Variations in asexual reproduction It has always been said that sexual reproduction produces offsprings which are superior to their parents, due to the variations which they acquire causing them to survive better in their environment. That's because we can think of meiosis occurring at some level of their life cycle resulting in the variations in the final offspring.
 But what when we talk about bisexual organisms, might they be plants, animals or any other life form? Can't there be variations in their offsprings if they produce them asexually? It's like when they undergo gamete formation in different male and female structure present in that single parent, they'll surely undergo meiosis(if the parent is not haploid undoubtedly) forming the gametes which are dissimilar in their genetic makeup. When these fertilize, shouldn't they show variations?

The question is rooted in a misunderstanding of what sexual reproduction is and is not.

Any good intro book to evolution has a chapter on the diversity of reproductive systems. Consider for example Evolution: Making Sense of Life. If you speak french, the book évolution biologique has a very chapter on the diversity of reproductive systems. If you want something more complete and more advanced, you can have a look at The Evolution of Sex Determination.

  It has always been said that sexual reproduction produces offsprings which are superior to their parents, due to the variations which they acquire causing them to survive better in their environment.

Who said that? The common simplistic idea and sex increases mean fitness because it increases genetic diversity is both wrong because sex does not necessarily increase genetic diversity and wrong because increase in genetic diversity does not necessarily result in increasing mean fitness.

You can have a look at the work of Nick Barton, Sally Otto and many others on the subject. The above misconception is well explained in the introduction of this talk from S. Otto's

  [..] But what when we talk about bisexual organisms, might they be plants, animals or any other life form?

I'm not sure what you meant here. You probably did not want to use the term bisexual. Maybe you meant dioceous.

Please note that sexual reproduction does not mean dioecy. Sexual reproduction does not even mean anisogamy and doe snot necessarily involved more than one individual (see selfing).

  Can't there be variations in their offsprings if they produce them asexually?

There is a whole range of reproduction mode and saying sexually vs asexually is making gross categories that make it sometimes hard to really answer the question. It is also hard to know what you mean by "variations" here. But shortly speaking:

Asexual reproduction does not necessarily mean total absence of recombination (see for example Narra and Ochman 2006) and definitely does not mean absence of mutations (see for example Sniegowski et al. 1997).

  It's like when they undergo gamete formation in different male and female structure present in that single parent, they'll surely undergo meiosis(if the parent is not haploid undoubtedly) forming the gametes which are dissimilar in their genetic makeup. When these fertilize, shouldn't they show variations?

If there is fusion, then there is sexual reproduction, even if it is selfing and even is they don't have genders (anisogamy).


Was life less colorful before color vision evolved? According to Wikipedia, we know that color-vision photopigments appeared in the common ancestors of tetrapods and fish at least 360 MY ago.  Would life have been less colorful before the evolution of color vision?

It is likely that the world have been less colourful before colour vision evolved, though that is my opinion, I will now back it up a little.

Certainly some of the colour we see in nature serves a function outside of the use of visual stimuli. For example plants have green leaves because of the way that functions with photosynthesis - it absorbs enough energy whilst not so much that the leaves burn. For more on the green leaves in plants see this classic Biology SE question with it's very good answers. Other examples could include functions such as thermal regulation or light contrast for camouflage (if anyone has other valid examples then please comment and I'll add them in).

However, there is likely to have been an increase in the prevalence of colour in nature since the evolution of colour vision. Colour is used as a visual stimulus in numerous ways. My first example is flower colouration. Flowers use coloured petals as a stimulant to attract pollinators. Another example is the use of colour in mate attraction. Peacocks tails, the orange bills of blackbirds, and the brightly coloured cichlid fish. All of these examples take advantage of colour vision, without it they simply wouldn't be as discernible from less colourful variants and given the cost of producing them it is unlikely they would evolve as often as they do. A third example is camouflage, the most striking example I can think of is cuttlefish which match themselves very well to their background.

Although I haven't provided direct evidence that the world was less colourful I have provided a potential theory. Hopefully the examples I've presented have convinced you that my theory of the world being less colourful, even possibly only marginally less so, is not developed without thought.

I will point out it is entirely possible the world was equally or even more colourful before - no colour vision would allow colours to drift around more, selection on colour in the context of camouflage would reduce the variety of colour we see as selection would favour colours matching the surroundings (if camouflage was necessary to survival in a grass environment we would expect most things to look quite green). To this end, I don't think we can currently answer your question firmly but we can put out theories as to how it would have been.


How important is non-binding site of protein? Just a curious question:

What will happen if i remove most protein sequence that encoded for non-binding site of Restriction Enzyme to make a new enzyme, can the new restriction enzyme still work?

As it seems with about everything in protein science, the answer is it depends on the protein.  Many proteins will lose activity if they are truncated; however, I've worked with GPCR's that were truncated down to the extracellular portion only and they showed consistent kinetic results.  Antibodies have been cut into pretty tiny chunks (scFv's) to create some drugs like Pexelizumab. Some proteins can be hacked down quite a bit, some can't be at all.


Biphasic T wave caused by digitalis toxicity Digitalis is a drug that can be used during coronary insufficiency to
  increase the strength of cardiac muscle contraction. But when
  overdosages of digitalis are given, depolarization duration in one
  part of the ventricles may be increased out of proportion to that of
  other parts. As a result, nonspecific changes, such as T wave
  inversion or biphasic T waves, may occur in one or more of the
  electrocardiographic leads. A biphasic T wave caused by excessive
  administration of digitalis is shown in Figure.

Therefore, changes in the T wave during digitalis administration are often the earliest signs of digitalis toxicity.

I was reading about it in Guyton and Hall Physiology (volume 1, heart , chapter 12) and there was nothing about this that answers my questions.

And my questions are:

Why is T wave more affected by digitalis toxicity?
Why does it cause Biphasic T wave?

Digitalis (which was by the way originally synthesized from Digitalis Purpurea) has two mechanisms of action:

The action by which digoxin improves contractility appears to be inhibition of the sarcolemmal Na$^+$K$^+$-ATPase "pump", normally responsible for maintaining transmembrane Na$^+$ and K$^+$ gradients
The major therapeutic electrical effect of digoxin occurs at the AV node, where it slows conduction velocity and increases refractoriness.

So it has a mechanical and an electrical mechanism. About the toxicity:

For example, in atrial and ventricular Purkinje fibers, a high dixogin concentration has three important actions that may lead to dangerous arrhythmias:

less negative resting potential

decreased action potential duration

enhanced automaticity

All quotes are from the book Pathophysiology of Heart Disease by Leonard S. Lilly, 5th edition.
So, I would assume one of the three (or a combination of them) is the reason for the biphasic T-wave. I hope someone more experienced can improve upon this answer.
This maybe has something to do with the relative refractory period ending during the T-wave.
Also, since the figure is from lead I, you can use that information for looking at where the net electrical axis is pointing at during the T-wave. Refer to the hexaxial system.


Bending your little finger without bending ring finger It is possible to bend each finger without bending any other, except one for most people. It is more difficult for the ring finger, but when I try to bend my little finger independently my ring finger bends as well. I don't know if this is because of the muscle or  bone configuration, but I'm interested in the answer.

  Is it possible to bend the little finger independently, and if so why is it so hard to do so?

This does not have to be the case always, For example if you are a pianist you need all your finger to work independently.

OK, So coming to the main question.

In simple words, They are all interconnected. See the image [Source: Google Images]

They share flexor tendons (The flexor tendons allow you to bend your fingers) , If you try to move one, other is objected to come along.

Yes it is possible, As I mentioned before if you are a pianist, you don't have much choice. It is possible by little bit training.


Why do cockroaches flip over when they die? This question has always mystified me since young. For beetles, I can reason that they flip over because they have a higher centre of gravity causing them to be in unstable equilibrium when they tuck in their legs when they are about to die. For cockroaches with a lower profile, I would expect them to stay upright. But why do they flip over? Is it more comfortable for them to die this way or is there a scientific explanation for this?

Edit:

As noted in some of the comments below, this is a general observation based on cockroaches being killed by insecticide. I haven't got the chance to observe (or notice) cockroaches that die in other ways and therefore do not want to limit the scope of my question to just insecticide poisoning.

It is a result from the insecticide you are using.  From this excerpt from the 10th Edition of the Mallis Handbook on Pest Control:

  Neurotoxic insecticides cause tremors and muscle spasms, flipping the cockroach on its back. A healthy cockroach can easily right itself, but without muscle coordination, the cockroach dies on its back. Cockroaches exposed to slow-acting insecticides that target respiration (energy production) also can die “face-down,” as they run out of energy without experiencing muscle spasms.

Here's also a website from UMass describing it in more detail:

  Most of these insecticides are organophosphate nerve poisons.  The nerve poison often inhibits cholinesterase, an enzyme that breaks down acetyl choline (ACh), a neurotransmitter.  With extra ACh in the nervous system, the cockroach has muscular spasms which often result in the cockroach flipping on its back.  Without muscular coordination the cockroach cannot right itself and eventually dies in its upside down-position.

And an entomology professor even answered this for Maxim:

  Most insecticides are poisons that target a bug’s nervous system. When you spray a roach, those neurotoxins cause tremors and muscle spasms, which flip
  it onto its back, and without muscle coordination, that’s the position it dies in


Eusociality and Natural selection? Eusociality, particularly focusing on the presence of certain altruistic sterile organisms within the social set-up creates questions as to why would the process of natural selection have favoured the persistence of such genes especially in hymenopteric species. One explanation (provided probably by Hamilton) pertains to very similar genetic constitutions of females of such species (owing to haploid nature of males), which increases genetic similarity between the female members of the social group. Thus it would be more "beneficial" (i.e., favourable for the persistence of similar genetic builds) for a female worker to help the fellow siblings, to which it bears greater genetic similarity, than its own offspring to which it bears a lesser genetic similarity. This might in a deeper way explain altruism in case of hymenopterans where the male is a parthenogenetic haploid and the female is diploid.

But why would the sterile condition of the workers in case of almost all eusocial groups be favoured by natural selection on grounds that it improves the 'fitness' of the 'genetic build' of the workers and ultimately the sterile altruists benefit the persistence of its genetic traits? Moreover the altruistic nature of the haploid males also goes unexplained.

