Can a second mass extinction by microbes happen? Science Daily reports that the mass extinction at the end of Permian period happened by the Methanosarcina archaea wiping out 90% of species:

Methane-producing microbes may be responsible for the largest mass extinction in Earth's history. Fossil remains show that sometime around 252 million years ago, about 90 percent of all species on Earth were suddenly wiped out […]. It turns out that Methanosarcina had acquired a particularly fast means of making methane, and the team's detailed mapping of the organism's history now shows that this transfer happened at about the time of the end-Permian extinction.

Is it possible by the global warming and all the spores of bacteria come out from melting glacier or anywhere else and mass extinction occur?

First of all, let’s consider your Methanosarcina scenario in specific.
Methanosarcina with those properties are still around. So, there is no reason to expect that introducing some ancient Methanosarcina into a suitable environment today would do very much – as they should already be there. Any existing (large-scale) environment providing a niche for Methanosarcina should already be occupied by it as it only needs a single organism to get there by chance at some point.
Moreover, there must be some reason why our atmosphere stopped being filled with methane by Methanosarcina.
For example some prerequisite resource could have been depleted, some other organism evolved that consumes this methane or controls the Methanosarcina population by feeding on it.
Whatever this reason is, we should expect that it still applies: A required resource would still be gone and a second organism controlling this activity should still be around (or resurface together with the Methanosarcina in question).
In fact, the hypothesis you mention maintains that the nickel required by Methanosarcina to produce methane was available in huge amounts due to specific volcanic activity at that time.
Finally, the current ice masses of the Earth are much younger and have not been around since the Permian period.
In general, if geologically cryostoring microbes were relevant, climate change should be the least of our worries as drilling a hole into the ice or local geologic activity could suffice to bring back a few individuals – which is all that would be needed.
Now, what about unfreezing microbes in general?
Due to lack of fossils, we have little knowledge about microbe extinction, except that it does happen.
However, my ecological intuition is that microbes either lose their niche to a fitter alternative (which either be more apt at causing problems or avoid them resurfacing) or survive in small amounts (ready to occupy their niche if it should resurface).
Microbes are considerably different from higher, sexually reproducing life forms here as it only needs a single individual to revive the species and individuals can survive for a long time in adverse conditions, not only by sporulation but also because they need little energy to maintain their state.
Finally, if a niche for disastrous microbes exists, there is the constant risk that it will be filled by some ordinary microbes evolving, which brings us to the next point.
Something that is conceivable to happen is that some microbes spontaneously evolve to fill a big niche and have some disastrous by product leading to a mass extinction.
It is hard to estimate this risk, but as far as I know, there is no historic precedent after the evolution of higher life forms.
(As elaborated above, the Methanosarcina hypothesis for the Permian extinction features additional factors.)
However, I consider it unlikely that climate change increases this risk.
While climate change undoubtedly has disastrous ecological consequences, tilting individual ecosystems, I don’t see how it creates some fundamentally new environment (that wasn’t already there in similar form somewhere else on the planet) that would stimulate a spontaneous disastrous microbial evolution.


Why do I have two kinds of pubic hair? I feel silly even asking this question, but there's a quirk of my anatomy that I find interesting, and I can find nothing about it online.  I am looking for information on whether this quirk is documented, and whether it has any biological role.

I am a Caucasian male, and my quirk is that I have two different kinds of pubic hair.  On my genitals and immediately above, I have a dark wiry kind of hair like that which I find under my armpits and on my chest.  Above this, there is a second bundle of hair which is fairer (similar color to the hair on my head) and curlier.  The color difference between the two hair types is marked.  There is also a small amount of hair continuing up to my navel, which appears to be of the first type (same as chest, armpits, and genitals).

So my questions are:

Is this a common feature?
If not, is it documented at all?
Does it serve a biological purpose?

My reason for asking 3, in particular, is that I've heard multiple explanations for the existence of pubic hair.  One theory is that it indicates sexual maturity.  Another is that it is related to hygiene.  My anatomy seems to suggest both might be true: Hair under armpits is presumably for some practical purpose, like wicking sweat out of an otherwise dank crevice, and the hair on the genitals would appear to have the same effect.  On the contrary, colored hair like that on the head is presumably a secondary sexual characteristic, and the fact that I have a bunch of colored pubic hair above my genitals (where there is no apparent practical purpose, as with the hair below) would seem to serve the same purpose.

Relatively interesting evolution question --- hypothesis regarding reasons for certain evolutionary traits can be debated (this particular question, scientists seem to have many theories). However, here is one possible explanation:

Pubic hair near the sexual organs is likely for hygiene function; especially for women infections from parasites were common in those areas. The hair would act as a protection barrier, and hence the different texture of that hair being a little thicker.
Pubic hair in arm pit regions may keep pheromones, or chemicals your body produces that send subconscious messages to other humans. Often, these chemicals are released from sweat, and hence it would make sense to have hair in those regions to trap them there. The texture of the hair in those regions probably evolved to be more effective in keeping oder.

https://www.self.com/story/why-you-have-pubic-hair
https://blogs.scientificamerican.com/bering-in-mind/a-bushel-of-facts-about-the-uniqueness-of-human-pubic-hair/


What is the expected amount of DNA shared by first cousins and the people between them in a family tree? What is the expected amount of DNA that is shared by all of the people between first cousins, including the first cousins, in a family tree?

To simplify your problem, let's just consider autosomal DNA. In this case,  your expected amount of shared DNA should be synonymous with genetic consanguinity, which can be conveniently checked from this image.
Thus, you share approximately 1/8 of DNA(I know saying so is not scientifically strict as there are recombinations and mutations that prevent the DNA to be exactly the same.) with your first cousins. Same is true between first cousins.
Source: Wikipedia image gallery.


What happens when the congenitally blind brain receives visual input? If a congenital blind person gets eye sight (either hypothetically, or in the near future due to advancements in technology), will their brain be able to handle that information, or will it become overloaded?

Short answer
Congenitally blind people can regain visual function at a later age.  However, the longer they were blind for, the lesser their visual function will be and the longer it takes for them to rehabilitate. Immediately after receiving first eye sight, the visual experience of congenitally blind people is not comparable to that of normally sighted people. They may need months of rehabilitation training to make sense of their newly acquired sight, especially when they were blind for many years.

Background
There are various treatments for blindness to date. Since you mention technology in the question, visual prosthetics come to mind. Visual prosthetics already exist, and there are at the time of this writing two retinal implant systems commercially available; the Argus II and the alpha-IMS (Stronks et al., 2014). Retinal implants are used to provide a crude form of vision to those with severe retinal degenerations, such as end-stage retinitis pigmentosa. However, visual prosthesis technology is still in its infancy and at the time of this writing, only people that lost their vision later in life are implanted. So there is as yet no data available on your question whether congenitally blinded people can benefit from it.

However, from a related technology, cochlear prostheses, we know that the earlier a congenitally deaf person is implanted, the better the result is. Early-implanted folks can learn to understand speech, and develop speech relatively normally. Nowadays infants as young as 3 months receive cochlear implants. Early implantation is critical, because the brain is plastic. When the auditory cortex is not used due to sensory deprivation, it will quickly be taken over by other cortical areas. Once this cortical recruitment progresses for too long, a person can never gain functional hearing at the level reached by early-implanted people (Teoh et al., 2012).

Very likely the same holds for visual prosthetics. A congenitally blind person should be implanted as soon as possible after birth. This, because it is known that cross-modal plasticity results in the visual cortex being recruited for tactile and auditory processing. As with the auditory system, once this restructuring progresses long enough, my educated guess is that a person will never be able to develop functional vision comparable to an early implanted subject. And this is the reason why at present, only the acquired blind receive retinal implants.

For example, a case report of a subject who was blind for over 50 years regained his eye sight after corneal surgery. Although the subject did develop visual function after the surgery, visual performance remained greatly compromised. This was particularly evident when the tasks targeted finer levels of perceptual processing Siki et al., 2013).

Important clues are being obtained in the "Project Prakash", an ambitious project to provide opthalmological support to the people in poor, rural parts of India. Routine cataract surgeries have been performed in people with cataracts, including in people with congenitally present cataracts, where the lenses in the eyes were opaque from birth. Older kids, like teenagers, that were blind from birth typically show non-functional vision after the bandages are removed after surgery. It is thought that these first moments for the newly sighted are blurry, incoherent, and saturated by brightness, akin to swirls of colors that do not make sense as shapes or faces or any kind of object. However, after months of rehabilitation, they do develop functional vision. The lower-level markers of visual function never reach normal values. Specifically, they continue to suffer from poor visual acuity - the gold standard to assess visual function. Nonetheless, some higher-order aspects of vision do seem to be improving. Within a week to a few months after surgery, the children can match felt objects to their visual counterparts (source: The New Yorker, August 28, 2014).

References
- Siki et al., Iperception (2013); 4(8): 498–507.
- Stronks et al., Expert Rev Med Devices (2014); 11(1):23-30
- Teoh et al., Laryngoscope (2004); 114(9): 1536–40


Introductory books about evolution This days I read some debates on evolution. That made me more interested to read something reliable on topic - I mean books.

I'm christian - although I think it doesn't matter on that topic - and I would like to read a book that presents all weaknesses and strengths (as much as possible) of evolution. I want that not to be presented as a debate on creationism, but to be a book on evolution theory explanation and presentation.

I also would appreciate if you know to give some details about the author that wrote the recommended book. I mean if he/she is atheist or a christian or a skeptic.

You won't find a good book that presents the 'weaknesses' of the theory of evolution, and for good reason. There has to date been no convincing challenge to the theory, whilst it has been supported by experimental and circumstantial evidence as well as clear logic over and over and over again, as well as actually being observed taking place numerous times. The closest to what looking for is a book which presents our best understanding of how evolution works, or which discusses competing ideas about how evolution works - there's no question about whether it works.

The Selfish Gene by Richard Dawkins, whilst it contains some errors, has some very clear thinking about evolution in it, and in particular explains why group selection is a misguided idea.

