How does GC-content evolve? Background

GC-content refers to the frequency of base pairs that are either C or G in the genome, or in other words the number of GC base pairs divided by the addition of the number of GC base pairs plus the number of AT base pairs.

$$GCcontent = \frac{N_{GC}}{N_{AT}+N_{GC}}$$

Question

How does the GC-content evolve and why does the GC-content differ between populations/species/lineages? Does it evolve under Genetic drift only? Under selection? Intuitively, I'd say that the ratio of the probabilities of mutating from A or T to G or C should be an important factor driving the evolution of the GC-content. Does it? Does the overall mutation rate influence the GC-content? What other traits/forces influence the evolution of the GC-content?

I think the key work here is 'evolve'.  Overall GC/AT ratios change by mutations, whose rate is constant.  The probability that given a mutation event that one base will be substituted by another one has been modeled in several ways where the probabilities of different mutations may or may not be the same.

Overall the GC content will tend to close to 50%.  What causes GC rich genomes to become GC rich (60-70%) are that mutations to GC base pairs have selective advantages either in regions or in the genome overall that cause them to be retained. The mutation rate may be no different (or even lower) in GC rich organism (many of them are deep underground or deep underwater.  GC rich genomes occur because AT->GC mutations convey an advantage and they stick around.

The reasons that the GC content migrates away from 50% fall into two categories I will call entropic and selective.

By entropic I mean specifically that coding sequences for genes and other features such as binding sites on the DNA or other features such as centromeres, which will cause the overall ratio to vary from 1 because the sequence is constrained by the information it contains.  While coding regions have a ratio higher than 1, GC content tends to hover around 54%.  Eukaryotes have GC islands and etc, but this also does not overall change the GC content

So gene rich genomes and typical functional features of the genome do not really explain some of the spectacularly high GC contents found; up to the 70% range.  While the link above looks at GC bias in coding regions, its a given that any part of the genome that is merely a spacer between elements with specific functions will freely vary to GC if it is useful.

Selective factors for high GC content include high pressure and temperature environments for instance, which usually strongly bias to high GC content by this mechanism.  You can imagine how this works: high GC content genomes are thermodynamically more stable and can survive the extra molecular collisions of higher energy of those environments more readily.

GC rich genomes are not simple adaptations to live with.  All the genes for DNA oriented processes such as transcription, chromosome packing, DNA polymerase have to adjust a lot. As the organism adapts to hotter temperatures or higher pressures, each individual protein produced will have to also change to be stable and function in the new conditions.  As such, these changes happen only over long evolutionary times.  This is probably a good part of the reason why the archaea niches have not been superseded by eubacteria in all 1+ billion years since life has been on Earth.


What type of tree is this? This is a tree that I have been growing. I'm wondering if this is a mulberry, and if so, what kind?  Location is Arizona.

It is a mulberry.  What isn't clear from the photos, and may not be clear without a DNA analysis, is whether it's a hybrid of the native red mulberry and the white mulberry imported from Asia in the hopes of starting a silk trade in North America (white mulberry is the main food source for silk caterpillars), or whether it's distinctly a red or white.  The berries won't always indicate this, and the leaves won't always indicate this.  At this point, our red mulberry has seen sufficient habitat loss that most new mulberry trees are hybrids.


Alternating Ovulation I have often heard that right and left ovaries alternate in releasing ovum.

Is it always true? What controls this rhythm? Is it simply because the other ovary is unresponsive to LH or FSH? If so, why?

Nope, not true.  It's a pretty common myth; that paper cites a  reference from 1932 in primates claiming to show that the ovaries alternate.  A few papers before this, in particular this one from 1991 showed that ovulation was not alternating, but this was the first to do so in actually fertile woman.  In particular,

  Alternate ovulation occurred in 61 of the 119 succeeding ovulations (51.3%, not significant) which means that there was no consistent tendency to alternation.

Alternation only occurred half the time.  Neither did they find a difference between side preference; right-side ovulation occurred in just over 50% of the cases, not significantly different.

FSH, follicle-stimulating hormone, and LH, luteinizing hormone, stimulate each ovary equally, but one ovary will get slightly ahead.  Ovulation (and indeed pregnancy at times) is a positive-feedback loop, meaning the response will be exponential; if one ovary is even just slightly ahead it will rapidly dominate the other.  The less-developed one quickly senses the other is ahead of the game and ceases to respond.