Group selection, in the extreme, yields eusociality due to the shared fate of the replicators in the group.  In a multicellular sexual organism, this "shared fate" of the "group" is the shared prospect that all replicators (alleles) have for making it into the next generation via the meotic lottery that produces the gamete.  Since they share this prospective fate they have an evolutionary incentive to cooperate in the construction of specialized cells that are, in effect, "sterile caste" members of the total "hive".  Similarly, if it is possible to subject all members of a group of individuals to a shared fate through multiple generations -- they will tend to evolve highly cooperative social structures.  However, one of the confusing aspects of the eusocial insect colonies is whether they evolved to be that way through shared fate of individual organisms, or some variant on the meotic lottery's shared fate of alleles.  The answer appears to be, primarily, that it is a peculiar form of meotic lottery in which the genes of the parents have extended phenotypes in the children that, in essence, parasitically castrate the vast majority of the children to help rear more offspring for the parents -- in particular the queen.  In this respect, one can view the evolution of eusociality in the social insects as a perverse form of individual selection where the genes of, say, the queen, cooperate in constructing not just the queen's body but, also, the entire hive.  The sterile castes are simply extended phenotypes of the queen (and the  drone with which she mates).

See "The Social Conquest of Earth" by E. O. Wilson for an in-depth treatment of eusociality and its evolution as set forth by Nowak et al in their recent paper "The Evolution of Eusociality".  See also "The Extended Phenotype" by Richard Dawkins -- in particular the chapter "Host Phenotypes of Parasite Genes".


confusion in types and kingdom system of classification I am a high school student and I want to ask: is the 'kingdom system' of classification (two-kingdom, three-kingdom etc.) different from artificial or natural classification? I am asking this because my teacher told me that these two are different things. He says that you cannot categorize the two-kingdom classification as artificial or any other type.
But I am little confused as to why we cannot categorize kingdom system classification into artificial, natural or any other type. For example, Linnaeus selected only a few characters to propose the two-kingdom classification. Then why can we not say that it is an artificial classification?

In earlier days, biological classification systems were often described as artifical or natural, with natural systems reflecting the 'real' relationships among living beings, and artificial ones allowing classification only for some limited purpose (Gilmour, 1937). Natural systems were supposed to be based on a large number of characters, with a focus on characters 'fundamental' to organisms.  Artifical systems were supposed to be based on fewer, arbitrarily chosen characters.
As an example, consider Linnaeus' works on the classification of plants. Linnaeus' Systema Naturae (1735) classified plants based on floral morphology alone. However, his later work Genera Plantarum (1737) included more characters, such as the morphology of fruits. Linnaeus therefore regarded the latter classification as being more natural. (See the Encyclopedia Britannica entry on Linnaeus for a more detailed discussion of this.)
As for the two-kingdom classification, I couldn't find any sources calling it either artificial or natural.
However, the natural vs artificial dichotomy is not always straightforward. For instance, how do we know which characters are 'fundamental' and will help us develop a natural classification system? To quote Judd et al (2008):
For hundreds of years, botanists tried to develop classifications that were "natural"... Unfortunately, the word natural has no fixed meaning; rather, authors have used it to mean something that agrees with their own ideas about nature or about constructing classifications or systems. Eighteenth-century systematists had ideas about nature that were very different from ours—they were certainly not evolutionary—and their systematic practice and classifications are best interpreted in terms of how they understood nature.

Thus, in modern biology, 'natural classification' and 'artificial classification' are better regarded as historical ideas than as useful descriptors. The focus is now on classification that integrates an understanding of evolutionary relationships, i.e. phylogenetic classification.


Strange Black-Brown Insect Identification Interesting Insect from Singapore. Around 0.5cm. Has 2 tiny pinchers at its tail. Insect is black for most part.

Please zoom in on scotch tape:

This is an earwig, an insect in the order Dermaptera that has notably robust cerci.

 Credit: Ron Yeo

Note that the name comes from an old wives' tale about these insects crawling into people's ears. They don't:

  Earwigs do get their name from the belief that they climb into human ears while individuals are asleep, however, this belief is fortunately untrue

Based on the sexing rules indicated here, your specimen's relatively straight cerci might be an indication that you found a female.

Earwigs are found worldwide, and with about 2000 species (source), it'll be difficult to narrow this down to species. If you can get access to a local dichotomous key or other accurate insect ID guide, you might be able to narrow further.


Are there more true codes found in biology besides the central dogma? I know each element of the central dogma is a code in the mathematical sense of finite-state machines. That is, DNA is transcribed into RNA, and RNA into proteins.  What other examples are there of codes that exist naturally in organisms?

DNA is a code that occurs via stepwise polymerization, like all major macromolecules. In respects to DNA, it is Nucleic Acid sequences that polymerize to create the DNA. In eukaryotic cells this happens at multiple replicons (regions of replication). So you can look DNA as code for itself. You also have rRNA, mRNA, and tRNA. All of these code for and do specific things. rRNA facilitates the creation and movement of the ribosome, where mRNA and tRNA "code" for the final protein. tRNA serves as the principle code strand for the correct Amino Acids. This is read as a series of three N.A's (codons) One codon for a respective Amino Acid. mRNA actually guides the synthesis of these polypeptide chains. You also have something called operons. These are groups of genes with related functions that are clustered together. This allows for rapid initiation and termination of gene expression. Im sure there are a few others but these are those that come off the top of my head. The term "code" and molecular bio are very much intertwined.


Does the anatomy of our hand result in (computer) mouse-accuracy that varies by direction of movement? First off, I apologize if this isn't the right stackexchange sub-site for asking thsi question.  I was torn as to where I should post this question: it could plausibly belong in Biology, User Experience or even Arqade.  However, given the root of my question has to do with the "wiring" of the human hand, I elected to post it here.

My hypothesis/question:
Let's assume that wrist adduction/abduction is responsible for horizontal movement of the mouse cursor and that finger extension/flexion is responsible for vertical movement of the mouse cursor.  (I am, of course, willing to revisit this assumption, if necessary.)  Would it be accurate to say that we are "hard-wired" to be capable of higher precision in vertical movement of the mouse cursor than in horizontal movement?

Description of mouse grip:
In making the above assumptions, I assume a fingertip-grip style of the mouse (as opposed to the claw and palm grips). The (corner of the) wrist rests on the table and acts as a pivot for allowing side-to-side motion (i.e., horizontal motion of the mouse cursor).  Meanwhile, flexing/extending the fingers allows for pulling/pushing the mouse away from us, (i.e., vertical motion of the cursor).  The main (admittedly unscientific) reason behind my hypothesis is that vertical movement of the mouse cursor uses similar finger motions as those used for hand-writing (which is, after all, a highly precise activity).

(I understand that my question makes the assumption that we are capable of more precise movement with certain muscles of our body than we are with others - please let me know if that's a flawed assumption.)

Why do I care about this?:
If my hypothesis is correct, there would be implications on mouse settings (namely, horizontal and vertical DPI*) that are conducive to both high accuracy and speed.  The key issue is that if we keep our wrist in place (i.e., no sliding/lifting of our pivot point) - then we're able to move the mouse a greater distance side-to-side (i.e., horizontal motion of cursor) than we're able to move it toward/away from us (i.e., vertical motion of cursor).  However, if there is evidence to support my hypothesis, than an appropriate adjustment (which wouldn't result in a loss of accuracy) would be to have a slightly higher vertical DPI than horizontal DPI.

*DPI = dots (i.e., pixels per inch).  For example, I have a resolution of 1366x768 (which is in units of dots or pixels) and a 600 dpi mouse, which means that my (physical) mouse needs to be moved ~2.3 inches (1366 divided by 600) in order for the mouse cursor to move the full horizontal distance of my monitor.  To put it simply, lower DPI results in higher accuracy but it is preferable for our wrist to remain in-place in the interest of speed.

Assuming the case where you move a mouse left and right with the wrist and up and down with the fingers, then yes, finger movements are more precise. The fingers and facial musculature are body parts with the most exquisite fine motor-control. The wrist, on the other hand, probably less so. The wrist is definitely involved in fine motor skills such as writing, but the fingers even more so.

I wasn't able to find a good reference about the level of precision for different body parts at the behavioral level. I can, however, approach the question from a neurophysiological point of view. The amount of motor control available for different body parts can be visualized by means of a motor homunculus. The motor homunculus shows how many neurons are available in the cortex for a given body part. The larger the cortical surface dedicated to a body part, the larger the corresponding body part is presented in the homunculus (Fig. 1).

Fig. 1. Homunculus drawn on the motor cortex (left) and the homunculus presented as a figurine (right). Sources: Conference on Human factors (1997) and Autism Index, respectively.

The fingers have a huge amount of motor cortex dedicated to them compared to the wrist. There are a lot of 'buts' to add, most notably the larger number of muscles in the fingers versus the wrist, which explains part of the difference. Nonetheless, the homunculus does show the relative functional importance of the fingers in motor processing power of the brain, while the wrist is virtually invisible on the homunculus (Fig. 1, left panel).

Lastly, you seem to be mixing up 'distance' and 'precision' in your question. While the wrist may cover a greater distance, it is not because of this that the precision is smaller. The fingers have more neuronal processing power behind them and can be exquisitely fine tuned. In other words, the precision is not determined by the dynamic range (distance), but by the processing power dedicated to the motor function.

As a side note, because of RSI, it is recommendable to use gross arm movements instead of fine wrist and finger movements.


What is an inclusion forming unit? What is inclusion forming unit load? I found it when reading this article.

What does this measure and what information can be gained form it? Does this represent the amount of bacteria within a person? What's the difference between inclusion forming units and colony forming unit?

I am from a mathematical background, so can someone please explain these in simple terms?

Depending on the development cycle of Chlamydia tend to appear in two forms, the elementary body and the reticulate body. As outlined in the excerpt below, the reticulate body can be found as inclusions in a cell's cytoplasm when stained with iodine. So yes, your initial guess of inclusion-forming units (IFUs) being a measurement of how much of Chlamydia spp is present in a sample (cell or tissue) is correct.

It is similar to the concept of Colony Forming Units (CFU) which is a unit used to estimate the number of viable bacteria or fungal cells in a sample. Viable is defined as the ability to multiply via binary fission ("division in half") under controlled conditions.

