Does evolution select against genetic diversity? Only the best genotype in a species will win. So it sounds like evolution selects against genetic diversity.

TL;DR

In a population, directional selection reduces genetic diversity.

Simple scenario

In a population, directional selection reduces genetic variance (at the loci that are under selection and other linked loci). Selection selects for variants that are associated with the highest fitness. Hence, selection reduces the number of variants (or at least the frequency of the variants that are associated with a lower fitness).

Note that, by reducing genetic variance, selection also reduces heritability (see this post for definition) for the selected trait.

Note that, for a correct terminology, you should not say that selection "selects for" low genetic diversity. Selection "selects for" variants associated with high fitness which causes a reduction in genetic diversity. Selection indeed does not "select for" any population-wide statistic but only for specific variants in the population which affect those population-wide statistics.

Selection vs evolution

You say

  Does evolution select against genetic diversity?

Please do not confound "evolution" with "selection". There are a number of "drivers" of evolution other than selection (e.g. genetic drift, mutation, migration). Both selection and drift reduce genetic diversity, however, mutation and incoming migration will typically increase it.

Balancing selection

Note also that there are types of selection that maintain genetic variance such as negative frequency-dependent selection, or heterozygous advantage for examples. Those types of selection that maintain genetic diversity are called balancing selection.

Multiple populations

Imagine a scenario where two populations are present in two different environments. If there is directional selection going into opposite direction in each environment (aka local selection), then selection will still reduce within-population genetic diversity but will increase the among-population genetic diversity.

Definitions of genetic diversity

Genetic diversity is a concept used in population and evolutionary genetics. The term genetic diversity is typically defined as the probability of non-identity by state of two alleles. In a single population, this is identical as the definition of expected heterozygosity. Let $p$ be the allele frequency in a population, the genetic diversity $\pi$ at this locus in this population is defined as $\pi = 2p(1-p)$.

More info about these definitions and their relationship to $F_{ST}$ (a widely used statistics of population divergence) in Nei (1973) and Charlesworth (1998).

Definitions of genetic variance

Genetic variance is typically a term used in quantitative genetics. One could say that genetic variance is defined by the phenotypic consequences of genetic diversity. See this post for the definition

For simplicity, above, I used the terms genetic diversity and genetic variance correctly but without highlighting that they take different definitions.

Intro to evolutionary genetics

Your question is a very introductory question in evolutionary genetics. You might be interested in some intro books (have a look at the post Books on population or evolutionary genetics).


Why does yeast react the way it does to water combined with sugar? I almost wanted to ask this in Cooking SE, but thought it would be better fit here.

So I understand than when you mix yeast with sugar and warm water, you get CO2. When using baking powder, it's a standard redox reaction, but what is it with yeast? Is the yeast still present after whatever reaction happens there? I don't think so, because that would mean that the reaction would go on forever. But what evolutionary sense is there for yeast to evaporate into CO2 when confronted with sugar and warm water?

Yeasts are living organisms, they do not evaporate. However it is true that in most fermented food we eat, yeast are no longer there. So why is it so?

It is not the reaction with sugar and warm water that makes them disappear. Most of the time they get killed later in the food making process. For instance, if you consider yeasts in bread, like french baguette for instance, after the dough raised, it goes to the oven where yeasts cells get heat killed.

For other processes, like brewering, yeasts used to stay in the final product. But then you had to drink it before it got spoiled by yeasts that were consuming all the sugar. So nowadays, industrially produced beers are filtered or pasteurized, or both, in order to get rid of the yeasts. Only artisanal beers are still "alive", with living yeasts in it.

EDIT:
As for the question "why/how do yeasts react with sugar?", sugar is actually fuel for yeasts. Yeasts oxidize sugar into CO2 in order to gain energy for their metabolism.


How fast is water transported from roots to leaves? I understand basically how water transport from roots to leaves through the xylem works, but I have no idea of the timescales involved.

How long does it take for water to get from root tips to leaves? How does this speed change in different parts of the plant? How does it differ between different plant types? How is it affected by plant size?

Also, I guess it changes from relatively fast in the middle of the day to almost zero at night, but how does it change during a normal sunny day (e.g. sinusoidal? More like a square wave?)

You can find some answers for your questions in this paper (it is only for Ricinus communis, but you may follow the cited by from google and find for other plants):

http://onlinelibrary.wiley.com/doi/10.1046/j.1365-3040.2001.00704.x/full

velocity in the phloem (0·250 ± 0·004 mm s−1)
xylem in the light (0·401 ± 0·004 mm s−1), in the dark (0·255 ± 0·003 mm s−1)

Graphs on daily change are on the paper.


Results of a complete DNA sequencing - are they 100% reusable? Is that correct that a complete DNA sequencing (the whole genome) need only to be done once (per person)?

After that is done, it the complete genome can be stored and once the new genes (and their purposes are confirmed) are discovered, the scientist can simply go back to a previously sequenced data and to find it this particular person has this new gene or not.

A single run of sequencing won't cover the entire genome, in most cases. That's why they do multiple rounds in order to increase horizontal (covering more regions of genome) and vertical (a.k.a depth; more reads per locus so that you can be more confident) coverage.

Edit by dd3:
In the cases where "a new gene is discovered", i.e. genome reannotation, it is possible to go back and look at previously stored sequence data to find out what alleles a person has (everyone has every gene, unless they have a deletion that spans the full length of the gene). This is a bioinformatics project, and if you are interested in learning more, I would recommend searching for recent publications on genome reannotation and remapping of sequence reads.

Whole genome sequencing is generally not recommended for prognosis of a specific disease like breast cancer. The common approach is to do a PCR of the biomarker loci and if necessary do a Sanger sequencing. However, if you have the money you can get your whole genome sequencing done :P

The number of runs required to increase the depth varies for different genomic regions. This article says that CpG islands require more runs. According to this article, the depth should be >3 per genotype marker.


How is the antigen against which autoantibodies are formed, identified? Say we suspect some new autoimmune disorder in a patient, and we collect blood for serology.

How are self antibodies differentiated from normal ones in the collected sample?
Once they are identified, how is the antigen towards which it is directed known?

Are there assays for this? Or is it identified by the structure of the variable region? Can a simple IHC be done on all body tissues using the purified isolated antibody to localise the protein?

I mean, what is the root for suspicion of an antigen? Like, what caused ANCAs (anti-neutrophil cytoplasmic antibodies) to be suspected in systemic lupus erythematosis (SLE)?

All of the above, basically. If it's a protein antigen, you can perform an immunoprecipitation with the auto-antibody and use any one (or more) of several methods (Western blot, various methods of sequencing, etc.) to identify the binding partner(s). DNA and RNA can be identified easily by biochemical means. You can also use ELISAs or similar methods like electrochemiluminescence which allow a greater degree of multiplexing.

Sequencing the autoantibodies' variable regions may give some information about the structure of the antigen, but not enough to actually identify the binding partner. Also, one key fact to keep in mind is that the antibody response in many autoimmune diseases is polyclonal (just as the T cell response often is), meaning there could be dozens to hundreds of different complementarity-determining regions (CDRs) to sequence, a very laborious process that may not yield much information.

Immunohistochemistry (IHC) can be useful for seeing which cell types the antibodies bind to, but it doesn't give great resolution on the subcellular level, and doesn't tell you anything about what the actual target is. Additionally, due to the amount of chemical processing a formalin-fixed paraffin-embedded (FFPE) tissue goes through, the antibody's antigen may not be exposed properly for the antibody to bind.

From what I can find, people suspected an association between ANCA and lupus due to the similarities in both diseases' clinical presentation. Here is a paper from 1996 talking about it, there are many others.


ECG wave names origin Why do electrocardiogram waves go  P, Q, R, S, T and not like A, B, C, D? Is there any specific reason behind this?

Interesting question! I searched briefly and came up with an answer from this short paper.

I won't repeat all the details of the paper, but to be not a completely link-only answer I will give a brief summary:

The technology used at the time was a lot different than modern ECG leads: it used a Lippman capillary electrometer that used moving mercury to detect brief current changes.

With this relatively primitive device, there were 4 apparent features in the trace, which were named A B C D (earlier, a different physiologist saw only two ventricular features that he logically named V1 and V2).

However, it was known that this primitive measurement was not showing the actual electrical signal, but rather a filtered version due to the physics of the mercury in the tube, which was subject to inertia and friction. When a physiologist used mathematics to essentially "deconvolve" the filtered signal to get the original signal back, he plotted both curves next to each other: one labeled A B C D, the other labeled P Q R S T (note that in this deconvolved version of the trace, there were 5 components rather than 4).

As for the choice of P Q R S T, the source I reference notes that these were the letters commonly used by Descartes, and since then have been commonly used to refer to series of variables when one needs to distinguish between ABCD, XYZ, etc.

Later measurements that directly displayed the 5-component PQRST wave continued to use that terminology.

Original: Einthoven W. Ueber die Form des menschlichen electrocardiogramms. Arch Gesamte Physiol.. 1895;60:101–123.
Reproduced in: Hurst, 1998

References:

Hurst, J. W. (1998). Naming of the waves in the ECG, with a brief account of their genesis. Circulation, 98(18), 1937-1942.


Why are C4 plants mainly tropical plants? Why is it that most C4 plants are tropical plants?

As far as I am aware the C4 cycle does not prevent water loss; so having it exist in tropical areas does not serve these plants any good other than preventing photo-respiration. Hence I do not understand why it is solely found in tropical plants and not plants from other areas as photo-respiration is a problem not limited to tropical areas

Reference:
http://lifeofplant.blogspot.sg/2011/10/c4-and-cam-photosynthesis.html?m=1

This is not my field, so the following is based solely on a brief reading of Internet sources.

The Wikipedia entry on C4 carbon fixation states:

  When grown in the same environment, at 30°C, C3 grasses lose approximately 833 molecules of water per CO2 molecule that is fixed, whereas C4 grasses lose only 277.

However it does not explain why this is so.