Building microtubules I have some questions regarding building microtubules:

Do alpha and beta monomers always exist as dimers when they are bonding to form tubulin?
When tubulin structure is destroyed, do alpha and beta monomers fall apart as dimers or monomers? and does it happen at the positive or negative end?

Microtubules polymerise from and depolymerise into alpha-beta-tubulin dimers.

Both happen on both ends, see this question: At which end does polymerization of microtubules occur?.


When does lactation occur? High levels of estrogens and progesterone antagonize prolactin’s effect on the mammary glands, and it’s only after the placenta has been removed and the levels of estrogens and progesterone has decreased that prolactin effectively stimulates milk production in the alveoli. However, I’m also aware that many hormones cause the maturation of the breasts and mammary glands during pregnancy—is anything produced then? When does lactation really occur—before birth or after birth? I ask this because I’ve heard things about milk leaking out of breasts during pregnancy, and there’s also the fact that the breasts seem very heavy and laden with milk during parturition.

Stage I lactation occurs from midpregnancy onward; stage II is the onset of substantial milk secretion associated with having given birth.

  In humans, stage I occurs at approximately midpregnancy... the gland is sufficiently differentiated to secrete milk, but secretion is held in check by high circulating plasma concentrations of progesterone and, possibly ...estrogen.

You ask,

  ...is anything produced then?

Yes. The mature primed breast produces colostrum, containing sodium, chloride, immunoglobulins, lactoferrin and other substances.

  I’ve heard things about milk leaking out of breasts during pregnancy...

Not at all common that I know of. I'm sure one can manipulate the breast to get a small amount of milky discharge, but that's a big leap from leaking. More common (again, that I'm aware of) is galactorrhea associated with early oral contraceptive pills, prolactinomas, and other conditions.

  the breasts seem very heavy and laden with milk during parturition.

The breasts mature during pregnancy in preparation to make milk; that's why they get bigger. They can get even bigger when they are actually full of milk. It may not be as obvious in a human, but in milk animals (goats, cows, etc.), well, a full udder is pretty obvious.

Different researchers divide lactogenesis into a different number of stages; this is a simple two-stage approach.
Lactogenesis: The Transition from Pregnancy to Lactation


Why dont "growing degree days" have units of degrees Celsius (or do they)? From Wikipedia:

  Growing degree days (GDD), also called growing degree units (GDUs), are a heuristic tool in phenology. GDD are a measure of heat accumulation used by horticulturists, gardeners, and farmers to predict plant and pest development rates such as the date that a flower will bloom or a crop reach maturity.

GDD is calculated as $\frac{T_{min}-T_{max}}{2}- T_{base}$ - so a quick check of the units would indicate that they are in the same units as T, i.e., degrees C. However, they are usually presented without units.

Why is this?

Actually, the units are °C days   or °F days. The units are mostly given in the typical name, Growing Degree Days where which temperature unit is meant is understood from the context.  Much more important is knowing the base temperature ("T_base") since this value can be different in different usages, even for the same type of organism.


Where does the initial action potential come from? When talking about action potentials we say that previous neurons caused an action potential in this neuron and that this neuron's action potential caused the same in further neurons.

But what is the origin of the first-ever action potential?
Maybe in a living organism, there are no action potentials initially because the brain is always "on" and some part of the brain can always initiate processes in an other. If that is the case then how is the brain turned "on" initially? If not, then how does the first action potential get triggered from the "resting state"?

The very first evoked spike is most likely triggered by spontaneous activity, as even neurons with no synaptic connections are able to fire action potentials (Luhmann et al. 2016). Later in life neurons can be excited by the external environment through sensory stimulation. At some point the central pattern
   generators also mature and, either by network synchronization or tuning of intrinsic neuronal properties, are able to maintain a self-sustained activity pattern.

The question is then what triggers spontaneous activity during development? It has to do with calcium signaling, both exogenous and from internal stores. The exogenous trigger is paracrine release of GABA and glutamate before the formation of synapses (Rosenberg and Spitzer 2011).


Gradualism vs. Punctuationalism TLDR? Just read the bold bits!

I started with Darwin's Origin of Species, and then read Dawkins's first three books The Selfish Gene, The Extended Phenotype, and The Blind watchmaker (I just started River out of Eden).

Dawkins talks of Gradualists and Punctuationalists as if their views are incompatible but my initial understanding of Darwin was that both of these are true. My understanding is that if you look at an individual line of heredity then you will see a very consistent and gradual change through the generations (at the mutation rate), but if you look at the population as a whole you will see "periods of rapid evolution".