The Logic of Chance: The Nature and Origin of Biological Evolution by Eugene Koonin is a more up-to-date coverage of our current understanding of evolution, in particular with insights from modern genomics.

There are plenty of terrible books about the weaknesses of evolution, but they are deeply flawed. Pick one and I'll be happy to debunk it for you.


Why can't the human eye focus blue light? I recently noticed that it is hard to focus on blue light sources, especially at night. When observing a blue light source, e.g. a neon sign, it looks somewhat blurry. A sign with a different colour right beside it looks sharp.

I already know about the three kinds of cone cells in the human eye (I'm not a biologist) with their spectral sensitivity peaks in in short (S, 420–440 nm), middle (M, 530–540 nm), and long (L, 560–580 nm) light wavelengths [1]. But does the spectral sensitivity correlate with focus? Or does our eye lens refract blue light in a different way?

When I screw up my eyes looking at a blue light, it becomes less blurry, but then all the other colours are blurred.

[1] http://en.wikipedia.org/wiki/Cone_cell#/media/File:Cones_SMJ2_E.svg

The same thing happens in photography when you see an image with colorful shadows of objects on it - this is called chromatic aberration. Check this wiki page if you're not familiar with. Now this happens because the lens in the objective has different refractive properties for different wavelengths or if go the other way around different wavelengths refract differently within the same material. This is why the famous triangular rainbow prism is capable of separating the sunlight to rainbow. So back to the question: in our eye there is the eye lens that is responsible for focusing. Let's assume that it is homogenous enough. So when light enters into our lens it refracts to separate colours and our lens is not complex enough to fully compensate for this. The second picture is a good approximation of the human eye lens in shape.

Edit: so when you focus one color perfectly the others will be blurry a bit since those will be out of focus due to different refraction.

taken from: http://commons.wikimedia.org/wiki/File:Prism-rainbow-black.svg

taken from:http://en.wikipedia.org/wiki/Chromatic_aberration#/media/File:Chromatic_aberration_lens_diagram.svg


What is the name of the category of viruses that affect only one side of the body? The Varicella zoster virus causes chickenpox in children and shingles in adults.
When the virus attacks as shingles, one of its distinguishing characteristics is that it only affects one side of the body. (As shown in the link and verbally identified by a doctor I spoke to). This happens because the nerve cells themselves are infected - and are partitioned on different sides of the body.

At first the rash appears similar to the first appearance of hives;
however, unlike hives, shingles causes skin changes limited to a
dermatome, normally resulting in a stripe or belt-like pattern that is
limited to one side of the body and does not cross the midline.[13]
Zoster sine herpete ("zoster without herpes") describes a person who
has all of the symptoms of shingles except this characteristic
rash.[16]
 From Wikipedia

My question is: What is the name of the category of viruses that affect only one side of the body?

Short answer: Viruses that affect only one side of the body are not categorized by this information.

Long Answer: For people who likes details

Several types of virus classification exists:

Baltimore: Classified by the type of DNA or RNA that is carried by the virus
Holmes: Classified by the target organisms of the viruses (plants, bacteria, animals)
LHT: Classified using several physical differences (More specific and complex)

For example, Shingles would be classified as:

Baltimore: Group I (double DNA stranded viruses)

Holmes: Group III Zoophaginae (animals)

LHT:

Order: Herpesvirales
Family: Herpesviridae
Subfamily: Alphaherpesvirinae
Genus: Varicellovirus
Specie: Human herpesvirus 3 (HHV-3)


How do dopamine agonists like amphetamine/methylphenidate affect acetylcholine signalling? Do they increase it, or is the effect mostly neutral?

Amphetamine and methylphenidate are not (direct) dopamine agonists.

Dopamine agonists are the substances that would specifically bind to dopamine receptors and activate them, thereby mimicking the effects of dopamine release.

Amphetamine/methylphenidate are so-called indirect sympatomimetics. This means that they stimulate the simpatyc nervous systems (with neurotransmitters noradrenaline and dopamine in CNS), but in indirect way: they don't bind to the receptors. Rather, they promote the massive neurotransmitter release from the presynaptic part. The released transmitter (DA, NA) then just diffuses to the postsynaptic membrane and binds to its own receptors.

There are some works done on investigating the effect of these substances on parasympatic system with acetylcholine as neurotransmitter.

Sympatomimetics like amphetamine generally lead to increase of acetylcholine release throurout the nervous system: in hippocampus and caudate nucleus, nucleus accumbens and generally in forebrain and cortex.

This effect of amphetamine is indeed in many cases mediated through dopamine receptors. Same time some direct dopamine receptor agonists were found to supress ACh release in some brain regions.


In vitro enzyme production I need to express a protein in vitro but I don't know where to start.  I will likely do a  T7 transcription protocol but for translation I am not sure what to do.  Are there any good kits?

New England Biolabs, which has an excellent reputation for well-tested, well-documented, and robust products, has a line of protein expression and purification products that I'd definitely take a look at. I've used the pMAL system for expression of fusion proteins in E. coli, and the PURExpress system looks just like what you're looking for. I have a personal (but not financial) connection with them, and I can vouch for their quality and technical support.

Pierce/Thermo is generally a good place to look when dealing with protein stuff. I've had good results with lots of their stuff, but I haven't done in vitro expression in ages, so I can't remember what I used. (BTW, I have no connection with them, I just tend to like their products.)

As Alan Boyd mentioned, lots of companies like Life Technologies, Promega, Qiagen, and Sigma have in vitro expression kits. Which one you pick will ultimately be influenced by what exactly you need your protein to do, the desired scale of expression, the type of tag(s) you want to put on it, what equipment and expertise you have in your lab, and how much time and money you want to invest.


What species of ant is this, and is it a queen? I found her underneath a big rock along with a bunch of much smaller Lasius niger workers, so
I suspect it might be a queen. I know Lasius niger doesn't have soldiers, so what could it have been doing there if it wasn't their queen? Also, sorry for the bad picture quality, I couldn't find a better camera, and also don't have a proper magnifying glass.

Country: Belgium

Environment: forest

Location: underneath big rock

Behaviour: calm when walking in lighted up areas

Species it was found with: Lasius niger workers running around frantically (note: this specimen was much bigger than the workers)

This ant looks very much like a Camponotus pennsylvanicus queen, but since it was found in a Belgian forest, I could be wrong. I am almost certain it is a Camponotus species though. I hope I could have been helpful to you!


Why is hydrofluoric acid so dangerous if it is a weak acid? I've read that hydrofluoric acid (HF) is extremely dangerous to touch, but what exactly makes it so toxic? It's weak acid ($K_a = 7.2 \times 10^{–4}$) and dissociates approximately 1/1000 as much as Hydrochloric acid does in water, so why is it so much more dangerous? Wouldn't a stronger acid cause more damage? What exactly happens when human skin comes into contact with Hydrofluoric acid that causes it to be so lethal?

The confusion arises from the term weak, which has only to be interpreted in chemical terms.

Weak acid, as you say, just means that the acid does not readily dissociate, not that its effects are weak! Just to say one, HF corrodes glass, something that not even smoking HCl does.

Wikipedia has a nice summary of HF toxicity (see also the references in the article itself):

  Hydrofluoric acid is a highly corrosive liquid and is a contact poison. It should be handled with extreme care, beyond that accorded to other mineral acids. Owing to its low dissociation constant, HF as a neutral lipid-soluble molecule penetrates tissue more rapidly than typical mineral acids. Because of the ability of hydrofluoric acid to penetrate tissue, poisoning can occur readily through exposure of skin or eyes, or when inhaled or swallowed. Symptoms of exposure to hydrofluoric acid may not be immediately evident. HF interferes with nerve function, meaning that burns may not initially be painful. Accidental exposures can go unnoticed, delaying treatment and increasing the extent and seriousness of the injury.
  Once absorbed into blood through the skin, it reacts with blood calcium and may cause cardiac arrest. Burns with areas larger than 25 square inches (160 cm2) have the potential to cause serious systemic toxicity from interference with blood and tissue calcium levels. In the body, hydrofluoric acid reacts with the ubiquitous biologically important ions Ca2+ and Mg2+. Formation of insoluble calcium fluoride is proposed as the etiology for both precipitous fall in serum calcium and the severe pain associated with tissue toxicity.


Silene virginica Endangered in FL Why is Silene virginica, colloquially known as Fire Pink, endangered in Florida? What factors besides human industrialization are affecting its survival there?

Various factors from different sources:

-- Diseases like Anther Smut Disease (reference).

-- Rampant use of herbicides.

-- Invasion of exotic pest species (reference).

-- Spatiotemporal variation in the pollination of Silene virginica by the ruby-throat hummingbird which is its principal pollinator (reference).


What is the effect of extra-cellular potassium concentration on heart rate and conduction velocity? If the extracellular potassium concentration surrounding a myocyte increases, then the potassium gradient accross the cell membrane decreases, and therefore the resting membrane potential will become more positive.  Similarly, if extracellular potassium decreases, the resting membrane potential will be more negative.

With this in mind, how does the heart rate change when extracellular potassium concentration increases/decreases?

Pathological potassium concentration promotes arrhythmia.
Increased extracellular potassium inactivates $Na^+$ channels and opens $K^+$ channels, causing the cells to become refractory [1]:

Increased extracellular potassium levels result in depolarization of the membrane potentials of cells due to the increase in the equilibrium potential of potassium. This depolarization opens some voltage-gated sodium channels, but also increases the inactivation at the same time. Since depolarization due to concentration change is slow, it never generates an action potential by itself instead, it results in accommodation. Above a certain level of potassium the depolarization inactivates sodium channels, opens potassium channels, thus the cells become refractory. This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Of most concern is the impairment of cardiac conduction which can result in ventricular fibrillation or asystole.

Decreased extracellular potassium leads to hyperpolarization [2]:

Lower potassium levels in the extracellular space will cause hyperpolarization of the resting membrane potential. As a result, a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential.
In the heart, hypokalemia causes hyperpolarization in the myocytes' resting membrane potential. The more negative membrane potentials in the atrium may cause arrhythmias because of more complete recovery from sodium-channel inactivation, making the triggering of an action potential less likely. In addition, the reduced extracellular potassium (paradoxically) inhibits the activity of the $I_{Kr}$ potassium current and delays ventricular repolarization. This delayed repolarization may promote reentrant arrhythmias.