In contrast, the section in Berg et al. focuses on the energy losses caused by photorespiration and makes the following initial point:

  …the oxygenase activity of rubisco increases more rapidly with temperature than does its carboxylase activity. How then do plants, such as sugar cane, that grow in hot climates prevent very high rates of wasteful photorespiration?

The answer to this (didactic) question is the C4 pathway (as described in full in that text), but the answer to the question posted here  is that “tropical plants employ the C4 pathway because of this increased wastage of energy through photorespiration at the higher temperatures in which they live.”


How to introduce predators to a simulated ecosystem? I made an evolution simulator and observed that when a marginally competent predator appears, it quickly multiplies and hunts down all of the prey animals, which leads to their own extinction soon after. This seem unlike the real world.

About the simulator
The animals are controlled by neural networks, herbivores must consume spontaneously generated food particles to obtain energy, predators can sap energy out of a prey without killing it, but this significantly hinders the prey's well-being. Animals reproduce asexually with mutations.

There are about 50 animals when the predator appears. All herbivores tend to resemble one another.

The ideal result
This simulator was initially meant to explore the development of individual organism through evolution, but the phenomenon I observed made me aware of the importance of whole ecosystems. I want a modified simulator to produce a ecosystems with multiple niches and stable final state, in short, I want biodiversity.

Some proposed modification

Add different habitats: different habitats vary in naturally spawned food particle, and their difference can be detected by the animals
larger population
arbitrarily increase the reproductive period of predators (?)

What you're trying to do sounds really cool. I feel that you can do the following:

1) Increase reproductive period of predators

2) Increase prey to predator ratio (see Lotka-Volterra equation)

3) Make the reproductive speed/ ability of an individual to be in relation with the number of energy 'points'

What kind of set-up are you working with, a unicellular model or a larger scale?

Maybe you could start with a solely herbivorous setup, but give all individuals the ability to harm/sap a small amount of energy out of another individual.

Is there some way you could send me your project? I want to have a look at it


Is it possible for two people to repopulate earth? Today I was wondering this question whether it is possible for two people to repopulate Earth.

What if everyone else disappeared, except for two people (man & woman)? Can they repopulate? In that case, what are the odds against and in favour of that ever happening?

Well, mathematically it might be possible. But, I would rather worry about the low amount of genetic diversity that the growing population would have, which would make it extremely sensitive to external stresses.

To repopulate earth from such a small pool of genetic material, one would need an organism that is much more sturdy as compared to humans in extreme conditions, multiplies fast and is much more prone to mutations that actually convert to a phenotypic significance so as to increase the genetic diversity of the total population.


How does gene affect organs development in eukaryotic cells? I'm totally new to biology and apologies if you find this basic. The central dogma insists that genetic information flows in this direction:

  DNA -> RNA -> proteins

So far so good, it is very clear to me. The question comes here. How does this flow contributes to creating/developing organisms. I want to zoom out from molecular biology to a bigger picture of an organ.
I want somebody to tell me, how does genetic code in a zygote, results in creating organs just in secreting different proteins by different active genes?

The question is very broad and I think can only be answered in very broad terms.

Proteins have metabolic functions. They do stuff! Their actions include catalyzing metabolic reactions, transporting molecules (incl. transport through the membrane), DNA replication, response to external stimuli and many other functions. Humans synthesize almost 30,000 different proteins Muller et al. (2002). The sum of their action put into a specific environment (such as a womb for mammals) end up building up and maintaining an individual.

Let's consider for example Hox genes. From wikipedia

  Hox genes, a subset of homeotic genes, are a group of related genes that control the body plan of an embryo along the head-tail axis. After the embryonic segments have formed, the Hox proteins determine the type of appendages (e.g. legs, antennae, and wings in fruit flies) or the different types of vertebrae (in humans) that will form on a segment. Hox proteins thus confer segmental identity, but do not form the actual segments themselves.

For more information, I would recommend you to have a look at an intro course to developmental biology. You might want to learn about HOX genes


Can exercise strengthen tendons and ligaments? Is is possible to strengthen tendons using exercise to prevent injury, for example preventing shoulder dislocation?

yes..It takes approximately 10 weeks of regular resistance exercise to strengthen your tendons, and it takes longer for them to thicken. You can expect up to 20 percent increase in strength and thickness of your ligaments and tendons with regular training.


What is lack in sense of smell called? People who lack the sense of hearing, vision and speaking are called Deaf, Blind and Mute.
But what is the person called if he/she lacks the sense of smell? Is there any case like that?

This condition is called 'anosmia', see these two links: Wikipedia and from the british National Health Service. They include a definition and reasons for anosmia.


Why do tattoos persist if body cells are regularly renewed? I am not quite sure if it is true, but I read somewhere that within 7 years all the body's cells are replaced with new ones. I am not quite sure if it is cells or atoms.

If it is then why do tattoos persist for so long? If the cells which were impregnated with the dye have been replaced, then why do the tattoos still remain?

First, tattoo pigment isn't injected into cells. If you were to puncture a cell with something the size of a tattoo needle, it would die - full stop. Many cells are destroyed in the process though, mostly by tearing, which initiates the wound healing process.

So what actually happens is the particles lodge in between the cells of the dermis (the layer below the epidermis, or outer layer of skin) and new cells crowd around it as damaged cells are replaced.

Since the particles in good tattoo ink are too big to be carried off by macrophages, they just sit there. That doesn't stop them from trying, though. Macrophages take up the pigment but are unable to escape with their garbage. Fibroblasts envelope the particles, both intracellularly and within the extracellular matrix they generate. At the end of a fibroblast's life, its contents are taken up by the same process - still too big to remove.

Smaller particles will be carried off by macrophages capable of both consuming the particles and migrating into the lyphatic system, which is why some ink fades more than other kinds. Ink composed of fine particles would be expected to fade severely. New tattoos are also sharper because some of the ink that was injected is lodged in the epidermis, which is the layer that grows out and is shed over time.

In this biopsy of a tattooed mouse, you can see how the epidermis has carried some of the pigment out of the skin while much of the dermal layer's pigment has been either removed lymphatically or enveloped:

Source: Tattooing of skin results in transportation and light-induced decomposition of tattoo pigments--a first quantification in vivo using a mouse model.

Thus, over time the pigment will be moved around a bit by this cellular activity, in fact deeper into the dermal layer on the whole.

The intent of using laser light to remove tattoos is to break those particles down into smaller pieces burst any cells containing them - again initiating the wound healing process. However, unlike in previous cases, when macrophages reach the site they can now sweep the remaining particles away to the lymph nodes.

Sources

General - Tattoos and tattooing. Part II: Gross pathology, histopathology, medical complications, and applications.
Process - Cutaneous Wound Healing

Secondary sources:

Fate of tattoo pigments in skin (pdf)
How Laser Tattoo Removal Works - Smarter Every Day


Public database of animal specifications I'm a math teacher looking for data to help my students interested in biology complete a quantitatively flavored study of animals. (As a math person, I apologize if I'm not using discipline-appropriate vocabulary in my request here.)

I'd like to find a publicly available database that lists different animal species along with their average measurements of various biological variables (body mass, heart rate, body temperature, length, lung capacity, etc.). Can anyone point me to something?

I'm interested in having my students study the relationship between pairs of variables (i.e. body mass and heart rate), to model this relationship via an appropriate function, and to use their function to make predictions. To hone their models, students will need access to known data about these variables for a number of different animals. I could have them look up all of this data in separate places on the internet, but I'm hoping to find one location that has all (or most) of it.

Thanks in advance.

You might be interested in the PanTHERIA database for several thousand mammalian species.  It has up to 53 characteristics for each species (but many fields have no entry).  It is available as two plain text files, each with one line per species (plus header line) and fields separated by tabs.  The files and data descriptions are available at http://esapubs.org/archive/ecol/E090/184/


What causes humans to be physically weak compared to animals like gorillas? Animals like gorillas seem to have a physical fitness and muscle mass that don't depend as strongly on how much exercise they get, compared to humans. E.g. gorillas living in the wild sleep and rest a lot. While they do get quite a bit of exercise (a lot more than the average human), they are not going to exert themselves much more than is necessary. So, they push themselves a lot less than people who exercise very hard. Yet the average gorilla would easily outperform even a well trained human being in bodyweight exercises.

So, there seems to be something fundamentally different about maintaining physical fitness in humans compared to gorillas.

Evolutionary tools that are not needed for increased survival rate of offspring of a certain lineage deteriorate with time. The deterioration might have a form of gene expression changes or mutation accumulation. For example, gene MYH16 encodes a protein that facilitates strong jaw muscles in primates, but humans carry a mutated gene that had lost its function (Stedman et al. 2004. Nature). We cannot bite hard, but we can articulate.

With respect to muscle strength, the common ancestor of apes and humans was likely stronger than we are now. Their descendants that formed a lineage diverging towards humans increased their survival by being smarter rather than stronger than their contemporaries.


Why do haemophillic females $X^hX^h$ die before birth? I just came across a statement in my book , while reading genetics, that haemophiliac females do not survive till birth (the reason not mentioned here why) . Before posting this question here I conducted quite a bit searching on the net but couldnt find any document on this. Can anyone tell me the reason why don't haemophiliac foetus make till birth ? I mean where is the problem, when a haemophiliac male having XhY can survive why not an XhXh  female ?

Haemophiliac females are rare but they can survive just like affected males do. However, the case is slightly more complicated in women because of menstruation.

I could not find an article from any medical journal but this site seems authentic enough for a reference.


What is range of the number of individual organelles in cells What is the range of the number of individual organelles in a cell?

I am not a biologist but I understand that there's one nucleus and sometimes lots of mitochondria, so I am after the total number.

I understand that different types of cell will have a different number of Organelles in them, (e.g. there might be some very simple cells with 10 but there might be some with many more than that) but I am after the range with some examples. (I need references)

This is for a computational model.

Thanks very much

BioNumbers is a database that contains exactly this sort of stuff.