Applying the concept of CFU to the above an inclusion-forming unit may be understood as a unit to estimate the number of Chlamydia cells in a sample. The difference between CFU and IFU would be as follows, CFU counts are normally taken for bacteria/fungi grown in a controlled environment. CFU counts also only account for viable cells, dead cells are disregarded. This is in contrast to IFU counts as we do not have a controlled environment as such and depending on what staining method you use, IFU counts may or may not account for dead cells too.

  Chlamydia may be found in the form of an elementary body and a reticulate body. The elementary body is the nonreplicating infectious particle that is released when infected cells rupture. It is responsible for the bacteria's ability to spread from person to person and is analogous to a spore. The elementary body may be 0.25 to 0.30 μm in diameter, and it mainly consists of C. trachomatis, C. pneumoniae, and C. psittaci. This form is covered by a rigid cell wall (hence the combining form chlamyd- in the genus name). The elementary body induces its own endocytosis upon exposure to target cells. One phagolysosome usually produces an estimated 100–1000 elementary bodies.

  Chlamydia may also take the form of a reticulate body, which is in
  fact an intracytoplasmic form, highly involved in the process of
  replication and growth of these bacteria. The reticulate body is
  slightly larger than the elementary body and may reach up to 0.6 μm in
  diameter with a minimum of 0.5 μm. It does not present a cell wall.
  When stained with iodine, reticulate bodies appear as inclusions in
  the cell. The DNA genome, proteins, and ribosomes are retained in the
  reticulate body.

Link to Wikipedia page - excerpt was taken from there.


If a trait does not appear to be advantageous to organism, why does the organism have it? Why do organisms have some traits that do not appear to have any evolutionary advantage?

There are many reasons why an organism might have a trait that does not appear to be beneficial.

The trait is actually advantageous even if it does not appear to be.
The trait is a byproduct of another trait, which is beneficial. Not all traits are the product of direct selection; traits that are byproducts of other traits are known as "spandrels", a trait coined by Stephen J. Gould and Richard Lewontin
The trait was fixed by some process other than natural selection, such as genetic drift. Genetic drift can fix traits that are neutral or even evolutionarily disadvantageous.


Is it possible to suffer from hyperthermia by spending too much of time in the hot springs? People may tend to spend time in a hot water spring. Is it possible to get hyperthermia (like a sun stroke) due to this?

You betcha!

  We report a case of acute hepatic failure combined with disseminated
  intravascular coagulopathy, acute renal failure, and neurological
  deficit caused by heat stroke after bathing in a hot spring.

Generically, the term you're looking for is non-exertional heat stroke.


HAR1 speedy mutation From wiki:

  Human accelerated region 1 (HAR1) is a segment of the human genome found on the long arm of chromosome 20. It is a Human accelerated region. [..] These 49 regions represent parts of the human genome that differ significantly from highly conserved regions of our closest [living relatives, the chimpanzees] in terms of evolution.

What could explain those differences?

A back of the envelope computation shows that in the course of 8mio years, at a rate of 64 mutations per generation, one can expect 1% of mutated basepairs. Indeed, the HAR1 of length 106 bp has 1.08 substitutions in the chimp. But humans have 13.93. (Data: see the table in this article.)

Substitution rate at neutral sequences

The rate of substitutions at neutral sequences is given by the mutation rate. It si a very simple and classic result. It is because the probability of each new neutral mutation to fix is $\frac{1}{2N}$ (which you can calulate from a Moran branching process as well as from a simple Wright-Fisher model of genetic drift) and there are $2N\mu$, new mutations at each generation (where $N$ is the population size and $\mu$ the haploid mutation rate), resulting in a substitution rate of $2N\mu\frac{1}{2N} = \mu$.

Substitution rate at non-neutral sequences

A beneficial mutation has a probability higher than $\frac{1}{2N}$ to fix, while a deleterious mutation has a probability lower than $\frac{1}{2N}$ to fix. Therefore, the more beneficial mutations there are, the higher is the substitution rate. There are a number of approximations to the fixation probability of a non-neutral mutation. For example, using diffusion equations, one can approximate the probability of fixation of a deleterious mutation with selection coefficient $s$ by $\frac{1-e^{-\frac{4s}{N}} }{1-e^{-4Ns}}$ from some Kimura paper.

This rate of substitution therefore depends upon the selection scenario. It is lower than $\mu$ in conserved sequences and it is high than $\mu$ in sequences that undergo positive selection. So, the reason for such fast evolving sequences is just that they are under positive selection.

How about HAR1?

Without looking for more accurate statement form the scientific literature, the same wikipedia article you cite says

  HAR1A is active in the developing human brain between the 7th and 18th gestational weeks. It is found in the dorsal telencephalon in fetuses. In adult humans, it is found throughout the cerebellum and forebrain; it is also found in the testes.[1] There is evidence that HAR1 is repressed by REST in individuals with Huntington's disease, perhaps contributing to the neurodegeneration associated with the disease

It already gives you a vague idea of potential selection pressures on those sequences in the human genome.


Biological basis of the science fiction story "The Dipteroid phenomenon" The science fiction novelette by Poul Anderson The Dipteroid Phenomenon describes a plot in which

   the protagonist Evalyth is one of the members of a space-faring civilisation which is rediscovering atavistic humans stranded on other planets following the fall of human civilisation from an interplanetary war in the past.

  The husband of the protagonist is murdered and cannibalised by the savage guiding him through the jungle, and she finds and captures the savage's whole family in revenge, intending to execute the savage. While doing so, she discovers that all of the humans on the planet, including the civilised city-dwellers, have a tradition of cannibalising humans. The savages hunt each other for cannibalism, while the city-dwellers hunt down the savages, which they then keep as slaves for consumption.

In the end of the story, it is revealed that:

   all of the male humans on the planet are unable to sexually mature normally due to a genetic mutation in their Y-chromosome, which results in them having to consume male genitals in order to reach sexual maturity.

The novel then further states that the phenomenon of having to consume males in order to mature is also found in terrestrial Diptera flies.

  'Hence a dipteroid phenomenon may have appeared in man on this planet. Such a thing is unknown
  among higher animals elsewhere, but it is conceivable. A modification of the Y chromosome would
  produce it. The test for that modification, and thus the test of the hypothesis, is easily made.'
  The voice stopped. Evalyth heard the blood slugging in her veins. 'What are you talking about?'
  "The phenomenon is found among lower animals on lower worlds,' the computer told her. 'It is
  uncommon and so is not widely known. The name derives from the Diptera, a type of dung fly on Old
  Earth.'

Is this "dipteroid phenomenon" a real biological phenomenon observed in Diptera dung flies on Earth? I was unable to find a scientific paper describing this rather interesting phenomenon.

After some research, it appears that the phenomenon being discussed was the consumption of Diptera flies by the dung fly, Scatophaga stercoraria. This paper describes their inability to sexually mature without consuming prey (for which Musca domestica flies were provided).

  Male  Scatophaga  stercoraria must prey on other Diptera before they
  display sexual behavior, develop  the  accessory cells  of  their  ejaculatory ducts, and
  achieve  full elongation of  the testes. The corpus allatum also becomes enlarged
  after predation and is  necessary for  the onset of sexual behavior and development
  of reproductive organs. The complex diet consumed  during predation apparently
  cactivates the corpus allatum, and the hormone released acts  independently on
  organ growth and sexual behavior.


Soft Agar Substitute I've got petri dishes with a base agar layer ready for E. coli culturing. However, I do not have soft agar in which to dilute the E. coli before pouring it on to the plate.

Any suggestions on what substance I can use to substitute for soft agar, or how I might be able to make it? I have the following at my disposal from the lab at school:

Tryptone base agar
Nutrient broth
MacConkey agar

The original soft agar medium had the following composition:

10 g Bacto™ tryptone
9 g Bacto™ agar
5 g KCl
1000 mL water

The good news is: You don't need any agar in your plating media, since the bacteria grow on the surface anyway and the plate can take up some additional moisture from your plating media.

What I usually do is to dry the plates for a while (and also let them warm up, since they are stored in the fridge) with the plate upside down and opened a bit. Contamination is usually not a problem here.

Then I dilute the cells in an appropriate volume of media, then plate about 50 to 100µl on the agar and spread it with a Drygalski spatula. Put the plate in the incubator and everything is fine.


Do all organisms have to die? I understand (a little) that there are biological clocks and reason that after a certain amount of time organisms die. I'm wondering if that is something inherent in our DNA or in biology/chemistry in general. EG, is it possible that there could be a complex organism that would not die and would just regenerate it's cells In Perpetuam? I'm specifically interested in mammals and even more specifically interested in humans. But, I would be interested in hearing about other organisms like bugs, fish, plant, algae, etc.

I'm not asking if this practical, do we know how to do this, etc.. I just want to know theoretically if living forever is biologically possible, as far as we know. If not, is there an estimated upper limit?

The immortal jellyfish can revert back to its immature polyp stage after reaching maturity, then mature again, over and over. You can read more on the wikipedia page, but this ability means it can potentially avoid senescence altogether.


Can we change the Eye/Hair color by knocking out the OCA2, HERC2 and MC1R genes using CRISPR in an adult human? This paper seems to describe the use of a plasmid delivered by a gene gun to depigment rat skin;

https://www.nature.com/articles/3302264
Published: 27 May 2004
Seeing the gene therapy: application of gene gun technique to transfect and decolour pigmented rat skin with human agouti signalling protein cDNA

Could a similar technique using CRISPR and chitosan change the eye and hair color of an an adult?

Let's first breakdown this question

What is CRISPR?

CRISPR is a group of DNA sequences that play a key role in the antiviral defense system of prokaryotic organisms such as bacteria and archaea.
They are derived from DNA fragments of bacteriophages that had previously infected the prokaryotes.
These sequences are used to destroy DNA from similar bacteriophages for future infections.

What is CRISPR-Cas?

The CRISPR-Cas system is an immune system seen in prokaryotes that provides resistance to foreign elements such as plasmids and phages. This is a form of acquired immunity.
Some factors allow Cas protein which is an enzyme to recognize and cut foreign pathogenic DNA making them act like a pair of molecular scissors.

What are OCA2, HERC2, and MC1R?

Now we know we can cut a specific part (Gene) of DNA. What do we accomplish by cutting out the genes which Andrew mentioned? To answer this we need to know what those three genes do.

