect assumption-- that all the genes on both chromosomes necessarily remain intact. It's possible that they do, and the the translocation is harmless.
But the transition point could be within a gene. This would usually lead to that copy of the gene becoming inactive, which can cause diseases just like any other loss-of-function mutation.
Alternately, the translocation can fuse two genes in a pathogenic way. While this might seem fantastically unlikely, the fact that the translocations are non-random means that there are patterns that recur frequently. The BRC-ABL fusion (https://en.wikipedia.org/wiki/Philadelphia_chromosome) is one of the most common causes of childhood leukemia. The fusion protein is constitutively active because the regulatory domain of the original protein has been replaced.
Finally, a translocation could separate a promoter element from the gene it controls, which could cause aberrant expression of that gene. The promoter element could also wind up proximal to a different gene and cause aberrant expression of that gene.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Can people with AIDS get tattoos?
When I do a Google search, most of the results are about whether or not people can get HIV / AIDS from getting a tattoo through dirt needles. I am, however, curious whether or not it is possible to get a tattoo if you have AIDS.
Quoting wikipedia's entry on tattoos:

Tattooing involves the placement of pigment into the skin's dermis,
  the layer of dermal tissue underlying the epidermis. After initial
  injection, pigment is dispersed throughout a homogenized damaged layer
  down through the epidermis and upper dermis, in both of which the
  presence of foreign material activates the immune system's phagocytes
  to engulf the pigment particles.

If your immune system is not working properly, I can imagine that the phagocytes might never respond to the tattoo ink and that the pigment might not ever enter the fibroblasts?

AIDS affects T-cells, I have never heard of it being particularly damaging to macrophages/neutrophils... So I would imagine AIDS would have no effect on the tattooing process.

@TheNightman. AIDS is the disease that is caused by the Human Immunodeficiency Virus, so AIDS is the result of HIV infecting T-Cells. The mechanism that it does this by is by glycoprotein 120 binding with high affinity to the CD4 surface receptor. It then binds to the CCR5 co receptor and fuses with the membrane to deliver the viral nucleocapsid and associated proteins. CD4 T-Cells, Macrophages, and Dendritic Cells all have CD4 and CCR5 (barring a mutation) and thus HIV can infect all three cell types.

@AMR - I edited my answer

@AliceD I saw, thank you for the acknowledgment. Was there something you wanted me to do further? This comment was related to The Nightman's comment...

@AMR - all is fine! Thanks for clearing matters up.

One of my interests is immunology, and I spent a good amount of time this Spring looking at the adaptive immune system and how HIV infections occur at the cellular level... I was actually kind of disappointed that I had to look some things up... What is it, we lose 70% after the first month?

Short answer
People with HIV can get tattoos.
Background
In Africa there are countries that tattoo people identified with HIV (Source: Kenya Today) and some people with HIV find comfort in tattooing biohazard symbols and related images on themselves to express their illness (Source: CNN).
However, as rightly mentioned by @AMR, macrophages  which are mainly responsible for ink fixation express CD4 and therefore can be infected by the HIV virus targets.
Hence, while I don't think HIV affects tattooing given the fact that HIV-infected people get tattoos, in theory HIV could reduce the ink fixation.

While it may not affect the ability to get a tattoo and have it fix in the skin, The HIV virus infects T-Cells, Dendritic Cells, and Macrophages. gp120 binds with high affinity to CD4 and then needs CCR5 to fuse with the cell membrane. Both CD4 and CCR5 are present on those three cell types and thus the virus can infect all three.

Posted due to certain inaccuracies in comments and answers provided to this question regarding the Human Immunodeficiency Virus.
It should be noted that while it may not affect the ability for macrophages in the dermis to phagocytose the heavy metals found in the inks used in tattooing, and thus not interfere with the fixing of a tattoo in an HIV+ person, the Human Immunodeficiency Virus, the virus responsible for Acquired Immune Deficiency Syndrome (AIDS) does in fact have the ability to infect any cell type that expresses the cell surface glycoproteins CD4 and CCR5.
Cells that express CD4 and CCR5, barring mutations seen in the bone marrow received by the Berlin Patient (Timothy Ray Brown), among them CD4 "Helper" T-Cells, Macrophages, and certain Dendritic Cells, are all capable of being infected by the HIV virus.
Glycoprotein 120, found on the surface of the HIV envelop, binds with high affinity to CD4. The coreceptor CCR5 then binds to the gp120 CD4 complex and allows the HIV envelop to fuse with the plasma membrane of the host cell. The fusion then delivers the viral nucleocapsid and associated proteins into the cytoplasm of the cell and the infection takes place.
If I had to venture guess, I would say that as Macrophages tend to be present within the dermis of the person for extend periods of time, there is likely enough of a population present in the skin to have the macrophages necessary to fix the inks used in tattooing.

