Analysis over single chromosome data I have no expertise in biology, I'm a data scientist, and I would like to know if it makes sense, from the biological point of view, to analyze data (SNP data) coming from a single chromosome, and not all 22 chromosomes, to predict the risk of a certain disease.

Should I obligatorily use data from all chromosomes? Why?

Thank you very much. And sorry if it is a very basic question, but I really would like to understand this.

You can analyse a single chromosome. All the bioinformatics tools I know, allow that. Consider only the reads that map to the desired chromosome (or any segment of the genome). However, most next-gen sequencing experiments sequence the whole genome and not just a single chromosome. You'll just end up losing information by not considering other chromosomes.


What flying insect is this? Resembles Wasp / Crane Fly / Moth? What insect is this?

Found this in southern Bangalore, India. Looked dangerous, flew really slowly with its body upright and legs spread out and landed on a wall.

Size: about 1.5 inches tall, 1.5 inches wide, when spread.

These photos are zoomed in and rather dull colored, but the actual color was a bright orange, like #FF9050 and dark black.

Pselliophora laeta, a species of crane fly (Tipulidae) in the Ctenophorinae subfamily.

Route to discovery: Reverse image searching my own photo on Google led me to a matching image on Naturalista (Familia Tipulidae), and in-turn to iNaturalist, which showed me to Genus Dictenidia. Further Googling for "Genus Dictenidia" brought up many families of crane-fly, which I visually scanned until I spotted it -- Pselliophora! That led to Wikipedia, and to this image, which mentions its source to be whatsthatbug, where the discussion cites Pselliophora laeta on India Nature Watch.

--

Source: https://www.inaturalist.org/observations/299363
Observed: Thiruvananthapuram, India; Jul 28, 2012 5:13 PM IST

Mating Crane Flies from India

Source: https://www.whatsthatbug.com/2010/09/30/mating-crane-flies-from-india/
Observed: Mumbai, India; Sep 30, 2010 1:43 AM IST


Could bone marrow transplants help make xenotransplants viable? So the immune system doesn't calibrate (for want of a better euphemism) to recognize it's own cells until fairly well along in fetal development & the major components of the immune system (antibodies, white blood cells, etc) are all produced by the bone marrow.

Those are the known details that cause me to wonder if this (below) might not be a viable approach.

Introduce the patients cells to a pig fetus before it's immune system has been set & it will be born with an immune system that recognizes both it's own cells & the patients cells as it's own.
Kill the patients own marrow (as per a normal bone marrow transplant) & transplant the pigs bone marrow into him giving him an immune system that recognizes both his cells & the pigs as it's own.

If my understanding is correct you should then be able to transplant any other organs from the pig into the patient without any tissue rejection issues.
I am only interested in the science so (any legal & moral issues aside) are there any major factors I'm unaware of to suggest this approach is a non-starter?

See Xeno: The Promise of Transplanting Animal Organs into Humans By David K. C. Cooper M.D., Robert P. Lanza M.D. Published 23 March 2000 by Oxford University Press, specifically the section on "The Induction of Chimerism Before Birth" from page 117 onward in this link.
That talks about my suggested first step (though in reverse), creating a human with immunity to cell rejection of a donor animals cells, which isn't much use to anyone who's already been born.
So I flipped the idea.

A Thymus transplant might be needed as well.

I feel I've enough sources & data to venture an answer on this one myself now, so here goes.
Step one: Can we produce the pig in the first place?

Fetal Inoculation With Donor Cells in Cardiac
Xenotransplantation 1996
Perinatal induction of immunotolerance to cardiac and pulmonary allografts July 1997
Induction of donor-specific tolerance to cardiac xenografts in utero: 1998 Sep
Cell Transplantation January 1 2003
IMMUNO-INTERVENTION FOR THE INDUCTION OF TRANSPLANTATION TOLERANCE THROUGH MIXED CHIMERISM: 2011 Aug 11
In utero hematopoietic cell transplantation: induction of donor specific immune tolerance and postnatal transplants: 2014 Nov 12

another link to the same article
In utero hematopoietic cell transplantation: induction of donor specific immune tolerance and postnatal transplants 12 November 2014

First human-pig 'chimera' created in milestone study 26 Jan 2017
Interspecies Chimerism with Mammalian Pluripotent Stem Cells 2018 Jan 26
Interspecies Chimeras and the Generation of Humanized Organs 3 Jan 2019

Yes, an animal can be produced with donor specific tolerance to the patients organs, it's a known procedure & observed effect that has been replicated numerous times in experiments, its immune system would not attack either the patients cells or its own.
Step two : Can we transplant this animals bone marrow to the patient?

Stem cell and bone marrow transplants

Yes, bone marrow transplants involving the complete removal of the original bone marrow is a long established procedure for the treatment of leukaemia.

And now being used for treatment of other severe autoimmune diseases in a way which may make this idea moot, I'll have to look into that further, not read that article in full yet.

Step three : Will we then be able to transplant other organs from this (or a genetically identical) animal to the patient without tissue rejection?
The immune system isn't seated entirely in the bone marrow & its products (the thymus, spleen & lymphatic system also have roles) so for best results some of these may also need to be replaced.
If so it must be hopped the lymph nodes play no role in in the development & tuning of the immune system, there are 500-600 of them around the body so replacing them all would be no small task.
Conclusion :
Still in progress / just saving work so far


Does vitamin D affect melanin concentration? I am aware of the affect on vitamin D production by melanin (in sunlight) but I can not find any information regarding a reverse connection.

Darker skin, as opposed to common belief, probably did not develop as cancer protection. Cancer is usually something that attacks the body in a subsequent life. Even pale individuals under the sun are likely to survive far beyond their reproductive era before they are wiped off by skin cancer.

Instead, it is believed that folic acid manufacturing is the highest selection pressure causing darker skin. Folic acid (vitamin B9) which is used all over the flesh, especially during pregnancy and childhood, will decompose in sunlight.

So the skin tone tries to discover the ideal equilibrium between vitamin D and minimal folic acid breakdown.

As a consequence, if you genuinely have enough vitamin D in your diet, there is no need for lighter skin (and further proof for the vitamin-d hypothesis). That is why the Inuit have lighter skin than expected for their extreme location: the intake of vitamin D is large, so the folic acid part of the equation "wins" and pale skin is not preferable. This is why Inuit individuals do not need so much sun.

Source:

scienceline.org/2007/06/ask-dricoll-inuiteskimos/

pnas.org/content/107/Supplement_2/8962


How do Kangaroo mothers deliver the correct kind of milk to the correct joey? Mother kangaroos are able to rear multiple joeys (young kangaroos) at different stages of development at the same time. According to Wikipedia, "the mother is able to produce two different kinds of milk simultaneously for the newborn and the older joey still in the pouch." What biological mechanisms are able to ensure that the correct joey gets the correct kind of milk? Do different teats produce different types of milk and somehow the joeys know which teat to suck from; or is each teat able to deliver both types of milk and the teat is able to tell from the mouth conformation (or something else) which type of milk to deliver?

The younger Joey remains attached to the teat from which it receives its milk for the period of nine months until it leaves the pouch. So that would be teat from which milk suitable for the newborn is available (reference 1 and reference 2). The older Joeys also have an incredible sense of smell by which it can detect the teat from which it gets the milk it requires but it stands to reason that they cant get milk from the teat to which the younger joey is attached. (reference)


What governs the size of animal bodies? Million of years ago there lived dinosaurs up to 36 m high. About 10,000 years ago lived Machairodontinae -compared to cats today they were huge. About 400,000 years ago lived Mammuthus trogontherii: it reached over 4 m at the shoulder. And these are just some examples.

Todays biggest living creatures look small compared to previous. So my question is, why are all creatures getting smaller? Why doesn't evolution generate any big creatures with size comparable to the dinosaurs?

I agree with other commenters that we are not necessarily living in a time of small body masses.
Here is a paper on a body mass distribution. It's quite mathematical, but the first author (Aaron Clauset) is good.
For individual body masses, you can look at Kleiber's law - this says that body mass and metabolism are related by a power law.


Why is elevated homocysteine considered a risk factor for angina? Elevated homocysteine levels are listed among risk factors for angina. How is homocysteine related to the heart? Or the coronary arteries? How do these relationships make it a risk factor for angina?

Homocysteine:

Causes endothelial dysfunction and damage
Accelerates thrombin formation
Inhibits native thrombolysis
Promotes lipid peroxidation through free radical formation
Induces vascular smooth muscle proliferation
Promotes monocyte chemotaxis

Many observational epidemiological studies indicate that individuals with higher Homocysteine levels have increased risks of cardiovascular disease.


Why aren't human babies considered larvae? I've seen people who are anti-baby describe babies, or children in general, as human larvae. This is generally done in order to make them seem weird. While I feel like this statement is wrong, I can't quite put my finger on exactly why.

Many definitions of "larva" specify that they must metamorphosize, or go through significant morphological changes on the path to adulthood. However, tadpoles gradually change form, rather than metamorphosizing, and hemimetabolic insects have larval instars that aren't substantially different from adults, aside from being sexually immature and smaller. "Sexually immature and smaller", of course, also describes babies fairly well.

Unfortunately, I'm no biologist and my knowledge of what defines animal young as larval vs. non-larval is rudimentary, at best, so I'm not sure if there's a more precise definition of "larva" than the one I found on wikipedia, which would disqualify human babies. What traits differentiate larva from non-larva, and which of those traits to babies lack?

For animals with a clear larval stage, the presence of such a stage indicates that there is a metamorphosis, a change in body morphology at some point in development.

Metamorphosis does not necessarily refer to an 'instant' transformation or one that requires a pupation step or something similar; gradual change can still be metamorphosis, as long as there is a clear 'before' and 'after.'

Human infants, on the other hand, don't go through much of a metamorphosis: sure, they grow quite a bit, but their general body plan does not change. Contrast this with insects, or your tadpole example, and it is clear there are major body plan changes from larvae to adult stages.

The Wikipedia page on larvae describes the characteristics of larvae fairly clearly. Like most traits in biology that vary across taxa, you are likely to find some intermediate creatures where the presence of a larval stage is somewhat controversial or depends on opinion. There could be a difference of opinion on how much of a change is sufficient to describe a juvenile form as a larvae. Humans don't have a postnatal stage that approaches that potential boundary.