References:

Wikipedia contributors, "Hyperkalemia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Hyperkalemia&oldid=612096441 (accessed July 12, 2014).
Wikipedia contributors, "Hypokalemia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Hypokalemia&oldid=612818488 (accessed July 12, 2014).


Which are the best apps and websites for insect identification? My kids keep asking me to identify some insects they found, and I am often caught off guard, as I have very little matter knowledge.

I have found the Insect Orders app quite useful, but still quite challenging.

Is there anything else, in terms of apps or websites, which is better for insect identification?

There are not many beginner-friendly apps that I am aware of. However, there are a few websites you can use.

BugGuide has a relatively nice picture-based search system. You will also gradually learn to easily identify various characteristics of an insect, thus making your search easier.

Insect identification is more beginner-friendly and more suitable to your kids.

You can also ask either here, or perhaps in the reddit community if you have trouble identifying a particular bug.

If they become interested I would recommend searching your local book store or library for a good field guide (depending on your location). Entomology can be a fun excuse to get out of your house and learn something in the process.


How animals maintain their body shape after development to maturity? I've recently read a book on evolutionary-developmental biology for laymen, and it described how a fetus is progressively divided into more refined zones of genetic activity. These zones, kinda like GPS coordinates define which genes will be activated at which time and at which location.

What interests me is - after development to maturity, what defines how animals maintain their body shape? Is it the same "GPS" system that defines boundaries of an organism? Or is it something else within the specialized cells that tells them to grow in certain directions and avoid others?

To clarify the question with an example - lets take blood vessels - what prevents blood vessel lining from growing forever in all directions, taking up all available internal cavity space?

Normally, cells do not proliferate without a "command". The "zones of genetic activity" you mentioned are defined by gradients of morphogenic molecules (and cell interactions). In the adult organism the original "map" of concentrations of these molecules is already realized and the pattern they defined before is no longer present.

Another closely linked idea is that most cells in mature tissues are not able to proliferate, because they have already undergone the process of differentiation. In contrast, stem cells maintain their ability to reproduce. [There are still some ways to de-differentiate some types of cells, i.e. to obtain induced stem cells in vitro.] Thus, embrya are composed of embryonic stem cells, while adult organisms have several restricted pools of stem cells (for example, in haematopoetic organs, where new blood cells are produced.)


Do leaves only appear on new growth? In some willows, there is a clear distinction between floriferous buds (out of which the catkins grow) and vegetative buds. I have observed this phenomenon myself on numerous occasions (in fact, I can ID several species and hybrids on floriferous buds alone). However, I never took it further and there are things I still don't understand. What about those vegetative buds. What grows out of them: twigs with leaves on them out of some and single leaves out of others? And would there be any noticeable difference between these two types of vegetative buds (if they both existed)?

To answer the question in you title, the leaves appear both on new and old growth. In addition to vegetative and floral buds, there are also dormant buds that activate themselves on old growth after leaves or branches are cut. You can read here a list of buds.

For the following questions in the text I think the answer is different for every species.


How likely is to develop an infection from a single virion entering a single cell? Is there any research (including mathematical or computational modelling) regarding how likely it is to infect an organism starting from a single virion entering a single cell?

I am interested in any virus and any multicellular organism (including immunocompromised).

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology! I'm glad we encourage such questions from curious people who want to learn more.

This is called the Independent Action Hypothesis, described here:

  The Independent Action Hypothesis (IAH) states that pathogenic individuals (cells, spores, virus particles etc.) behave independently of each other, so that each has an independent probability of causing systemic infection or death.

Zwart et al. (2009) tests this theory, and their results support the hypothesis that a single virus particle can infect a cell:

  The ‘independent action hypothesis’ (IAH) states that each pathogen individual has a non-zero probability of causing host death and that pathogen individuals act independently. IAH has not been rigorously tested. In this paper, we (i) develop a probabilistic framework for testing IAH and (ii) demonstrate that, in two out of the six virus–insect pathosystems tested, IAH is supported by the data.

The modeling done in this paper may be worth reviewing.


A 10mm long creature in the California dust I observed this tiny creature burrowing through the dusty soil of Cachuma Lake Recreation Area in Santa Barbara County, California, on June 8, 2014, about 7 a.m. I have really no clue what it could be, other than an annelid, or newly hatched type of legless lizard or snake. But it seems too tiny for the latter. Yet, I would think an annelid would need more moisture, or different soil. Do worms live in dust? I watched it for about five minutes, maybe more. Burrowing under and re-emerging. So that seemed to be its normal environment.

Here's a closeup, and a link to a Youtube page I put up for it. Video on Youtube of animal's movement

I'm going to answer this question and close it. Based on the location, the environment, its appearance and behavior, I'm 90% sure that this creature was a Stiletto Fly (Therevid) larva. Most likely an Acrosathe sp., as those tend to be very common in the area. Thanks to all for your help in clarifying and narrowing it down for me.


Whether de novo mutation can be inherited or not? Think about the following scenario: A child is diagnosed as having long QT syndrome, an autosomal dominant disease. However, neither of his parents is affected. This may be due to a new mutation in the embryo, which would explain the son having the disease with normal parents. Next, this de novo mutation could be inherited to off-spring of the child? or not?

And there are additional questions. Why do so many genetic tests performed by blood samples represent all germline mutations? Except for cell free DNA, blood cells are not germline cells. Therefore, the mutation found in the blood sample test may be a huge somatic mutation (except blood cancer). For example, for mutations that occurred early in embryo development, many cells may have been affected, and I think this might be in the form of somatic mosaicism. Doesn't it mean that it's a germline mutation if it's found at 50% or 100%?

I asked you a little more, is there only a family test (segregation test) that checks to see if it's a germline mutation?

Thank you so much in advance.
Please answer these long question, because no one answer me about this question.
If you answer me, I 'll always love you somewhere in the earth.

Thank you very much!! And I love you forever :)

And you say, in other words, de novo mutations can occur in postzygotic embryos or by germline mutations in parents.

Then I want to go further and conclude. In this case, an autosomal dominant disorder was detected as a heterozygote on a blood test. If it occurs in the embryo after conjugation, two possibilities are conceivable.

It could happens a heterozygous allele in the whole cell of a postzygotic embryo, Or can occur in one of the cells as a homozygous mutation when there are only two cells in the early embryo. In the latter case, autosomal dominant mutation would be lethal, so the child is likely not lived.

So in conclusion, if I thought that the whole cell of the child had the heterozygous mutation of the long QT syndrome, it was probably the result of the parent's germline mutation.

Am I thinkin right?

De novo mutations can be inherited if they occur in the germline cells, those responsible for making the sperm or the egg. If you have a de novo mutation in a blood cell or a skin cell, this doesn't pass on to the next generation. But when you test the blood for mutations, it can also mean that the same mutation is present in the germline! However, if the parents are not sufferers of the dominant disease, it means this mutation is not present in their somatic (non-germline) cells. It's likely that the mutation occurred de novo in either the parent's germline during their lifetime (during the production of their sex cells in adulthood).

If your parent has a mutation in their germline, and it is passed on to you, the zygote is formed from both your parents (half of your alleles are from the mutated parent) and this zygote creates ALL of you, including your blood cells and your skin cells. This is why we can test your blood to guess what must have been the case in your germline. Of course, you may have accumulated mutations independently in the germline in the meantime, or accumulated mutations independently in the blood cells! So it's not completely the case that testing blood will tell you about the state of the germline. But you must understand that ALL of you is created from a single cell, the zygote, so at this point there is a 'bottleneck' that forces all somatic and germline cells to share the same genetic makeup.

Also, please consider that humans are diploid, i.e. have one copy from the mother and one copy from the father. And that these recombine and only one copy goes into the sex cell. This may help you think about your problem.

I trust this will help you better understand your questions.


Cats, Dogs and Bears - how are they related? What is the ancestral relationship between cats, dogs and bears?

I presume they are more closely related to one another than other paraphyletic clades of mammal.

Which came first?
What did their common ancestors look like?
What are their geographical origins?

Cats, dogs and bears all belong to the Carnivora clade of mammals, but they are not the only ones belonging to this clade.
For instance, cats are more closely related to mongoose and hyenas than to dogs or bears, who in turn are more closely related to raccoons, weasels, and walruses.

Their common ancestors likely displayed various adaptations to a carnivorous diet, as the name of the clade suggests, and which are still present in many extant Carnivora (the panda being a well-known exception).

Together with many other groups of mammals, Carnivora are part of a clade named Laurasiatheria thus named because they may have originated in the Laurasia supercontinent, which comprises nowadays north America and Eurasia.


ChIP-seq and the output of SPP I have been processing some ChIP-seq data with the R package spp. I looked through the literature (ENCODE uses it) and it seemed that spp is indicated as a good program to use.  I have found and adapted the two tutorials I found for using spp (first and second), and read the original paper. I have also e-mailed Prof. Karchencko and posted on the bioconductor listserv - all with no response. My question is about the MSER and the predicted sequencing depth - additional output of spp. So what I think the MSER is, is the score value above which a peak is authoritatively determined? When I look at peaks above this score value they are very well defined. Also, is the predicted sequencing depth is a prediction of the number of additional "tags" necessary so that the MSER and the FDR value coincide? It is hard to find decent information about this program.  Any advice or additional information is greatly appreciated!

TIA

I found the answer to this question and some more interesting details that people who stumble upon this might also need. First look at this paper, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3191340/ and especially this figure, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3191340/figure/F3/. The MSER is a ratio of the fraction of discovered peaks to the fraction of the sampled reads to recapitulate them, so if you are able to return all of the peaks with a small sample of reads then you have excellent coverage. Now even though you have great and well defined peaks you need another sample to confirm that they are indeed significant, and you can do this with the IDR, see this website - https://sites.google.com/site/anshulkundaje/projects/idr. The IDR is laid out pretty well in the supplemental material for this ENCODE paper, http://www.nature.com/nature/journal/v489/n7414/full/nature11245.html. Beautiful!!