For example, I took this from this site:

Number of mitochondria per cell:

Yeast Cryptococcus neoformans cell: ~34

Human HELA cell: ~6000

Mouse L cell: ~1000


How essential is vitamin B3 to the diet? I know this might seem contradictory since by definition a vitamin is an essential part of the diet but I have read that nicotinamide, a form of vitamin B3, can be synthesised from L-tryptophan. Is it possible for a person to synthesise all their vitamin B3 requirements from one's dietary intake of L-tryptophan?

According to one study:

  It was calculated that if the excretory percentage of niacin metabolites in the urine were 60%, of the tryptophan ingested, the conversion factor would be a value of 67, meaning that is 67 mg of tryptophan is equal to 1 mg of niacin.

However, the study has a pretty low power with only 10 participants and an indirect measure of niacin.

Is it possible that a person could get all of their niacin from tryptophan? Probably - you just need to eat enough tryptophan, which is also an Essential Amino Acid. The body may preferentially keep Tryptophan (which it does not store) until Niacin runs out (which also cannot be stored).


Why do many people seem to prefer unhealthy compared to healthy foods? I don't have any concrete statistics on this but many of us seem to love the taste of food that is unhealthy for us.

Over the centuries, wouldn't it have been a non negligible advantage to those who preferred (and hence ate) healthier food?

So, why don't most of us inherently find healthier food to also be tastier?

Apologies if this is a silly question or something that is frequently asked. I know very little about biology in general.

It's a very simple answer. "Unhealthy" foods, for example potato chips, sugary drinks, and other fatty, cheesy or sugary edible items, have only been around a few hundred (at most) years. In prehistoric times (before agriculture, when the primary source of food was hunting and gathering), when food was scarce, fatty and sugary foods would be of great importance. They would supply the body with large quantities of energy (a gramme of fat gives about 9 calories, a gramme of carbs gives around 4 calories). Since we survived mostly on fruits, vegetables, meat, and whatever roots we could find, something as energy rich as, say, a serving of deep fried cheese covered bacon would have sustained us for days. So eating anything with high calorific value, like a fat rich tuber would release 'feel-good' chemicals, like dopamine and serotonin, among others, which make us feel happy (dopamine is also released in response to hugs and accomplishing goals, serotonin is released, in very large quantities, during nicotine consumption).
Our body these days just isn't used to our relatively sedentary lifestyle with  guaranteed food. Our body still hoards fat like it did during our time as hunter-gatherers, and our body still secretes dopamine everytime we dig into a sumptuous serving of cake.
A couple of good sources:
http://www.ncbi.nlm.nih.gov/pubmed/8697046

Serotonin-releasing brain neurons are unique in that the amount of neurotransmitter they release is normally controlled by food intake: Carbohydrate consumption--acting via insulin secretion and the "plasma tryptophan ratio"--increases serotonin release; protein intake lacks this effect. This ability of neurons to couple neuronal signaling properties to food consumption is a link in the feedback mechanism that normally keeps carbohydrate and protein intakes more or less constant. However, serotonin release is also involved in such functions as sleep onset, pain sensitivity, blood pressure regulation, and control of the mood. Hence many patients learn to overeat carbohydrates (particularly snack foods, like potato chips or pastries, which are rich in carbohydrates and fats) to make themselves feel better. This tendency to use certain foods as though they were drugs is a frequent cause of weight gain, and can also be seen in patients who become fat when exposed to stress, or in women with premenstrual syndrome, or in patients with "winter depression," or in people who are attempting to give up smoking. (Nicotine, like dietary carbohydrates, increases brain serotonin secretion; nicotine withdrawal has the opposite effect.)

http://www.scientificamerican.com/article/addicted-to-fat-eating/

Like many pleasurable behaviors—including sex and drug use—eating can trigger the release of dopamine, a feel-good neurotransmitter in the brain. This internal chemical reward, in turn, increases the likelihood that the associated action will eventually become habitual through positive reinforcement conditioning.

http://www.ncbi.nlm.nih.gov/pubmed/8697045

There is an intimate relationship between nutritional intake (eating) and serotonin activity. ...
Traditionally, serotonin has been linked to the macronutrient carbohydrate via the intermediary step of plasma amino acid ratios.

TL;DR:
You would have starved if you didn't eat fatty foods back before we had food so readily available, so your body automatically stocks up in case you ever run out.
Watch this video for more information:
Why our brains love junk food


Under what conditions do dendritic spines form? I'm looking for resources or any information about the formation of dendritic spines and synaptogenesis, especially in relation to how new connections are formed on a daily basis.

Does the electrotonic signalling along the axons and through the spines cause new connections to be made based on some kind of spatial condition (maybe an electrical or chemical attraction), or is there some larger heuristic here?

Dendritic spines are thought to grow and recede under LTP and LTD, respectively. See (Bosch and Hayoshi 2011) for a review.

From there, much of the synaptogenesis occurs due to surface molecules present both on the dendrite and the presynaptic axon in the growth cone.  Localization and guidance are achieved through gradients of growth factors in the developing nervous system  See (Kolodkin and Tessier-Lavigne 2011) for a review of all of these mechanics.

How this maps back onto the human CNS and thinking/learning/memorizing is still up for debate, but some of these mechanisms must have been preserved in higher species.

References:

Bosch M, Hayashi Y. (2012) Structural plasticity of dendritic spines. Curr Opin Neurobiol.,22(3):383-8. (Epub 2011 Sep 28).

Kolodkin AL, Tessier-Lavigne M. (2011). Mechanisms and molecules of neuronal wiring: a primer. Cold Spring Harb Perspect Biol., 3(6). [DOI]


Is this tall, white tree in central Australia a kind of Eucalyptus? This is near Alice Springs NT, Australia, about -24°S latitude, 550m. Area is arid but it's in a maintained park.

I don't know the exact size, but the photo is hand-held from the ground and clearly the tree is quite tall.

I only have this one photo to work with (it's not mine). I've added some cropped sections of the same original image below for easier viewing.

It reminded me of the tree I saw in the linked video below, which is likely a Eucalyptus considering the koala context.

I don't need an exact species, just confirmation of my genus hunch.

Oh! No koalas were seen in the tree eating leaves at the time, which would have made a "differential diagnosis" easer.

From Koala Bears and Eucalyptus - Periodic Table of Videos at about 02:10 (Sir Poliakoff reminds us a few times in the video (himself as well) that koalas are not "bears"!)

This is Eucalyptus apodophylla, the so called whitebark.

Further information can be found here


Applying drugs to brain via scalp (transdermal) Many medications are intended only for the brain, but are taken orally. Hence <10% finds its intended target, while the remaining >90% is at best wasted, and at worst causes unwanted side-effects.

Valproate is a classic example; it is medicated as an antiepileptic, but only a small fraction crosses the brain blood barrier to make it into the brain. Because of this, a large dose is required, and unwanted side-effects are common.

However, certain (small molecule?) drugs (e.g. Ibuprofen) can be applied transdermally.

For a drug intended for brain tissue that allows transdermal application, is there any sense in applying on the (preferably shaved) scalp?

Is this a known mechanism of administration? If so, does it have a name?

Is there any way of correctly scaling the dosage? For example, if experiment shows that 50% of substance X taken transdermally reaches the bloodstream, if it is administered to the scalp is there any way of figuring out how much ends up in the brain and how much ends up in the rest of the body?
Since this is a tricky and obscure question, may I also ask this: how to go about finding an answer to this? Where else can I ask?

The short answer is no, it will take forever for a drug to pass through skull bones.

The usual reason to apply drugs on skin is if you want them to act right there, on the skin. Acne creams fit here. You need less drugs, you get where it is needed sooner, and you have fewer off-target effects, when compared to taking them by mouth. The brain is not "right there", so this scenario does not apply.

The second reason is convenience. Some drugs cannot by taken by mouth, because they would be degraded by the stomach or guts. In most cases, the drug has to be given through painful, expensive injections. But if such a drug does pass through skin (usually when it is a fat-loving small molecule), you may get away with applying it on skin. Testosterone is one such drug. However, it usually doesn't matter whether the skin you are applying on is close of far from the target organ. The drug will be taken from the skin by blood, get to the heart through veins, and then spread to the whole body, eventually reaching the target. There is no reason to shave your head, since it will go through the same detour before reaching the desired destination.


What happens when you mix type A with type B blood (and v.v) What happens when you mix different blood types that are not compatible?

For example, if a patient has type A blood and receives type B blood, or v.v.?

The blood type of people is determined by proteins which are anchored into the surface of the red blood cells. Cells can either express the A, B, A and B or no marker, resulting in the blood groups A, B, AB and 0. People which have a certain blood type (for example A) have antibodies against the other blood type (in this case B).

This will lead to the attachment of antibodies against the subtype which you don't have (so B for people with A and vice versa) on the transfused blood cells and their lysis. Depending on the amount of blood transfused, this can also lead to a very serious immune reaction. This works like in the figure below (from here):

To avoid this reaction a sample of the blood, which is about to be transfused is mixed with blood from the patient before the transfusion takes place. This looks like this:

For more information look here:

Acute hemolytic transfusion reaction
Transfusion reaction - hemolytic
Genes and Blood Type
Adverse reactions to transfusion


How does boiling water release dyes from vegetables? Why does boiling water always seem to release and become the colors of whatever vegetables I am boiling?

For example, beet root and red cabbage both vividly color hot water.

I'd assume it's something to do with collisions with water particles breaking down cell walls and releasing anthocyanin, but how would this work on a cellular level? I.e., how does boiling water succeed in breaking through (correct assumption?) cell walls?

Why boiling water releases dyes from vegetables:

In general, one would need a solvent to extract compounds from the vegetables. Water is a solvent for the coloured pigments. In air or oil, the same pigments are less or even not at all soluble.
Hot water can damage cells. Proteins, which give structure to cells and membranes, denature at hot temperatures. Cell walls, by the way, are much more robust than membranes.
But even in cold water, some pigments can pass through membranes or membrane channels by diffusion. This will only take more time.

There are possibly other factors that are more case (vegetable) specific.