+1 thanks for your careful analysis. I adapted my answer to be in line with yours.

Yes.. If I am not wrong HIV strains are classified as M-Tropic (macrophage) and T-Tropic (T-cell).

The same infection in initial stages is more m-tropic and later turns in the late stages, more t-tropic


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What is this fish?! Is it even real?
According to a guy in a Facebook group I belong to, this fish was caught in the Missouri River near Omaha, NE, US. I have never seen one like it in my life, not in person or photo or anywhere. What on earth is this fish?! Is it even real? I've not seen it in person, only the photo below, but he says its real.

Welcome to Biology.SE. I added a small coma to make sure you don't "belong to the fish" but to the "Facebook group". To ESL like me ponctuation is appreciable!

@Remi.b I hope it was a comma instead of a coma ;)

I thought it looked a lot like a sea robin which didn't make sense in context. Glad to find out sculpins and sea robins are very close in appearance indeed!

@Andy, we're discussing a different fish down in chauxvive's answer, and we may need a change of best answer!

Original Answer

It looks to me like a species of sculpin, for example, the "short-horned sculpin" Myoxocephalus scorpius.

http://www.luontoportti.com/suomi/en/kalat/short-horn-sculpin

Best answer

After some deliberation, and it appears the other very good answer was for some reason removed: the OP fish appears to be a northern sea robin Prionotus carolinus.

This conclusion comes from the aid of user chauxvive, so much thanks for the identification, though his answer is oddly gone. The conclusion is based off of (1) the morphology of the head and face plate, (2) the longer and tapered pectoral fins, (3) the distinguishing long feelers at the sides anterior to the pectoral fin, and (4) the more probable distribution.

It indeed looks like a sculpin +1 However, would you expect to find this species in the Missouri river? (Caution: very bad naturalist and bad ichthyologist is commenting!)

You know, my background doesn't give me any expertise here either, I'm just particularly good at acquiring information as needed. So to answer you, I'm really not sure out of experience. You definitely find sculpin in the Missouri River, but the distribution for the short-horned sculpin is certainly further north, which is why i could only provide it as an example, rather a clear-cut ID.

It definitely looks like what your answer says it might be, but I looked that up and it says its habitat is arctic coast! how would it have gotten to the Missouri River?! https://en.wikipedia.org/wiki/Myoxocephalus_scorpius

It's a really good question. I added a link to some info on sculpins, and there's a query to geographic distributions, you can use it to find a distribution for the specimen above and related. None seem to be endemic to the Missouri river if we're considering spiny sculpins, based on information I can find here

I think this is most likely it. Maybe it was an aquarium fish someone let go. Very odd though!

I think this is probably the mottled sculpin (Cottus bairdii) which is found in freshwater in NA, including the Missouri river.
http://www.fishbase.us/Summary/SpeciesSummary.php?ID=4065&AT=sculpin
https://en.wikipedia.org/wiki/Mottled_sculpin

Sculpins are a good candidate at this point, but I hadn't considered the sea robins at first. Taking a look at Prionotus carolinus, this fish is in my opinion a better fit than a sculpin. The morphology of the face and mouth, and the presence of what appear to be feelers at the bottom of the fish (as opposed to horns) confirm this, I believe.

I'm glad to see it may be indeed be a sea robin. Please vote for my answer here, if you don't mind, since my other post is gone. The pectoral fins were what I noticed first- robins have such unusual fins!
here's a great image, looks much like our fish here.
here's another anatomy of the sea robin. As you can see, it has pectoral fins much closer to this mystery fish than the sculpin.
This is an interesting discussion of the sea robin types and habitat The common sea robin is much larger than the northern and apparently the northern can stand much fresher water. Obviously this is outside of their range (which is along the coast and up brackish rivers of the Eastern US) but mystery fish could be a release. This isn't a popular tank fish, but you can buy and order them online (reference) They are pretty common in new england, apparently.