The part in your question about people who are "anti-baby" sounds a bit judgmental, but I think what you are describing is just a phrasing meant to be somewhat humorous and to evoke images of "gross" larvae; I wouldn't take that for any biological meaning and I wouldn't focus your time on proving it "wrong" - the actual difference of opinion you have is something entirely different.


Is there a notion of RMSD for two different molecules? The (least) Root Mean Square Deviation is used for comparing different conformations of the same molecule. However one may be interested in comparing the conformations of two different molecules e.g. two proteins of different backbone lengths. So is there any method for comparing conformations different molecules such as a generalized RMDS?

PyMOL ("align molecule1, molecule2" returns aligned structures and RMSD). TM-align (returns aligned structures and TM-score; tmalign.py is a python module for running TM-align using PyMOL).


What is Pan for in pan-caspase? A simple question (I could not find it on internet): What is Pan for in pan-caspase? Is it any different from the term 'caspase' ?

The term pan, in my opinion, is perhaps one of the most vague that exists in science! I can partley answer this question (ironically as vague as the term pan) by referring you to the term pan-neuronal. A pan neuronally expressed genes has features, which include the expression of many "generic" genes required non-specifically for neuronal function, such as components of the synaptic vesicle machinery, so pan-neuronal genes are not neurone class specific (http://www.wormbook.org/chapters/www_specnervsys/specnervsys.html). So with that token pan-caspases are a term referring to a general caspase activity/function/structure and not a specific caspase type activity but I would welcome any corrections or edits to this response.


What is this black insect? I found it in my computer but I don't know what it is

It appears to be a Boxelder bug, which are common in areas of North America with maples, ash, or other host trees:

 (photo by Katja Schulz via Wikimedia Commons)


How can I determine the purity of cells isolated from rat brains if I cannot use FACS, Immunohistochemistry or SEM anaysis? Please help.

I know how to isolate the different cells (astrocytes, other glial cells, neurons and synaptosomes) from brain tissue using a Ficoll-based separation but how do I determine the purity of the fractions that I have isolated if I cannot use immunological techniques, FACS or SEM analysis.

You can do qPCR for certain markers from the extract. GFAP for astrocytes, Tuj1 for neurons, Myelin for oligodendrocytes etc and calculate their percentages to have an estimate of the relative populations. If you are quite used to microscopy and studying these cells then you can identify the different populations of cells with normal light microscopy as well; this is not quantitative and is susceptible to bias.


Tools I can use to find similar genes What tools are available to estimate the function and purpose of a gene ? I think the right approach is to find similar sequences of genes that we know the function of.

All the information I have on a gene is (for example):

KXN84633.1

and

>lcl|Query_208731:23119-24312
CTACAGACATATCCCATCCAGAAGAAATCTTTATCTATCGAATACCTTCGCGATAACGCGTATCTACGCG
CTCGAACAGGCCAAATAGCTGCAATGTTAAGGCTGAGGGATAGTATTTCCAAAAACCTATCCCGGCATTT
TGAGGTACATTTACTTTCTTCCGTATCTGGCCTGACTAAAAATCCTGCGTAGTCTCAAGGGTTTACATAT
ACTCATACGCCTATAATAACAGCTAGCGATTGCGAAGGCGCAGGCGAAGCATTTCGCATATCACCTATCC
AACCTACCACCCCCTCTCTCTCAAAAACTGACGCAAGTTCAGACGCAAATACCCCTATAGAGTTCTTTTC
ACGTCCTGCATATCTCACAGTCTCGCATCAACTTCATCTAGAATCCTTCACCACGGCTCTCTCTCGCGTG
TATACCCTTTCACCATGTTTTCGTGCGGAACGATCTATGACTGGACGACATCTGGCCGAGTTCTGGATGC
TTGAGGCCGAGTGGAACCTTGCAACGCGTTGCGATAGCTTAGAAGAAATTTGTGCCTTTGTGGAAGGCTT
AATTCGGACGTCGGTAGATCATGAGTCGCAGGATGTCAAGGCTCTGTGGGCGGAGAAAGGAGCGGAAGTA
GAGGAATTCAAGATGTTTCGTGCCGCATTTGACAACGCTCAGCCTTGGAGGCGATTAACATACTCGGATG
CAGTCGAGGCGTTGAGCACGGCTTATGTCAACGGACATCCTTTCGAATTCAAACCTGTCTGGGGCGAATC
ACTCTCGAGCGAACATGAACGTTGGCTGGCAGAGGTGTACGTTGGTGGACCAGTGTTCGTGACAGACTAC
CCTATCAAACTTAAACCGTTTTATATGCGGGTCAACGAAGATGGGAAAACCGTTGCGTGTTTCGATTTGA
TTGTACCTCATGCTGGTGAACTTGTGGGTGGAAGTGTGAGGGAGGAGAGATGGGATGTCCTCTCAAAACG
GATGGCAGAGCATGGATTGTTGCCTCACCCTGACCAGAATGAGGGTGCCCCAACTGATTCGACATATGAA
TGGTATCTGGATTTACGCAAGTATGGTGGAGCGCCGCATGCAGGGTTTGGTCTTGGGTTTGAAAGGCTGG
TGAGCTGGGTTGGAGGGATTGACAATGTGCGAGAATGCATCGGCATGCCTCGGTGGACTGGGAGAATGAT
TATG
>lcl|Query_208731:22646-23071
ATGCTCCTTCGCAGGTTATACTCGACTGCTGCACATCCTGCCAGGTTCAAACTACCGCCGACAATCAAAC
AGGTGCTTTCAGCTAATGGCAGCGAAAGTTCAGCGACATCAGTGACTGGCTGGATTAAATCTATCCGTAA
ACAGAAAAACATAACCTTCGCTGTAGTCAGTGATGGTACAACACCAGAGGGCCTGCAAGCAGTTGTGTCA
AAAGAACAGGGTACTTCCCCAGAAATGTTGAAAAGGTCAGTTCATCTCTCACAGCTCGAAACCGGAACAC
TCACCAATTGAAGACTTACGAACGGTACAGCAGTGCGGCTCACAGGAAATCTAATTCAGTCTCCTGGCCG
AGGTCAAGAATGGGAGCTTGTCATTCAAGAAGGTGACAAGAACGCTATCGAAATCCTCGGCGACTGTGAT
ATTGAC
>lcl|Query_208731:c22559-22323
ATATCACATTCAACATCCAGGGTAATGACATCGCCATGTCGCTAGACAGCGTCGACAATGACTTCCAAGA
AACACTCGTTCCCATCTCCACTGGAATCTCTCTGGAACTCGATCTTATCAAACCCCGTCAACCGCAAGAG
CAAGAGTCCAAACTAGCAATCTGTCTTCACCCCTGGTCTCGACTCGGAGGACGCAAAAGCGACCCGTGCG
GTGTCTTATTCCACGAGCTCAGGTCGA
>lcl|Query_208731:c23949-23902
CACGAACACTGGTCCACCAACGTACACCTCTGCCAGCCAACGTTCATG

obviously I am new to this :)

I personally do not find the second part with the queries helpful without greater context.

The first part appears to be an accession number (more information on these can be found here: https://www.ncbi.nlm.nih.gov/Sequin/acc.html). By going to NCBI (https://www.ncbi.nlm.nih.gov/) and searching that accession number, you can get a lot of information quickly and easily.  Searching this particular number shows it to be a Asparagine-tRNA ligase from the fungal genus Leucoagaricus (https://www.ncbi.nlm.nih.gov/protein/KXN84633.1/).

If you simply have a DNA or protein sequence and no accession number, you can perform a BLAST (https://blast.ncbi.nlm.nih.gov/Blast.cgi).  This will search your sequence against a massive database of annotated DNA or protein sequences. The specific type of BLAST to run and the ideal parameters will take some reading on your part to determine.  However, if you're just starting out, nucleotide BLAST for DNA sequences, protein BLAST for protein sequences, and default parameters will often suffice. This search will provide you with the best "hits" to the database which you can then follow up on to get an idea of the function of your original sequence.


Are there any documented cases of extinction of a species of fungus? Are there any documented cases of extinction of a species of fungus? I imagine it would be hard to detect something like this.

Edit: documented by humans when it happened and/or induced by humans.

According to the International Union for Conservation of Nature’s Red List there are many endangered fungi, but none that are documented to have become extinct within the time frame of interest to you.

However, it seems likely that some fungi have gone extinct with their plant hosts — according to the IUCN there have been 133 documented extinctions of plant species. In particular, mycorrhizal1 (and other) associations between plants and fungi are prevalent and some of these associations appear to be specific (i.e. the fungus only associates with one plant species). For example, there are reported to be 28 species of fungi that only associate with the shrub Lantana camara.2

References:
1: Hoeksema, J. D., Bever, J. D., Chakraborty, S., Chaudhary, V. B., Gardes, M., Gehring, C. A., ... & Lajeunesse, M. J. (2018). Evolutionary history of plant hosts and fungal symbionts predicts the strength of mycorrhizal mutualism. Communications biology, 1(1), 116.
2: Hawksworth, D. L., & Rossman, A. Y. (1997). Where are all the undescribed fungi?. Phytopathology, 87(9), 888-891.


Preventing paracetamol overdose Paracetamol overdose is one of the most common drug toxicities. It may be treated by intravenous N-acetylcysteine which replaces the glutathione that is used up in paracetamol metabolism to prevent the harmful effects of NAQBI.

Why can glutathione, NAC nor an inhibitor of the alternate cytochrome metabolism be added to paracetamol to prevent the possibility of acute liver failure? I imagine there is a reason as this is too obvious a solution.

I assume you mean "why can't glutathione, NAC .. be added"

From lef.org

  There is one problem. The FDA prohibits combining existing drugs and
  dietary supplements unless a New Drug Application is filed, tens of
  millions of dollars of clinical studies are performed, and the FDA
  agrees to allow the combination to be sold. The whole process can cost
  upwards of $100 million and take a decade to complete.

It's sad that would would be very likely an effective solution for the deaths and liver damage is not available or made more widely known.

Only about 10% of acetaminophen is metabolised through the glutathione conjugation pathway via NAQBI (the other 90% is direct sulfation and glucuronidation of acetaminophen). Many people take NAC supplements regularly (I used to).  While high does can have some side effects, a typical supplement level dose of a few hundred milligrams daily are well tolerated.