What is meant by nucleated in this context? Hi I am little confused in one of my classes; because the teacher will say that " the actin is nucleated by the ARP 2/3 complex" or "microtubles are nucleated by the centrosome". Unless I am misunderstanding, I don't take this as having anything to do with the nucleus as in the nucleus inside a cell. ( or does it). so what does this really mean than?

Thank you

Cytoskeletal nucleation refers to the de novo formation of cytoskeleton filaments. If microtubules are nucleating, that means microtubules are being polymerized from lit. "From the beginning" by α/ß-tubulin dimers. So literally, and we see in the image below, Arp2/3 complexes act as progenitor sites so to say for new actin filaments by the "nucleation" of actin:

From wikipedia for Nucleation: "Nucleation is the first step in the formation of either a new thermodynamic phase or a new structure via self-assembly or self-organisation."


Difference between Premature Atrial Contraction and Atrial Fibrillation what is the difference between Premature Atrial Contraction and Atrial Fibrillation. I know that both have irregular heart beat but have normal QRS complex. Both have abnormal or absence P waves but a normal T waves.

Can PAC be considered as an isolated event? and AFib be considered as chronic event?

Atrial Fibrillation is a dysrhythmia while PAC is an early depolarization coming from the atria. An occasional PAC can be normal for some people. In that case their heart rhythm would be a sinus arrhythmia instead of a normal sinus rhythm.

In AF, the atrias don’t contract/pump at all, but they quiver/twitch due to the many simultaneous ectopic foci that are being discharged from random cells; similar concept to Ventricular Fibrillation. Due to the atrias not fully depolarizing, you won’t see any P waves on the EKG. If/when an electrical discharge reaches the AV node, it goes through the normal electrical condition system from there, forming a narrow QRS complex. AF is the only irregularly irregular rhythm, meaning that the QRS complexes have no regularity at all, and have no pattern to their irregularity.

Video example of AF.

Rhythm Strip

As for PACs, the atrias depolarize earlier than expected creating what looks like an early beat. The next beat though will be later than expected. The pacemaker cells “reset”, returning to their pattern after this early beat.

Both AF and PACs can be acute or chronic depending on the person.


Can a zombie apocalypse really occur? Now, before you flag this question as blatantly off-topic, I claim to have a scientific basis for this(!): not some drug or remote control, but parasitic infection.
While reading about behavior altering parasites and parasitoids, I found this:

Parasites that induce behavioral changes in their hosts often exploit the regulation of social behavior in the brain...For example, Toxoplasma gondii attaches to the hypothalamus rather than target a specific cellular pathway; this broad targeting leads to a widespread increase in host dopamine levels, which may in turn account for the loss of aversion to cat odor...This rise in dopamine levels induces a loss of aversion to cat odor in the rats, increasing the risk of predation by cats, T. gondii’s definitive host.

Now, if a parasite can prevent mice from being afraid of cats, how hard would it be for another parasite to prevent humans from caring about each other's life(!)? Can a parasite develop some method by which it can alter behavior of humans in such a way that they just start killing each other for no reason? How easy/hard would it be for a parasite to do so?
Note: although it is just a curiosity question about whether it is possible or not, giving some description of neural pathways which stimulate social behavior in humans and how they are regulated would be much more appreciated.

There are many examples of parasite manipulation in nature, if you want more examples you can look up the paper of Lefevre and Thomas (2008). I think the key is, in order for a parasite to develop such behaviour, that it should be giving them a fitness advantage. So I don't think it would ever happen for no reason. The paper discusses a few examples where the manipulation results in a higher transmission rate by the parasite.

I guess that because parasite manipulation is happening in many other organisms, it's probable that it happens to some extent in humans too. There are for example indications that when we are infected with  malaria, the malaria parasites can change our odour profile to make us more attractive to mosquitoes, thus increasing it's transmission (Batista et al. 2014, De Moraes et al. 2014). There are also indications that our gut microbiota have an influence on our brain and behaviour, regulating anxiety, mood, cognition and pain, by communicating with our CNS (Cryan and Dinan 2012).


Does suffocation pain involve nociceptors? I never suffocated myself so not entirely sure, but when you suffocate, it's painful, right? But of course different kind of pain than being injured or sick. What I'm wondering is, if the "painful" (or suffering) experience of suffocation involves the standard pain pathway mediated by nociceptors? Or is it some other kind of pain pathway due to a lack of oxygen? I don't mean psychological pain.

This is more of a hypothesis

I am not sure if suffocation per se would cause pain. Asphyxia, as RoryM indicated in their comments, can lead to anxiety and panic but not really pain. However, forceful breathing may lead to muscular fatigue which may result in pain. Pain induced by muscle fatigue is called myalgia. Myalgia is possibly triggered by low pH generated by lactic acid, via ASIC3 (Acid Sensing Ion Channel) receptor. Carbon dioxide has no role in this process either directly or as a synergist.

Reference:

Alan R. Light, Charles J. Vierck, and Kathleen C. Light. (2010) Translation from Mouse Sensory Neurons to Fibromyalgia and Chronic Fatigue Syndromes. Boca Raton, FL: CRC Press; Chapter 11 (Myalgia and Fatigue)


Does cocaine bind competitively or non competitively to DAT? I was just wondering whether cocaine, once reaching a synapse, binds to a DAT (Dopamine transporter) competitively or non competitively, or neither of them?

Cocaine binds competitively to DAT, though not in precisely the same binding site, rather there is overlap, and many of the same amino acids are involved in binding of each.

Amphetamine and benztropines also bind in the same region.

Beuming, T., Kniazeff, J., Bergmann, M. L., Shi, L., Gracia, L., Raniszewska, K., ... & Loland, C. J. (2008). The binding sites for cocaine and dopamine in the dopamine transporter overlap. Nature neuroscience, 11(7), 780-789.


Simple interpretation of effective population size? I'm looking for alternate ways to explain effective populations size, in more conceptual terms. These need not be perfectly accurate "definitions" but should at least be generally accurate in non-edge cases.

For example, if I have a population with a supposed effective population size of 1000, what (if anything) can I conclude about the amount of genetic diversity present within a single individual sampled at random from the real (census) population?

Like, would it be overly simplistic to say that the sampled individual could be expected to contain ~1/1000 of the population's standing variation? Or to say that a given (observed) nucleotide state has a 0.001 probability of being   fixed?

Again, I'm looking for anything that is not the standard way to explaining Ne
to somehow get a student's head partly into the game without being wholly misleading. Thank you

Like, would it be overly simplistic to say that the sampled individual could be expected to contain ~1/1000 of the population's standing variation?

It is a little unclear what you mean by "variation" here. If you mean "genetic diversity" aka "expected heterozygosity", then it would not just be simplistic, it would be wrong to say that!

  Or to say that a given (observed) nucleotide state has a 0.001 probability of being fixed?

Ah that one is pretty good. If the effective population size $N_e = 1000$, then the probability of fixation a a new neutral mutation is $1/2N_e$ (assuming diploidy). The probability you indicate would be correct in a haploid population if you are talking about a new neutral mutation.

Another simple statistic you might want to consider is that, in absence of mutations, the genetic diversity would decrease by a factor $\frac{2N_e - 1}{2N_e}$ at every generation (assuming diploidy again).

You can derive a whole bunch of statistics of interests. For example, the expected genetic diversity in the total population at a locus at which the mutation rate is $\mu$ is $\frac{4N_e\mu + 1 }{4N_e\mu}$. You can derive many other statistics you might be interested in such as the expected number of segregating sites in a sample of size $k$ or the expected coalescent times for examples.

For more information just have a look at an intro course to population genetics. You'll find book recommendation in this post.


Is this an ectopic beat? First of all, I am unclear as to whether the answer to this question is a matter of fact or of opinion.
Nevertheless, I hope to find the answer.

In the image below, is the green beat considered ectopic?

For reference: a normal P QRS from an EKG

from https://www.healio.com/cardiology/learn-the-heart/ecg-review/ecg-interpretation-tutorial/qrs-complex

The question and the different looking beat: one cannot say it is ectopic because the strip represents some sort of atrial arrhythmia.  Atrial fibrillation is the most common of these.  The beats are not regularly spaced and there is no sign of a P wave (the one produced by the atrium).

From link

  Atrial Fibrillation occurs when multiple electrical impulses occur
  within within the atria. This chaotic electrical activity results in a
  chaotic wave form between the QRS complexes. P waves are absent. They
  are replaced by lower case "f" waves. No P waves means there is no PR
  interval measurement. This rapid electrical activity overwhelms the AV
  node causing impulses to enter the ventricular conduction system at
  irregular points. This results in irregular R to R intervals.

"Ectopic" beat suggests there is a regular beat going on and some rogue beat elbows its way in.  In A fib they are all rogue beats - "multiple electrical impulses".  The one you see is not in structure different from the rest - there is a T for every QRS and so they are all coming from the atrium.  It is just that with that beat the S wave is deeper.  Maybe because it is so close to the T?   I bet if you ran that strip a while you would see others comparably deep.

I am betting this is homework.  What exactly is the question?


Why doesn’t p53 cause the repair of cellular DNA that has been altered experimentally? When scientists mutate bacteria or even embryos of lambs and other animals, why doesn't the p53 reverse whatever mutation the scientists cause? I know that the p53 stops the DNA from mutating and since the restriction enzymes essentially mutate the DNA, why doesn't the p53 stop it? Does the p53 gene have to be temporarily turned off?

I am no expert in this area, and this answer is only based on a reading of the Wikipedia article on p53, which you should perhaps have read carefully. I welcome edits or correction by persons more knowledgeable than me on this topic.

First, although the Wikipedia article neglects to mention it, you can forget about bacteria as the protein is only found in eukaryotes.

Second, one needs to consider what exactly p53 does in relation to protection of DNA from mutation, how it is activated to do this, and hence whether this would occur in the circumstances of the introduction of mutated DNA into a eukaryotic genome.