Your answer still looks like a comment and in its current form deserve being converted into a comment. You should edit it to include a picture and the reasons that make you think it is a sea robin and not something else. You can consider @kendall's answer as an example. Not however, that it is a little worthless to repost an answer that already exist (even though I understand you were first to suggest it a sea robin but again your answer just looked like a comment).

Also you should not use answers to complain about how the StackExchange sites work. You can use the meta-sites (either Meta-Biology.SE or the more general meta.SE) to ask question about how the SE sites work and suggest improvements.

I looked your strange fish and I think that it is a short horned sculpin because of its spikes.So, don't imagine that it is a sea robin because sea robins live in very deep waters (500 meters depth aproximately).In fact, I think that this sculpin was trapped in the river while it was going to the sea and the fishermen caught it.


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Does polyploidy always isolate the polyploids from the diploid source population?
I am receiving conflicting information while researching polyploid speciation. On the one hand, some sources state that a polyploid can only reproduce sexually with polyploids having the same number of chromosomes. But I am also finding information claiming tetraploid x diploid reproduction in orchids, or tetraploid x triploid reproduction of orchids (for example,see  American Orchid Society, AOS.org).
Is polyploid sexual isolation always the case, sometimes the case, or never the case? Can someone clarify this?

Welcome to Biology.SE. That would help if you could link to all your sources.

Ploidy and reproductive isolation in plants
Speaking generally, there is simply no question that for flowering plants there can be a sexual pathway between diploid and polyploidy levels. The question is how wide is the bridge and how much flow is there in either direction. In other words the questions become "How much flow?", "How meaningful the flow?", "How much flow back to the original diploid and polyploid populations?", and "How often over the last 200 million years has such interaction been an important factor in the evolution of flowering plants?".
Examples from Rhododendron
In the following, I will give a number of examples from the plant genus Rhododendron to show how ploidy level can function in relation to sexual isolation. In this taxa, diploid X tetraploid normally produces triploids although occasionally a tetraploid or even a diploid offspring is produced. The triploid offspring of diploid deciduous azalea species X tetraploid deciduous azalea species often look very similar to the tetraploid pollen parent.  'Margaret Abbott', which is a seed fertile tetraploid deciduous azalea, has a fragrant white flower produced by crossing a fragrant pink flowered diploid seed parent with a non-fragrant yellow flowered pollen parent.
Our research on hybrid elepidote Rhododendron indicates that triploids, although reluctant to reproduce sexually, can produce diploid, triploid, tetraploid, and pentaploid offspring when crossed with pollen from diploids, triploids, and tetraploids. 'Phyllis Korn' is an example of a fourth generation triploid. 'Graf Zeppelin', which exhibits polyploid characteristics, is an example of a diploid offspring of a triploid. 'Countess of Derby' is an example of a tetraploid offspring where both parents are triploids. 'White Ginger' is a an example of a pentaploid offspring of a triploid. 'Pink Pearl' is an example of a triploid that has produced diploid, triploid, and tetraploid offspring from interaction with diploids.
In deciduous azaleas triploid X tetraploid crosses often produce aneuploids between triploid and tetraploid. Such crosses can on occasion produce pentaploids.
Our limited experience working with triploids and pentaploids as seed parents indicates that in general pentaploids are better seed producers than triploids.
An interesting finding is neotetraploids can produce diploid offspring in the first generation. In general tetraploids can produce diploids, triploids, tetraploids, and pentaploids when crossed with pollen from diploids, triploids, and tetraploids.
Triploids are common in natural contact zones where diploid deciduous azalea populations overlap with tetraploid deciduous azalea populations. There is strong evidence indicating there is gene flow from the diploid population to the tetraploid population in these contact zones. There is some evidence of gene flow from the tetraploid population to the diploid population. There is some evidence to suggest multi-generational triploids exists in these contact zones.
Worth noting is that the meiosis for triploid deciduous azaleas that do set seed is distributed around 1.5x gametes ranging from 1x to 2x with an occasional 3x gamete. This uneven distributed splitting of triploids is what produces aneuploid offspring between 3x and 4x when semifertile triploids are crossed with pollen from stable tetraploids. Cyril Dean Darlington in the late 1920's and early 1930's documented this uneven distributed splitting of triploids during meiosis. Evidence suggests that neotetraploids can also undergo uneven distributed splitting during meiosis.
Darlington's history of the garden hyacinths showing a triploid pathway from diploid species to tetraploid hybrids parallels the history of the hybridization of the tetraploid elepidote Rhododendron 'Countess of Derby'.
We have some evidence for deciduous azaleas that 3x X 4x can produce aneuploids close to 5x indicating that some of the "3x gametes" are coming from first an uneven splitting of the triploid followed by a failure to reduce in a later phase of meiosis. However this result of aneuploidy near pentaploid has not occurred often enough to be certain that is what is happening.
In general for deciduous azalea species;