When was the first exception to Mendelian genetics discovered? In addition to the the question in the title I'd like to know , how scientists reacted to the exceptions?

I would say that first exception might be White gene in Drosophila Melanogaster, described in 1910 by Thomas Hunt Morgan and Lilian Vaughan Morgan. At least, is the first exception we study in genetics since sex linkage its so fundamental. These experiments established the chromosomal theory of inheritance.

Thomas Hunt Morgan, an embryologist who had turned to research in heredity, in 1907 began to extensively breed the common fruit fly, Drosophila melanogaster. He hoped to discover large-scale mutations that would represent the emergence of new species. As it turned out, Morgan confirmed Mendelian laws of inheritance and the hypothesis that genes are located on chromosomes. He thereby inaugurated classical experimental genetics.
After breeding millions of Drosophila in his laboratory at Columbia University, in 1910 Morgan noticed one fruit fly with a distinctive characteristic: white eyes instead of red. He isolated this specimen and mated it to an ordinary red-eyed fly. Although the first generation of 1,237 offspring was all red-eyed but for three, white-eyed flies appeared in larger numbers in the second generation. Surprisingly, all white-eyed flies were male.
These results were suggestive for hypotheses of which Morgan himself was skeptical. He was at the time critical of the Mendelian theory of inheritance, mistrusted aspects of chromosomal theory, and did not believe that Darwin's concept of natural selection could account for the emergence of new species. But Morgan's discoveries with white- and red-eyed flies led him to reconsider each of these hypotheses.
In particular, Morgan began to entertain the possibility that association of eye color and sex in fruit flies had a physical and mechanistic basis in the chromosomes. The shape of one of Drosophila's four chromosome pairs was thought to be distinctive for sex determination. Males invariably possess the XY chromosome pair (Morgan used a more cumbersome notation) while flies with the XX chromosome are female. If the factor for eye color was located exclusively on the X chromosome, Morgan realized, Mendelian rules for inheritance of dominant and recessive traits could apply.
In brief, Morgan had discovered that eye color in Drosophila expressed a sex-linked trait. All first-generation offspring of a mutant white-eyed male and a normal red-eyed female would have red eyes because every chromosome pair would contain at least one copy of the X chromosome with the dominant trait. But half the females from this union would now possess a copy of the white-eyed male's recessive X chromosome. This chromosome would be transmitted, on average, to one-half of second-generation offspring—one-half of which would be male. Thus, second-generation offspring would include one-quarter with white eyes—and all of these would be male.
Intensive work led Morgan to discover more mutant traits—some two dozen between 1911 and 1914. With evidence drawn from cytology he was able to refine Mendelian laws and combine them with the theory—first suggested by Theodor Boveri and Walter Sutton—that the chromosomes carry hereditary information. In 1915, Morgan and his colleagues published The Mechanism of Mendelian Heredity. Its major tenets:
• Discrete pairs of factors located on chromosomes like beads on a string bear hereditary information. These factors—Morgan would soon call them genes—segregate in germ cells and combine during reproduction, essentially as predicted by Mendelian laws. However:
• Certain characteristics are sex-linked—that is, occur together because they arise on the same chromosome that determines gender. More generally:
• Other characteristics are also sometimes associated because, as paired chromosomes separate during germ cell development, genes proximate to one another tend to remain together. But sometimes, as a mechanistic consequence of reproduction, this linkage between genes is broken, allowing for new combinations of traits.
Morgan's experimental and theoretical work inaugurated research in genetics and promoted a revolution in biology. Evidence he adduced from embryology and cell theory pointed the way toward a synthesis of genetics with evolutionary theory. Morgan himself explored aspects of these developments in later work, including Evolution and Genetics published in 1925, and The Theory of the Gene in 1926. He received the Nobel Prize in Physiology or Medicine in 1933.

quoted from: http://www.genomenewsnetwork.org/resources/timeline/1910_Morgan.php
see more: http://www.esp.org/foundations/genetics/classical/thm-10a.pdf


What is the name of the critter depicted in the attached image? I found a critter on my bathroom towel. It's really tiny. Maybe 2 milimetres? I placed it on an envelope for the photograph.

Can someone identify what it is?

That is the larva of a carpet beetle.

  Larvae feed on natural fibers and can damage carpets, furniture, clothing and insect collections.

"Anthrenus verbasci - larva side (aka)" by André Karwath aka Aka on Wikimedia

Related question: What kind of caterpillar is this?, though I think that the larva photographed in that example is either of a different species or at a different time period within the larval stage.


Bacteria resistant to antibiotics? If I use antibiotic on a specific type of bacteria, some will survive because it is resistant. Was this bacteria resistant to this antibiotic before it was even used, or did the bacteria develop resistance after the antibiotic is used?

How or why some bacteria can simply mutate to form beneficial alleles which will help in survival and others can't?

Antibiotic resistance comes from selection pressure: any bacteria that are resistant will survive and replicate, so in the next generation of bacteria you will find more resistance.

Bacteria do not simply mutate to form beneficial alleles, the alleles or genes that confer drug resistance must already be in the population; by using antibiotics, however, you're killing off their competition by killing the bacteria that don't have the resistant allele(s)/gene(s).

It's very unlikely that one individual using one antibiotic for one illness will lead to detectable antibiotic resistance. However, antibiotics aren't used in just one individual: they are used repeatedly, in many individuals, often in multiple species, etc. It is this broad use of antibiotics over time that eventually "finds" strains that are antibiotic resistant. Once these strains with resistant alleles become more prevalent, it becomes more likely that they will be present in some quantity to be selected for in the future.


Who gives a newly discovered microbe its name? Assuming a hitherto unknown microbe is found - who gives it its name?

I sthere any reason for your question to be specific to microbes? Whether a microbe or multi-cellular organism is found, the problem is the same. Who name it?

  Who name it?

Whoever discovered it. Of course, discovering a new species is not as easy as just taking a picture. One has to provide a very thorough description of the species morphology and eventually argue that it should be considered as a new species and not just as a subspecies or something else. See here for discussion on the definition of a species.

  How does the discoverer name it?

If the new species is considered part of an already existing genus, then the author has to keep the genus name. The species name the author chooses is mainly to up himself / herself. Consider for example Macrocarpaea dies-viridis (dies-viridis means "green day") was named like this because the researchers were listening to Greenday when they found it!


What animal has fat with the highest energy density? Fat is more energy-dense than protein and carbohydrates, it is not only an energy deposit but also an organ with many functions such as cushioning and metabolism regulations. I want to know are animal fats similar across species (composition & function), specifically what animal has fat with the highest energy density?

In both humans and animals, the body fat stores appear as triglycerides, which can be composed of different fatty acids, but they all have about 9 kilocalories per gram (USDA).

There can be different amounts of fat in different fat cells, so there can be slightly different amounts of fat in 100 grams of different types of fat tissue.

Calories in 100 g of fat from different animals:

Lard = 902
Beef tallow = 902
Chicken fat = 900
Turkey fat = 900
Goose fat = 900

The fat mentioned above was white fat, which appears as a single fat droplet in a fat cell. Humans and some animals, especially rodents and bats, also have different amounts of brown fat in which the fat cells contain a lot of mitochondria and the fat is present in multiple droplets, so, logically, brown fat tissue has lower energy density.


Confused about definition of bulk flow of water by osmosis As a teacher of high school and introductory college chemistry, I used textbooks that defined osmosis as a flow of water (only) through a membrane that prevents other substances such as dissolved salts from passing through.  But in more advanced text, discussing osmosis through aquaporins in the plasma-membrane, bulk flow by osmosis implies that the water carries along dissolved substances.  So which is it:  pure water or a solution that moves by osmosis?  (I'm somewhat naive about biology, as my degrees are in physical chemistry and metallurgy.  Biology is way more complicated!)

Bulk flow and osmosis are different; I'm guessing your text might be talking about using osmosis to drive bulk flow, but they are occurring at different stages.

For example, if you get your water from a water tower, your house's water pressure is driven by gravity. However, the water tower could be filled by an electric pump. You could say your water pressure is driven by an electric pump, but the pump isn't really pushing water into your house, it's just pushing water up a tall tower so that gravity can act, and if you didn't realize this fact you might be confused about how you can still have water pressure even when the power goes out.

Similarly, you can drive bulk flow by osmosis. If you have a closed space (e.g., a "tube") and pump salt (or anything else water soluble) into it, it can pull water from the surrounding tissues via osmosis. As the pressure of water increases in that closed space, it can now flow in bulk through that tube. Plants can use this mechanism to deliver nutrients up a stem: they pump in ions/molecules inside the stem, which pulls in water from the soil around. Because the space is rigid, instead of expanding the water goes up the stem in "bulk": anything else carried in the water will be pushed up with it. Then, when target tissues pull in solutes, osmosis again causes water to follow, and by only pumping solutes in one place and out another you produce a bulk flow of water.


Why are cancer rates low in large animals? Large animals generally have more cells and live longer than smaller animals. For example, bowhead whales live up to 200 years and weigh up to 100 tonnes, as opposed to humans (living ~71 years and weigh ~75 kg) and mice (10–25 g, <1 year in the wild). Hence, whales have an immense number of cells and those cells are subjected to environmental carcinogenic influences (chemicals, UV) for a longer period of time.

Cancer is caused by random mutations and those random mutations are basically stochastic processes. Given their long life span and larger number of cells, shouldn't larger animals have a substantially higher chance to develop cancer? In fact, story goes that bowhead whales in fact only very rarely contract cancer, and less so compared to humans?

Short answer
Large animals do get cancer. They may contract cancer with an incidence less than that estimated by absolute cell numbers, but there seems to be a lack of data on cancer rates in large animals to support this hypothesis conclusively.

Background
Whales contract cancer (Martineau et al, 2002). There does, however, seem to be a lack of correlation between body mass and cancer risk, which is counterintuitive since larger animals have more cells. This is known as Peto’s paradox (Caulin & Maley, 2011), after epidemiologist Richard Peto of Oxford University in the UK, who noted it in the 1970s. He reasoned that larger organisms have more potentially carcinogenic cells, tend to live longer and require more ontogenic cell divisions. Therefore, statistically, cancer incidence should scale with body size (Nagi et al., 2007).