From the article it appears that “It (p53) can activate DNA repair proteins when DNA has sustained damage”, and that “p53 becomes activated in response to… stressors, including… DNA damage (induced by either UV, IR, or chemical agents such as hydrogen peroxide)…”

The manipulation of animal DNA will be performed outside of the target organism, and the modified DNA re-introduced into the genome by one of several mechanisms that are unlikely to evoke the stress signals that are evoked by agents that damage DNA ‘naturally’. Hence there is no reason to expect the activation and action of p53 in response to this type of experiment.


Does anyone know what are these birds? Never saw them before, they appeared suddenly , the day my father died.
Place is Serbia in Europe.
Does anyone know what are these birds?

Looks like European Starlings (Sturnus vulgaris).  They are often seen in large numbers and are native to most of Europe, including Serbia.  They were introduced to North America (Central Park, New York City) as a project to introduce species of birds from works of Shakespeare and are now widespread.

Source: https://www.allaboutbirds.org/guide/European_Starling/id


do tumour cells begin with abnormal characteristics? At what point in the cell cycle do cells start to become tumorous? Do they have abnormal characteristics to begin with; if so what are they?

Cancer cells don't start to become cancerous at a specific stage of the cell cycle; you will find that while uncontrolled proliferation is a hallmark of cancer, different cancers acquire alterations in different phases of the cell cycle. BRCA-deficient cancers for example have a compromised G2-M checkpoint [1], while Rb deficient cancers have a compromised G1-S [2] checkpoint in the cell cycle.

The cell cycle is simply a property of proliferating cells and the same broad phases of the cell cycle are universal to both normal and malignant cells.

As for when abnormally growing cells actually become a cancer - this has nothing to do with phases of the cell cycle, and everything to do with the ability to break through the basement membrane of the original site (indicating the potential to be invasive/spread), because the ability to invade is a hallmark of cancer [3]

References

[1] http://cancerres.aacrjournals.org/content/67/13/6286

[2]  https://www.ncbi.nlm.nih.gov/pubmed/16936740

[3]  https://www.ncbi.nlm.nih.gov/pubmed/21376230


What's the difference between morphospace expansion and packing? I'm reading an article that talks about morphospace and niche expansion or packing.

  Differences in slope above and below zero indicate dominance of
  morphospace expansion versus morphospace packing, respectively.

What do the terms mean? What's the difference?

The way I understand it is that morphospace expansion is the change in morphology from the perspective of a population, but morphospace packing is, from the perspective of the ecosystem, the process where organisms are occupying the ecosystem space entirely so that no niche are available anymore. Is that correct?

The "packing" seems to refer to the density of the different "regions" of morphospace. Or said differently, you could "pack" different morphotypes in an environment. Is this a probable explanation?

I haven't found an answer looking at the history and definitions of niche.

You're almost there--both terms concern the relationship between increases in species richness and morphological diversification. They're two opposing patterns:

Morphospace expansion indicates that a lineage is occupying new areas of morphospace with increasing species richness. (The slope is more or less relating density of morphospace occupation to speciation rate--so > 0 means new species tend to go farther away in morphospace.)

Morphospace packing indicates that a lineage is not expanding its morphospace with increasing species richness, so the existing region of morphospace that it occupies is getting more densely filled, instead of expanding.

The relationship between functional/ecological diversity and morphological diversity isn't always clear cut, though, so you have to be careful when relating the two. If you're going to use these concepts, especially if you're going to use morphological diversity as a proxy for functional diversity, it's best to state that assumption outright.

This paper includes a nice discussion of the two concepts (and is cited by the one you list): http://rspb.royalsocietypublishing.org/content/283/1822/20152013


Calcium ions and bacterial transformation What is the mechanism by which calcium ions and heat treatment allow the bacterial membrane to become permeable, allowing the uptake of plasmids?

DNA has an overall negative charge. The phosphate heads of the lipid molecules that make up the cell membrane, along with the LPS molecules on the outer membrane, are also negatively charged. This means the plasmid is normally repelled by the cell membrane.
What Ca2+ ions do is shield the negative charges on each side, making the overall situation electrostatically neutral.
This site has a nice animatic for this process: http://www.dnai.org/b/index.html


Making sense of enzyme Km comparisons I have encountered comparisons of the Michaelis-Menten constant ($K_m$) a few times. Generally speaking if the $K_m$ of an enzyme is higher, then its affinity to its substrate is lower. How does this make sense?

Maybe the maximum velocity ($V_{\mathrm{max}}$) of higher $K_m$ enzymes is higher? Then of course, $K_m$ can have a higher value. Because $K_m$ is the substrate concentration at half of the $V_{\mathrm{max}}$. But I think we cannot determine affinity with $K_m$.

Since the Michaelis-Menton constant Km is the concentration of substrate at 0.5Vmax, it is an inverse measure of its substrate affinity, because a lower Km indicates that less substrate is needed to reach a certain reaction speed. Hence, a low Km means a high substrate affinity.

Your statement

  "Maybe the maximum velocity (Vmax) of higher-Km enzymes is higher? Then of course Km can have a higher value."

is incorrect. Km characterizes how steep reaction speed increases with substrate availability; it does not determine maximum speed.

Lastly, to address your title question, comparing affinities can make a lot of sense. For example, consider the case where enzymes catalyzing similar reactions in different species of organisms are compared. Very low Km means optimal use of small substrate levels, while a high Vmax shows optimized reaction speeds. This in turn may tell you something about optimal habitats and evolutionary pressure.


Is there any source for raw data of SNP genotype frequency? On sites like SNPedia, some pages contain the frequency of the SNP in question in different populations, based on published research. I'm trying to write a script that takes 23andme data and compares it with SNP frequency to find rare SNPs that the user possesses. I'm thinking that the only way to do this might be to scrape it from a SNP database. Is there anywhere you know of that makes this information available in a more accessible format, ideally preformatted for parsing?

You might be able to get some raw data on SNP frequency by batch querying the dbSNP database.  I have not used it myself, though.


How is antibody production stopped? Once clonal selection is done, B cells would start dividing and producing antibodies. So, after an antigen is eliminated, what stops the division of B cells and antibody production?

Upon activation plasma B cells upregulate death receptors as part of being activated. Presence of the antigen overcomes the death signal, thus the cell survives. When antigen is lost, the death signals overcome the survival signals as there is no antigen, so the B cell dies via apoptosis.

Memory B cells don't do this. They survive and continue to produce antibodies for years, although this slowly wanes. Antibodies have to be produced as antibody mediated immune mechanisms are extremely important for memory and the reason why a subsequent infection is cleared so rapidly. Furthermore for the example of HPV, antibodies induced by the vaccine prevent the virus even infecting cells (so called neutralising antibodies).


.Net DNA/Codon Parser Does anyone know of an .NET (C#,VB.NET, maybe F#) DNA parser?  If not I will probably make one, it doesn't seem like it would be hard.  My general idea was to generate something that would report the codon biases and go back and adjust the bias for engineering.

I realize the later part is a bit specific, but if anyone knew about an open .NET program that annualized/parsed the codon bias, I'd be interested.

Thanks.

I don't know much (read: anything) about the .NET framework but a little search turned up Microsoft's .NET Bio:

  .NET Bio (formerly Microsoft Biology Foundation [MBF]) is a language-neutral bioinformatics toolkit built as an extension to the Microsoft .NET Framework—initially aimed at the area of Genomics research. Currently, it implements a range of parsers for common bioinformatics file formats; a range of algorithms for manipulating DNA, RNA, and protein sequences; and a set of connectors to biological web services such as NCBI BLAST.

Free (as in beer) and open source!  And from this it looks pretty cool.


What is the name of the bond between phosphate and the sugar in a nucleotide? I am slightly confused about what the name of the bond is between the phosphate and sugar within a nucleotide. All my research comes up with is a phosphodiester bond being the backbone of DNA. But within a single nucleotide, would we perhaps call it a phosphoester bond (all of my searches of phosphoester bond correct it to phosphodiester, so I don't think the term 'phosphoester' is in use...); or maybe it would be an O-glycosidic bond as it is a sugar molecule covalently bonded to another molecule via an O atom?

Phosophoester is a valid term. There are at least a 1000 peer-reviewed articles that use this term. IUPAC Goldbook defines nucleotides as:

  Compounds formally obtained by esterification of the 3 or 5 hydroxy group of nucleosides with phosphoric acid. They are the monomers of nucleic acids and are formed from them by hydrolytic cleavage."

Phosphoester or phosphoric ester means an ester of phosphoric acid.


How much of the weight of yoghurt is due to bacteria? I recently started making all kinds of bacteria-processed foods by myself (such as yoghurt, but also Sauerteig and so on), and I found myself wondering how much of the weight of these products is actually due to the bacteria themselves in the end. But I couldn't find anything useful on the internet.

So, specifically for yoghurt, how much of its weight is due to the bacteria, i.e. dead and/or living bacterial cells, but not including the products of their metabolism outside the cells?

I would also be happy about numbers on other bacteria- or fungi-processed foods, but I wanted to keep the question simple.

Interesting question and it will only be possible to do some estimation. The problem is to know the exact bacterial composition as well as the mass of the bacteria. To start, it is necessary to know the number of bacteria in a defined amount of yoghurt. There are scientific publications on this topic, but the numbers in fresh produced yoghurt are in the area of 108 bacteria per gram yoghurt and declines over time. Based on the numbers in  reference 1 and 2 I use 2x108 bacteria per gram fresh yoghurt.

The other number we need is the mass of one bacterium. This is complicated, as bacteria are very light due to their size and cannot be easily weighted. There are some numbers available (we imply here that all bacteria weight the same, which is of course not the case), and according to them, one bacterium weighs about 1x10-12 grams.

Mutiplying both numbers gives the amount of bacteria in one gram of yoghurt, around 0.0002 gram or 0.2mg. One typical sized yoghurt of 150 gram therefore contains about 30mg of bacteria. The weight of the bacteria can thus be neglected against the total weight.

References:

Survival of Yogurt Bacteria in the Human Gut
Handbook of Food and Beverage Fermentation Technology
Mass of a Bacterium


Do ribosomes read mRNA? So I understand that tRNA bonds to a codon (with an anticodon) in the translation process. I read in my biology textbook that the ribosomes "read" the mRNA strand.