diploid X diploid normally produce seedpods and high percentage of
viable seed.
tetraploid X tetraploid normally produce seedpods and high percentage
of viable seed.
diploid X tetraploid normally produce seedpods but a highly variable
percentage of viable seed.
tetraploid X diploid almost never set seedpods.
triploid X tetraploid sometimes produce seedpods and a low percentage
of viable seed.

For hybrid elepidote Rhododendron, 2x X 2x, 2x X 3x, 2x X 4x, 3x X 2x, 3x X 3x, 3x X 4x, 4x X 2x, 4x X 3x, and 4x X 4x are all documented to have occurred.
For deciduous azaleas, we have produced viable seed from 2x X 2x, 2x X 4x, 3x X 4x, 4x X 4x, 4x X 6x, 4x X 8x, 5x X 4x, 6x X 4x, and 6x X 6x.
The flow cytometry for this research on the genus Rhododendon was performed by Dr. João Loureiro, Dr. Silvia Castro, José Cerca, and Mariana Castro
Plant Ecology and Evolution Group,
Centre for Functional Ecology,
Department of Life Sciences,
Faculty of Science and Technology,
University of Coimbra, Portugal.
The ancestry for 'Phyllis Korn' illustrates that triploids can be multi-generational.

The diagram below illustrates how the triploid 'Pink Pearl' has produced diploid, triploid, and tetraploid offspring when interacting with diploids and has produced a tetraploid offspring by interacting with another triploid.

The family tree for the Rhododendron elepidote hybrid 'The Duchess' illustrates that interploidy interaction can be multi-generational.
\
Picture of 'Margaret Abbott' with a quote from Frank Abbott.

Picture showing how much the offspring of a diploid crossed with a tetraploid looks like the tetraploid pollen parent.

Picture showing the successful development of seedpods from crossing a diploid by a tetraploid.

Picture showing the failure in developing seedpods from crossing a diploid by a tetraploid.

Picture showing interploidy hybrid swarm at Audra State Park, WV.

References
Meiosis in Polyploids
by W. C. F. Newton and C. D. Darlington
in Journal of Genetics 1929
The history of the garden hyacinths
by C D Darlington, J B Hair and R Hurcombe
in Heredity 1951
Rules of Engagement: Have Pollen—Will Travel
by John Perkins · Sally Perkins
in Azalean 2010
Frank Abbott's Village of Azaleas
by John Perkins · Sally Perkins
in Journal American Rhododendron Society 2011
Ploidy level estimations in deciduous and elepidote hybrids of Rhododendron
by José Cerca de Oliveira, Mariana Castro, Francisco J. do Nascimento, Sílvia Castro, John Perkins,Sally Perkins, João Loureiro
in Jornadas Portuguesas de Genética, Coimbra, Portugal; 05/2011
Weighing in: Discovering the ploidy of hybrid elepidote rhododendrons
by Sally Perkins, John Perkins, José Monteiro de Oliveira, Mariana Castro, Sílvia Castro,  João Loureiro
in Rhododendrons, Camellias and Magnolias, Royal Horticultural Society, Editors: Simon Maughan, pp.34-48 2012
Untersuchung des Ploidiegrades elepidoter Rhododendron-Hybriden
by Sally Perkins, John Perkins, Mariana Castro, José Cerca De Oliveira, Silvia Castro, João Loureiro
in Rhododendron und Immergrüne , Deutsche Rhododendron-Gesellschaft e.V. , Seite 21: pages 21-42; 11/2013

Very comprehensive and well referenced +1. I edited your answer to bring the general conclusion (for plants) to the forefront, and added a couple of headings. I hope you are fine with my suggestions - otherwise feel free to edit or rollback.