It is thought that larger animals use protective mechanisms that many smaller animals do not. For example, blue whales have 1000 times more cells than us, if they would contract cancer at rates 1,000 times higher than humans, they would die before they were able to reproduce and the species would quickly go extinct. However, the paradox itself has been scrutinized, because there may simply be a lack of data on cancer rates in large animals (Source: Nature News, 2013). In addition, it is thought that malignant tumors are disadvantaged in larger hosts. In larger organisms, tumors may need more time to reach lethal size, so tumors have more time to evolve without becoming lethal. Hence, in large organisms, cancer may in fact be more common, but less lethal (Nagi et al., 2007).

The persistent myth that sharks don't get cancer seems to stem from clinical evidence that cartilage has antiangiogenic properties, i.e., it inhibits the development of blood vessels, which are crucial to the growth of many cancerous tumors. Since shark skeletons are made of cartilage, it was thought that they can't get cancer. Recent studies have found that while the incidence of cancer in sharks and related fishes such as rays does seem to be low, cancerous tumors, including chondromas (cancers of the cartilage), have in fact been found in sharks. The reasons for the apparently low incidence are not necessarily related to their high cartilage content, but may simply be a matter of lack of directed research on cancer in sharks and related fishes (Source: American Museum of Natural History). Indeed, tumors have been found in 23 species of sharks, measuring up to 30 cm in a Great White (Source: Scientific American, 2013).

References
- Caulin & Maley, Trends Ecol Evol (2011); 26(4): 175–82
- Martineau et al., Environ Health Perspect (2002); 110(3): 285–92
- Nagi et al., Integr Comp Biol (2007); 47(2): 317-28

P.S. All animals, including whales, age and die, otherwise the oceans would've been pretty crowded, at least before whaling started.


Can someone identify this brown spider in California Spider found on transit case from California. Approx 1 1/2 inches leg span. Is it poisionus?

It looks a lot like a Kukulcania hibernalis, or southern house spider. This one appears to be a female and if it were to bite you then it would be painful, but not dangerous. These spiders typically keep to themselves so unless you find one hanging in a really bad place it's better just to leave them alone.

For further information you can look here:

https://spiderid.com/spider/filistatidae/kukulcania/hibernalis/


Why would a python go after such large prey? I read that most Pythons would go for smaller prey, around the size of a house cat, but that larger species enjoy crocodiles, deer and even a bit of antelope for dinner. But why?

Now, I realise that evolution is ongoing, and that even in the year infinity evolution can't be expected to result in any subjective measure of "perfection". But, even so, it seems odd to me that this behaviour could have survived the eons.

Perhaps I'm misunderstanding the animal's physiology and it's more mobile in this state than I expect, but isn't this animal utterly defenceless for the next couple of weeks while it digests its tasty snack? Couldn't something else now come along, rip open the snake, steal its crocodile then leave the snake for dead, all without encountering much in the way of effective resistance?

One possible answer I thought of was that other animals may not much like the taste of half-digested crocodile. Conceivably, one could stalk the snake waiting for it to start swallowing the croc, then grab it while the food is still relatively fresh. But I doubt any animal that's not already substantially stronger than the snake would feel too comfortable stalking it in the first place. Is that enough to explain why Pythons have gotten into the habit of apparently making themselves sitting ducks for protracted periods of time rather than simply eating less more often?

It's hard to answer your question directly. But one might start by noting that pythons are hardly alone - snakes in general have evolved the ability to swallow prey that is much larger than themselves. It's probably not unusual for opportunistic carnivores to stumble across gorged snakes and make a meal out of them.

But there's a flip side: Consider an animal that has to feed daily. If it doesn't gorge itself snake-style, then it will never be in such a vulnerable state. But it still has to venture out of its shelter or hiding spot to feed EVERY DAY, putting itself at risk each time.

If a snake eats just once a week, then it can spend six entire days hiding from predators.

In summary, it would appear to be a numbers game, and the statistics obviously favor snakes, which have been around for millions of years.


Simultaneously using both hands - How does that work? Is some part in one hemisphere the decision maker and "calling the shots" - controlling the opposite side's hand "directly" and controlling its own side's hand through the corpus callosum. Or: is there some "Gestalt" of parts in both hemispheres working as one making the decision?

If the latter - it would seem counter intuitive to have a deciding part which is not "unified" in one region, having to go back and forth through the corpus callosum for deciding.

I am not sure I fully understand your question, it's a little unclear. But if I understand the question correctly it is how to we coordinate movement on both sides of the body?

Well this can occur because we have connections between both hemispheres of the brain. The major connection is called the corpus collosum, this is a white matter tract that allows signals from one side of the body to pass to the other side of the body.

In some rare cases there have been individuals who have had this connection severed, for these individuals each side of the body may perform tasks of which there other side of the body is unaware.


What is the name of this black-ochre striped snake? I've seen the following snake (?) near Calvi (on Corsica):

I guess it was about 50cm long.

What is the name of this type of snake?

Great find!  Based on the picture and location, I believe this is the Corsican grass snake (Natrix natrix corsa).  It is a pretty rare subspecies, and is listed on Annex IV of the European Union Habitat and Species Directive.  Worth mentioning that it's nonvenomous.

Photo cred to Frank Deschandol/Philippe Sabine

Unfortunately, I was not able to find too much more info on this subspecies.  I know Natrix natrix are pretty widespread throughout Eurasia, but this subspecies is much more restricted.


Is it still true that C. elegans has no known natural viruses? I read in a 2009 review that

  While mammals and C. elegans each have a single Dicer that makes both miRNAs and siRNAs, Drosophila has two Dicers: Dcr-1 makes miRNAs, whereas Dcr-2 is specialized for siRNA production. The fly RNAi pathway defends against viral infection, and Dicer specialization may reduce competition between pre-miRNAs and viral dsRNAs for Dicer. Alternatively, Dcr-2 and Ago2 specialization might reflect the evolutionary pressure on the siRNA pathway to counter rapidly evolving viral strategies to escape RNAi. In fact, dcr-2 and ago2 are among the most rapidly evolving Drosophila genes. C. elegans may achieve similar specialization with a single Dicer by using the double-stranded RNA-binding protein, RDE-4, as the gatekeeper for entry into the RNAi pathway. However, no natural virus infection has been documented in C. elegans. In contrast, mammals may not use the RNAi pathway to respond to viral infection, having evolved an elaborate, protein-based immune system.

Is it still true that no know natural virus infects C. elegans? And is this [thought to be] due to the effectiveness of its viRNA (virus-derived small interfering RNAs) immunity/defense mechanism?

It has a natural virus, an Orsay virus.
https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1000586
is the paper of the discovery. found by searching "virus infecting C elegans"


Why does photosynthesis occur even in blue light when the photocentres are activated in red light From Engelmann's experiment

  Engelmann used this device to illuminate a strand of Cladophora (not Spirogyra) with light from the visible spectrum, exposing different sections to different wavelengths (or colors of light). He added the oxygen seeking bacteria B. termo to this setup and noted where they accumulated (Note: Four years later, Hauser concluded that B. termo had been mislabeled and was not one, but three species of bacteria of the genus Proteus [2]). Their clumping allowed him to see which regions had the highest concentration of oxygen. He concluded that the most photosynthetically active regions will have the highest concentrations of bacteria. The bacteria accumulated in the regions of red and violet light, showing that these wavelengths of light generated the most photosynthetic activity.

It can be concluded that the photosynthetically active regions of light are present at the blue-violet region and the red region

What I am unable to understand is , if photosystems I and II are activated at light wavelengths of 680nm and 700nm (primarily at the red region of the spectrum) then what type of photosynthesis is happening at the blue region due to which there is oxygen evolution?

My attempt:

The antenna molecules (light harvesting complex) which absorb majorly at this wavelength are transferring energy to the photocentre due to which there is excitation of the photocentre and thus OEC gets activated.

Even if this were true, then should'nt blue light be as effective as red light in helping in generating the quantum yield?

While it is true that strongest activity of Photosystem I and II happens with 700nm and 680nm light, these are not the only wavelengths that can be used for photosynthesis.

The green color of plants comes from chlorophyll, which is the main light absorbing component in the photo systems. If chlorophyll had only a single absorption peak at 680-700nm, it would have a blue(-ish) color instead of a green one.

Looking at the absorption spectrum of chlorophyll (which wavelengths it can absorb how well), you can see that there is a a second peak around 400nm:

This both explains the results of Engelmann's experiment and the green color of chlorophyll (with both red and blue colors removed only green remains)

Picture taken from: http://hyperphysics.phy-astr.gsu.edu/hbase/Biology/ligabs.html


Mathematical representation of "gene signatures" According to Wikipedia's definition, "a gene signature is a group of genes in a cell whose combined expression pattern is uniquely characteristic of a biological phenotype or medical condition."

While the above definition is very useful to understand the concept, I am looking for a "more practical" definition or, rather, a mathematical representation (e.g., a vector) of gene signatures. Hence my question.

There are mathematical definitions of "gene signature". Please have a look at the supplemental material of Subramanian et al. PNAS 2005, one of the first papers on "gene signatures", and a method and tool which is still commonly used in basic research.

Note that Subramanian et al. have multiple definitions and that copying them here would exceed the scope of this page.


Is "Cisternal Twins" an actual classification of twin types and if so, describe it I always assumed my brother and I were identical twins. Now my mother, in her eighties, says we are cisternal twins, but I cannot find any references on the matter. Is there such a thing? If so, what traits make them so?

appended: also, we've been called mirror twins. In a study by a student, we learned that our fingerprints are nearly exact opposites.

Cisternal doesn't make sense in this context, so either your mother is using an obscure term (quite possible, these things change a lot) or just has the wrong word.

However, mirror twins are a known thing (and quite cool): http://www.twinsuk.co.uk/twinstips/4/140/twin-pregnancy--multiple-births/types-of-twins--identical-fraternal--unusual-twinning/.

She may have meant something like "chiral twins" or "cis-trans twins", which would be borrowing from a similar concept in chemistry to describe your mirror-image nature (but is, again, not a phrase I've heard in the twin literature.)


On which part of the DNA will the new DNA nucleotide connect? My question is:

  Where will the new DNA nucleotide connect on the (part of the) DNA shown on the picture? Will it connect to the phosphate group?

What does the 5' --> 3' mean?

Thank you in advance.