OCA2 (P-gene): Provides instructions for making a protein called the P protein. This protein is located in specialized cells
(melanocytes) that produce a pigment called Melanin.
Melanin is a natural skin pigment. Hair, skin, and eye color in people and animals mostly depends on the type and amount of melanin
they have.
HERC2 (E3 ubiquitin ligase HERC2): Protein ligase which helps in DNA repair regulation, pigmentation, and neurological disorders.
MC1R (Melanocortin 1 receptor): Proteins involved in regulating mammalian skin and hair color.

In short, these Genes affect the Eye and Hair Colour and Andrew is suggesting to us that by removing/modifying them using CRISPR we change the Eye/Hair Colours.

Can we knock out OCA2, HERC2, and MC1R?

Yes, it has been done before and there are sequences available to target these genes within the genome. An example would be the gRNA sequences developed by Sigma-Aldrich and Genscript. I'll provide links of articles which has knocked out the respective gene and links to the gene sequences.

OCA2: (Article: https://pubmed.ncbi.nlm.nih.gov/29555241/ | Sequence:
https://www.genscript.com/gRNA-detail/4948/OCA2-CRISPR-guide-RNA.html)

HERC2: (Article:
https://jmg.bmj.com/content/early/2020/06/22/jmedgenet-2020-106873 |
Sequence: https://www.sigmaaldrich.com/catalog/genes/HERC2)
MC1R: (Article:
https://www.genscript.com/gRNA-detail/4157/MC1R-CRISPR-guide-RNA.html
| Sequence:
https://www.genscript.com/gRNA-detail/4157/MC1R-CRISPR-guide-RNA.html)

Can we change the Eye/Hair Colour by modifying the above genes?

An Interesting article from MIT Technology Review called Engineering the Perfect Baby gives you a nice idea of what I am going to tell you.
In Theory: It's technically possible. We can put up a convincing theory and there is a huge chance that this can be successfully done.
In Reality: Well, Reality kinda sucks cause most of the genetic engineering breakthrough starts from failures. Killing a rat for scientific purposes won't make any big difference but what about killing a fetus? It's almost impossible to get the permissions required to use CRISPR to edit the human genome even if it is to find a cure for a deadly disease that would actually improve the human race significantly. Due to its obvious ethical questions, people always stand against it. I said "almost impossible" cause there are few people who actually got the permissions and there are indeed few ongoing trials experimenting with CRISPR on Human Genome.
A popular Example would be He Jiankui who gave rise to the first-ever gene-modified human babies "Lulu and Nana". He had to forged ethical review documents, misled doctors into unknowingly implanting gene-edited embryos into two women, and many more things which haven't come out yet. What are the consequences? He's bloody missing!
The point is, there is absolutely no way they would approve the usage of CRISPR for modifying something as silly as Eye/Hair color.
I mean we all like our babies to look like Megan Fox but I totally doubt if anyone would dare to modify a human genome for changing mere appearance cause people would start protesting if they find out someone is putting all those innocent fetuses at unknown and uncalculatable risk for changing external traits.
We want people to use CRISPR for things like this - Scientists edit gene for blood disease in human embryos and not for things like this - The rise of the designer baby: Parents who paid $16,500 to choose the sex of their child.
TL;DR (Too Long; Didn't Read):

What is CRISPR-Cas?

Technique in which we can edit genes relatively more precise than before.

What are OCA2, HERC2, and MC1R?

Genes which control the color of Eyes, Hair, Skin, and has other purposes.

Can we remove OCA2, HERC2, and MC1R genes using CRISPR?

Yes

Has it been done before?

Yes

In Humans?

Nope cause we got all those ethics and stuff.

What are we trying to accomplish by removing those genes?

To change the Colour of the Eyes/Hair of a human being.

Can we change the Colour of the Eyes/Hair of a human being?

In theory, it'll work. In Reality, nobody would allow it. They'd be better off with Hair Dye and Contact Lenses than to risk the lives of innocent fetuses.


Why are Merkel cells innervated by an axon, and not a dendrite? Here are two images from Google. Afferent neurons receive input and send it to the central nervous system. Input is received by the neuron's dendritic end and send away centrally via axon terminals that are sheathed with Schwann cells. Axon terminals synapse to motor neurons (muscles and glands).

How is it possible that Merkel cells, which supposed to be a sensory cell, synapse with an axon, and not with a dendritic end?

There is nothing out of the ordinary with the Merkel cell, as it functions in the same way as photoreceptors and hair cells (see Further Reading #1).

Fig. 1. Merkel cell. Source: Gallery for Share.

The Merkel cell depicted in Fig. 1 is a specialized receptor neuron. It has no axon. It relies on a secondary sensory neuron (a somatosensory afferent) onto which it synapses to direct the touch signal to the brain.

Note that neural information flow goes from dendrite to axon. An axon terminates into a synapse. The Merkel cell, which does not have an axon, features a synapse directly onto the dendrite of the secondary neuron (See Further Reading #2).

Further Readings
1. Can axons act as receptors?
2. What are the functions and differences between axons and dendrites?.


Transcription Factor expression level Could someone explain me in detail what is meant by "TF expression LEVEL", what does it represent and how is it measured? This is for example used in figure 3 of this paper: A census of human transcription factors: function, expression and evolution.

Transcription factors are an important cellular regulatory mechanism to control gene expression. The expression of TF is important for cell function, differentiation and also for responses to environmental signals.

We know quite a number of different TF, but only for a little part of them their exact function (in terms of which in which tissues they are expressed, when and which genes they regulate) and this is where the paper you read comes in.

They test for the expression of roughly 1400 TF in a number of different tissues, to see where they are expressed (figure 3 from the paper):

The group used micro-arrays to analyze the expression levels (in this case how much transcript from the genes is made assuming that this also translated). The quantification was done using the signal strength of the array - the more transcript you have, the stronger the signal is.

The expression of a certain TF in a specific tissues shows its involvement in gene regulation (either direct or indirect) there.


What is the genetic difference between two cone branches? As we can see on this larch, male and female cones are sometimes directed to grow on the opposite side of the branch. We were told in school that this mechanism works against self-fertilization. Also they flower in different times, so they are mostly fertilized from the other conifers.

When I saw this picture, I got that idea, that maybe they face the branches on above by design: To decrease the genetic uniformity at least a little.

But how important this effect actually is? And how big is the genetical difference between two branches? Are there any other factors taking effect in the tilt of the cones?

I don't understand your hypothesis. But the number of pairwise differences between two cells assuming neutrality ($\pi$) in the two different branches in $\pi = 2 \mu L t$, where $\mu$ is the somatic nucleotide mutation rate (around $10^{-11}$ on average), $L$ is the length of the sequence of interest (eventually the whole genome). $L$ can therefore be of the order of $10^9$. $t$ is the number of cell generation since the two cell lineages split. $t$ depends on the relative positions of the two branches but it could be $10^4$ cell generations. With these very quick approximations, we can estimate the number of pairwise differences as

$$\pi = 2 \mu L t \approx 2 \cdot 10^{-11} \cdot 10^9 \cdot 10^4 = 200$$


How does heat shock transformation work? What exactly happens when competent cells like DH5ɑ are heatshocked with DNA present? How does the DNA get inside the cells?

Specifically, why are all the steps necessary? What if you heatshock right after adding DNA? What if you don't put on ice after heatshock? What does the calcium chloride do? What actually happens when cells are "competent"? What governs transformation efficiency (besides obvious things like amount of DNA or cells)?

To make it clear what I'm talking about, I use a protocol like the following:

Take cells out of -80C and thaw on ice for 5 min.
Add 1 ul (~500 ng) plasmid DNA to 50 ul cells, mix gently with pipette tip.
Leave on ice for 30 min.
Put in 42C water bath for 45 sec.
Put on ice for 10 min.
Add 950 ul LB, put in 37C for 1 hour.
Spread 300 ul of the culture on LB-agar plates with appropriate selection.

I usually get thousands of colonies from this (in fact, often 1:10 or 1:100 dilution is necessary so I can actually get isolated colonies). Even if I skip the outgrowth, I still get hundreds.

I don't have my competent cell protocol, but basically I use that one rubidium chloride that everyone uses: DH5ɑ cells are washed with some buffers, suspended in a solution with CaCl2 and RbCl, then frozen in liquid nitrogen. I never actually measured, but usually the concentration of cells in the frozen aliquots is about 10 times as many as you would get from an overnight liquid culture (they are spun down and resuspended in a small volume).

Heat shock transformation alters membrane fluidity creating pores:

  A sudden increase in temperature creates pores in the plasma membrane of the bacteria and allows for plasmid DNA to enter the bacterial cell.

Reference: Journal of Visualized Experiments. Bacterial Transformation: The Heat Shock Method. 2014. http://www.jove.com/science-education/5059/bacterial-transformation-the-heat-shock-method

  The change in temperature alters the fluidity of the semi-crystalline membrane state achieved at 0oC thus allowing the DNA molecule to enter the cell through the zone of adhesion.

Reference: Anh-Hue T. Tu. Transformation of Escherichia coli Made Competent by Calcium Chloride Protocol. 2008-2013. American Society for Microbiology

  ... heat-pulse (0 degrees C42 degrees C) step of the standard transformation procedure had lowered considerably outer membrane fluidity of cells. The decrease in fluidity was caused by release of lipids from cell surface to extra-cellular medium. A subsequent cold-shock (42 degrees C0 degrees C) to the cells raised the fluidity further to its original value and this was caused by release of membrane proteins to extra-cellular medium.

Reference: Panja S, Aich P, Jana B, Basu T. How does plasmid DNA penetrate cell membranes in artificial transformation process of Escherichia coli? Mol. Membr. Biol. 2008 Aug;25(5):411-22. doi: 10.1080/09687680802187765. PubMed PMID: 18651316.


Why does ammonium oxalate cause swelling of RBCs? From Pre examination procedures in laboratory diagnosis by Walter Guder :

  ...It consists of three parts by weight of ammonium oxalate which
  causes swelling of erythrocytes balanced by two parts of potassium
  oxalate which causes shrinkage...

This is regarding use of oxalates as anticoagulants.
To me, it makes sense that potassium oxalate causes shrinkage of erythrocytes but i don't understand why Ammonium oxalate causes swelling. Is it because it converts to Ammonia in alkaline pH of blood, diffuses into the RBC and converts back to ammonium.