Why is the DNA helix anti-parallel? Why is it that DNA strands are running in anti-parallel fashion? Given the chemical base-pairing, they could have been parallel just as well.

Parallel nucleic acid double strand is possible but it is not as stable as the antiparallel form (Szabat and Kierzek, 2017). This is because the nucleobases are not aligned in a way that is conducive for the Watson-Crick (WC) type base pairing. In parallel conformation, the bases can form Hoogsteen (HS) and reverse Watson-Crick (RWC) type base pairing (see below).

You can see that these base pairs are not as strong as that in WC base pairing:

No triple bond between G and C in RWC base pairing
GC pair occurs in HS base pairing only when C is protonated at low pH

Formation of parallel helices, therefore depends on the sequence.

  In general, the formation of duplexes with parallel strand orientation
  is determined mostly by the sequence context and pH conditions.
  Fragments of RNA or DNA capable of forming a parallel duplex are often
  rich in A and C, which is related to their ability to become
  protonated, in middle acidic conditions.

However, it is not as simple as RNA/DNA base pairing with its complement. Parallel helices would not follow the WC base pairing rules and therefore predicting whether they will form is not that straightforward. However, parallel helices can form in vivo (see references 23–25 of Szabat and Kierzek, 2017).

You can also check out this article by Leontis et al. (2002) for hydrogen bond patterns in parallel and antiparallel helices.


human anti-mouse antibody I have heard about human anti-mouse antibodies (HAMAs) and read that HAMAs neutralize murine antibodies, therefore decreasing the effectiveness of those murine antibodies. Is this true that HAMAs neutralize the murine antibodies? How?

It's common for the human immune system to create antibodies against many proteins, even some human proteins. Hemophiliacs who receive regular doses of clotting factor proteins often develop neutralizing antibodies against the clotting factor proteins, even though they are a human protein1.

Therefore it's not surprising that antibodies would be developed against mouse antibodies. There are differences between mouse and human antibodies, and human antibodies may bind to these different regions. I found the amino acid sequences for human2 and mouse3 immunoglobulin gamma heavy chain constant region and aligned them by hand and marked the matching amino acids:

Human: MELGLSWVFLVAILEGVQCEVQLVESGGGLVQPGGSLRLSCAASGFTFSSYWMSWVRQAPGKGLEWVANIKQDGSEKYYVDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCARECDNWF DPWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHT CPPC      PAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK
       |   |  |||| || |||||||||||||||| ||||  ||||||||||| | | |||||| ||||||| |       || | |||||||||||||| |  || ||| |||| ||||||      | |||||  ||||| |  ||| ||||    | |    |||||| |||| ||| |||| | | |||||| ||| |||  || ||||||    ||  | | |  | | |||| ||     |   ||||      ||| | |||||| |||  || |||| || |||||||||  || |   | |  |||| | |    | |||| |||| |   ||||  ||| |||| || || ||| |||| ||  | |||| |||    |    ||||||| || | || ||| ||   | ||| | |||||||| | ||||    | |     ||| | || | | |  |  | ||||
Mouse: MDSRLNLVFLVLILKGVQCEVQLVESGGGLVKPGGSRKLSCAASGFTFSDYGMHWVRQAPEKGLEWVAYINSGSTTIYYADTVKGRFTISRDNAKNTLFLQMTSLRSEDTAMYYCARELWLRRIDYWGQGTTITVSSAKTTPPSVYPLAPGCGDTTGSSVTLGCLVKGYFPESVTVTWNSGSLSSSVHTFPALLQS GLYTMSSSVTVPSSTWPSQTVTCSVAHPASSTTVDKKLEPSGPISTINPCPPCKECHKCPAPNLEGGPSVFIFPPNIKDVLMISLTPKVTCVVVDVSEDDPDVQISWFVNNVEVHTAQTQTHREDYNSTIRVVSALPIQHQDWMSGKEFKCKVNNKDLPSPIERTISKIKGLVRAPQVYILPPPAEQLSRKDVSLTCLVVGFNPGDISVEWTSNGHTEENYKDTAPVLDSDGSYFIYSKLDIKTSKWEKTDSFSCNVRHEGLKNYYLKKTISRSPGK

As you can see, there are a lot of matching residues, but several differences. Keep in mind that antibodies also contain light chains, and that there are several other types of antibodies, I just used the IgG heavy chain as an example.


What is meant by increase in information embodied in the system? From Ecosystem Ecology
edited by Sven Erik Jørgensen

After the initial capture of energy across a boundary, ecosystem growth and development is possible by

an increae of the physical structure(biomass),
an increase of the network (more cycling)
an increase in the information embodied in the system.

What is meant by increase in information embodied in the system?
Does it mean increase in diversity of the genes (genetic information)?

Table 1 on the next page (p. 36) lists a number of properties for each of the three "growth forms".

For information, properties include:

Life history types
Diversity (taxonomic & ecological)
Body size
Stability

I have to admit that some of these properties doesn't really make sense to me under these headings (at least from the common use of these terms). However, I suspect that they are used in a very specific sense that might make sense if you read the entire book. And systems ecology isn't really my thing.

Note also that exergy (which is used in relation to these three growth forms in the book) is a term borrowed from thermodynamics (ie physics), and it describes potential/available work. Exergy is also negatively related to entropy, so when exergy decreases, entropy increases. Since higher entropy is related to disorder, the opposite goes for exergy, so high exergy means a higher amount of order (within the system), which can be translated into "structural information". I suspect that this is the form of information that the book is referring to, as one of the "growth forms".


What is the distance between the sciatic nerve and the colon at the closest point? Is it possible that a full colon impinges on the sciatic nerve? Is there anything that physically separates the sciatic nerve from the colon?

Short answer
Sciatic nerve pain cannot be caused by a full colon.

background
The sciatic nerve runs at the back of the pelvis down the the leg. The sciatic nerve exits the spine from the lumbar spine to S3 in the sacrum (Fig. 1).

Fig.1. Left: sciatic nerve overview. Right: Sacral plexus. Source: Manchester Bedford Clinic

Hence the sciatic nerve does not come into contact with the bowel and intestines located ventrally in the abdominal cavity (Fig. 2).

Fig.2. Left: sciatic nerve in detail showing dorsal location. Right: Intestines ventrally situated in abdominal cavity. Source: Manchester Bedford Clinic and University of Maryland

Pain in the sciatic nerve (sciatica) is often caused by compression or entrapment by muscles, tendons, and other soft tissues along the nerve path Manchester Bedford Clinic.


What use a pair of lips? Pardon my ignorance ... A lip is apparently a very sensitive tactile device - as it at-least serves to warn it's owner they may just be about to consume something that could cause injury. Primates (including humans), dogs, cats, sheep, buffalo, elephants, some fish, octopodes - to name a few, have a lip.

How have lips evolved to be nearly ubiquitous across animals? Why have they evolved into a beak/bill in some birds & fish? What niche/purpose do they fulfill?

I think what you are looking for can be found https://en.wikipedia.org/wiki/Lips#Functions_of_the_lips and https://en.wikipedia.org/wiki/Beak#Functions pretty easily.

To summarize, lips:

Mainly useful in mammals
Food intake
Articulation
Tactile organ
Erogenous zone
Facial expressions

Beaks:

Found in birds
Feeding
Defense
Manipulation of objects
Communication
Heat exchange


Where do biologists get information about mouse genes? From this article https://ui.adsabs.harvard.edu/abs/2005Sci...308.1909S/abstract

“We created transgenic mice that overexpress human catalase localized in the peroxisome, nucleus, or mitochondria (MCAT).”

How exactly do such changes occur step by step? Those. how did they find which genes needed to be changed in order to get the result in overexpression of catalase and in mitochondria?

I am new to biology, and although I understand, for example, how CRISPR works, it’s not clear where people get such data "this gene in the mouse is responsible for the expression of catalase in mitochondria. "Where to find such data?

Hi Potion and welcome to Biology Stack Exchange and biology in general!

To answer your questions, these changes do not occur. The authors of the publication have engineered "new" genes (also called transgenes in this context).

They have done so by fusion a portion of a of another gene (also called domain) to the beginning or the end of the sequence of the catalase gene. If your gene of interest is localized to a given organelle (for example mitochondria), you can also swap the domain which is responsible for the targeting to this particular organelle with one from a different gene you know goes for let's say peroxisomes.

If you want to know more details for this particular work I encourage you to check the supplementary material here: https://science.sciencemag.org/content/sci/suppl/2005/06/23/1106653.DC1/Schriner.SOM.pdf

Hope that helps!


Do male skunks have teats? Simple question.  Do male skunks (striped skunk, eastern US/Canada if it matters) have teats?  Occasionally want to identify road-kill, but don't know if teats are diagnostic for females.  I believe they are for racoons.

Petrides, 1950, writes:

  Male skunks have tiny nipples which are considerably smaller than those of juvenile females.

and also:

  Female skunks which had bred could easily be distinguished from those which had not by differences in the size of the teats

So it sounds like the mere presence of teats is not sufficient to sex skunks, but the size is sexually dimorphic and is probably a reasonable guide with practice, though the differences may be more subtle for female juveniles vs. males.

For pelts, Petrides recommends sexing based on the presence of a penis scar; I presume that genitalia is likely a more reliable guideline than teats.

For roadkill where damage might make it hard to sex animals based on genitalia, Fuller et al found canine size to be highly predictive, though they suggest that a comparison group of sizes from animals of known sex be used for a particular region, so that might not be too helpful for sporadic sexing.

Casey & Webster 1975 discuss sex identification based on presence of Barr bodies in the hippocampus, but their technique would probably not be applicable to your use case.

Casey, G. A., & Webster, W. A. (1975). Age and sex determination of striped skunks (Mephitis mephitis) from Ontario, Manitoba, and Quebec. Canadian journal of zoology, 53(3), 223-226.