To me this seems easy to reconcile. Imagine a gene for fur thickness in polar bears, if each nth generation has a 'random' mutation for thicker or thinner then for each line of heredity you'll see a random walk about the starting point. Most of them will go up a bit, then down a bit, and end up close to where they started, some will be a bit further away, and a small number will be far away (much thicker or thinner fur) in a Gaussian distribution. So any random sample from the population that happens to become a fossil is most likely to be in the middle (i.e. unchanged over many generations).

Now if there's a sudden environmental change, or a one-off freak event such as a very cold winter, say that only the 10% with the thickest fur survived this cold winter (and perhaps a very small number of others who got lucky). Now very quickly within a few generations, that thick fur gene will dominate and as the population grows back to whatever size the environment can sustain it will be present in much greater absolute numbers than before the selection event. When looking at random samples of the population throughout this period, you might conclude that there has been a "period of rapid evolution". If the change is more gradual than a single sudden event, for example it gets colder over 500 years, each year the ones with the thinnest fur die off and the thicker fur genes get more popular in the population. This would appear to be a very rapid period of evolution, but really all the evolving happened gradually, long before the selection event.

My question really is what's wrong with this view of things? Dawkins seemed to anticipate all my thoughts and objections while I read his books and provided explanations, except for this one. This kept nagging at me the whole time and he never mentions it at all. I can't imagine I'm the first person to think this way (especially since Darwin himself pretty much said this) so why doesn't Dawkins explain it (either as correct or as incorrect with the reasons why)? Can someone please explain it to me either way?

If I understand your question correctly, you are essentially distinguishing between the timescale on which the variation in the character of interest is generated, and the timescale on which selection prunes the population based upon that variation. The argument is then that "all the evolving happened gradually, long before the selection event" because that is when the variation was generated.

To me, this seems to be a misuse of the term "evolution", which is usually defined as a change in trait or allele frequencies in a population over time. Under that definition, much of the evolution does occur via the selection event. Before, you have a wide range of trait values; after, only a narrow selected set of trait values. In such a model, selection indeed is the major cause of allele frequency or trait value change.

In practice, both processes are usually acting in concert; variation is being produced by mutation and recombination and eliminated by selection at comparable rates so that the net amount of variation in the population is at an approximate steady state. This is essentially the model Darwin espouses, though note that Darwin does not have our modern understanding of heredity and therefore is not able to explain how variation is generated or preserved.

Additional note: When thinking about models of the kind that you describe, it is also key to understand that if you have a large number of loci affecting your trait (e.g. coat thickness), then the Gaussian distribution prior to strong selection will not include the extreme phenotypic values. If there are 20 diploid loci interacting additively to determine coat thickness and the mean individual has 20 thickness alleles and 20 thinness alleles, no individuals in a reasonably sized population will initially have all 40 thickness alleles, or even 39 or 38 etc. Selection for thickness will change the mean, and will also result in individuals outside of the initial range of variation. If the mean is 30, you may well get an individual with 38 or 39 or even all 40 thickness alleles. So once selection occurs, new more extreme phenotypes will suddenly appear. Nothing strange has happened in terms of rates of generating new variation; in fact this is just a consequence of reassorting the current alleles under the new allele frequencies.


Is there any possibility that gender is determined by Temperature? One day I was watching TV show. It was based on Fire Dragon. They stated that if the dragon provide greater warmth to the egg, then a male Dragon will hatch. And if the Dragon provide less warmth to the egg it will be female Dragon.
This was totally Science Fiction!!

But is there any possibility that, the Temperature decides the Gender of progeny.

It is definitely more than science fiction. Many species have sex determination that depend upon the temperature.

As a rule of thumb, when it comes to sex, not much has been invented in fictions. The diversity of reproductive system is HUGE! I will not mention 1% of the existing complexity in sex systems. For simplicity, below I will limit my concepts and examples to big animals only. I won't talk about

double fertilization
cloning
parthenogenesis
dosage compensation
Mating types
Cases of multinucleated cells typically in fungi but not only
Asexual reproduction
Systems with more that two genders or with coexisting hermaphrodite along with a single other gender
Liability factor
Reaction norms for sex determination
How reproduction relate to all that
How dosage compensation relate to all that
How the concept of individual relate to all that
etc...

Sex Determination System: GSD vs ESD

There is a great diversity of sex determination system. The standard is to classify them in two

Environment Sec Determation (ESD)
Genetic Sec Determation (GSD)

Of course, the reality is more complex. In many species a mixture of both genetics and environment clues matter.