Depending on the species the hability of generating hybrids will be different.
Some can, others don't. However generating a hybrid of a diploid and a tetraploid will give rise to a triploid, usually sterile plants (as it happens with seedless whatermelons, which are a cross between tetraploid and diploid).
This is where most of the isolation comes from, as these triploid hybrids are sterile (they can't undergo meiosis because of the control systems that require an even amount of chromosomes) they are not a viable species, and thus a genetic barrier begins.
I don't know specifically on the Orchids though.


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What exactly is extreme heterozygosity and how does it work?
What does the concept of "extreme heterozygosity" mean?
I first encountered this concept in "The Drunken Botanist". They describe that when planting a seed from, say, a 'red delicious' which was pollinated by another 'red delicious' does not guarantee growing another 'red delicious' tree. The author goes so far to say that the new tree may have almost none of its parent traits, and may barely resemble any other breed whatsoever. They argue this is caused by extreme heterozygosity.
I later found the concept of extreme heterozygosity the Wiki page for "apple"

This is because seedling apples are an example of "extreme heterozygotes", in that rather than inheriting DNA from their parents to create a new apple with those characteristics, they are instead significantly different from their parents.

On a PNAs article on Extreme genomic variation referencing extreme heterozygosity

We conclude that the extreme heterozygosity in C. savignyi is caused by a large effective population size and not an elevated mutation rate.

My understanding of population genetics (allele frequencies and patterns of dominance)
I understand homozygous diploid pairs, like pp or PP, and heterozygous pairs like pP and Pp, and hetero/homozygous dominance and recession. I also found an interesting paper on sea squirts to work through later that suggests why extreme heterozygousity is popular in large population sizes.
What I can't seem to find is exactly how "extreme heterozygousity" works. How is this different than ordinary heterozygous? Is there an entirely different context I'm missing out on? The only way I can imagine a more "extreme" heterozygosity is with triploid mismatched pairs, which can't be right. So how does the process work and what exactly defines it?

Can you please link to your article? I have never heard of "extreme heterozygosity" and it is pretty hard to say anything without seeing the paper.

Large population size tend to have higher heterozygosity and there is less drift to wipe out genetic variance. I guess this is what your paper is refering to given that you say extreme heterozygousity is popular in large population sizes. The term popular seems a little inappropriate though. You should cite correctly.

I am voting to close as you're asking to comment on a claim and a concept without providing the claim or the context in which you found this concept. Of course, I'll remove my vote close as soon as you link to the article.

Please take a look at my edits.

Thank you! That is much better with the links. I am surprised that even in the PNAs paper, they don't seem to offer any good working definition.  I voted to reopen. I also made important edits to your post. Feel free to roll back or make any further modifications.

I appreciate your edits as I'm new to the site and do want to make positive contributions. Although I've read the faqs, these changes are helpful in context, thank you.

@yingw response was right, but I will try to explain it a bit better.
Say that you had a gene, let's call it the plumb gene. This presents two alleles: P and p. Those alleles behave in a way that gives three different phenotypes depending on the genotype: PP, Pp and pp all have different phenotypes, for example, yellow, green and blue color.
If the P and p frequencies are each 0.5 on the total gene pool of the population you would expect a Hardey-Weimberg equilibrium if the reproduction and survival was random (there would be no selection).

$0.5^2=0.25$ of homozygous (PP and pp are each a 1/4 of the total population)
$2*0.5^2=0.5$ of heterozygous (Pp would be 1/2 of the population)

For what you say, extreme heterozygous would mean that the rate of heterozygosity in the population would be much higher. For example, if we found 90% of green and only 5% of blue and 5% of yellow, that would mean that there is a selective advantadge for the green individuals.

It is also my intuition that "extreme heterozygosity" would refer to any heterozygosity higher than $0.5$. That'd be great if you'd have a reference for this definition!

From the article the OP linked: extreme heterozygosity in C. savignyi is caused by a large effective population size and not an elevated mutation rate.. It doesn't seem to match your definition as large population size and (reasonably) high mutation rate won't cause a heterozygosity that is greater than 0.5.

Without reading the article, given the context that you have mentioned, I think extreme heterozygousity means that most of the individuals in the population are heterozygous (much higher than 50%). So there might be some kind of selection pressure that gives heterozygous individuals a reproductive benefit.