Fuller, T. K., Hobson, D. P., Gunson, J. R., & Schowalter, D. B. (1984). Sexual dimorphism in mandibular canines of striped skunks. The Journal of wildlife management, 48(4), 1444-1446.

Petrides, G. A. (1950). The determination of sex and age ratios in fur animals. American Midland Naturalist, 355-382.


What are limitations on the number of objects the eye determine at a glance? Take two people Sam (average human) and Jack.

Jack says to Sam "I'm going to show you some skittles (or other object) and I want you to tell me as quick as you can how many I'm holding." He opens his hands and there are three. Sam can instantly tell there are three. Then Jack shows five to Sam, who takes a little longer, as he knows there are around 4/5 but can't tell so has to count.

As the number of skittles increases, Sam takes longer and longer to answer to the point where he needs to count the skittles one at a time to be sure, and sometimes to even recount them.

Why is it that we can instantly if we are looking at three maybe four objects but any more than this we cant? It gets harder and harder to estimate?

The answer to this question is complicated, but assume it's not for the moment. The easy answer is that our eyes can detect patterns we're familiar with and "produce" an answer in the form of a number. Unfamiliar patterns do not produce this 'number'.

Take a die. We are immediately aware of the number of dots in the typical arrangement of one to six. We need expend no counting to do so. If the skittles are arranged in the familiar die pattern, we will have no problem knowing if there are 4 or 6 skittles.

Given a pair of dice, any gambler can tell you what number any two faces adds up to without counting the spots. Do it long enough, and your brain is on auto-recognize. In your example, if Sam is a gambler, and the skittles are arranged like the spots on two dice, again, no problem telling between 2-12 skittles.

If you arrange things in a comfortable pattern, this can go on into the hundreds.

The above was easily recognized by you as nine, I presume.

Someone good with pattern recognition will know that the above left is 25 dots. However, they will not know that there are 25 dots in the above right.

So, the easy answer is that the eye can grasp high numbers of things if they are presented in a familiar pattern. The normal mind, however, is not able to do so with higher numbers arranged in a random pattern. And, random is how most things present themselves. So, we need to count.


Why do crocodiles have a high concentration of lactic acid in their blood? Crocodilians have high concentration of lactic acid in their blood. This is the cause that prevents them from prolonged intense activity, since prolonged intense activity causes the muscles to secrete more and more lactic acids, up to the stage where the lactic acid level become lethal - even for the crocodile.

So the shortcomings of high level of lactic acid are clear, it restricts activity and endangers the croc to death.

So why in the first place crocodiles have high level of lactic acid? What is the advantage of this?

As far as I can tell from a brief literature search, the explanation for the high concentration of lactic acid in the blood of crocadilians is two-fold:

The lactic acid is generated from the anaerobic muscular activity involved in capturing their prey.

In a gloss from Science Daily a journalist writes:

  Concealed below the water's surface, crocodilians stealthily approach animals that have come to drink, spring upon their prey, and drag them into the water and drown them. This powerful burst of activity generates an extraordinary amount of lactic acid in their muscles…

It is maintained at a relatively high concentration in blood so it can be used to acidify the stomach for the digestion of its meal.

I am less sure about this. Certainly the crocodile needs to acidify the stomach, and the scientific article glossed by the Science Daily shows how the lungs are bypassed to allow carbon dioxide to reach the stomach:

  During this period of digestion crocodilians divert blood through a special vessel that bypasses the lung, named the left aorta… …when crocodilians are digesting a meal, they chose to shunt and direct CO2-rich blood straight to the stomach where glands make use of the CO2 to form gastric acid and bicarbonate. Consequently this shunt enables crocodilians to secrete gastric acid at a rate that is approximately 10 times the highest rates measured in mammals.

My supposition is that lactic acid also contributes to the acidity, but I may be wrong on this point. If anyone has information about this, I shall be happy to add it to my answer.


How do you estimate global species richness? I know how estimates of species richness in a small area are made. But how do you estimate the total number of species on a global scale?

One example of such a method can be found in Mora et al. 2011.

You might be interested in the below works as well as the references that they cite.

May, R. M. (1988). How many species are there on Earth? Science, 241(4872), 1441–1449.

Millennium Ecosystem Assessment. (2005). Ecosystems and Human Well-Being: Synthesis (p. 137). Washington, D.C.: Island Press.

It's worth noting that many estimates of species richness at large scales are based on the use of the species-area relationship to upscale richness measurements from small scales to large scales.


How can I generate a random DNA sequence? I've found this paper which involves the construction of 19-bp random DNA sequences, but I don't know enough biology to understand how this method works.  Could someone explain it to someone who is highly technical, but has knowledge of only introductory, undergraduate biology?  How do the authors know that their resultant sequence is truly random?

If you want to synthesize a specific DNA sequence chemically, you start by attaching your first nucleotide (one letter in your DNA) to a solid phase. You can then continue adding individual letters to it. Because it is bound to a solid support material, you can wash the whole thing without washing your growing DNA away.

So if you want to synthesize AGC, you would first only add A to your reaction and then wash away all the A that hasn't reacted. Then you'd add G, which binds to your previous A, and again wash away all the G that hasn't reacted. Then you'd add C, and do the whole thing again.

If you want to create a random or semi-random sequence, you simply add multiple letters at once. If you always add all four letters in each step, you'll get a completely random sequence. You can also randomize only specific positions, and only there add all letters.

The result is random, but I don't think it is as random as e.g. a cryptographically secure pseudorandom number generator. There are various factors that can affect the randomness, variations in the concentrations of your nucleotides, variations in the quality or composition of your reactants and probably a lot more.

See also Oligonucleotide synthesis on Wikipedia


Do men have significant hormonal cycles? I know there's a similar question here. But that discussion dissolved into lunar cycle and a correlation with it.  I want to find more towards the original question of is there a periodic hormone cycle in men.
The links i have read suggest that there's probably a daily one for sure. But few hint at monthly ones too.
 That link seems to have very shaky science, but my biology is too weak for me to find the actual studies. Anyone else with more informed opinions? Any studies tracking purely hormone levels in men over a period of couple of months/years?

[EDIT]
   I understand it's clear there are cycles within the day or around the 24-hr mark now. I still am looking for studies focusing on longer term cycles like week,months etc.

Short answer: yes.

Although clearly the infradian changes in steroid hormones in females are quite "obvious", other changes are less evident, but happen nonetheless in males as well as in females.

Most of the hormones produced by endocrine organs such as the hypothalamus (a region at the base of the brain) or the hypophisis are not secreted in a continuous manner but rather in pulses. The exact frequency/amplitude etc. of these pulses can be different depending on the species considered, but (as fare as we know) the undelying mechanism are fairly conserved.*

In general, you can find circadian (~24 h), ultradian (<24h) and infradian (>24h) rhythms.

For instance these graphs show the concentration of cortisol, aldosteron and renin in a man, showing a strong circadian rhythm.

From: Charloux et al. - Am J Physiol Endocrinol Metab 1999

You can see that on top of the circadian rhythm, an ultradian pulsatility (every ~2-3h) is also quite clear.

Another example is that of GH (growth hormone): here you see secretion of GH in an healthy women (top) and an healthy men (bottom)

From: van den Bergh et al. - J Clin Endocrinol Metab. 1996

Many other hormones show this type of rhythmicity in males, such as testosterone, LH, GnRH, and probably many other.

I am not aware of long term studies on this matter.

* Actually, the mechanisms underlying pulsatility are still poorly understood.


Displaying nucleotide at a single position from RNA-seq reads in a BAM file How do I display a single nucleotide position from reads in a BAM file? I have been looking at variation using samtools mpileup, but I want to actually just display the nucleotide at the position I am interested in. This seems like you should be able to do it but I can't figure out how.

To be clear I have a BAM file of a bunch of reads. I'm looking to do something like samtools magic reads.bam chr3:10000 where I get back something like:

T T T T T T T T T T T T T T T T T T T A A A A A A A A A A A A A.

I just want to sanity check the output of bcftools by actually looking at the base calls.

Your best option is to create a tab delimited position list file:

chr3    1000

You can then use the samtools mpileup -l pos.txt option

-l FILE      list of positions (chr pos) or regions (BED)

This file can also be in bed format if you are interested in specific regions


Terminology of the sequences of promoters in relation to DNA strands I'm studying molecular biology and I'm trying to understand an experiment which shows the importance of promoters in the relative transcription level (RT). The image below comes from Rolf Knippers' book "Molekulare Genetik" (8th edition).

The legend says (among other things):

  Die erste Zeile gibt die normale "Wildtyp"-Sequenz der 5'-flankierenden Region wieder.

Which, in english, means something like:

  The first line repeats the normal wild-type sequence of the 5' flanking region.

The column on the right gives the relative transcription (RT) level, 1.0 being the highest possible level of transcription. As we can see, the lines where some parts of the "5' region" have been deleted give quite low RT levels, since some regions of the promoter are missing.

My questions are the following:

1) According to this and this, I understand that RNA polymerase reads and uses both coding and non-coding strands in order to synthesize RNA. Therefore, how did they manage to use the sequences strands regions had been deleted to make a polymerase "read them" and perform transcription?

2) If the polymerase reads the template strand in the 3' -> 5' sense, shouldn't we talk of "ATAT box" or "TAAC box" instead of "TATA" or "CAAT" boxes? Does it mean that the "promoter" regions they are using on the graphic above are actually on the coding strand?

Thanks a lot for your help.

It appears that this question is one of terminology, so I am answering it as such.

Convention for representing features in DNA sequences

The convention is that in indicating any sequence feature† in a protein-coding gene on double-stranded DNA, a single strand‡ is represented — the one from which the amino sequence could be read using the genetic code (conceptually, with T substituted for U). Like any other nucleic acid sequence§, it is always written in the 5ʹ to 3ʹ direction in the same manner as the mRNA transcribed from it, without this being explicitly stated.

† An exception might be hemi-methylation, in which case both strands would be shown.

‡ I call this the sense strand. I discuss the nomenclature further below.

§ An exception is that tRNA anticodons are sometimes written in the 3ʹ to 5ʹ direction for ease of comparison with the codon, but in this case the directionality is indicated.