After a lot of search I think the following seems a satisfactory answer.

You are correct in thinking that outside the RBC, $\ce{NH_4^+}$ converts to $\ce{NH_3}$ and once inside the RBC, it again converts to $\ce{NH_4^+}$. But this does not explain how $\ce{NH_4^+}$ swells up the RBCs. For that, let us look at the process from the beginning.

As described by Hemker et al, 2003, an important part of this process is the enzyme carbonic anhydrase (an absolutely important constituent of RBCs). Hemker et al, while studying how the Rh complex in RBCs exports $\ce{NH_4^+}$ ions out of the cell (although they used $\ce{NH_4Cl}$ in their study, it doesn't matter since blood already contains enough $\ce{Cl^-}$) they came up with the following scenario:

$\ce{NH_4^+}$ breaks into $\ce{NH_3}$ and $\ce{H^+}$ and enters inside the RBC. $\ce{H^+}$ combines with $\ce{OH^-}$ (coming from $\ce{HCO_3^}-$, we'll talk about this later) to give $\ce{H_2O}$.
Due to increased osmotic pressure (by $\ce{NH_3}$), $\ce{H_2O}$ enters inside the RBC where it is again broken into $\ce{H^+}$ and $\ce{OH^-}$. $\ce{NH_3}$ combines with $\ce{H^+}$ to give $\ce{NH_4^+}$ again (and we're done with $\ce{NH_4^+}$ here, though Hemker et al took this further).
The $\ce{OH^-}$ (from water) combines with $\ce{CO_2}$ (via carbonic anhydrase) to give $\ce{HCO_3^-}$. This $\ce{HCO_3^-}$, via Hamburger shift, is exchanged with a $\ce{Cl^-}$ while the $\ce{HCO_3^-}$ outside converts into $\ce{H^+}$, $\ce{OH^-}$ and $\ce{CO_2}$ (providing $\ce{OH^-}$ to $\ce{NH_4^+}$). See the diagram below for visual representation:

So, where does the swelling effect come in? It turns out, it is due to the increasing concentration of $\ce{NH_4^+}$ and $\ce{Cl^}-$ inside the RBC which keeps on generating higher and higher osmotic pressure. Hemker et al also found that Rhnull RBCs (lacking Rh complex) became victims to osmolysis much faster than the normal RBCs, suggesting that increased concentration of intracellular $\ce{NH_4^+}$ is the main cause of swelling and osmolysis of RBCs (in their research, they concluded that Rh factor indeed exports $\ce{NH_4^+}$ outside the RBCs).

Reference: Hemker, M. B., Cheroutre, G., Van Zwieten, R., Maaskant-van Wijk, P. A., Roos, D., Loos, J. A., Van Der Schoot, C. E. and Von Dem Borne, A. E. G. Kr. (2003), The Rh complex exports ammonium from human red blood cells. British Journal of Haematology, 122: 333–340. doi:10.1046/j.1365-2141.2003.04425.x


Has anyone used Crispr/Cas to induce a knock-in in MEF cells? Does anyone have experience with the CRISPR/CAS9 platform performed on MEF? Or does anyone recall any relevant articles?

From this paper:

  We chose to test for Cas9-driven targeted mutagenesis on the
  endogenous Trp53 gene in mouse embryonic fibroblasts (MEFs), a cell
  line in which the biology of p53 has been thoroughly characterized and
  where the gene is structurally intact.

Furthermore:

  Seventy-two hours post-transduction, cells were cultured in the
  presence or absence of Nutlin-3a, a specific inhibitor of the MDM2–p53
  interaction (Tovar et al. 2006). Cells were scored for the fraction of
  GFP+ cells after 4 d of Nutlin-3a exposure using flow cytometry (Fig.
  2B). Nutlin-3a potently activates a p53-dependent anti-proliferative
  cellular response, which strongly and specifically selects for any
  cells with disrupted Trp53 function (Efeyan et al. 2007). Much like
  MLP-p53.1224 infected cells, the pQCiG-p53 GFP+ cells were rapidly
  enriched for in the presence of Nutlin-3a, suggesting that
  CRISPR-mediated gene disruption had initially occurred in at least a
  proportion of the initial Cas9-expressing cells.


Where can I find the pZ189vector plasmid vector sequence? I need this sequence since it was used in this paper https://onlinelibrary.wiley.com/doi/pdf/10.1002/em.1046. They say that the plasmid was prepared as in this paper http://www.jbc.org/content/271/16/9637/F1.expansion.html (see figure below)

However, they do not seem to be reporting the sequence of the pZ189 vector. Does anybody know where can I find this sequence?

Turns out the sequence is not actually written down anywhere. I asked one of the original authors of the plasmid (not the paper above) and he said that nobody ever did it because at the time when the plasmid was used it would have been a laborious task with little utility. Bummer :(

He also said that plasmid pSP189 is sort of the same but much more efficient and what it does, and is also more studied, with the sequence freely available around the internet.


Dry Bulb Temperature VS Dew Point, which one is most relevant to insects? I study insects that are leaving freely on my campus. The campus weather station has two different measures of temperature, the Dry Bulb Temperature and the Dew Point Temperature. Which one is the most relevant when studying insects? Are they very different? In other words, can you state the main differences between the two that are relevant when studying insect biology.

Insect development and activity are strongly associated with dry-bulb temperature. Development rate is usually predicted using degree-days (Links here: http://ipm.ucanr.edu/WEATHER/ddconcepts.html and https://entomology.ca.uky.edu/ef123). Basically this takes advantage of the nearly linear relationship between development rate and temperature in almost all insects (in some the type of food available can also be limiting). At temperatures above a certain threshold -- usually around 50 F or 10 C --  the warmer it is, the faster development will take place, up to a certain temperature cut-off above which development is drastically slowed (varies widely from species to species).

Insect activity is also strongly associated with dry-bulb temperature. In general most insects cannot fly at temperatures much below about 50 F or 10 C. They cannot generate energy fast enough at lower temperatures. The species that do fly at lower temps are generally Hymenoptera or Lepidoptera that use group or individual muscle movement to generate heat. Those that do fly in cooler weather or at night are often covered with fur or hair, which allows them to retain more of the heat generated by their flight muscles.

Wet bulb temperature generally relates to relative humidity, which has little to do with insect activity except in extremely hot, dry environments, wherein insects will be much more active during higher relative humidity (as it helps them retain more moisture) times of day such as morning or evening.

I hope this helps.


Why are sushi proteins called "sushi"? What are the origins of this name? Does anybody know why complement control proteins (also short consensus repeats) are called "sushi" proteins? Is there any special reason for their name?

Because their shape reminded researchers of rolls of Sushi (Ichinose et al, 1990):

  These repeats were initially called GP-I structures because they were first identified in $\beta_2$-glycoprotein I. More recently, they have been called short consensus repeats or sushi structures because of their shape.


Books on population or evolutionary genetics? I have recently been involved in collaborations that require me to model the population genetics of eukaryotic populations. I fear I may either be "re-inventing the wheel" or making conceptual mistakes (e.g. simplifying assumptions) in many of the techniques and decisions so far.

I would very much appreciate recommendations of books about population/evolutionary genetics or micro evolution to deal with these fears. Preferable criteria are:

Intuitively introduces key concepts.
Emphasis on modelling with examples of problems and their solutions.
Relatively short (I'm planning to read from cover to cover).

TL;DR
I'd recommend Population Genetics: A Concise Guide (Gillespie) for an introduction to population/evolutionary genetics (thanks AGS for highlighting this big miss of mine on the first version of my answer).
I'd recommend A Biologist's guide to mathematical modelling in evolution and ecology (Otto and Day) if you want to ensure your knowledge in mathematics by learning their application to evolutionary biology.
General Entry Books to Population Genetics
There are several books that offer an introduction to population genetics. I read Principles of Population Genetics (Hartl & Clarke). I appreciated it but if I were you I think I would rather try Elements of population genetics (Charlesworth) or Population Genetics (Hamilton). There is also Genetics of Populations (Hedrick). I would tend to think that this last book presents lots of empirical population genetics data and doesn't take as much focus as the others in theoretical concepts (but I might be wrong). Gillespie's book Population Genetics: A Concise Guide is a classic. It is short, very easy to follow and pleasant to read. Gillespie's book might eventually be a little bit outdated but I would still highly recommend it.
Emphasis on Analytical Modelling
A Biologist's guide to mathematical modelling in evolution and ecology (Otto and Day) is a very good and very accessible book. It makes a good review about all subjects that are usually taught to first year students in Biology such as linear algebra for example. It is highly accessible and in the meantime it goes pretty far as it ends up talking about the application of diffusion equation in population genetics (Kimura's work among others). This book presents some important models in population genetics but as it aims to provide the tools for mathematical modelling in ecology and evolution it may under-considerate some fields of ecology and evolutionary biology. For example, the book does not talk about population structure nor about evolutionary game theory and there is little about Coalescent theory.
Other books treating specific subjects within population genetics
Coalescent Theory: an Introduction (John Wakeley) is a good book. I haven't read it completely for both time issues and because the math are a bit complicated for me. Coalescent theory offers a very important set of mathematical tools in evolutionary biology.
There's also Mathematical population genetics (Ewens). I am currently reading it. It is definitely not an introductory book and it really doesn't cover much of the most common fields in population genetics.
If you are particularly interested in age-structured population, Evolution in age-structured populations (Charlesworth) is a very good book.
Modeling evolution (Roff) offers some discussion on how to mathematically define fitness from phenotypic traits. While it is interesting I would not counsel you to buy it. Moreover, all the mathematics are quite basic and it aims to explain how to perform mathematical modelling with R which is to my opinion not essential to learn as other languages make a better job at dealing with math (Mathematica for example).
Evolutionary Conservation Biology (Ferrière, Couvet and Dieckmann) is a very good book of conservation and conservation genetics. It develop some mathematical models that are of special interest to conservation of populations and communities.
Ecology, Genetics and Evolution in Metapopulations (Hanski and Gaggiotti) is a book that may interest you as well. However it focuses much more on ecology than the other ones I cited above. Note: I haven't read it entirely.
If you are interested in kin selection and level of selection, you might want to have a look at Major Transitions In Evolution (Maynard Smith and Szathmary) which is a classic (I have not read it though) or The Major Transitions in Evolution Revisited (Calcott and Sterelny) who encompass the opinion of many authors on the subject. Evolutionary Dynamics: Exploring the Equations of Life (Nowak) is also of interest esp. for those interested in epidemiology. Finally, you might want to have a look at the extremely well written and easy to read books by Dawkins such as The extended phenotype (Dawkins) for example. The Dawkins book are very popular and very very introductory. It offers more a way to think than the actual science behind evolutionary biology.