Within ESD species, there is quite a bit of variety. Some species use temperature (e.g. crocodiles, Nile tilapia, Australian skink lizard), others use social cues (e.g. clownfish, swordfish, boa constrictor).

Within GSD, there is also a great deal of diversity. By far not all species use the XY system used in mammals.

Related post

Do males of all sexual species have Y chromosomes?
Have there been any theories put forward as to the reasons behind Temperature-Dependant Sex Determination in reptiles?


Photoreceptors and light with mixed frequencies I am interested in how the activation of a, say, blue cone depends on the incident light. Wikipedia tells me this:

 ,
which describes how strong the activation of the blue cone is for light with a single wavelength and a given intensity. But what happens if the incident light has several frequencies?

My question is: given the intensity i(f) of the incident light at frequency f, what is the activation of the blue cone?

(A natural guess would be that if b(f) is the activation curve in the figure, then the activation of the blue cone should be the integral of b(f)*i(f) over f. But I have not found any confirmation of this guess. For example, in the reference for the picture above, only pure light was used in the experiments.)

Yes, current color models assume a linear response in the spectrum.

Given a light with mixed spectrum $\Phi(\lambda)$, the response of a cone with spectral sensitivity $\Psi_i(\lambda)$ is a (nonlinear) function of the L2 inner product:

This is how CIE XYZ color space is defined.

Reference:

M. D. Fairchild. Color Appearance Models, 3rd edition. 2013 (p.63)
https://en.wikipedia.org/wiki/CIE_1931_color_space


What kind of factors determine how someone looks according to their race or ethnicity? From what I read, race is considered the biology, the physical traits inherited by ancestry. Ethnicity and nationality have to do with social construct and cultural identity. This is almost the same things as sex and gender, where the former means the biological characteristics, and the latter refers to the social identity.

So, is there any relationship between race, ethnicity, and nationality? For example, Asians have a different cuisine than Europeans, which consists of whole grain and wheat, which explains why they are generally shorter? What makes them have slanted eyes? Is it because they have been known to look up at the sun constantly that they developed that characteristic over time?

What makes Mexicans have black hair, brown eyes, and medium skin, or have higher foreheads? Again, does this have to do with the cuisine that they have, or something else?

The only explanation I have heard about race is that melanin affects the colour of the skin. It is always sunny in Africa, which is why Africans have really dark skin, despite the fact that all of humanity derived from Africa. Europeans lived in more cloudy weather, so their skin became paler. I'm sure there's more to these findings.

Concept of race

The concept of race often poorly represent the genetic structure of populations. There is therefore an important socio-cultural aspect to the concept of race. The first sentences from wikipedia > race make this point clear

  Race is a concept used in the categorization of humans into groups, called races or racial groups, based on combinations of shared physical traits, ancestry, genetics, and social or cultural traits. Although such groupings lack a firm basis in modern biology, they continue to have a strong influence over contemporary social relations.

What explain why people of different race look different?

You should most definitely have a look at the post Why is a heritability coefficient not an index of how “genetic” something is?

Your question can therefore be rephrased as "What is the heritability of the phenotypic trait X in humans?", where trait X could be anything of interest such as hair colour for example.

The answer for such question is always the same. It goes in three points

It depends upon which phenotypic trait you are looking at
For whichever trait you consider, it will most certainly be a combination of both genetic and environmental factor.
The evolutionary reasons for the existence of such distinction among groups will again depend upon which trait you're looking at.

If there is one particular trait that is of interest to you, you might want to open a new post to ask what is the heritability of this trait and whether there is any selective reasons for why different ethnic group differ for this trait.

You might be interested in a short and easy intro course to evolutionary biology such as Evo101 by UC Berkeley


Does our nose detect only if there is change in odor? If I enter a room with certain odor, I can sense the odor. However, if I stay there for some time I cannot sense it anymore. A new entrant to the room can still smell it or I have to leave the room for some time and upon returning I can sense it again. Does our nose detect only if there is change in odor?

Senses in general adapt to continuous stimulation due to various processes. One such process is simply the exhaustion of the reserves of a receptor, or secondary neuron, due to a depletion of neurotransmitters. Entering a room activates a fresh pool of chemical receptors, thereby generating a clear sense of smell. However, this dims due to adaptation. Exiting and re-entering the room after a while revives the neuronal response. More central adaptive responses may also play a role. A comparable effect is seen in the tactile sense. For example, the awareness of wearing a ring or watch fades quickly. Changing its position revives the percept. So yes, sensory systems like olfaction and touch are more responsive to differential stimuli.