The numbers come from the numbering of the carbon atom of the ribose in the backbone of the DNA. The ribose is numbered as shown in the figure below:

In the nucleotides the phosphate groups are attached to the 5' carbon atom and new nucleotide will be added at the 3' carbon atom. See the image below:

First you have a OH-group at the 3' position which is then "replaced" by the new nucleotide.


In cell division, are daughter cells identical? I understand that after a cell replicates, there will be two daughter cells instead of one. But wouldn't one of them be the old cell that created the second one?

The old cell having gone through G0, interphase, and mitosis and after dividing wouldn't it be somewhat different from the new cell (the old cell's telomeres having shortened, having already undergone the cell cycle and so on)?

Actually, the answer is not obvious. @RoSiv gives the textbook case of symmetric cell division, where the two new cells can indeed be considered identical, and this is valid in many cases. But there are also cases of asymmetric cell division, where the "mother" and "daughter" cell are clearly different.

In asymmetric cell division, the parent cell is polarized already before division by gathering certain proteins at one end of the plasma membrane. Therefore, during replication one of the the two new cells obtains certain proteins while the other does not, which makes them distinct. See this article for details.

Asymmetric cell division occurs among other things during embryo development, where it is important to establish body plan asymmetry. It is also the basis for the stem cell concept: stem cells are thought to divide asymmetrically so that the "mother cell" remains a stem cell (stays immortal) while the "daughter cell" becomes mortal and differentiates.


Why is marginal reconstruction "more correct" than joint reconstruction in some cases? When reconstructing the ancestral states on a phylogenetic tree given the states at the tips, there are a number of methods for performing the reconstruction. This question is about marginal and joint maximum likelihood reconstruction.

To quote the wiki, marginal reconstrucion "is akin to a greedy algorithm that makes the locally optimal choice at each stage of the optimization problem", while joint reconstruction "find(s) the joint combination of ancestral character states throughout the tree which jointly maximizes the likelihood of the data"

Pupko et al. (2000) describe an algorithm for performing joint reconstruction.

I have a question about a paragraph in the discussion of this paper, where they discuss the differences in the results between the joint and marginal reconstructions.

  Deciding which is ‘‘ more  correct ’’ depends  on  the  question
  asked.  For instance, if one wishes to count the number of threonine-
  to-methionine replacements over the entire tree, then the joint
  reconstruction should be used to obtain this number (2,  in  our
  case,  on  the  branch  connecting  node  24  to node 3 and the branch
  connecting node 32 to node 33). However,  if  one  wishes  to
  synthesize  the  hypothetical cytochrome b sequence  of  the  ancestor
  of  Cetartiodactyla,  then  one  should  use  the  marginal
  reconstruction approach. We emphasize that both methods compute op-
  timal reconstructions by using all of the available data.
  Discrepancies originate not from misuse of information, but from the
  difference in the nature of the probabilistic questions asked

I don't understand why you would use marginal reconstruction for estimating the ancestral state at one node, or how the question you ask affects which method you should use. There is only one true ancestral state, I would think that the correct method for any question is the one that most accurately estimates the true ancestral state. Can someone shed some light on why the marginal reconstruction method is preferable in this situation?

I know this is too late, but since this is something I'm struggling with too I thought I'd post here in case others also find there way here. I don't have an answer but, here are some quotes that might help (I found them at least partially helpful).

Yang (2004): "Marginal reconstruction is more suitable when one wants the sequence at a particular node, as in the molecular restoration studies. Joint reconstruction is more suitable when one counts changes at each site."

http://aracnologia.macn.gov.ar/st/biblio/Yang%202006%20Computational%20Molecular%20Evolution.pdf

Revell (2014):

"Joint reconstruction is finding the set of character states at all
nodes that (jointly) maximizes the likelihood."

"Marginal reconstruction is finding the state at the current
node that maximizes the likelihood integrating over all other
states at all nodes, in proportion to their probability"

http://www.phytools.org/eqg/Lecture_5.1/Revell.ancestral-state-reconstruction.pdf

Joint reconstruction is "not (necessarily) equivalent to picking the state at each node with the highest probability" (Revell 2014), but is the method of picking the tree with the overall highest MLE.


Is this 12+ foot plant a sunflower or hogweed? I'm trying to determine what this is. The plant is well over 12-feet tall, had huge leaves, and a very thick stalk. People near me say it's a giant sunflower plant, but it hasn't bloomed or shown sign of flowers. My moral ag-knowledgeable friends say it's hogweed, which is very dangerous. Thoughts?

This is the plant .

Here's another picture .

The plant in your photo is a sunflower (Helianthus annuus).  The large, heart shaped leaves and stiff, hairy stem are very characteristic of the sunflower as seen in your plant. These form a single flower head on top when mature - about 90 days after planting.  They typically grow to 10 feet in height, so 12 feet would not be unusual.  The tallest recorded specimen was apparently 30 feet in height. Please see links below for more information.

https://en.wikipedia.org/wiki/Helianthus_annuus#Cultivation_and_uses

https://homeguides.sfgate.com/time-year-sunflowers-bloom-67915.html

http://www.illinoiswildflowers.info/prairie/plantx/an_sunflowerx.htm


Is chocolate poisonous? I have heard that chilli peppers and coffee evolved to contain toxic chemicals which help to protect them from predators.  And recently I learned that star anise, liquorice and aniseed are not actually related plants, but each independently developed the ability to produce anethole, which can also deter predators.

However humans have evolved resistance so they can ingest all these substances, and tend to enjoy their extreme flavours.  Some more examples are onions, garlic, peppercorns and tea (for its stimulative effect rather than for its flavour).

It made me wonder:

Did the active ingredient in chocolate also evolve to deter predators?

And I am also curious, are there any other foods which I haven't mentioned that humans also enjoy due to their toxic or deterrent components?  (I'm thinking more about flavour than psychoactive effects here, as I know there are many examples of the latter.)

Alkaloid synthesis is energy consuming for plants and have complex metabolic pathway.

If their evolutionary history is not known with certainty, they have numerous uses and are often toxic to potential plant or animal aggressor.

Chocolate contain many alkaloids including caffeine and theobromine. But apparently do it with a different pathway and is the result of convergent evolution.

It is safe to assume these alkaloid protects cocoa plant in the same manner it protects coffee and that the benefits of such poisons allowed poisonous cocoa plant to become predominant.

However, alkaloids of chocolate are solely responsible for its bitter taste. (Cf. Wikipedia page "Alkaloids" for more info).
If bitterness is part of its flavour, we prefer its fats the numerous volatile compound gained during fermentations of the beans. According to this article published on academy.org :

  The distinctive chocolate flavor evolves throughout its production. Odorless, tasteless “precursors” form during fermentation, and these precursors react during roasting to form taste and aroma compounds.

Also many essential oils are poisonous to insects, fungi or bacteria. These properties are sometimes used by humans : for instance cinnamon oil is toxic to mosquito larvae


Why do sloths come down from the trees to defecate? I'm under the impression that most sloths exhibit this behavior, but why? They are slow moving and so have no way of escaping from predators when on the ground. Not to mention the energy they expire to break from their normally sedentary lifestyle.

They may only have to defecate and urinate once a week, but it strikes me as an unnecessary risk.  Why not let gravity do all the hard work?

From Wikipedia:

  Sloths go to the ground to urinate and defecate about once a week, digging a hole and covering it afterwards. They go to the same spot each time and are vulnerable to predation while doing so. The reason for this risky behaviour is unknown, although some believe that it is to avoid making noise while defecating from up high that would attract predators. Consistent with this, they reportedly relieve themselves from their branches during storms in the rainy season. Another possible explanation is that the middens provide the sloths with one of their few methods of finding one another for breeding purposes, since their sense of smell is far more acute than their eyesight or hearing. It has also been pointed out that individual sloths tend to spend the bulk of their time feeding on a single "modal" tree; by burying their excreta near the trunk of that tree, they may help nourish it. [Source]


Are aquatic filter feeders effective at cleaning water to a safe level? I've been raising Daphnia magna cultures over the last few months as feedstock for freshwater aquarium fish. From my reading, Daphnia feeds on bacteria and single-celled algae, as well as other small crud suspended in the water column.

Practically, yeast or soy flour can be suspended in water and poured into a tank containing a population of Daphnia, and the critters usually clear the water in a few days. The clarity of the resulting water is quite impressive. Which leads me to...

My question: How effective are these types of organisms at removing harmful bacteria and substances from a volume of water? Lets say you only needed a few gallons of clean water each day, could you have a tap that drew from a tank containing a dense culture of Daphnia, and use that water as drinking water?

I've not found information that studies the quantities of bacteria in the water column before and after introduction of Daphnia or other filter feeders.

P.S. I thought about posting this question in the Sustainability SE but figured I'd get more accurate information here.

My answer from the top of my head is that they will not be very effective at cleaning the water. One reason is that if the substances and organisms are harmful to the filter feeder as well, they will avoid eating them or they will die from them or have their health reduced. In either case they will be filtering less.

Another reason is that if you use the tap and replenish the water with new contaminated water regularly, the filter feeders will probably not filter all water in the tank, and the outflow from the tap will still contain the contaminant. This is certainly the case if the tank is also the culture vessel for your filter feeders. In this case, the tank has come close to being a continuous culture. There are decades of science (including R* theory) which show that resource levels in such systems settle at a positive level (and you propose that the harmful micro-organisms are used as resource or at least eaten in proportion to the resource if the filter feeder cannot be selective). This positive level will then thus also be present in the effluent from the tank (your tap water).

An alternative is to grow the filter feeders in a dedicated tank, and than add them later in high concentrations to your drinking water. This would not be efficient because you need to feed your filter feeders with something.

Finally, the harmful substances may be absorbed by the filter feeders, but also be excreted, in which case the will end up in your drinking water anyway.

For getting rid of the harmful micro-organisms, it is probably more efficient to boil your water!


How can I find the most studied SNP of a gene? How can I find the most studied SNP of a gene and diseases that the most studied SNP has been related to?

I search in dbSNP database but I can't find it.

What is the process?

Can you provide the gene of interest?

You can usually search Entrez for the gene symbol in the dbSNP database, which will pull up a NCBI Entrez page for SNPs located in the gene and will also give an indication of their clinical significance (benign or otherwise).

Alternatively, if you have a specific disease in mind, you can check more specific databases for a SNP, such as COSMIC for cancer-related SNPs.