Why do the ribosomes need to read the mRNA strand? Are the ribosomes able to intepret the message and bring the correct anticodon to it? Or is the main function of the ribosomes just to join amino acids to make polypeptides? I'm just confused why the ribosomes read the mRNA strand when it seems like there is no need to.

The first two sentences of the Wikipedia Ribosome article say:

  The ribosome... serves as the site of biological protein synthesis (translation). Ribosomes link amino acids together in the order specified by messenger RNA (mRNA) molecules.

Slightly later, in the Overview section it says:

  Ribosomes can bind to a messenger RNA chain and use its sequence for determining the correct sequence of amino acids for generating a given protein. Amino acids are selected, collected, and carried to the ribosome by transfer RNA (tRNA) molecules, which enter one part of the ribosome and bind to the messenger RNA chain. It is during this binding that the correct translation of nucleic acid sequence to amino acid sequence occurs.

And it then tells us "The attached amino acids are then linked together by another part of the ribosome."

So, the function of the ribosome is to make sure each codon of the mRNA is matched up with the correct tRNA, and then to catalyze the linkage of the associated amino acid to the growing chain of the protein being built.


How to find the amino acid in the DNA protein 3' A T A G T A C C G C A T G T A C G G G C G A G A C A T T C G A G C A T T C A T 5'

This a Template DNA.

How to find the number of amino acids amino acids in the protein encoded by the above gene?

The answer is $7$.

My Try:

First I converted the above DNA to RNA and got

   5' U A U C A U G G C G U A C A U G C C C G C U C U G U A A G C U C G U A A G U A 3'

Then I found the start codon which is A U G

5' U A U C |A U G| G C G U A C A U G C C C G C U C U G U A A G C U C G U A A G U A 3'

From here I am not understanding how to proceed.

Can anyone please explain how to solve this?

Then you just have to read the codon until you reach a stop codon. There are three stop codon UAA, UGA and UAG. So, in your example..

             Start                                                   Stop
5' U A U C | A U G | G C G | U A C | A U G | C C C | G C U | C U G | U A A | G C U C G U A A G U A 3'

Your protein is therefore 7 amino acids long (incuding the starting methionine). The genetic code is

Therefore the 7 amino acids are

Met Ala Tyr Met Pro Ala Leu

In case you are confused about having an AUG codon in the middle of an open reading frame, then you should have a look at the post Effect of a doubling of the start codon in a gene.

Of course, I assumed that the region is indeed transcribed and that the first AUG is indeed the start codon and not just a methionine in the middle of an open reading frame.


What is the criterion for genetic similarity among siblings and humans in general? I just started reading Blueprint by Robert Plomin. He makes some well-known statements about genetic similarity which we all have read somewhere but I would like to know what the criteria for genetic similarity actually are:
He writes that all humans are the same for 99% of the 3 billions base pairs of our DNA. I take that to mean something like this: If our DNA had only 100 base pairs and we compare two individuals, those two individuals' DNA would differ in only one place out of the 100 base pairs.
But he also writes that siblings are (on average) 50% similar genetically. I know the rudimentary story of two chromosome pairs, one from mother, one from father, etc. My question is simply how this can be spelled out precisely. I mean, if any two humans are 99% similar in terms of their DNA, how can two siblings be only 50% similar genetically?
I have a slight suspicion: 99% similarity between the DNAs of any two human beings leaves out 30 million base pairs where they are different. Two siblings then are, in addition to the 99& similarity in base pairs, also 50% similar regarding the remaining 30 million base pairs. Thus, two siblings differ from each other in only 15 million base pairs. SO the 99% shared DNA is what makes us human, as opposed to apes, and the rest constitutes the arena in which individual differences take place?

Your slight suspicion is close to correct. There are two different ways to discuss 'proportions of shared DNA' (identity by state, versus identity by descent). If two individuals share an allele that is identical by descent, it must by identical by state, but the reverse isn't true.
The 99% figure comes from comparing all of the base pairs and follows the concept of 'identity by state', where 'state' is A, T, C, or G. If individual 1 and individual 2 both have an A at position 39, they match. Average over all positions in the genome, and there's your 99% figure.
The second part of your suspicion is not quite correct, largely because of assortative mating and drift within local populations. The 50% figure comes from classical theory of Fisher, Haldane, and so on. They were trying to solve the mathematics starting from pedigrees and Punnett squares. They didn't have access to the high-throughput DNA sequence data that is common today, but you can follow a rare allele through a pedigree if it causes some observable outcome in its carriers. As a consequence, the classical theory is defined in terms of 'rare' alleles and follows the concept of 'identity by descent', and is tightly linked to the sorts of things you can observe in a pedigree. Having examined many pedigrees, you can generalise the patterns to derive classical population genetics theory. The key thing to remember here is that this branch of theory is expressed in terms of limit formulae: 'as variant A becomes rare, statement Y becomes closer to true'. In that context, the 50% figure is approximately the probability that your full-sibling has a rare allele, given that you have it.
That 50% is a direct consequence of the mechanics of meiosis: you have two copies of each allele. One copy of each allele was inherited from your mother, and the other from your father, at random. As a result, offspring have an exact 50% chance of inheriting any rare allele carried by one of their parents, and so are exactly 50% identical by descent to each of their parents. By the same reasoning, individuals are 50% identical by descent to their full-siblings, on average. In contrast, all humans are 99% identical by state, because a large portion of the genome is shared by all humans.


Screen brightness for reading in dark room While searching online I did not find any conclusive article on whether it is good or bad for one's eyesight to read on a computer screen in a dark room. Most mention that it will cause strain that will go away after some rest (sleep).
My question is does reading in dark room has any long term effect on one's eyesight and what screen brightness setting (low of high) should one prefer if trying to read in a dark room?

Not an answer, but just a suggestion:

If you are in a position where you must read off of a computer monitor without ample ambient light, I'd suggest you try setting your monitor/reader/whatever to have a dark background and light/wight text so it doesn't feel like you're staring into the sun.


where does genetic material for antibody production come from? All antibodies are proteins and like every other protein, mRNA codes for them. So acquired immunity, is acquired, which means that information was not previously present in our DNA before exposure to the pathogens.

So my question is, does our DNA in some way get modified or something else? Where does the new genetic material come from?

Does our DNA in some way get modified or something else?

Yes. The DNA gets modified. VDJ recombination and somatic hypermutation are the mechanisms by which this happens.

You can find an entire book chapter/review on these topics. So I shall not elaborate further.


haplotype data for 1000 Genomes I need to get haplotype data for HapMap or 1000 Genomes for CEU, MKK, TSI, CHB and JPT for ± 1 Mb at LCT gene. I'm quite new in the area. Actually I don't know the meaning of "± 1 Mb". From which sites and how do I get the data? Do I need a program?

As far as I understand, LCT gene is on Chromosome 2. That's why I used following code:
wget -r --reject="index.html*" http://ftp.1000genomes.ebi.ac.uk/vol1/ftp/release/20130502/ALL.chr2.phase3_shapeit2_mvncall_integrated_v5a.20130502.genotypes.vcf.gz
Now I have a vcf file.

I also obtained a vcf file from Data Slicer ( http://grch37.ensembl.org/Homo_sapiens/Tools/DataSlicer ). I chosed populations and wrote 2:135,787,840-135,837,200 for region lookup. What does this file contain? How can I see the file content? What else do I have to do to get haplotypes? I will try to cluster and visualize haplotypes accorgind to populations. If you can guide me, I am very happy.

Thanks!

To obtain population related vcf files I created the respective (CEU, MKK, ...) samples list first using the samples file you can also download the 1000 genome ftp site.

grep CEU integrated_call_samples_v3.20130502.ALL.panel | cut -f1 > CEU.samples.list

Then I installed vcf tools (https://vcftools.github.io/index.html) and used the vcf-subset command.

I got the commands from this faq page:
http://www.internationalgenome.org/faq/how-can-i-get-allele-frequency-my-variant/

I did not compute haplotypes from the files, but I read in another post, that you can do that with PLINK. Have you checked that?


How can sequence analysis establish whether a genomic sequence is a functional gene or a pseudogene? BLASTX of a query gene shows 5 hits in my subject, how can I find out which of these are expressed and which are pseudogenes (using DNA sequence or by sequence analysis)??

There is no good single answer genes which long have been though to be pseudogenes may have function in a very narrow set of cells.

That being said, some of the best indicators are; destruction of the ORF, accumulation of C->T and G->A mutations (methylation/deamination in mammals).

Expression is probably not a good indicator, because once you start including long non-coding RNA, pseudogenes may be transcribed, but may not have a protein-encoding function (if any).

You can also measure loss of introns and a poly-A tail in the DNA sequence which is consistent with a retro-pseudogene, but that doesn't mean that the 'pseudogene' doesn't have it's own function.

Overall, evolutionary conservation is the fastest and most reliable indicator, but ultimately genetic knock-out would be required.

If you have more information about the pseudogene, there may be other useful information which could help distinguish the two.


Book on current state of knowledge on the genetics of intelligence I'm looking for a book that gives a good summation of the current state of knowledge on the genetics underlying intelligence.

I have read textbooks on human population genetics but I'm looking for something more specific.

I'd be happy for pointers to any books on neuroscience, developmental psychology, genetics that give some coverage to this topic.

I am not really looking for a popular science book.

A very recent review has been written on this. See

Plomin, von Stumm (2018): The new genetics of intelligence.

For some of the latest genome-wide association studies, see:

Hill, et al (2017): A combined analysis of genetically correlated traits identifies 187 loci and a role for neurogenesis and myelination in intelligence.

Savage, et al (2017): GWAS meta-analysis (N=279,930) identifies new genes and functional links to intelligence.

However, as Robert Plomin and Sophie von Stumm report, newer genome-wide association studies are on the way which account for a larger portion of the variance. So there is constant progress at the moment.

If you're interested in the neuroscience aspect of intelligence, I recommend Richard Haier's book The Neuroscience of Intelligence.