Origin and justification for this convention

Historical. The amino acid sequence of the protein (the product of the gene) is central to this convention because knowledge of the genetic code, and hence representation of the region of the mRNA that encodes protein — and by extension the DNA — was the first sequence information to be known.
Logical consistency.  Later other sequences features were identified (some of which initially may have just been genetic features), e.g. ribosome binding sites, polyadenylation addition signals, transcription start sites, promoters, transcription factor recognition sites. It was logically consistent to represent them on the same strand as the coding sequence.
Functional agnosticism. In many cases the function of a sequence followed its description, so there was no reason initially to place it on any particular strand. However, even if it were thought that the function of some sequence were to be recognized on the opposite strand (what I would call the anti-sense strand), it would be unwise scientifically to  change the representation to indicate this. Science progresses and interpretation changes. Better to separate concrete descriptive features from conclusions about their function.

It couldn’t ever be an ATAT box

Even if you represented the TATA box on the anti-sense strand, it could never be called an ‘ATAT box’ (as suggested by the poster) because, according to the basic convention, ATAT is 5ʹ-ATAT-3ʹ, and on the antisense strand the sequence is 3ʹ-ATAT-5ʹ, i.e. TATA!

Terminology for referring to the two strands of dsDNA

Whereas the above is the convention followed universally, the following is just my opinion. In science terminology is important to communicates ideas unambiguously, so I think it worthwhile explaining the ambiguity in some of the terms, the use of which I discourage.

Sense and anti-sense
This is my preferred term because, although not perfect, it avoids the pitfalls of the others. The idea seems to me clear that when you read the string of codons that encode the amino acid sequence from this strand they ‘make sense’. (Anti-sense is used in preference to non-sense, as ‘nonsense’ was the term used historically for mutations that converted amino acid codons into stop codons.) It can also be extended to non-protein coding genes (e.g. for tRNA), where ‘sense’ correlates with the sequence of the gene product.

I shall use ‘sense’ and ‘anti-sense’ as reference terminology in discussing other terms.

Coding and non-coding
This has the disadvantage that it cannot be extended to non-protein coding genes. However my primary objection is that it can cause confusion, as coding only unambiguously refers to mRNA. As the anti-sense strand is the template for RNA polymerase, one might make the mental association between this and ‘coding’, whereas it is the sense strand that is meant in this (admittedly common) usage.

Template and non-template
Template might be a more logical term for the anti-sense strand as this is the template for transcription by the RNA polymerase (although mRNA is also a template — for translation). However it is used only infrequently.

Plus and minus
This terminology is used for single-stranded (especially RNA) viruses to represent the whole genome, where in plus-strand viruses the genome is also the mRNA, i.e. the sense strand. One problem here is that it can be confusing for the beginner, who by extrapolation may assume that in double-stranded DNA genomes one strand is the sense strand for all genes. It is not.  Which brings me to my final point…

…whatever terminology you use, it is better to make sure it is clear that you are referring to the sense or anti-sense strand of a gene, not of the whole genome. You need to employ some other terminology to distinguish between the two strands of e.g. bacterial or plasmid DNA if it is necessary to distinguish them.


Strength of Female Chimpanzees vs. Male Chimpanzees? Where can I find studies done on the strength dimorphism between male chimps and female chimps?

For example, "one-arm pull strength is 300 pounds for male chimps and 200 pounds for female chimps"

I searched for "chimpanzee strength" on PubMed and followed links from

O'Neill et al. PNAS 2017 "Chimpanzee Super Strength and Human Skeletal Muscle Evolution"

to

Bozek et al. PloS Biology 2014 "Exceptional evolutionary divergence of human muscle and brain metabolomes parallels human cognitive and physical uniqueness" where I found this figure:

which shows pulling strength normalized by individual body weight, with circles for females and diamonds for males.  In fact, the Excel spreadsheet given in supplementary materials shows there were two males and three females, tested in three sessions; in each session weight and pull strength were listed. The ratios of max pull to weight for males were 3.44 and 3.49, for females were 2.9, 3.14, and 3.25 (one of the males was quite small ...)

O'Neill et al. give a few other references, you could follow those as well and see what you come up with.  (I found that "chimpanzee strength" gave better results as a search term than terms including "sexual dimorphism", which tended to be swamped by more general discussions of the evolution of dimorphism in apes.)

@jackaidley notes in a comment that

  extreme caution is needed in interpreting these results for Chimp sexual dimorphism, quite apart from the very low number of individuals, there is a significant problem with these measurements - as the paper itself notes "The inability to control nonhuman primates' motivation hinders the exact quantification of the muscular strength difference between humans and nonhuman primates, even in a highly controlled experimental setup." This problem equally applies to male/female differences.

In other words, male chimpanzees might pull harder at least in part because they are more motivated than females in this particular setting, rather than because of intrinsic differences in strength. (That may or may not matter for what you are trying to do with this information.)


What is heteroduplex? I fail to understand the what exactly is heteroduplex due to unavailability of a suitable diagram. According to wikipidea:

  A heteroduplex is a double-stranded (duplex) molecule of nucleic acid originated through the genetic recombination of single complementary strands derived from different sources, such as from different homologous chromosomes or even from different organisms.

Should the following highlighted structure be called heteroduplex?

What you've circled is not a heteroduplex. A better name for it would be "crossover" or "junction". Instead, the two duplexes at the bottom of your diagram are what should be labeled heteroduplexes. Your diagram shows one process by which you could generate heteroduplexes starting from homoduplexes.

Here's a better picture from the NCI Dictionary of Genetics Terms that more clearly shows the difference between homo- and heteroduplexes:

The two strands in a heteroduplex still have to have a high degree of sequence identity or they won't be able to form into a duplex in the first place. However, because they come from different sources there's likely to be many short subsequences in which one or more base pair is mismatched, causing a deformation as shown.


Tapeworms and their effect on humans I've read that some people in some countries actually use tapeworms as a form of losing weight.  What are the dangers to these people?

I haven't really found much on this topic (besides popular sites) but I can summarize it here:
There are quite some tapeworms (or cestoda), I found numbers of up to 3500 species. They attach to the intestinal wall of the humans and then start to take up predigested food through their skin. With that, they reduce food from their host and start to grow, some get as long as 15 meters!

Some of the worms seem to be relatively harmless (besides stealing food), but this is more true for the first world. In poor countries, where there is not enough food, tapeworms can cause severe malnutrition.

Some tapeworms can migrate into the blood stream and from there into other tissues or organs like muscles, eye and brain. There they can cause cysts which can lead to organ failure and death.

For more information see this CDC webpage and this article: "Biochemistry and physiology of tapeworms.". This popular article is probably also interesting.


Why doesn't Fenoxaprop-P-ethyl damage cool season lawns? For controlling bermudagrass, Cynodon dactylon, a serious perennial grassy lawn weed in my area, I use the herbicide Fenoxaprop-P-ethyl. It kills the bermudagrass rather well, without damaging the cool season lawn grass in the least.

I believe Fenoxaprop-P-ethyl acts by inhibiting the synthesis of fatty acids in the meristematic tissues of the weedy grasses (designed especially for bermudagrass).

How does this mode of action not affect the 'good' grasses (the fescues, bluegrasses, and ryegrasses popular in my area)?

A number of studies have been done that investigated resistance to Fenoxaprop-P-ethyl and related compounds. Most of these studies focused on resistance in crops (e.g., maize) or black grass. One of these studies (Kay et al., 1999) was particularly interesting as it focused on several possible mechanisms of herbicide resistance in Alopecurus myosuroides (Black-Grass). I quote from the abstract:

  [...] Resistance at the whole-plant level correlated well with reduced acetyl Co-enzyme A carboxylase sensitivity (target site resistance) in two of the populations (one from the United Kingdom and one from Germany) but enhanced metabolism appeared to be the primary mechanism of resistance in the majority of the other populations. [...] We suggest that resistance in Lincs E1 may be explained by multiple resistance mechanisms—the expression of both insensitive acetyl Co-enzyme A carboxylase and an increased rate of detoxification. However, resistance in the population Clay from the United Kingdom could be explained neither by target site insensitivity nor by an enhanced rate of metabolism. These results provide conclusive evidence that a single resistance mechanism alone cannot explain insensitivity to fenoxaprop-P-ethyl in European resistant black-grass populations and that additional, as yet uncharacterized, mechanisms must also be present.

So based on these data, I think several mechanisms may play a role in the cool season lawn grass resistance (a species name may help to specify my, admittedly, broad answer).

Interestingly, Fenoxaprop-P-ethyl is an acetyl CoA carboxylase (ACC) inhibitor (Kay et al., 1999). Note that Haloxyfop (as mentioned in your question "How does Haloxyfop control young grassy weeds in fields of broadleaved crops?") is also an ACC inhibitor. From the answer on that question it appears that ACC inhibitors inhibit cell membrane formation and that monocots (grasses) are most susceptible and dicots less. Dicots are less sensitive because they have two ACC types at their disposal, one being insensitive to ACC inhibitors. Not surprisingly then, Bermuda grass, being a monocot is killed by this herbicide. Interestingly however, other monocots seem to survive, such as the cool-season lawns you mention.

I was not able to find conclusive evidence as to why some monocots survive ACC inhibitors. An educated guess is that resistance can be conferred by mutations in the ACC enzyme (Letouzé & Gasquez, 2001) that make the enzyme less sensitive to the herbicide. These mutations can be caused by repeated exposure to these herbicides, whereby strains become resistant to the material, much like the way in which (multi-) resistant bacterial strains emerge after repeated exposure to antibiotics.

References
Kay et al. Pesticide Biochem Physiol 1999; 65:169–80
Letouzé & Gasquez, Theoretical Applied Genetics 2001; 103:288-96


What are the evolutionary reasons behind men being taller than women? Human men and women are sexually dimorphic: there are some phenotypic differences between men and women.
Men being taller than women is an accurate stereotype. Overall, men are on average 13 centimeters taller than women. The most extreme example is Macedonia, where the average man is 18.5 cm taller than the average woman.