Lastly, merely Googling the gene of interest (for example, "EZH2 SNP") in Google Scholar will bring up articles that present SNPs of interest.

Some combination of those methods should yield what you want, but I might be able to provide a better answer with more info.


Machine learning for light microscopy -- problems to solve? I would like solve some biological problems that would improve the state-of-the-art of biology or bioinformatics. In particular, I want to apply machine learning on light microscopic images. The equipment and experience I have are:

Bright-field, dark-field, and phase-contrast microscopy
Modern laptop
56-core super-computer with >100 GB of memory (on request)
Intricate knowledge of machine learning algorithms and signal processing
PhD-level research skills
Programming skills that would get me to work at Google
Limited knowledge about biology, bioinformatics, and microscopy (yet)

I want to do some publishable research free from all academic hassle. I will do this solely on my own time, without hurry to publish, in an attempt to do something good for the mankind. I can throw a few hundred dollars on the project every two months (or abour 1000 USD per year).

Much of the biological research published in Science, Nature, PNAS, Cell, etc. are so specialized that I find it difficult to detect important problems I could have a good chance of solving given my skill set. Thus, I am asking your help:

What kind of software you always wanted for light microscopic research, but did not know how to build?
What are some important biological problems you would like to get solved? (For machine learning, problems with a binary decision task are particular well suited -- e.g. "does this person have malaria or not"?)
What are some recent, high quality reviews on open problems in biology?
Something else?

While my question is a bit broad, I think this goes under the "good intention" (or whatever it is called) SE policy.

I know this question is going to close. But, if you want to work something you can work on:

Cryo super-resolution fluorescence imaging

  Highlights

  CryoFM allows imaging of vitrified biological samples with fluorescence microscopy.
  There are significant challenges to achieve high-resolution cryoFM imaging.
  Fluorophore characteristics at low temperature offer additional advantages.
  Cryo super-resolution fluorescence imaging will give dramatic resolution improvement.

Source: Fluorescence cryo-microscopy: current challenges and prospects.


Identify this Harvestman I spotted this guy in Switzerland. It's clearly an Opilione (Harvestman), but I really know nearly enough about this diverse group to be able to identify the species.

Sorry, I didn't think to place any reference near it for scale. Can anyone tell me the species or at least the genus? (Bonus points if anyone can guess what it's feeding on)

It is probably Daddy Longlegs (Leiobunum vittatum)

this invert color image show the resemblance.

Source:
http://www.insectidentification.org/insect-description.asp?identification=Eastern-Harvestman

http://bugguide.net/node/view/840130

Might be eating a cockroach:

UPDATE:

OR

It might be Mitopus morio(modern harvestman)


Is it possible to prove that a hand sanitizer can kill 100% of a person's germs? We have a project for Economics, and we need to advertise something that consumers will be willing to buy. My group thought of "improved" hand sanitizer. So, instead of it killing 99.9% germs, we would make it kill 100% germs. Although, we are having a hard time trying to prove that our hand sanitizer can, but we can't change what our product is anymore, since we only have a couple more weeks until we pass the commercial.

Can anyone help us? Thank you in advance.

There's no realistic way to prove that your hand sanitizer can kill 100% of a person's germs. In fact there's probably no realistic hand sanitizer that can do that. The reason is that there are just so many germs. There are billions of germs on your hands. To compare, there were only a few hundred thousand people in Hiroshima when it was hit by the atomic bomb in 1945, and even that did not reach 100% fatality.

It's because it's hard to kill all germs that antibiotic resistance is a problem.


Pink growth (aka pink slime) in bathtub or shower I was wondering if anybody had studied or was knowledgeable about the pink growth that people often find around water fixtures in their homes, especially bath tubs and showers?

My understanding is that this pink growth is actually a bacteria and not a fungus as many assume (source1,source2). Supposedly, the bacteria, Serratia marcescens is airborne and thrives in areas of retained moisture and fatty residue.

My main questions are:

How ubiquitous is this bacteria? What is the bacteria's geographical range of occurrence?

For example, is this species more prevalent in more humid environments?

Are there other species of Serratia that can create similar pink biofilms in tubs? (Are the sources of "pink" separated by geographic location?)

Is S. marcescens even forming a biofilm in these pink stains??

What likely introduces S. marcescens into a bathroom?

I ask, because I've seen this bacteria both present or absent from similarly clean or dirty bathrooms, and thus far have not really seen any consistent patterns in the bacteria's spatial occurrence.

Any other interesting facts or sources on S. marcescens would be great!

I live in St. Louis, MO and get this in my bathtub over time, but not in my other sinks. I actually think @Christiaan is correct here, but with a few additional observations:

I don't think it's bacteria. When dry, it's not slimy, nor does it grow back quickly when wiped away. It feels much more like a mineral deposit.
It was no longer pink when using a different shampoo. Upon returning to an older brand, the color returned to pink.
It's only directly around the drain, it isn't on the walls or anywhere else.

These lead me to think it's a mix of mineral deposits from the hard water and potential reactions with certain soaps/shampoos, at least in my case. These are only based on my own observations though, there very well could be a pink bacteria/fungi that tends to inhabit damp areas.


Is there differences in components of saliva among species Are there differences in the components of saliva among species? Also, do the functions of saliva differ between species?

It could be better answered if you specified which species you were interested in. Broadly from Wikipedia, snakes have venom, some swifts have gummy saliva to help in the building of nests, spiders produce their web from salivary glands etc. This is too broad a topic. The human salivary composition is found on the Wikipedia page I have linked. Salivary compositions can change with habits which have been detailed in this article. To compare, I am also providing the link to an article on the saliva composition of an assassin bug.


How to do a nucleic acid or genome and amino acid search I have been looking to find a database where i can search for genome and amino acid search. Are there any open source databases available for the same.

In my experience the most popular sequence database is https://www.ensembl.org/ (other databases are available, eg. NCBI).  If you have a sequence of either nucleotides or amino acids that you want to find matches for then the BLAST/BLAT search is probably what you want.


Which ORF will be translated I've a question about ORF and translation into protein. Say I have an RNA transcript that contains two ORFs, one in phase 1 ; one in phase2 ; as:

ORF number 1 in reading frame 1 on the direct strand extends from base 529 to base 759.
ORF number 2 in reading frame 3 on the direct strand extends from base 849 to base 1223.

So ORF number 1 comes earlier in the transcript, but ORF number 3 is longer ..
Is it always the first ORF that is translated ?
Edit >

It's in an eukaryoytic organism and same gene (it's the same transcript)

I use ORF finder (http://www.bioinformatics.org/sms2/orf_find.html) on my transcript sequence and it gives me two potential ORFs (ORF 1 and ORF 2 within two different frames)

Thanks

If both of the ORFs that the web tool predicted start with an AUG initiation codon, then the textbook answer is that the 5' cap on eukaryotic mRNAs is the first feature that is recognized by the translational apparatus, and the ribosome scans along until it finds the first AUG (it is a simplified description). However, if there are several AUGs near each other then the one that matches the best to the Kozak PWM (position weight matrix) will be preferred. The Kozak sequence can be approximated by: CCATGG which is also recognized by the restriction enzyme NcoI. Highly expressed genes tend to match most closely to the Kozak consensus.


Is "muscular attachment" synonymous to tendon? (when talking about the insertion of glutei medius and minimus to greater trochanter of the femur) I have read the following two terms in an MRI report (both points refer to the insertion of gluteus  medius/minimus to greater trochanter of the femur):

mild degeneration of the muscular attachment of the left gluteus medius
mild tendinosis of the left gluteus minimus

Is muscular attachment (to a bone) synonymous to tendon? Or does the muscular attachment designate the muscle part that attaches to the tendon? Or something else?

The tendon and muscle attachment are not the same. In your example, both are affected, so they are described separately.

A muscle extends into a tendon and this into an enthesis - an actual attachment site where the muscle is attached to the bone (PubMed).


Why do cockroaches and flying beetles survive high levels of radiation? Apparently it's a fact that cockroaches survive nuclear radiations.

How can they survive this?

Cockroaches have slow cellular replication rates and radiation is known to be the most dangerous to replicating cells, thus making cockroaches (and several other insects) more resistant to radiation than us, but not immune.

This was the subject on a Discovery episode of MythBuster


Why is saltatory conduction in myelinated axons faster than continuous conduction in unmyelinated axons? How does spacing apart sodium and potassium channels allow the action potential to travel faster down the axon? This is the reason always cited for saltatory conduction and myelination, but my mental model of conduction tells me that the density of ion gates along the axon should not affect the speed of the AP.

To illustrate, consider a myelinated axon. A wave of Na$^+$ from action potential site 1, a node of Ranvier, rushes into and quickly diffuses down the axon. (It travels in both directions, but backwards is still in the refractory period.) It diffuses through the myelinated region, its concentration always diminishing. Before it attenuates too much, however, it happens upon node of Ranvier 2, where it triggers another action potential. A new wave of Na$^+$ rushes in and the cycle repeats. This should be plain so far.

Now imagine that there is actually a node of Ranvier halfway between node 1 and 2, called node 1.5. The wave of Na$^+$, on its way to node 2, happens to trigger an action potential at node 1.5, from which a wave of Na$^+$ pours in and either boosts the original wave or replaces it by taking its momentum. Now the reinforced wave proceeds to node 2 and triggers it just as soon as, perhaps even sooner than, if node 1.5 had not existed. Repeatedly insert nodes at higher densities until the situation is simply lack of myelination, and we conclude that unmyelinated axons can transmit an action-potential-triggering wave of Na+ as fast as or faster than a myelinated one.

In short, my point of confusion is this: I cannot see how a higher density of gated channels can possibly slow down the wavefront of Na+ that triggers action potentials. If anything, the additional influxes of Na+ should speed up the all-important wavefront, assuming that new waves really "either boost the original wave or replace it by taking its momentum", and also assuming that the wavefront of Na$^+$ is really all-important for signal transmission, and also assuming that the mere presence of (voltage?) gated ion channels in the membrane does not significantly retard the wavefront.

But the usual explanation for why saltatory conduction is faster than continuous conduction (a fact I hope is empirically and unambiguously established) relies on the putative slowing effect of ion channels on the signal fore. Please explain this effect in more detail, if it is not a misconception.

Short Answer
Myelination acts as an electrical insulator and allows saltatory propagation.