Great insight- So the likelihood of homozygous pairs would be highly unlikely? But in diploid pairs, would that mean that rather than two options like r and R, there would be more alternatives, like say r, R, d, and D for one spot? so you would be less likely to get rr, and more likely to get rD or something? The article isn't relevant to my question. I had heard of extreme heterozygousity in apples and couldn't find any other explanations of exactly what that meant in Punett square vocab.

I think you might be confusing a couple of things. r and R would be two different alleles. Alleles can often be thought of as different mutations (ex. R represents the original A allele, r represents an A->T mutation, D represents an A->C mutation. Its possible that the A base pair is dominant to T and codominant with C). If you find that R allele appears in 0.5 fraction of individuals, r in 0.2 and D in 0.3 then if population is in equilibrium you expect RD = (2* 0.5 * 0.3), RR = (0.5 * 0.5), Rr (2* 0.5 * 0.2), etc. If you observe fewer RR/rr/DD then there is some selection for heterozygous

According the this article: Extreme genomic variation in a natural population

There is increasing evidence that many animal species exhibit high levels of heterozygosity (1–4), which, according to the Neutral Theory, should be caused by elevated mutation rates or large effective population sizes (5).

This would imply in addition to the fact that even in a single genetically homogeneous orchard the offsprings are still very heterozygotous, that apple trees have a high mutation rate from the parents to the children.


text:
Looking for university/graduate-level texts on RNA
Although I was not a biology major in college, I took the biology introduction sequence, as well as organic chemistry and biochemistry.
I would like to learn more about RNA and ribozymes. What texts/textbooks are currently used? Perhaps it's best to begin with a genetics textbook.
The scope of the book should cover be at a undergraduate level or higher, and should cover the dynamics and purpose of ribozymes.

I'd start with the most recent edition of Watson's "Molecular Biology of the Gene". The problem with RNA books is you go too old (which may still be relatively new), you could be in the dark ages of RNA. I'd say newer is better, and there's a new edition of Molecular Biology of RNA set to release in '16. Textbooks are perhaps more unreliable than literature in this respect given some of the good ones date back to 2011.

Jennifer Doudna is probably the preeminent researcher in RNA today. I would say that reading her papers would give you graduate level coverage of the topic. Watson's MBOG may be a little too generic if you are focused solely on RNA, and there are better choices of advanced level genetics texts if your interest in more general genetics.

Please read the tag-wiki for book-recommendation. You should address all the mentioned points in detail, otherwise your question would be considered broad/opinion based.

@AMR "there are better choices of advanced level genetics texts if your interest in more general genetics." Do you have a suggestion? Thanks

I hesitate to recommend this Text because it is difficult to read... but Lewin's Genes XI. This is the Amazon.com page. Even in their description they say it is designed for Upper Level or Graduate Genetics, and they are not exaggerating. The material is excellent, but it is difficult to use as a textbook. They will make references to topics in other sections, but they reference by name, so you have to go to the TOC to figure out where in the book you need to go...

... I had the physical edition... An electronic version may be easier if they properly designed it with links. The Kindle version is overpriced compared to paperback or used copies. Watson is probably the way to go if you need an introduction, I was responding to your suggestion that it should be at a graduate level. Our graduate level genetics course is using Genetics, From Genes to Genomes by Hartwell, however I have not yet reviewed it so can't comment definitively.

As suggested by others, you can start with some basics on molecular biology. Genes - Benjamin Lewin and  Molecular Biology of the Gene - James Watson et al. are good books for the basics.
I haven't seen any book dedicated to RNA-biology and most of my understanding has come from reviews.
You can start by studying RNA secondary (and higher order) structures which is essential for understanding how riboswitches function. I would suggest that you first begin with the wikipedia article on this (it is not that great). The above-mentioned books would also cover the basics. You may then have a look at this review which is about thermodynamic and kinetic aspects of RNA-hairpins:
       Structures, Kinetics, Thermodynamics, and Biological Functions of RNA Hairpins
For Riboswitches you can refer to these reviews, which are quite comprehensive:

Ribozymes, riboswitches and beyond: regulation of gene expression without proteins
Riboswitches: Emerging Themes in RNA Structure and function

This is another comprehensive review on ribozymes:
        Ribozyme Structures and Mechanisms

PS: Some of these articles may not be freely available. You can mail the corresponding author (email address would be mentioned in the article) requesting for a reprint.