When you look at animals, I think it's pretty intuitive to think that females are often larger than males from the same species. Spiders, fish, insects, some birds, there's an endless list of examples of bigger females than males. This is explained by a variety of different reasons depending on the species, from mate competition to the ability to bear children. So why would human males be so much bigger than women?

We all know that there are a lot of factors behind the height - and, on a related subject, strength - differences between the sexes. There are some genetic factors, as pointed out in this interesting Quora post about the topic. We also know that nutrition has a large impact in growth. In a word, we know what causes the height difference between men and women. There is a great post about it here. But I couldn't find any conclusive evidence as to why men are taller than women.

Is this because women naturally like tall men? Did prehistoric men have to be taller than women in order to thrive? Or is it just genetic drifting that, more or less randomly, led to this height difference?

The motivation behind my curiosity is feelings-driven. A while ago, my dad said during a conversation that he once "saw a documentary in which they explained that early men stole all the good proteins from the women, so they could grow taller and stronger unlike the poor females." As much as I love and respect my dad, I have a hard time believing that men are natural culprits and thieves. I am by no way making this post just to "prove him wrong" - I am absolutely interested by the topic and would love to know more. Also, if anyone knows the documentary he was talking about, I would be glad to give it a watch.

All apologies for any bad English you might find. Please tell me if I make recurring grammar mistakes.

I assume by asking why, you are asking about the distal evolutionary causes, and not the molecular mechanisms that account for these things.

(Important disclaimer: these causes are difficult to be certain about; they require a fair amount of informed speculation.)

With that said: it is widely agreed upon in evolutionary biology that human males, as in other mammals, are thought to be larger mostly due to sexual selection. In other words, size is sexy, and sexy individuals fare better with respect to mate choice, on average. Sexual selection can also work via male-male competition. There may be other causes that are relatively minor contributors compared to this one.

Notice, however, that in humans, females evidently do not remain tiny with respect to males, but they get 'dragged along' in terms of their height, so that males are not drastically different in height (unlike, for instance, in elephant seals). This too may be a result of sexual selection, quirks of physiology across the sexes (e.g. genetics of dimorphism), or even natural selection. Think hip size and the size of human skulls.

Additionally, differences in development time (e.g. length and onset of puberty) can skew body size. Humans certainly exhibit dimorphism with respect to development.


Palaeontology and Palaeobotany Could someone please clarify the roles and differences between palaeontology and palaeobotany. My textbook says the palaeobotanists study plant and animal fossils, but other sources say that this is incorrect.

Thanks

Paleontology is the main scientific branch, which study fossils and prehistoric times.

Paleozoology studies the fossils and biology of prehistoric animals.
Paleobotany studies fossils and biology of prehistoric plants.
Paleobiology studies the biology of prehistoric organisms.
Paleoecology studies the prehistoric ecological systems and ecology.

In fact, putting the prefix "paleo-" turns every scientific branch of biology to a branch concentrating on this subject but in prehistoric times.


What causes the elongation of Genome down the evolutionary time line Theory of natural evolution says that complex life forms arose from simpler ones e.g. starting from Eubacteria to modern day multicellular eukaryotes. {If we try to reduce these changes happening at molecular level, it should be like, from Eubacteria like E.Coli. (20 kilobasepair genome/DNA strand size ) evolving, over time, to Multicellular Eukaryotes ( 3 Gigabasepair genome size) e.g. (humans and other hominids.)}
Now if we see molecular changes happening inside cells, the molecular changes are within nucleus as extra nuclear changes are largely function of nuclear information (and a smaller extent external stimuli). For biochemical changes to take place inside cell Nuclear information is the major guiding force. But according to Central Dogma elongation of DNA shouldn't have happened as there is no scope for it in either doubling, translation or transcription. But actually it is not so according to evolution. So what allows changes to be imbibed in the DNA that also increases it's length ?

DNA misreplication events can lead to accidental duplication of DNA (even the entire genome), misalignements in recomibination events, integration of DNA from extracellular sources e.g. viruses. All these events can lead to large scale changes in the genome size of an organisms, smaller scale changes can be insertions and deletions in the DNA from repair pathways such as non homologous end joining.


Immunofluoresence and vaccines Can you use indirect immounofluoresence to verify if a vaccine will work against a virus?

Using the vaccine antibodies against the virus, plus a second antibody with fluorophore that will join the first.

A vaccine isn't antibodies.  It's bits of virus or microbe that elicits a response from the immune system, the most important component being the creation of specific memory cells which are ready to react if the real invader is introduced.


Need help with ImageJ thresholding I'm trying to measure the colocalization of two proteins in a .tiff image taken with a wide-field fluorescence microscope. In ImageJ I have split the image into the two channels (red and green), and now I have to apply a threshold, however when I threshold both channels the bright areas corresponding to the cells are located in the darkest part of the histogram instead of the brightest part, as you can see in this image for the red channel:

https://www.screencast.com/t/QO2iVt0JM

Why ImageJ is assigning darker values to the cells rather than to the background? I'm having problems with this as I cannot properly select these cells for the colocalization analysis.
Anyone does have any clue? Any help would be greatly appreciated.

Check the "dark background" checkbox that is unchecked if the background is dark and you want to select the bright cells. Right now it is assuming the background is bright.


Neanderthal/Human Genetics "According to preliminary sequences, 99.7% of the nucleotide sequences of the modern human and Neanderthal genomes are identical, compared to humans sharing around 98.8% of sequences with the chimpanzee."
https://en.wikipedia.org/wiki/Neanderthal_genome_project

What precisely is the issue with the supposed 2-4% of Neanderthal genetic material, how does that connect with the general near-total-identity of genetic material?

Does the 2-4% refer largely to analysis of haplotypes, which I take to mean clusters of alleles/ groups of specific traits, which reveal direct contact between the populations?

The 2-4% of Neanderthal genes refer to alleles, as you guess.  If, for a super simplified example, a human genome has

ALLELE_1__ALLELE_2__ALLELE_3__ALLELE_4__ALLELE_5__ALLELE_6__ALLELE_7

and the Neanderthal equivalent had

ALLeLE_1__ALLELE_2__ALLELe_3__ALLELE_4__ALLELE_5__ALLELE_6__ALLELE_7

(note the two lower-case 'e's), then they are 97.1% identical (67/69 characters), but if we sequenced a human and found

ALLELE_1__ALLELE_2__ALLELe_3__ALLELE_4__ALLELE_5__ALLELE_6__ALLELE_7

then we might infer that "ALLELe_3" came from Neanderthals and that that genomic region was 14.2% Neanderthal (1 of 7 alleles).

(Obviously with only 7 alleles there would be other interpretations, but I don't feel like typing out 10,000 alleles right now.  You can see how you'd get enough information in a longer stretch of DNA.)

This is exactly the same as when you say "Half of my DNA is from my father and half if from my mother."  Obviously (one hopes) your parents were both human, and their genomes were virtually identical, but it's still possible to identify -- through allelic variation -- which segments came from which side.


How do high-throughput/NGS sequencers calculate quality scores? I am confused as to how quality scores are actually calculated by DNA sequencers like Illumina. For each base call, some quality predictor value is computed, based on various properties of the sequencing machine, like intensity of light during the read.

Do we know exactly how these quality scores are computed? Exactly how many factors go into computing these QUAL values?

I'm restricting this answer to Illumina. Even then, I don't know about the exact details of the raw data analysis (it is a proprietary software).

Basically Illumina records the sequence based on photographic images. Each nucleotide has a distinct fluorescent label. In a cycle, a nucleotide is pumped and unincorporated nucleotides are washed off (this is repeated for all nucleotides). A laser excites the fluorophore and the emitted light is recorded in the form of a photograph. The template DNA is present in the form of clusters of strands (at a given location), which enables easy visual identification of the fluorescence.

Base calling is done using image analysis. Each image is analysed for intensities of different colours and based on this the quality score is calculated. The quality score is basically the log likelihood of a occurrence nucleotide at a given position (based on its colour intensity) compared to other nucleotides.

This is the most simple explanation of how Illumina does base calling. There are different kinds of errors and biases and there are different statistical approaches to correct for them.

Have a look at following references for more details:

Ledergerber, Christian, and Christophe Dessimoz. "Base-calling for next-generation sequencing platforms." Briefings in bioinformatics (2011): bbq077.
Illumina MiSeq Imaging and Base Calling course
Genome Analysis Wiki


Lab marker for labelling cell culture plastics? I am a lab manager trying to ask other lab biologists what brand/make of markers their labs use for labeling tissue culture plastics, which need to be repeatedly wiped down with 70% ethanol to maintain sterility. (Most "permanent" markers wash off in 70% ethanol.)

I have been looking for an equivalent to the Sharpie Industrial Extra-Fine point marker, which seems not to be on the market anymore. The supposedly solvent-resistant Fisher extra-fine point marker leaves almost no trace when wiped with ethanol.

Does anyone have suggestions?

This is hardcore going to come across as a SPAM answer, but I simply did a Google search:

Laboratory Marking Pens from Ted Pella

Statmark Pen™: resistant to formalin, ethanol isopropanol and xylene

Secureline® Marker: water resistant; autoclavable; not suitable below 0°C (32°F)

Secureline® II / Superfrost: resistant to xylene, ethanol, acetone and formalin; service temperature -15°C to 100°C (5°F to 212°F)

You can try a Sample Pack of all 3 for $8 USD to see which you like the best.


How does Sanger sequencing resolve two bands with equal size? In Sanger sequencing, how can we read the sequence if we have 2 bands with the same size?

It happens if your sample contains a mix of two DNA molecules, with different bases at a certain position.

In your case, you would have a mixture of ACTGGCTA and ACTGTCTA.

In real life, the "double band" would be half as intense as the other single bands, as the signal is "divided by two".


Have there been studies done to test Immortality of cancer cells in culture? This website on cultured cancer cells () says cancer cells may be immortal.

I am wondering if there has been any research done to find if cancer cells are really immortal.

How old is the still maintained living oldest culture of cancer cells?
Has there been any research done on replicative senescence of Cancer Cells invitro?