By reducing membrane capacitance and increasing membrane resistance, myelination increases the velocity of signal (i.e., Action Potential) propagation.

If you want to see a really wonderfully simplified explanation, see this Quora post by Edward Claro Mader. Four great figures that Edward created show this phenomenon simply:
Decreased Membrane Capacitance:

Increased Membrane Resistance:

 Long Answer
So you're right: myelination speeds up electrical conduction. Unmyelinated axon conduction velocities range from about 0.5 - 10 m/s, while myelinated axons can conduct at velocities up to 150 m/s -- that's 10-30x faster!!
But why? ...
 Let's Look at Action Potentials & Signal Propagation:

You can get a background of this process in numerous places (e.g., here), so I will just mention this briefly:

When the neuron is at rest, ions are distributed so that the inside of the neuron cell is more negatively charged than the outside. This creates an electrical potential, called the resting membrane potential, across the cell membrane.

Sodium and potassium channels in the cell membrane control the flow of positively charged sodium (NA$^+$) and potassium (K$^+$) ions in/out of the cell to maintain this negative charge.

During depolarization, the cell membrane essentially becomes more permeable allowing NA$^+$ to enter the cell. This causes that section of axon to have a positive charge relative to the outside.

When this positive voltage is great enough (i.e., when an action potential is created), the influx triggers the same behavior in the neighboring section of the axon. Gradually, this positive charge on the inside of the cell moves down the length of the axon to the axon terminals.

 The Main Takeaway:
In this process, action potential generation occurs repeatedly along the length of the axon.
It's important to note two things about action potential propagation:

Each action potential takes time to occur.
The charge (i.e., voltage) that is created dissipates with $ \uparrow $ distance.

 Time for some Math & Physics:
In fact, we have equations to calculate both the time a voltage change takes to occur and how current flow decreases with distance.

You can read more about the mathematics behind this and passive membrane properties in general here and here.

Importantly, these equations rely on two constants: length and time.
The time constant, $\tau$, characterizes how rapidly current flow changes the membrane potential. $\tau$ is calculated as:
$$\tau = r_mc_m$$
where r$_m$ and c$_m$ are the resistance and capacitance, respectively, of the plasma membrane.

Resistance? Capacitance? Huh?...

Resistance = the measure of the difficulty to pass an electric current through a conductor.

Capacitance = the ability of a structure to store electrical charge.

A capacitor consists of two conducting regions separated by an insulator. A capacitor works by accumulating a charge on one of the conducting surfaces, which ultimately results in an accumulation of oppositely charged ions on the other side of the surface. In a cellular sense, increased capacitance requires a greater ion concentration difference across the membrane.

The values of r$_m$ and c$_m$ depend, in part, on the size of the neuron:

Larger cells have lower resistances and larger capacitances.

Importantly, however, is that these variables also rely on membrane structure.

c$_m$ (the capacitance of the membrane) decreases as you separate the positive and negative charges. This could be the result of additional cellular structures (e.g., sheaths of fat) separating intracellular and extracellular charges.

r$_m$ (the resistance of the membrane potential) is the inverse of the permeability of the membrane.

The higher the permeability, the lower the resistance.

Lower membrane resistance means you lose ions quicker and therefore signals travel less far

But why? This is where that length constant becomes important. The length constant, $\lambda$, can be simplified to:
$$ \lambda = \sqrt {\frac {r_m}{r_e + r_i} } $$
where, again r$_m$ represents the resistance of the membrane and r$_e$ and r$_i$ are the extracellular and intracellular resistances, respectively. (Note: r$_e$ and r$_i$ are typically very small).
Basically, if the membrane resistance r$_m$ is increased (perhaps due to lower  average "leakage" of current across the membrane) $\lambda$ becomes larger (i.e., the distance ions travel before "leaking" out of the cell increases), and the distance a voltage travels gets longer.
 Why am I telling you all of this??
How are the time constant and the space constant related to propagation velocity of action potentials?
The propagation velocity is directly proportional to the space constant and inversely proportional to the time constant. In summary:

The smaller the time constant, the more rapidly a depolarization will affect the adjacent region. If a depolarization more rapidly affects an adjacent region, it will bring the adjacent region to threshold sooner.

Therefore, the smaller the time constant, the more rapid will be the propagation velocity.

If the space constant is large, a potential change at one point would spread a greater distance along the axon and bring distance regions to threshold sooner.

Therefore, the greater the space constant, the more rapidly distant regions will be brought to threshold and the more rapid will be the propagation velocity.

Sooo....

If you increase the layer of cells around the membrane, you decrease the electric field imparted by extracellular ions, which allows intracellular ions to move more freely in the axon. In other words, you decrease the capacitance.

As a result, you have more cations available to depolarize other parts of the membrane.

If you decrease the permeability of the membrane (i.e., if you prevent ion pumps from moving ions in/out of the axon), you increase the resistance of the axon membrane, which allows for the voltage created in the action potential to travel farther before dissipating.

By allowing the voltage to spread farther before necessitating the generation of another action potential, you reduce the time it takes for signal propagation.

In other words, if you "block" ion pumps and decrease the concentration of anions near the axon membrane, you increase  membrane resistance (r$_m$) and decrease membrane capacitance (c$_m$), respectively. Together, this decreases the time of electronic conductance through the axon (and thus increase conduction velocity).
 Finally, to Myelin!
Myelin greatly speeds up action potential conduction because of exactly that reason: myelin acts as an electrical insulator!

Myelin sheath reduces membrane capacitance and increases membrane resistance in the inter-node intervals, thus allowing a fast, saltatory movement of action potentials from node to node.

Essentially, myelination of axons reduces the ability for electrical current to leak out of the axon. More specifically, myelin prevents ions from entering or leaving the axon along myelinated segments. As a result, a local current can flow passively along a greater distance of axon.

So instead of having to contantly generate new action potentials along each  segment of the axon, the ionic current from an action potential at one node of Ranvier provokes another action potential at the next node. This apparent "hopping" of the action potential from node to node is known as saltatory conduction.

 So Why not Just Myelinate the Entire Axon??
The length of axons' myelinated segments is important to the success of saltatory conduction. They should be as long as possible to maximize the speed of conduction, but not so long that the arriving signal is too weak to provoke an action potential at the next node of Ranvier. The nodes also can't be too frequent because, although adding a new node to the axon would increase its ability to generate sodium current, it would also increase the capacitance and thus diminish the effectiveness of other nearby nodes.

Sources:

Purves D, Augustine GJ, Fitzpatrick D, et al., eds. (2001). Neuroscience. 2nd edition. Sinauer Associates, Sunderland, MA.

The Brain: Understanding Neurobiology

Byrne, J.H. Chapter 3: Propagation of the Action Potential. Neuroscience Online. Univ. Texas.

Understanding the Passive Properties of a Simple Neuron

Quora

Wikipedia


Effects of having too much vitamin D? I saw there was another question about vitamin D; however, I do not believe this is a repeat.
What are some of the effects/side effects of having too much vitamin D in your body?

That is a rare condition that can only occur when taking too much doses of vitamin D. It has nothing to do with sun exposure.

High levels of vitamin D stimulate hypercalcemia and all its negative consequences. It can also exacerbate liver and kidney chronic diseases.

Reference: Katherine Zeratsky, What is vitamin D toxicity, and should I worry about it since I take supplements?


Many black people I've met have bigger lips than white people, why? I noticed that many black-ish people I've met have bigger lips than the white-ish people I've met. However, not all black-ish people have big lips.

Is there any explanations in terms of natural selection, geographic localisation, common ancestors, or something else that could explain why a subset of dark skin people have bigger lips on average than pale skin people?

Edit: This question is different from the other one because the answer talks about the nose and its function (air temperature) linked to the environmental factors. I don't see how this applies to lips.

Regard this one as a comment

I prefer to cite some text form this website instead of providing the link only (as it could be removed).

  In general, this pattern can be observed across the planet with the
  size of lips and nose decreasing as we move away from the equator
  towards the poles. So what could the reason be?

  For someone living in hot climatic conditions, cooling down the body
  is critical for their survival. Our body has many cooling mechanisms
  and one of them is simply disseminating heat when it comes in contact
  with colder air (simple thermodynamics). This however requires larger
  surface area so that more heat can be disseminated.

  Given that a significant portion of breathing also happens through the
  mouth (especially when exposed to heat), lips are pretty much like the
  gateway for colder air being inhaled and exhaled. So, the larger the
  lips, the more heat that can be disseminated. Thus, people living in
  hotter climatic conditions gradually evolved to have bigger lips.

  The opposite is true for people in colder climates. They get a
  survival advantage if they are able to retain as much heat as possible
  and so they gradually evolved to have smaller lips thus limiting the
  amount of heat that can escape when cold air brushes past their lips
  while inhaling and exhaling.

Notably, there was no scientific source provided for this claim, however intuitively this could make sense.


Disadvantage of using Drosophila for breeding experiment What should be the disadvantage of using Drosophila for experiments?

a)small size of larva.
b)short life cycle.
c)mating soon after emergence of flies.
d)large number of offsprings.

Options (b) and (d) should be advantages.

I think that the answer should be (a) as small larvae would be difficult to maintain.

Given answer is(c).

Why is that?

All options given have advantages but become disadvantageous depending on experiment you are trying to do. Here question is asked for "breeding experiment". In these experiments it is very important to keep track of genetics. If females mates with males of some undesired genotype, it will ruin your experiment objective.

As option (c) is 'mating soon after emergence of flies' , females and males from same vial (which is generally maintained as single genotype) will start mating soon. Generally this time period is 4 hours. Drosophila melanogaster starts mating after 4 hours at room temperature. This is the precise reason in Drosophila, virgin collection is done within 4 hours of eclosion.

Imagine you want to set up cross between wild type and some mutant. You will grow them initially in separate vials. Now for crossing , assume you need females from wild type and males from mutant. In this step it is important that females should be virgin else it will be difficult to track your genotype later on. Now if Drosophila starts mating soon after emergence of flies, it is disadvantage for your breeding experiments.

Note: There is sperm competition but that is special case


Is it trivial to assume a version of Hamilton's rule that applies for numerous generations? Is it trivial to assume that a version of Hamilton's rule that applies to numerous generations is:

C > rB

C = lineage fitness lost by an actor,

B = lineage fitness gained from the act, and

r = relatedness between actor and those that gained lineage fitness?