Does the yolk sac for Danio rerio form at the vegetal pole? Does the yolk sac in general form always at the vegetal pole?
If so, is this the case for Danio rerio (the zebrafish)?

Generally, yes, yolk is at the vegetal pole. There may be exceptions but I am not aware of them.

You can read about zebrafish (Danio rerio) embryology in great detail in this paper. Figure 3 from this paper (see image) shows the immediate post-fertilization zygote, in which the animal-vegetal axis is first set up by the migration of non-yolk to the animal pole.

UPDATE: very explicitly labeled yolk figures.


Growing crops on the Moon The short version of my question is this:

  It's some time in the future. I go into my back garden and focus my telescope on the Moon. The surface is virtually covered with giant greenhouses, growing food to support the cities that have sprung up there. The question is: what plants are they growing in those greenhouses?

Factors such as temperature, water, soil quality etc. can be controlled easily enough if you already have the ability to build sealed greenhouses in a vacuum. There are also a number of experiments on growing food in closed systems where air and water are recycled (the Biosphere 2 project being the best known). The low gravity can't be controlled, but there have been a number of experiments on plant growth in microgravity conducted on the international space station, so growing plants in Lunar gravity should be possible. There have also been some interesting results from growing plants in an Earth-based approximation to Lunar soil.

However, another important issue is the length of the Lunar day, which is 28 Earth days long, meaning that the Sun shines continuously for two Earth weeks, followed by two weeks of total darkness. I'm interested in what's known about how plants could adapt to this, but I haven't been able to find any research papers on the subject. Of course it would be possible to simulate an Earth day using artificial lighting, but the energy costs of doing this on a large scale would be rather high, so for economic reasons future Lunar farmers would likely want to keep it to a minimum.

So my first question is, has any research been done on the effect of extreme changes in day length on plant growth?

Secondly, is there any type of food plant that would be particularly likely to cope with such an environment (perhaps with some suitable genetic modifications)? For example, would normal crop plants such as cereals be able to build up enough sugar reserves in two weeks to survive the next two weeks in total darkness? If not, is there another type of plant that's more likely to be able to adapt to this? Or as an alternative strategy, is there any crop that grows fast enough that its shoots could be harvested after only two weeks of continuous sunlight? (Some individuals would have to be grown to maturity under artificial light in order to produce seeds, of course.)

Finally, I'd be grateful for pointers towards research on any other issues that I might have missed that are relevant to the problem of large-scale Lunar agriculture.

Plants are adapted to the conditions we have here on earth, therefore, for them to grow on the moon we would have to recreate the conditions found on earth (or at least find conditions that we can create and they can grow in). To do this we would need to replicate climate (temperature, air pressure, humidty etc.), provide (sun)light at the necessary intervals and intensity, provide water, air, and nutrients of the right composition, intervals and intensity. That is a simplified version...

In reality there is great variation in how plants require these things. Some cope with long dark periods better than others, some cope with drought better than others, some cope with chemical variation in the soil better than others so answering this question is hard. But generally growing plants on the moon will require the ability to recreate (to some degree depending on the sensitivity of the plant) the conditions a plant has evolved under on earth.

Thus to answer your questions:

Length of day can have strong effects on growth patterns, two weeks of darkness is likely to be a major upset for plants! Just transplanting plants of the same species from different latitudes can affect the growth patterns because of changes in length of day. Try putting some plants in darkness for two weeks and see what happens.

Plants all vary in their ability to meet the requirements of space growth. There will only be a short list of plants that could with "small" modifications to the moon's environment, the more we adapt (adding artificial light, watering, adding nutrients etc) the longer that list would become - the limitation is in our ability to adapt the moon.

See above for reasons why plants might struggle. Oh and we would need to consider the effects of reduced gravity too...

Here's a little something from nasa about how plants are used in space vehicles. And another on light and gravity.


Reason behind using DNA primer in PCR techcnique while RNA primer use in replication in vivo? I have went through Lehinger ( biochemistry book) and cooper ( cell Biology) but i didn't find my answer.
plese help me

The (very) basic answer to your question about in-vitro vs. in-vivo primer usage is:

In-vivo - Although either (DNA or RNA primers) can be used for in-vivo primer extension biochemistry, DNA primers are not available (not made) in living cells. Therefore all natural in-vivo primer chemistries utilize RNA primers.
In-vitro - DNA primers are easily synthesized, inexpensive, functional, and substantially more stable (less likely to be degraded). DNA primers are therefore primarily used for most in-vitro purposes (i.e. PCR and other in-vitro primer extension applications).

Beyond that, all other reasons (complex evolutionary reasons vs. human choices in-vitro); involving subtle differences between RNA and DNA chemistry, structure, and function, similarly can play a role. The links below may be helpful to address some of these differences.

https://en.wikibooks.org/wiki/Structural_Biochemistry/Nucleic_Acid/Difference_between_DNA_and_RNA

https://en.wikipedia.org/wiki/Primer_(molecular_biology)


Where can I find disease diagnosis datasets? For an epidemiological study, I'm looking for datasets for any kind of vector-borne disease (i.e. West Nile Virus, Malaria, etc.), or any parasites that are dependent on intermediate hosts (i.e. Schistosoma spp., which have snails as intermediate hosts).

The data should include day or week and location of each diagnosis. I have been able to find diagnosis data for individual countries for each year, but I'm looking for daily or weekly data for city-wide resolution or at least smaller regions inside countries.

Additionally, it does not matter what country/continent the data is for, as long as there are many data points (i.e. at least 10,000). For example, if there is a lot of good data for Brazil, that's fine.

Does anyone know if such information exists, and if so, where I can find it? I've been searching for it for the past month but have had little luck with finding anything useful. Any help and guidance is appreciated!

CDC Wonder, a health database of the US Center of Disease Control and Prevention (CDC), has weekly data for Nationally Notifiable Infectious Diseases and Conditions, United States: Weekly Tables from 1996 to 2020 on the state level for antrax, brucellosis, dengue fever, leptospirosis, malaria, meningococcal disease, Q fever, rabies, etc.

Weekly tables since 2014 are available on Data.CDC.gov.

Weekly tables for 1952-2017 published in the MMWR are available at CDC Stacks MMWR and weekly tables starting in 2018 are available at CDC Stacks NNDSS.

HealthData.gov has two weekly datasets for malaria by US states - here is one.

Open Government Data (OGD) Platform India has data on a district or state level, for example, for malaria.

Keywords that can help in further search:

infectious disease
week or weekly report or data
MMWR (Morbidity and Mortality Weekly Report)
surveillance

Keywords, like diagnosis or outbreak, can limit your search too much.


Can you identify this mystery bur? I found this strange bur on a stray cat in my neighborhood.  I've never seen anything like it, and Google reverse image search thinks it's an earring.  Found in in northern California, just south of Clearlake.  (38.90 N, 122.60 W)

The spike structure is almost exactly one inch long.

A friend has informed me this is from the redstem Filaree, and there are some cool time-lapse videos on Youtube of their spinning behavior when they are exposed to water, which is thought to help them burrow into the soil.  (I'm just glad it didn't get a chance to burrow into the kitty!)


Living intermediate species? Hypothetical question regarding three animals 'species' {A, B, C}.

Are there any examples in nature where {A and B} cannot regularly produce viable offspring, however {A and C} and {B and C} can regularly produce viable offspring.

I imagine that such a situation could arise if {A, B, C} have a common ancestor, but {A and B} are sufficiently different from each other, but not from C.

The hybridization situation you describe could be found in ring species, and is partially related to this concept.
For instance, the three species A, B and C could have partially overlapping distributions, such as:

In such a situation (assuming that the relative distributions have been stable over evolutionary time), A and C might be able to produce offspring, as well as B and C, while A and B might not produce viable offspring if they would meet.

Here is a picture from the wikipedia page for a similar situation, showing interbreeding between seven gull species in the genus Larus:

However, I also know that the ring species concept has been challanged, mainly by the fact that there are very few good empirical examples of ring species. See for instance the nice blog post "There are no ring species" by Jerry Coyne, which may also include a couple of examples of species groups that are relevant to your question.

Also, the hybridization patterns that you describe can be caused by other processes, for instance specific reproductive barriers between groups of species (molecular or behavioural). My answer is therefore merely mentioning one possible explanation for the hybridization patterns you ask for, but there are many other processes to consider.


What is Growing on These Tree Leaves? (Image) I found a seemingly diseased tree when I was out playing tennis yesterday... What is growing on this tree leaf? Is this a disease? If so, is it contagious? I have zero knowledge in botany, but I'm curious about what is happening to these trees. :)

This is actually not a gall as other answers have suggested.
This is likely a fungus called Cedar-apple rust (Gymnosporangium juniperi-virginianae).

The fungus only thrives in the presence of both Juniperus virginiana (Eastern red cedar) and apple (Malus spp.) trees.

The leaf in the picture belongs to some species of the apple genus and the growths are aecia of G. juniperi-virginianae. You can read about this interesting fungi through Rutger's Plant & Pest Advisory here.

You can see a picture of the fungi here, and I've included Sabrina Tirpak's (Rutgers PDL) photo of its aecia below:

http://plant-pest-advisory.rutgers.edu/3859/

Below is a visual of the telia of the rust fungus on J. virginiana:

 (Photo source: Ada Hayden Herbarium)


Does Pseudomonas aeruginosa have any common name at all? Pseudomonas aeruginosa is the fifth most written about¹ binomial name of all species. I'm having trouble coming to terms with the possibility that such a well researched and studied organism has never been given a shorter vernacular name. I can't find one listed anywhere.

Is there any short common name for it? Even a colloquial one? Maybe a pet name common to microbiologists or students in the labs of some particular region? I'm mostly interested in English but how about in other languages?

I am aware it can be abbreviated to P. aeruginosa. I don't consider that a common name. Pseudomonas by itself refers to a genus of around 191 species.

¹ "most written about" meaning mentioned in the most books or volumes of Google Books' English corpus (ngram data), according to my own research. The top five are: Homo sapiens, Escherichia coli, Staphylococcus aureus, Candida albicans, Pseudomonas aeruginosa.