Why "broad" instead of "large" cross-immunoreactivity? From the articles I read, expressions like "broad cross-immunoreactivity" pops up a lot. So, I was wondering, why "broad" is used here instead of large? Is there a specific reason?

Broad means wide as in a wide range. Normally, antibodies have one epitope they recognize, i.e., one specific target; they are said to have a narrow range of targets.

Some antibodies, however, recognize multiple targets, i.e. the number of targets they recognize is larger and their target range is widened. They are said to have a broad cross-immunoreactivity.

A 'large' cross-immunoreactivity, however, is ambiguous, as 'large' can also imply 'large reactivity', and then 'large' becomes synonymous to 'strong'. Wide is unambiguous as it always implies a large range.


How to read cladograms/phylograms? I understand the difference between cladograms and phylograms; the latter can show the evolutionary linkage over time. However, I am having trouble finding out which two organisms are most closely related.

In the image above for example:

Referring to the cladogram, would these following statements be correct

-Bacteria 1 is least related to Eukaryote 4 (the furthest branch is always the least related as there common node is furthest away, correct?)

-The most related organisms are Bacteria 2 and 3, and Eukaryote 2 and 3

Referring to the phylogram

-Is Eukaryote 2 the least related to Bacteria 1 as its branch is the furthest away? Or is it Eukaryote 4 as it is the furthest away (bottom of list)?

-Is Eukaryote 1 most closely related to Eukaryote 3?

-Bacteria 1 is least related to Eukaryote 4 (the furthest branch is always the least related as there common node is furthest away, correct?)

In terms of relative relationships, eukaryote 4's least-related relative is Bacteria 1. Bacteria 1's least-related relative is the entire rest of the tree

  -The most related organisms are Bacteria 2 and 3, and Eukaryote 2 and 3

You cannot actually answer this question because a cladogram only shows relative relationships. To know which species pair is the most related (has the least total distance between them), you would need to know the branch lengths.

  -Is Eukaryote 2 the least related to Bacteria 1 as its branch is the furthest away?

To determine relationships, you want to look at the total branch length between two species. Therefore, this is correct

  Or is it Eukaryote 4 as it is the furthest away (bottom of list)?

Avoid this way of thinking. A phylogeny is not a 'list'. Pay no attention to the order the species labels appear: you only want to pay attention to how the species are connected. The same phylogenetic tree could be drawn differently, placing Eukaryote 3 at the bottom, for example.

  -Is Eukaryote 1 most closely related to Eukaryote 3?

Eukaryote 1's closest relative is Eukaryote 4: the distance from Eukaryote 1 to Eukaryote 4 is the shortest out of all possible pairs with Eukaryote 1.


Are there genetic similarity between humans and pigs that don't exist in chimps? Chimps are our closer relative.

Any genetic similarity between humans and chimps must exist on the common ancestor.

Pig branch out sooner. So, any genetic similarity between humans and pigs must be on common ancestor between humans and pigs. That must be on common ancestor between humans and chimps.

But chimps may evolve differently.

Hmmm... I am confused.

Actually is there any?

Yes there are!

I think it would make more intuitive sense to you if you would have switched the words chimps and humans in your question:

  Are there genetic similarity between chimps and pigs that don't exist in humans?

Then, you would directly answer, of course, there are genes concerning bipedalism, brain (FoxP2 for example), digestive track (adult production of lactase for example) and so, and so… which are different in humans but might not have much reasons to be so different between pigs and chimps. Those mutations occured on the human lineage after the split between human and chimps.

To answer your question:

  Are there genetic similarity between humans and pigs that don't exist in chimps?

Yes. Most of these difference are due to mutations that occurred in the chimps lineage after the split of the original lineage into human lineage and chimps lineage.

The following are improbable but would also allow to explain such similarities:

Genetic admixture or introgression between human and pig after humans and chimps lineages splitted.
Convergent evolution.

Maybe pigs and human got the same beneficial mutation that never appeared in the chimps lineages.
Maybe pigs and human, due to the fact that today live in cold climates evolved the sequence ATTCGCTGA which cause them to produce a more efficient shivering!


Do mosquitoes allow for DNA transfer between unrelated species? A mosquito can bite individuals of different species and eventually allow for some blood of one species to enter into the bloodstream of another species which I suppose may eventually cause DNA transfer, that is horizontal gene transfer

Do mosquitoes increase horizontal gene transfer among the species they parasitise? If yes, is it considerable or negligible?

In general foreign materials may be transferred from one organism to another in a mosquito, as is obviously the case with malaria, but for DNA to make it from inside the cells of one organism to inside the cells of another organism is exceedingly rare. In general DNAses and RNAses are present anywhere around living cells so when DNA is released it is quickly chewed up into useless fragments. Most likely this happens readily inside the digestive tract of a mosqito (Evolutionarily this makes sense as it would be extremely bad if a mosquito started absorbing genes from any of the organisms it was feeding off of!). Furthermore, DNA is an enormous charged molecule and does not easily pass through a cellular membrane. In a laboratory setting, DNA may be transferred into organisms with the help of electroporation or "gene guns" but this requires large amounts of identical genes to be effectively forced into cells, and even then, efficiencies of gene transfer are low. In short, no, it would be effectively impossible for a gene to be transferred from one organism to another by a mosquito. However, if a virus gets transferred by the mosquito...


Why Is Gray Matter Gray? When I researched I found  different reason for this, the  popular
ones are

1) white matter is mylinated .this reason was given in reference books and   this website

while others say

2)cell body concentration causes grayish appearance ,as in brain the cell body is concentrated outside. As mentioned in this .i.e cell body orientation.

also my teacher agrees with 2nd one, that the nissls granules contribute to the grayish appearance.orientation causes the effect of gray matter and white matter

I feel 1st reason to be more appropriate as there are billions of it couldn't be arranged as depicted in the second reason.

kindly help  me out to choose the accurate one, with appropriate reason of-course!

The terms gray and white matter relate to their color in gross specimens (i.e., not microscopic specimens) that have been formalin fixed. Nissl granules describe a microscopic structure, the rough endoplasmic reticulum, and aren't directly related to the color of gross specimens. Here's an example of a frontal cross section from a University of Utah slide set:

You'll see it's generally a tannish-yellow (at least on my monitor, this image is a pretty good representation of what it looks like in person), but there are lighter "white" parts in the white matter areas, and darker "gray" parts in the cortex.

A live, or a recently deceased and not formalin fixed brain has different qualities, including color and consistency.

The color of the formalin fixed tissue is an artifact of the process of fixing, so it's not necessarily accurate to describe the gray color as something inherent to the cells in the gray matter, but generally yes, the whiter color in the white matter of formalin fixed brain is because of the high lipid concentration. The grayer color of the gray matter is because of the lower lipid concentration. This lovely old JBC article from 1929 discusses some of these issues, mostly regarding white matter in response to staining after fixation, but also gray and white matter before staining.


How do researchers know that a species is at risk of extinction? Recently researchers present evidence that the platypus is at risk of extinction.

Source

How do researchers know that a species is at risk of extinction?  I mean Earth is so large, said species could be deep in the Pacific ocean or somewhere else that has been thoroughly explored.

The to assess the extinction risk of a species, Researchers first study the ecology and global populations of the species.

Then mathematical models are applied to  simulate the population dynamics and estimate extinction risk.

The results are collected in the IUCNs Red list.

https://www.iucnredlist.org/


Do Pthirus gorillae remain in gorilla leaf nests after gorillas migrate and abandon them? Gorillas build leaf nests to sleep in. Do the lice which parasitise gorillas, Pthirus gorilla, remain in gorilla leaf nests after gorillas migrate to new regions (and abandon the old nests)?

From the Wikipedia page on Pthirus gorillae: "Researchers theorize that humans acquired the parasite while butchering or scavenging on gorilla corpses, or sleeping in the abandoned sleeping nests of gorillas".

So yes, they are believed to remain.


Life on other planets first of all I'm not sure if I should post this here or in the astronomy stack. I think biologist are more likely to answer my question. To make it short:

Why when looking for any sort of life on other planets, we keep looking for similar conditions we call "life friendly", like nice temperature, oxygen level, pressure etc...

Is there some rule in biology that says life can only exists under these conditions? Why nobody supposes that evolution did not have enough time yet on our planet to generate other living mechanisms, and that on other planets even if the conditions are not suitable for us, there might be something well evolved through time there. After all if we can conceive electric robots that can survive to radioactivity and to high pressures and temperatures, why nature shouldn't be able to?

We might imagine living things that are very different from what we know. There is no conceptual reason for limiting life in its relation to water for example. Moreover, the definition of what is alive is really unclear. We classified more or less arbitrarily objects we know on earth as being living or not living but this does not give any clear definition of what is life and therefore it would not allow an exobiologist to even know what he's looking for!

But if you had to seek in billion of planets/natural satellite a living creature somewhere where what planets would start looking at? Probably those that look alike yours because you already know that life is possible the kind of conditions these planets offer. I think the answer is as easy as that.


Are humans hardwired to continue gathering resources after the costs outweigh the benefits? An animal will stop foraging in a berry bush if the perceived cost of searching for berries remaining is greater than the cost of finding another bush which isn't as picked over. People do the same thing on websites. We'll stay on a website searching for our information berry if we feel it costs less than jumping to another website bush.

If we had significant resources such that the cost of predatory/foraging behavior out-weighed the energy benefit from gaining more resources, would we stop? There seems to be a biological and cultural drive to keep getting more stuff. As people, could we ever reach a point where we're satisfied? The logic says yes, but common sense says we're hardwired to feel compelled to never stop gathering resources.

The answer to your question is very sensitive to the time frame you are interested in.  Assuming the costs and benefits you describe are referring to fitness (i.e., survival and reproduction), then the situation you are describing is one in which a particular behavior has lowered fitness (i.e., costs outweigh benefits).