Or does this rely upon a particular derivation of Hamilton's rule?  If so, does anyone know of a citation in which this derivation is made?

Thank you very much.

I am not sure what you mean by "applies to numerous generations". If the following does not help, can you please clarify what you meant?

Hamilton's rule expresses the condition for which, under a prisoner's dilemna game (see game theory), the stable equilibrium that will be reached is the one where everyone is cooperating. Hamilton's rule is, therefore, a condition to determine the directionality of a dynamic system (the system is dynamic because the state of the system varies over generations).

EDIT

  what if the values of B and C differ depending on [the generation]

In other words, you are asking

  What if the (social or not) environment is changing over time?

Well, under such circumstance, of course, the simplistic rule that consider B and C as constant won't hold.

You could not simply replace B and C by the the arithmetic mean (or by the geometric or harmonic or any other mean) as the system as two stable equilibriums and upon reaching one there would be no way to get out of it (at least as long as the game remains a prisoner's dilemna).


Which books give data on how humans grow physically from birth till death? I am searching books on how humans grow physically from the birth till death. I am not a biology student, and don't know any technical terms. I searched amazon but didn't find any such books. I need book to be precise. Even if the book is a textbook, it would be helpful.

If it is not possible to get all the data in one book, is there any other alternative reading to be made via multiple source reading.

The 'Illustrated textbook of paediatrics' by Lissauer et al. (ISBN 9780723438717) contains a section about the average growth of children from birth up until puberty. After puberty humans don't grow anymore unless there is a medical condition. However it is important to understand that growth is influenced by many factor including ethnicity, sex, socioeconomic status and health and therefore precise numbers are hard to find.

For the most accurate information you should look for scientific publications for you specific population.


Expression of an ancestral gene Why would the expression of an ancestral gene and comparing the product to a modern protein give misleading conclusions about heredity?

Update:
By ancestral gene I mean a gene which was used by an ancestor but than changed slightly through evolution, though it still serves the same purpose. And by the misleading conclusion I mean that using this similarity between the product of the ancestral gene and the modern protein as evidence that the organism is descended from the ancestor.

Your updated question is still very vague, but I'm going to assume it is basically: "Why would the ancestral version of a gene be mistaken for a more recent version than the modern gene?"

If this is incorrect, please let me know and modify your question to clarify.

The simple answer to that question is that the mutations that occurred after the Ancestral gene resulted in less apparent divergence than the LCA (last common ancestor), which would cause the Ancestral gene to seemingly have more polymorphisms - and the general assumption is that the more polymorphisms (mutations) that a gene has undergone, the more recent it is.

So let's say you have the following DNA sequences:

5' - AAAT - 3' = LCA (Template)

5' - AAAG - 3' = Sample 1 : # Differences = 1 Nucleotide

5' - AACG - 3' = Sample 2 : # Differences = 2 Nucleotides

The general assumption is that the larger the difference from the LCA, the more mutations have occurred over time. So, under the general assumption, Sample 2 is probably the most recent version of the sequence.

However, and this is what I think is the answer to your question, because mutations can occur in any order and at any place in the genome, it is entirely possible for the third (from left) Nucleotide to have followed this mutation path: A -> C -> A

That would make Sample 2 appear to be more recent than it is because it essentially mutated "back" to the LCA version of the gene, despite being a linearly older version than Sample 1. In this way, an Ancestral gene can be mistaken for a more recent evolution of a gene. This is also why genomic data is never as strong as when paired with fossil records or other corroborating data that also aligns with the genomic data's proposed timeline; though the odds of a mistake being made grow exponentially less as more of the genome is compared and analyzed.

With very recent mutations; on the scale of hundreds to thousands of years, it's sometimes necessary to analyze thousands of base pairs to calculate an adequately confident answer.


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

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

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

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

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

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

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

Part of the problem is that chromosome is a slippery word. Really it should refer to a single DNA molecule, but since chromosomes came before DNA this sometimes gets a little loose.

This explanation refers to the five Figures in your question as 1-5 from the top.

Figure 1 A pair of homologous chromosomes from a diploid cell  drawn to illustrate their relationship in terms of genes, alleles, centromeres etc. This doesn't really correspond to any biological event. Colour coding is to emphasise that they originated from different parents. I suppose this is what you see in a karyotype.

Figure  2 An homologous pair again, different colours again, but they aren't closely side by side. When each one replicates we end up with pairs of sister chromatids joined at the centromere. These are four homologous chromosomes. At mitosis each of the pairs of sister chromatids will be pulled apart with one chromosome going to each daughter cell. So the daughter cell will end up with a pair of homologous chromosomes, one maternal, one paternal.

Figure 3 is very similar to Figure 2, nothing to add really.

Figure 4 is similar to the right hand half of Figure 2 except that the chromatids are shown not joined at the centromeres. This image is being used to show that recombination can take place between chromatids. This would be during meiosis, but the pairs of sisters would actually  be joined at the centromeres

Figure 5 Up to now the images have been designed to illustrate one chromosome either individually, as an homologous pair or as a pair of sister chromatids. But of course most organisms have more than one chromosome. Leaving aside the X and Y chromosomes your cells have 22 pairs of homologous chromosomes or 44 individual chromosomes. When these replicate the cell  will have 88 chromatids, forming 44 pairs of sisters, corresponding to  22 homologous sets of four.


Is there a hypernym for enzymes that "cut" other molecules? I have searched on Google for a hypernym/umbrella term that encompasses all enzymes whose function is to cut other molecules, but I have yet to find such a term. The term I am looking for would encompass enzymes groups such as proteases, nucleases, and lipases.

Is there such a term in molecular biology?

Hydrolases can "cut" other molecules using hydrolysis (see proteases), and Lyases can catalyze "cutting" with other reactions (see aldolases). These are umbrella terms for families of enzymes classified by function.

I think this is a fair open-access review of enzyme classification.


Is every part of a virus important for replication? Is every component of a virus absolutely essential for its infection and replication in a host cell? Or can you just have parts of it to cause infection?

Unless you have a specific virus in mind, I can speak generally about viruses. It seems that the viral genome is reduced to just essential genes. Many viruses segregate their genome into periods of expression: early, mid and late. The early proteins are so-called because they encode for proteins that help their entry into cells (what is called infection). Middle and late genes tend to help the virus co-opt cellular machinery to aid in viral replication. Late genes are then useful for final stages of viral assembly and ultimtely their exit from the cell (lysis) and the newly made viral particles can go on and infect more cells. When viewed in this manner, it follows that removing even one coding region from the viral genome would inhibit the overall infection/reproduction/assembly process. In fact, if you remove the gene encoding for a viral envelope protein, purified virus added to cells in culture are able to infect cells, but not produce complete and functional viral particles. In this sense, they are infection-competent, but reproduction-incompetent.


How is CO2 related to acidity in plant cells? Why does increase in concentration of CO2 in a plant cell increase the acidity of the cell sap?

Thank you

CO2 is a Lewis Acid.  CO2 is a double carbonyl carbon which is electron deficient, and we know that Lewis Acids readily accept electrons, so when present in H20 it forms carbonic acid (H2CO3).  Christiaan posted the balanced equation of the formation of the acid.


Is this "Sympathetic fight response" axis accurate? Peripheral sensory cell > Preganglionic cell > Dorsal root ganglia cell in the ''Sympathetic chain'' > Ventral root ganglia cell in the ''sympathetic chain'' > Post-ganglionic cell that activates an organ such as the pancreas (or a muscle).

The typical axis of the fight response is depicted in Fig. 1.

Fig. 1. HPA axis. Source: Social Psychology principles

This axis is the hypthalamus-pituitary-adrenal axis, or HPA axis. It mediates not only the fight response and is typically referred to as the fight-flight-fright response. It is the central stress response system that prepares the body in a fraction of a second for survival, basically under the influence of adrenalin and cortisol produced by the adrenal glands.

The circuit you are describing, by the looks of it, is more typical for a reflex arc (Fig. 2.).

Fig. 2. Reflex arc. Source: Sweetibnotes

A typical example of a reflex arcs is the pain-withdrawal reflex. Although the sensory stimulus triggering the reflex arc may also trigger the HPA axis, the basic circuitry of a reflex arc does not include the HPA axis. The pain-withdrawal reflex, for example, is basically designed to jerk a limb away as fast as possible in the presence of acute pain as a protective mechanism.


Why Rh conflict happen but no ABO conflicts? I wonder why Rhesus conflict can happen during pregnancy and mother can make antibodies against Rh protein (I think the correct name is D protein), but it doesn't happen if mother has different ABO type than the child?

It happens, but it is very rare.

Anti-A and Anti-B antibodies are IgM type. They do no cross the placenta. Sometimes IgG can be produced and lead to the hemolytic disease of the newborn.

Anti-D antibodies are IgG type and can pass through the placenta.


Are epigenetic modifications the most stable mechanisms for cell differentiation? Wondering what the general take is on what are the molecular mechanisms that are mostly responsible for cell type differentiation stability; ie, for a cell's identity to actually become 'locked in' and progressively less susceptible to extracellular cues (for example, in heterotopic transplantation experiments such as Sue McConnell's).

I'm pretty convinced it really comes down to DNA methylation / chromatin remodelling / histone modifications in order to reach those truly stable, self-perpetuating, differentiated cell identities, but haven't been able to find a paper or review that actually discusses this. Your suggestions and opinions are welcome.

Also posted on reddit/labrats

Edit: I suppose another way to ask this is: Are Waddington's stable "attractor cell states" most likely or most easily explained by epigenetic modifications such as DNA methylation?

Epigenetic marks are reversible (you might be aware of induced pluripotent cells). Many animals can regenerate organs with high tissue complexity (such as a limb) and this involves de-differentiation in some species (Sandoval-Guzman et al., 2014). Even otherwise, cells can respond to extracellular/environmental cues to modify their epigenetic state (for e.g. EMT involved in wound healing). I would still consider epigenetic marks to be more "stable" than simple regulatory mechanisms.

Only way for a cell's identity to actually become 'locked in' is by genetic changes. The maturation of lymphocytes (especially the B-cells), would be a good example. These genetic changes happen via V(D)J recombination, class-switching recombination and somatic hypermutation.

L1 retrotransposons are also known to contribute to somatic heterogeneity in the brain neurons. However, the frequency of insertions is not very high (Evrony et al., 2012).