I think there's a difference between a vernacular or common name ("tiger", "cat", "pigeon", "elm", "pine") and a pet name or nickname as you use it here. The former are names in human languages for a particular kind of animal or plant, while the latter are a colloquial name used by professionals to refer to a particular species, often based on its scientific name.

I can't think of many micro-organisms that have a true vernacular name -- most micro-organisms were given fancy scientific names, and those were used consistently thereafter. The only proper microscopic common name I can think of is "slipper animalcules" -- but I'd be happy to be proved wrong!

Lots of micro-organisms have pet-names -- E. coli, C. diff., "smallpox", "Ebola", "white nose", even Pelagibacter ubique -- but they're either based on the scientific name or on the disease the organisms cause. AFAIK (and based on the comments), Pseudomonas aeruginosa doesn't have one. However, of the list of species you list, only H. sapiens has a vernacular name, while the others only have nicknames based on their scientific name, so I'm not sure it's that surprising! IMO it's mostly macro-organisms that get vernacular names.


Can sugar alcohols, and glycerol in particular, cause intoxication? I'm mostly curious about glycerol, which I use as a sweetener. I've been told that it can cause intoxication, because it is an alcohol. Is this true?

If so, are there any good sugar alcohols which can be used safely without intoxication (or nasty side effects)?

Well, I was intrigued by this, and my intuitive response was that it would never be toxic at reasonable doses, but I was wrong.
A quick Google search led me to this paper:

Andresen, H. et al. (2009) Severe glycerol intoxication after Menière's disease diagnostic--case report and overview of kinetic data. Clin. Toxicol. 47: 312 - 6

Apparently in the Klockhoff test for Menière's disease the patient is given an oral glycerol dose of 1.2 - 1.5 g/kg (50% in water) then observed over a period of 4-5 h. The other details of the test don't concern us here. In this case report a patient suffering neurological symptoms was found to have previously undergone a Klockhoff test at another hospital, and it was estimated that he must have received a dose of 3.88 –3.95 g/kg.
Here are two sections from the paper's introduction (references removed).

Glycerol is well known as a nontoxic substance (LD50 > 25 g/kg in the rat). Possible side effects of the Klockhoff test include headache and nausea. During treatment of brain edema, additional adverse effects such as diarrhea and vomiting were reported, symptoms comparable to those reported for intensive osmolar diuretics. The GESTIS database ranks glycerol in general as a substance with very low toxicity. However, severe symptoms after oral ingestion of glycerol have been reported to occur. Doses exceeding 0.7 g/kg BW have been regarded as potentially toxic for adults. After doses of up to 1.4 g/kg BW, only mild symptoms such as headache, nausea, and diuresis appear. Reportedly, these symptoms are also associated with glycerol treatment of brain edema. In individual cases, an oral dose of 100 g of glycerol has been reported to cause drowsiness, cyanosis, renal pain, and bloody diarrhea.
Martindale Reference Desk reports headache, thirst, nausea, and hyperglycemia as adverse effects. Glycerol may also produce cardiac arrhythmia and hyperosmolar nonketonic coma. These effects are mainly based on its dehydrating properties. Hemolysis has been reported to exclusively occur after intravenous infusion. In fact, most of the major toxic effects of glycerol, such as hemolysis, hemoglobinuria, and renal failure, seem to strictly correlate with serum concentration of glycerol and the route of administration.

It appears then that any toxic effects of glycerol are not due to its alcohol nature per se but rather because it can become elevated in the blood leading to osmotic effects. The authors estimated that 10 h after administraion of the glycerol the concentration in the patient's serum was approximately 39 mM, compared to a physiological basal level in the range 0.05–0.3 mmol/L. The patient's serum level fell to the basal level over a period of 30 hours.
Just to put this in some perspective, in the UK the legal alcohol limit for drivers is 80 mg/100 mL which corresponds to 17.4 mmol/L.
I think that recommending sugar alcohols would fall under the heading of medical advice (not that I have any such recommendations).


What is the difference between a human being, a Homo sapiens, and a Neanderthal? I know that the Neanderthals were part of the genus Homo. How do they relate to other members of the genus, such as Homo sapiens?

Homo sapiens / Homo sapiens sapiens
Human being, in the popular culture generally refers to modern humans, called either Homo sapiens or Homo sapiens sapiens. The existence of the two names will make sense when talking about the Neanderthals. In the term Homo sapiens, Homo indicates the genus and sapiens indicates the species. In the term Homo sapiens sapiens, the second sapiens refers to the subspecies.
Homo neanderthalis / Homo sapiens neanderthalis
Neanderthals (or Neandertals) is sometimes referred to as a species in the same genus (Homo) as H. sapiens and sometimes as a subspecies of H. sapiens. When considered as a different species then, they are called Homo neanderthalensis. When Neanderthals are considered as the same species as H. sapiens but different subspecies, then they are called Homo sapiens neanderthalensis and modern humans are then called Homo sapiens sapiens.
Related Post
The post How-could-humans-have-interbred-with-neanderthals-if-were-a-different-species will probably be of interest to you.


Are agave plants perennial? If I were to harvest an agave plant for its nectar, would it kill the plant? I have watched videos of the process and it seems quite invasive.

When harvesting agave nectar, generally the whole plant is harvested at once to get to the core, where most of the sap is. There isn't exactly an easy way to continually get nectar from the agave plant since it is herbaceous, whereas something like maple trees can be tapped because the wood can support the spigot.


Perception of white in the absence of rods If the retina would not have any cones, one would be color blind. If white is the presence of all colors (in the matter of color mixture, not addition), then what would white look like without rods?

Short answer
Cones mediate the perception of white in photopic conditions. Rods mediate the perception of white in scotopic conditions. The rod system is not needed for cones to mediate white perception and vice versa.

Background
Cones code for red, green and blue. The remaining colors, as you rightfully state in the question, can be generated by mixing these three colors, as shown in Fig. 1.

Fig. 1. Color mixtures. Source: Davidson College

The millions of different color hues that we can perceive are generated by the retina and the brain by mixing colors and adding the weight that each cone class adds to the color percept (Fig. 2).

Fig. 2. Color Triangle. Source: Wikipedia

As you can see in Fig. 2, when all three basic colors are present in equal amount, perceptually a white color is perceived (the middle point of the color triangle). That is, the combination of co-activation of each cone class yields the perception of white, i.e., without the need for rod activation. Rods are not needed for color vision, including the perception of white or black. In fact, under photopic (well-lit) conditions the rods are adapted to high light levels and are less responsive; their photopigments are said to be bleached and the rods become unresponsive to light. Hence, under photopic conditions the contribution of rod-mediated vision is low (Ambler, 1974).

Rods mediate vision in low-lighting conditions (scotopic vision), as opposed to photopic vision where sufficient amount of light is present to feed the photon-hungry cones. While rod-mediated vision operates at much lower lighting conditions than cone-vision, it only mediates the perception of low-resolution gray-scale images.

References
- Ambler, Perception & Psychophysics (1974); 15(3): 586-90
- Gouras, Color Vision. In: Kolb et al. (eds). Webvision. The Organization of the Retina and Visual System. Utah (2012)


When streaking microbes on a plate to test growth after uv exposure, does how I streak make a difference? I've been working on what I think might be a special strain of E. coli, I've been streaking it on LB agar plate and exposing it to varied times of UVC via the germicidal hood.
I'm wondering if how I streak, as in too heavily, vs very lightly, or diluted culture, etc would make much effect in survival.
If I'm putting too much onto the plate, the e coli could be self-shielding, or some ecoli dying off, but the rest underneath being protected from the light.
I've done several generations of surviving colonies, I'm now comparing to wild type to see if my streaking method results in survival in both.
This test will also rule out if the lamp is failing and my surviving colonies are just the tougher ecoli compared to the growth on the control.
tldr
Should I lightly streak or dilute my culture to ensure all ecoli are being hit with the UVC?

I work with e. coli myself though I do not know if your special strain has anything drastically different than my own so I'll just give advice that I've gotten from post docs and other PhDs on how to handle cultures.

(Note: This is methodology that I can't really find a "source" for so take with a grain of salt and change for your needs)

Typically when streaking I try to ensure that I make the streaks light enough so there aren't colonies within vicinity of each other. It's hard to really give a quantitative answer on how to do this so you will have to experiment on your own so your streaks aren't laden with massive amounts of colonies next to one another. It should look like consecutive "beads" on a string. This is generally what I try to accomplish with my colonies. Keep in mind I am focused on cloning plasmids so I'm not really concerned about experimenting on the e. coli themselves, just getting individual populations that do not have mixed variations of my plasmid. This is why having colonies with good separation is important for my particular project.

As for making sure they are all being affected by the UVC, I'm not entirely sure if having them to heavily grouped together would "shield" from UV. I feel as though UV can easily penetrate through e. coli colonies but I guess its not out of the question. Best bet is to keep your colonies well spread out, enough so you can pickup a single colony with a pipette tip and nothing else. This will make any genetic experiments you may want to do a lot easier as well. Which I think would be interesting if you are interested in the mutations occurring.

Is there something about your project that requires you to streak these out on agar plates? I saw comments suggest liquid broth. Maybe that's easier to do to make sure everything is exposed and then streak them out on a plate to see growth and/or test for mutations.


DNA modifications other than 5-mC/5-hmC/5-fC/5-caC in vertebrate genomes? Other than 5-Methylcytosine and the more recently discovered 5-Hydroxymethyl, 5-formil and 5-carboxylcytosine DNA modifications found in DNA sequences, what are other DNA modifications present in vertebrate genomes? There is apparently a whole bunch of modifications that can be found in prokaryotic and eukaryotic genomes, but I would like to know which ones have been found relevant in vertebrate/mammalian genomes of the eukaryotic ones.

There can be other modifications resulting from DNA damage (oxidising agents etc). Those may include Xanthine and Hypoxanthine (caused by chemical deamination of guanine and adenine).
There are no other known modifications resulting because of a physiological process.