There are several possible outcomes in this case.

Evolution. If the behavior is not plastic (i.e., it cannot change in a single individual), the there would be selection pressure against those individuals that exhibit the behavior.  If the behavior is heritable then evolution would cause a reduction in the frequency of the behavior over time.
Lowered Fitness. If you are not interested in evolutionary time scales but the behavior is not plastic, then the outcome would be no change in behavior but a reduction in the survival and reproduction success of individuals with the behavior.
Change in Behavior. If the behavior is plastic (i.e., it can be changed by a single human) and the current situation provides the appropriate information about the state of the behavior, then the behavior will change.  The key here (as with optimal foraging models) is that the appropriate cues have to be present to change the behavior.  Often organisms use proxy cues to trigger behavioral shifts.  For example certain caterpillars use day length to trigger shifts in developmental pathways (diapause vs pupation) when what really matters is temperature.

So the real answer to your question lies in the further questions of whether consumption is plastic (or hardwired as you say) and if it is, whether a situation provides the appropriate cues to indicate that we have acquired enough resources.  Those are rather complex questions that, as far as I know have not been answered definitively in the general sense that your question implies.


What does 'kinetically accessible' mean in protein folding? The hydrophobic collapse model discusses this term in the energetics section. What does this actually mean?

At some point during protein folding, there may exist lower energy states from a thermodynamic perspective (lower ΔG free enegy) which are actually unreachable in a given environment, because the required activation energy is too high. These are kinetically inaccessible states, conversely accessible state are those that can be reached.

For example, that could mean a protein could reach a lower energy state by unfolding a bit, but exposing hydrophobic amino acid even temporarily would require too much energy. So the lower energy state is not kinetically accessible.

This is somewhat similar to the concept of kinetic and thermodynamic reaction products in chemistry.


R Stringdb bioconductor I 'm using STRINGdb package from biconductor to manipulate String database of ppi
I'm newbie and I don't find the documentation of the package useful for me .
I wanna extract the associated network of cancer fo example ,
I tried to used this function s <- string_db$get_term_proteins(terms_id,string_ids =NULL , enableIEA =TRUE )
and I don't know  what that terms_id attribute stand for .

second , is there a simpler way to get the full network using R interface  given in the url as an example

https://string-db.org/cgi/network.pl?taskId=2hQuabKoXe02

The terms_id is meant to be a vector of GO or KEGG IDs that annotate to the proteins of interest. As it's described, the method get_term_protein:

  Returns the proteins annotated to belong to a given term.

My substantiation in part comes from the vignettes for STRINGdb that use terms in a separate set of functions like so:

>head(enrichmentGO, n=7)
term_id proteins hits pvalue pvalue_fdr
1 GO:0048545 383 15 2.337593e-07 0.000368020
2 GO:0006952 1286 28 3.806997e-07 0.000368020
3 GO:0002252 405 15 4.756829e-07 0.000368020
4 GO:0010466 234 11 1.767763e-06 0.001025745
5 GO:0045861 330 12 8.407161e-06 0.003765892
6 GO:0010951 228 10 9.735179e-06 0.003765892
7 GO:0002443 141 8 1.224368e-05 0.003839606
term_description
1 response to steroid hormone
2 defense response
3 immune effector process
4 negative regulation of peptidase activity
5 negative regulation of proteolysis
6 negative regulation of endopeptidase activity
7 leukocyte mediated immunity
>head(enrichmentKEGG, n=7)
term_id proteins hits pvalue pvalue_fdr
1 04115 66 6 9.969204e-08 1.475442e-05
2 04610 68 5 3.577966e-06 2.647695e-04
3 05168 174 5 3.254067e-04 1.605340e-02
4 01100 1161 12 5.277721e-04 1.952757e-02
5 04380 123 4 8.399948e-04 2.486385e-02
6 00590 61 3 1.197959e-03 2.638087e-02
7 05161 139 4 1.322517e-03 2.638087e-02
term_description
1 p53 signaling pathway
2 Complement and coagulation cascades
3 Herpes simplex infection
4 Metabolic pathways
5 Osteoclast differentiation
6 Arachidonic acid metabolism
7 Hepatitis B

And so usage would follow, for example, I want proteins that associate with cell growth, I can use c("GO:0016049") as my terms_id to retrieve that list.

library(STRINGdb) #load package

string_db <- STRINGdb$new(version="10", species=9606, score_threshold=0, input_directory="") #set environment, 9606=human

string_db$get_term_proteins(c("GO:0016049")) #use new environment variable to query the database, 0016049 refers to cell cycle just as an example.

Output (annotation column w/ text descriptions removed for brevity):

               STRING_id    term_id preferred_name protein_size
1   9606.ENSP00000002829 GO:0016049         SEMA3F          785
2   9606.ENSP00000211998 GO:0016049            VCL         1134
3   9606.ENSP00000212355 GO:0016049         TGFBR3          851
4   9606.ENSP00000216037 GO:0016049           XBP1          261
5   9606.ENSP00000216911 GO:0016049          AURKA          403
6   9606.ENSP00000221930 GO:0016049          TGFB1          390
7   9606.ENSP00000225792 GO:0016049           DDX5          614
8   9606.ENSP00000230732 GO:0016049         POU4F3          338
9   9606.ENSP00000238682 GO:0016049          TGFB3          412
10  9606.ENSP00000239462 GO:0016049            TNN         1299
11  9606.ENSP00000245479 GO:0016049           SOX9          509
12  9606.ENSP00000255448 GO:0016049          DCLK1          729
13  9606.ENSP00000256951 GO:0016049           EMP1          157
14  9606.ENSP00000258106 GO:0016049           EMX1          290
15  9606.ENSP00000258743 GO:0016049            IL6          212
16  9606.ENSP00000261023 GO:0016049          ITGAV         1048
17  9606.ENSP00000261918 GO:0016049         SEMA7A          666
18  9606.ENSP00000262017 GO:0016049          ITGB3          788
19  9606.ENSP00000263713 GO:0016049        EPB41L5          733
20  9606.ENSP00000263980 GO:0016049         SLC9A1          815
21  9606.ENSP00000264057 GO:0016049           DGKD         1214
22  9606.ENSP00000264279 GO:0016049          NOP58          529
23  9606.ENSP00000265136 GO:0016049           COBL         1261
24  9606.ENSP00000265362 GO:0016049         SEMA3A          771
25  9606.ENSP00000265371 GO:0016049           NRP1          923
26  9606.ENSP00000266058 GO:0016049          SLIT1         1534
27  9606.ENSP00000268182 GO:0016049         IQGAP1         1657
28  9606.ENSP00000270221 GO:0016049           EMP3          163
29  9606.ENSP00000272134 GO:0016049         LEFTY1          366
30  9606.ENSP00000276416 GO:0016049           BIN3          253
31  9606.ENSP00000278671 GO:0016049        LAMTOR1          161
32  9606.ENSP00000281321 GO:0016049         POU4F2          409
33  9606.ENSP00000283027 GO:0016049          NUBP1          320
34  9606.ENSP00000284981 GO:0016049            APP          770
35  9606.ENSP00000296388 GO:0016049         LEPRE1          736
36  9606.ENSP00000296755 GO:0016049          MAP1B         2468
37  9606.ENSP00000296875 GO:0016049           GDF9          454
38  9606.ENSP00000301067 GO:0016049           MLL2         5537
39  9606.ENSP00000303351 GO:0016049          ITGB1          798
40  9606.ENSP00000305133 GO:0016049          SOCS5          536
41  9606.ENSP00000306157 GO:0016049           IL7R          459
42  9606.ENSP00000306662 GO:0016049         ADRA1B          520
43  9606.ENSP00000307156 GO:0016049          LAMB2         1798
44  9606.ENSP00000307272 GO:0016049          RPTOR         1335
45  9606.ENSP00000316357 GO:0016049          USP9X         2570
46  9606.ENSP00000316543 GO:0016049          RAPH1         1250
47  9606.ENSP00000317257 GO:0016049          CPNE1          542
48  9606.ENSP00000322957 GO:0016049           PAK7          719
49  9606.ENSP00000324549 GO:0016049         CYFIP1         1253
50  9606.ENSP00000324560 GO:0016049           ULK1         1050
51  9606.ENSP00000324856 GO:0016049          STK11          433
52  9606.ENSP00000329623 GO:0016049           BCL2          239
53  9606.ENSP00000330382 GO:0016049          PDGFB          241
54  9606.ENSP00000332643 GO:0016049            NDN          321
55  9606.ENSP00000333982 GO:0016049          NDEL1          345
56  9606.ENSP00000334458 GO:0016049          GATA4          442
57  9606.ENSP00000335246 GO:0016049         ENTPD5          428
58  9606.ENSP00000337146 GO:0016049          ENOX2          610
59  9606.ENSP00000337332 GO:0016049          SIRT6          355
60  9606.ENSP00000337697 GO:0016049            DCX          441
61  9606.ENSP00000339740 GO:0016049         CAMK2D          499
62  9606.ENSP00000340820 GO:0016049           MAPT          776
63  9606.ENSP00000341940 GO:0016049           CAV3          151
64  9606.ENSP00000347906 GO:0016049          PRMT2          433
65  9606.ENSP00000348769 GO:0016049          ARIH2          493
66  9606.ENSP00000351049 GO:0016049           PAK4          591
67  9606.ENSP00000351591 GO:0016049          NLGN3          848
68  9606.ENSP00000351905 GO:0016049         TGFBR2          592
69  9606.ENSP00000353362 GO:0016049        CACNA1A         2506
70  9606.ENSP00000353582 GO:0016049           NRP2          931
71  9606.ENSP00000354558 GO:0016049           MTOR         2549
72  9606.ENSP00000354829 GO:0016049          SGMS1          413
73  9606.ENSP00000354877 GO:0016049           ULK2         1036
74  9606.ENSP00000355627 GO:0016049            AGT          485
75  9606.ENSP00000355785 GO:0016049         LEFTY2          366
76  9606.ENSP00000355896 GO:0016049          TGFB2          442
77  9606.ENSP00000357288 GO:0016049        LAMTOR2          125
78  9606.ENSP00000357470 GO:0016049           IL6R          468
79  9606.ENSP00000357494 GO:0016049           ROS1         2347
80  9606.ENSP00000359095 GO:0016049          PRMT6          375
81  9606.ENSP00000359729 GO:0016049         SLC9A6          701
82  9606.ENSP00000360973 GO:0016049          AGTR2          363
83  9606.ENSP00000360988 GO:0016049          LUZP4          313
84  9606.ENSP00000361423 GO:0016049           ABL1         1149
85  9606.ENSP00000362092 GO:0016049          RRAGC          399
86  9606.ENSP00000362717 GO:0016049           LHX2          406
87  9606.ENSP00000363822 GO:0016049             AR          920
88  9606.ENSP00000365663 GO:0016049           NPPA          151
89  9606.ENSP00000366396 GO:0016049           XRN2          950
90  9606.ENSP00000367123 GO:0016049         SLC3A2          631
91  9606.ENSP00000367830 GO:0016049          PRKCZ          592
92  9606.ENSP00000368030 GO:0016049         ATAD3A          634
93  9606.ENSP00000368169 GO:0016049           DVL1          670
94  9606.ENSP00000368683 GO:0016049           EDN1          212
95  9606.ENSP00000369014 GO:0016049           NDNF          568
96  9606.ENSP00000369816 GO:0016049           SHBG          402
97  9606.ENSP00000369960 GO:0016049         ADRA1A          475
98  9606.ENSP00000370330 GO:0016049        ERBB2IP         1371
99  9606.ENSP00000376800 GO:0016049           MTPN          118
100 9606.ENSP00000377823 GO:0016049          NDRG4          391
101 9606.ENSP00000377947 GO:0016049           RARG          454
102 9606.ENSP00000378306 GO:0016049         PPP3CB          525
103 9606.ENSP00000379003 GO:0016049          NUPR1          100
104 9606.ENSP00000385610 GO:0016049          MEX3C          659
105 9606.ENSP00000395359 GO:0016049          CADM1          442
106 9606.ENSP00000411672 GO:0016049       ATP6V0E2          213
107 9606.ENSP00000414303 GO:0016049           BDNF          329
108 9606.ENSP00000419782 GO:0016049           CDK5          292
109 9606.ENSP00000422591 GO:0016049          SLIT2         1529
110 9606.ENSP00000427941 GO:0016049       ATP6V0E1           81
111 9606.ENSP00000430333 GO:0016049          SLIT3         1523
112 9606.ENSP00000465742 GO:0016049        RASGRP4          673