Edit 1:

If there is some data relating to the number of replications the cells have undergone, it will be very useful

The HeLa cell line is undoubtedly the most used and investigated human  immortal tumor cell line. Extracted from a cervical tumor from Henrietta Lacks in 1951 at Johns Hopkins hospital, Baltimore, MD these cells proved immortal and are still used in many, many labs worldwide today. It is the oldest human cell line in use and, therefore, the oldest human tumor cell line (Callaway, 2013).

In terms of senescence of immortal cells; HeLa cells are immortal, and hence do not grow old as such. However, they are subject to mutations and the genetic profile of HeLa cells does change over time. Hence, although they may not be growing old, they do age in the sense that mutations are accumulating in continuous cell lines.

References
Callaway, Nature (2013); 500: 132-3


Do Alzheimer's patients have spaces in their brain with low interstitial space? Lulu Xie et al write in their paper Sleep Drives Metabolite Clearance from the Adult Brain:

  Using real-time assessments of tetramethylammonium diffusion and two-photon imaging in live mice, we show that natural sleep or anesthesia are associated with a 60% increase in the interstitial space, resulting in a striking increase in convective exchange of cerebrospinal fluid with interstitial fluid. In turn, convective fluxes of interstitial fluid increased the rate of β-amyloid clearance during sleep.

Given that Alzheimer's patients have more β-amyloid in their brains, do they also have less interstitial space?

It's hard to judge whether interstitial space changes are due to beta amyloid accumulation or because the Alzheimer's brain has suffered such profound cell loss and neurodegeneration as a result.

The Nedergaard paper you quote is more about a daily cycle of increase/decrease in interstitial space related to the sleep/wake cycle [Ref 1]. Specifically, that during sleep, there is more space to flush out the brain including beta-amyloid.  One interesting hypothesis from that being that perhaps the accumulation of these aggregates is actually due to inefficient sleep -> inefficient flushing of plaques which go on to give symptoms.  So even if the interstitial space in what's left of the Alzheimer's brain remained the same as a healthy brain, the problem of beta amyloid clearance could still be present.  It remains to be seen if one could restore normal clearance whether degeneration could be slowed and symptoms abated.

[Ref. 1]: Paper from Nedergaard group


Roles of creatine and bilirubin in foetus circulation I think they are not inputs from maternal placenta.
I think they are the results of foetus metabolism.
However, I do not understand it how and where exactly.

What are the roles of creatine and bilirubin in foetus circulation?

Creatine is an important energy source for body, especially for the muscles, so it is no wonder you can finde it there. I don't think it has a special role besides that. See the Wikipedia article for more information.

For bilirubin this is different, this substance is a breakdown product of the heme metabolism (basically hemoglobine). It is not water soluble and needs to be conjugated to a carrier protein (albumin). In this way it is transported to the liver, where the glucuronyltransferase conjugates it to glucuronic acid. This step makes the bilirubin water soluble and it can be excreted from the body.

Newborns have a higher bilirubin level, since their glucuronyltransferase activity is at about 0.1% of that of adults. This can lead to the typical newborn jaundice. For more details about bilirubin, see here.


Simple experimental design of a chemostat without pumps A chemostat is a device to maintain a cell culture in equilibrium, by continually pumping nutrients in and pumping excess cells and nutrients out.

What's the simplest design of a chemostat one can make? Has anyone tried to mount one without pumps?

A particularly sensitive issue here is sample taking, because you risk contamination of the culture.

Here is a link to a design in which electrolysis is used to generate gas which displaces liquid from the reservoir into the culture chamber, which in turn displaces culture into an outflow (where samples could be collected). The design does however require a pump for aeration, and I can't think of a way in which this could be avoided, although there is a reference cited in this article which apparently describes the use of gravity flow (I haven't checked it out).

Just for interest, this link is to a design which does require a peristaltic pump and a vacuum line but it looks to be achievable.


Can plant fruit and seeds be albino like animals? There are numerous examples of albino animals, including snakes, birds, fish, mammals---humans too. Apparently this comes from some a genetic defect that results in lack of pigment.

What about plants? Obviously a lack of chloraphyl would be fatal for a plant, so I'm imagining the seed or fruit being white. Does this exist in nature?

Edit: I'm thinking of fruit/seeds that are not normally white.

Note the wiki page I cited has only 2 paragraphs on this:

  In plants, albinism is characterised by partial or complete loss of chlorophyll pigments and incomplete differentiation of chloroplast membranes. Albinism in plants interferes with photosynthesis, which can reduce survivability.[4] Some plant variations may have white flowers or other parts. However, these plants are not totally devoid of chlorophyll. Terms associated with this phenomenon are "hypochromia" and "albiflora".[5]

That last part seems what I'm interested in, but the cite is a dead link.

Later in the article:

  The primary function of pigments in plants is photosynthesis, which uses the green pigment chlorophyll along with several red and yellow pigments including porphyrins, carotenoids, anthocyanins and betalains.

No cite there and not much info anyway.

So are white seeds or fruit found in nature?

If you're curious, I originally thought of this as an alternative way of getting white chocolate from an albino cocoa bean, and maybe even a white coffee bean too.

When thinking of albinism in fruits, the only thing I could think of is strawberries. Yes, there can be albinism in strawberries! They are nearly always assocoated with excess nitrogen and are usually tasteless. According to a research by Lieten et al, their mineral composition also differes. Albino strawberries contain higher N:Ca and K:Ca ratio than normal fruits. Another study by Sharma et al shows that albino strawberries show less lipoxygenase activity. Also, Hwang et al and team found that presence of more than normal silicon also causes, among many other things, albinism.

You can get more information here, here, here and here. Obviously, there could be numerous other examples, but albino strawberries is all I could remember.

PS the exact genetic cause and mechanism of albinism in strawberries is not known yet. When searching online, I only found a study by Plante et al which suggests presence of mixoploid cells over a critical number which might have an effect on it.


Does the cranial dura consist of the periosteum? and if not, then is there a mistake in my textbook? My textbook (Neuroanatomy an illustrated colour text) states that:

  The spinal dura and much of the cranial dura are separate from the periosteum, which forms the inner lining of the surrounding bones.

However, as far as I am aware the cranial dura has two layers, one of which is the outer periosteal layer or the periosteum, so I'm not sure why this is mentioned separate to the cranial dura.
The textbook later states that:

  At certain locations, however, such as on the floor of the cranial cavity, the dura and periosteum are fused and the cranial dura is tightly adherent to the interior surface of the skull.

This would make sense if they were referring to the pericranium, but the first quote suggests that the textbook is referring to the outer periosteal layer (or the inner periosteum).

Please could you shed some light on this. Thank you.

First about the terms:

The outer side of the cranial bones is covered by a single layer of  periosteum that is specifically called pericranium.
The inner side of the cranial bones is covered by dura mater that has 2 layers:

the periosteal (or sometimes called endosteal) layer that is attached to the inner side of the bones
the meningeal layer that covers the periosteal layer and, at places, folds into the skull to make extensions

Image 1: Dura mater with its periosteal and meningeal layer (source: Idris Siddiqui, SlideShare)

Image 2: Extensions of the meningeal dura mater (falx cerebri, falx cerebelli, tentorium cerebelli) (source: Wikipedia, CC license)

The cranial dura mater has the periosteal and meningeal layer, but the spinal dura mater has only a meningeal layer, which encloses the spinal cord. Vertebra have no additional periosteal layer. The periosteal layer of the dura mater that covers the cranial bones does not extend to the spinal canal:

  The periosteal or endosteal layer of dura mater is simply a layer of
  periosteum that covers the inner surface of the skull. The layer does
  not extend beyond the foramen magnum to become contiguous with the
  dura mater of the spinal cord. The spinal cord dura mater has no
  periosteal layer.

  The meningeal layer of dura mater is a durable, dense fibrous membrane
  which passes through the foramen magnum and is continuous with the
  dura mater of the spinal cord. (V. Kekere, Dura mater, StatPearls)

Both quotes from the book mentioned in the question suggest that the periosteum and dura are two separate things: periosteum being a part of the bone (as elsewhere in the skeleton) and dura consisting of a single layer. The other  explanation, which I presented here, is that the periosteum on the inner side of the skull is a part of the dura (its periosteal layer) that has another layer (the meningeal layer). So, they are two ways how you can look at the structure of dura mater, and I believe, the second one is more widely accepted.


Are there organisms which have compartments of different body temperature? I was wondering if there are organisms which have compartments(inside the body) with different body temperatures. To clarify are there organisms which have tissue/organs which are surrounded by something (other cells, tissues) which have an other temperature.I'm not talking about fluctuation in body temperature, such as in ectotherm organisms. I have never heard about something like this and nor I could find information or articles about this (the reason why this question doesn't provide much background research). However I'm still wondering if there are organisms like this (or at least come close to this)?

Ps. please edit this question or comment if you can provide more background information regarding this topic

For most of the multicellular organism; different part of body would exist in  different temperature; however there are more extreme/ drastic examples too.

Bombardier beetles; a group of beetles; that have a specialized reaction chamber in the body; where they can produce a hot and noxious reaction-mixture. They project it towards the enemy; and can throw by bending their pygidial region to wide range of directions. They do it as a defense mechanism.

Wikipedia image of bombardier beetle. They are some members from the tribes  Brachinini, Paussini, Ozaenini, Metriini of family Carabidae.

The reaction mixture can attain a temperature up to 100°C , more than enough to cause thermal death of normal protoplasm. But the reaction take place in a specialized compartment inside their body... and nothing else happen to the life of the beetle.

Here are some image of the anatomy of bombardier beetles (from here)

pygidial glands within a Bombardier Beetle; highly diagrammatic.

 more detailed diagram of the gland, however, diagrammatic.

 this is a more realistic diagram of the gland in bombardier-type carabid beetles; whole diagram showing forms of this glands in other-type carabid beetles  is available in the main website.

This paper includes a simplified diagram of chemical reaction in the chamber. reaction summary.

Here is an image from BBC showing bombardier beetle in action.

  Reference: Wikipedia