regarding evolution of ears and sense organs How could we(or any other organism) have developed ears through evolution when before having ears we did not know that sound waves existed or there was anything such as hearing? How did the first hearing organ develop? The same can be asked for the other sense organs as well.

When you are asking about the evolution of organs, you are already five steps ahead of yourself. To have sensory organs, you need cells that react to some stimulus:

Hearing, Touch: Mechanical stimulus
Smell, some pain: Chemical stimulus
Sight: Optic stimulus
Other (non-human) organisms can also sense electric fields, magnetic fields, ...

As soon as you have those, having 'organs' that house a lot of those cells surrounded by tissues that aid in the reception of these stimuli, is relatively trivial.

But isn't a sensory cell totally complicated? It is. But: A simple neuron already is a sensory cell of sorts: It reacts to electrical and chemical imbalances.

But isn't then a neuron totally comlicated? It is. But: A simple non-neuronal cell already has a lot of the intricate machinery that a neuron does - a neuron mostly has some special parts and structures that make it a neuron. A simple cell also does react to chemical and other stimuli (this is why hormones work, and how little one-celled animals can orient themselves towards the light or food, or away from dangerous chemicals)

But isn't a run-of-the-mill cell totally complicated? It is. But it actually is just the workings of several archaic cells crammed into one (one of the more popular theories on Eukaryote evolution has them result from a very intense partnership of several more basic cells). And those archaic cells can also react to stimuli (they manage their metabolism according to the available food, for instance)

But isn't a basic cell totally complicated? It is. But is actually is just the interaction of several molecules that have some very interesting properties - DNA/RNA can function as an information storage, but are at the same time tools that can cowork with other DNA/RNA, and also interfaces/interferes with proteins in interesting ways.

But aren't big molecules totally complicated? They are. We still need supercomputers to reliably model all of the intricacies of any given Protein-Protein or Protein-RNA interaction. Many proteins behave differently in different environments (electromagnetic field strengths, chemical environment, temperature and mechanical factors (e.g. ultrasound)) - they could be said to 'react' to certain triggers. But they are actually just chains of repetitive elements (so called polymers of so called monomers).

But aren't those monomers totally complicated? Some are, but here we slowly get into the realm of 'mostly modellable on a hefty home computer'.

So we have systems of systems of systems... All of them very complicated.

But evolution is not a process that involves understanding ot planning. It is simply the result of coincidences and inheritance. You can see colors that many animals cannnot. You have the requisite molecules in your sensory cells in your eyes. Some people can see more colors than you, an inheritable trait. Some people can see less colors. Currently those people have no evolutionary profit from this - they reproduce and die with the same probability as the rest of us. Likewise there are a million (possibly billion?) such traits in every human. Traits that are different from the rest. Little things. Ineffective things (= having no net effect). But there might come a time where seeing one color or not seeing it (= not being distracted by it) will give a continuous net positive or net negative effect on the reproduction of those people carrying that trait. That is the time when that trait will start to  be present in a larger piece of the population (over many generations). The people carrying that trait will also be different from one another. And the ones carrying the traits with the most positive net effect will multiply the most, etc. Humans in some distant future then can eye-sense some X-factor we cannot even describe currently (try describing different colors to a blind person) and thus have, say, Xeyes.


Is infrared photosynthesis possible? The post-apocalyptic science fiction novel Dark Universe by Daniel F. Galouye has some plants living inside bunkers that use infrared light for photosynthesis. There are speculations that extraterrestrial plants might use the same trick on planets orbiting red dwarfs and that their leaves would be totally black. Would this type of photosynthesis be possible and are there any plants on low-light environments from Earth that might do this already?

I would hardly ever say never where biology is concerned.  In this case that utilizing red rather than blue light for a plant would require many of the basic assumptions of photosynthesis in terrestrial plants to be revised, but since we're talking about another planet, that might not really be an issue.

If we are asking only about how we could change our plants to work with IR light, I'd say that might take a few hundred million years of selection and its harder to imagine.

Firstly photosynthesis in another planet doesn't have to fix carbon or produce oxygen - both of these chemical processes utilize the relatively greater energy produced in blue and red light photosynthesis we see in plants here.

Secondly using IR would have its particular questions associated with it.  In this case the energy quanta are very small and in fact in the same range as chemical bond vibrational energies.  Such energy might be hard to capture with any efficiency since simple heat would tend to compete with the photon, so this would work better if the entire system were at a relatively low temperature.

The leaves could be black or they could be completely clear by the way.


Why are we able to differentiate between colored objects without the presence of light? Rods help us to see during the dark.

We can see colour of the object when it reflects light.

But in a dark room(room of any color but the light is switched off and it is night),we still can differentiate between colored objects if we open our eyes for sometime.(although not very much clearly)

How the colors are seen when there is no light?

Do we see as the brain remembers their colour?

You seem to have many misconceptions about how we see and how that relates to light. I'll address them one sentence at a time:

  Why are we able to differentiate between colored objects without the presence of light?

Answer: the premise of the question is wrong: we aren't able to differentiate between colors without the presence of light, because we aren't able to see without the presence of light. Light is what allows us to see. "Seeing" is the act of detecting the light coming from the environment and using it to derive what the environment is like.

  Rods help us to see during the dark.

It sounds a bit like you think rods help us to see during the dark... without light ? This is not the case: BOTH rods and cones absorb light and thus allow us to see. Rods help us see in low light because they are more sensitive (to light !) than cones. Nothing can help us see with no light.

  We can see colour of the object when it reflects light.

It depends on how much light it reflects ! The correct form of that sentence is "We can see the object when it reflects light". (even more correct would be "when it reflects enough light to trigger the light receptors in our eyes, i.e. rods and cones). Whether we can see its colour depends on whether it reflects enough light to trigger the cones specifically.

  But in a dark room(room of any color but the light is switched off and it is night),we still can differentiate between colored objects if we open our eyes for sometime.(although not very much clearly)

Indeed; this is because no room is completely dark. Even more so in our artificially lit world, but even in a moonless cloudy night you may have a few errant photons coming from the stars and Sun (via diffusion in the atmosphere), fireflies, what have you; to be fair in our artificially lit world I haven't experienced it. As far as I know you can get true pitch darkness in things like underground caves (once you're far enough from an exit of course).

Basically, if you can see anything then there is some light. (well, short of your optical cortex confabulating stuff, which in fairness it will do).

  How the colors are seen when there is no light?

As I hope you understand now, they aren't.

  Do we see as the brain remembers their colour?

I think that may actually be one reason we perceive colour in low-light environments. I'm sure some of it is that there's enough light to trigger the cones a little bit, but I wouldn't underestimate our brain's ability to show us the world as it knows it is as opposed to as whatever information it's receiving right this second says it looks like.

EDIT

Some references :

The state of seeing things in such low light that we only use the rods is called "scotopic vision" :
https://en.wikipedia.org/wiki/Scotopic_vision

Some sources for how "dark" environments still contain low amounts of light (one word for "amount of light" being "illuminance", measured in Lux) :
http://www.engineeringtoolbox.com/light-level-rooms-d_708.html
https://en.wikipedia.org/wiki/Aphotic_zone (thank you to @Johnny for that one)

HOPEFULLY LAST EDIT

On reflection I thought I'd say some more about scotopic vision since it's very relevant to the question. It turns out "scotopic" vision is opposed to "photopic" vision (the vision we have in full lighting, where the cones do the work because the rods are saturated), and in between there is an intermediate range called "mesopic" vision, which is likely the kind of vision we experience when it's dark but we still see color (this is ignoring our brain filling in colors, which could also be a factor and in that case could also happen with scotopic vision - but I didn't find any sources on that).

Mesopic vision is used under lighting conditions that seem to range from low indoor lighting or streetlights to starlight; scotopic vision is used with luminances darker than that. This page is all about it and includes a very nice drawing, sadly it's a pdf so I can't show it in the answer:

http://www.visual-3d.com/Education/LightingLessons/Documents/PhotopicScotopiclumens_4%20_2_.pdf