Neuronal Architecture of the Brain To what extent do brains (e.g. of humans) contain recurrent  connections?

I am studying artificial neuronal networks and frequently encountered the statement, that recurrent neural networks are closer to biological neuronal networks than for example feed forward networks. But I didn't find information on the question if feed forward or recurrent architectures dominate the brain architecture.

The recurrent patterns of connections in a network are known as network motifs.

You can check this paper out. They have identified common network motifs in different types of real networks including neural networks (of C.elegans though).

Apart from feed forward loops, bi-fan is also a common network motif in neural networks.

Perhaps the connectome project has data for human brain which you can analyze for identifying network motifs. You would have to request for the data, though.


Why are Birds and Reptiles with abundant yolk sac polyspermic? I was given an explanation that birds and reptiles are polyspermic because they have an abundant yolk sac. But how does it explain the thing?

Chicken as an adult is not using in my opinion yolk as an energy source.
Yolk is used during embryogenesis as the primary energy source with blastula and gastrula -stages and during organogenesis, since the embryo needs proteins and energy somewhere.

How does abundant yolk sac make birds and reptiles polyspermic?

My professor says that

  The yolk sac is not connected to the mechanism of polyspermy or
  monospermy. [Amount of yolk inside the oocyte is then again.]  The
  oocytes of reptiles and birds are yolk rich  - polylecithal  for instance.

where
lecithal = yolk containing and some pieces of information about here.


Are the bacteria in the stomachs of unborn babies beneficial? Babies are born with bacteria in their stomachs. I heard on The radio that when a child is given antibiotics for the first time unique bacteria in the stomach are destroyed and cannot be replaced. Is this true, and, if so, does this have negative effects on the health of the newborn?

Closely Related, but different: What bacteria do unborn babies contain?

It's a fascinating topic! While most of the bacteria known to colonize babies comes from the vaginal tract during birth and then later, through breastfeeding, although there is evidence to suggest that microbial colonization may begin before birth.

Regarding what these bacteria are, our microbiomes are composed of probably hundreds of species of bacteria from at least four major phyla: actinobacteria, proteobacteria, firmicutes and bacteroidetes (see the review for more on them).

As for taking antibiotics, I find it highly unlikely that taking antibiotics would completely destroy any native gut flora species. I certainly can't find any evidence to suggest that that might be the case. In general, when we have to take antibiotics, the offending bacteria are a relatively small population, compared to our native species and are less well-adapted to our body environment. Antibiotics work with our own immune defenses to clear our system of pathogenic species. Antibiotics also hurt our native flora, but less so than the ones that make us sick.

As for your last question regarding health, I wouldn't exactly say that having a microbiome promotes better health, so much as that your microbiome is critical for survival and health. There are actually nutrients that we need for survival that we cannot digest without our microbiota and a wide number of diseases, from immune disorders to potentially depression, can arise from an unhealthy microbiome.

As a fun bit of trivia to ponder in parting, our bodies are composed of 90% bacterial cells by count. Sweet dreams...  :-)


How can seedless fruits not be GMO? Biology is the closest I could find to botany on SE.  Grafting can not occur naturally and so if a fruit does not have seeds there is no way it could reproduce in nature.

That logic makes complete sense to me so I am wondering why seedless fruits claim to not be GMO?

Take for example, Satsuma oranges.

Were they somehow crossed like a mule?  See here.  And then grafted over and over again?

It appears they occur naturally and are then grafted.  See here.

So the deeper question is does grafting create a "clone" of the grafted organism?

And deeper yet, what defines genetically modified ( GMO ) from simple genetic variation?

GMO stands for Genetically Modified Organism.

Grafting a plant to a rootstock of another plant is a form of plant husbandry -- a farming technique -- but this isn't changing the DNA code of either of the plants. Sort of like you receiving a donated organ wouldn't be the same as Genetically Modifying you. When a desired trait arises in a plant this is a way to keep reproducing it without having to wait for cuttings or seeds to grow.

There are some plants such as seedless watermelon that are reliably made by crossing two seed species. You take two species of watermelon, Species 1 and Species 2. Both of these are normal -- they make seeds. When you cross them, you get seeds that grow into AB hybrids, seedless watermelons. These AB are infertile, so you have to cross A and B again each year to get more seeds to plant.

Species 2 has twice the number of chromosomes as 1. They are able to cross and make seeds that grow. But when the [1x2] plants grow and try to form seeds, those cells have an odd number of chromosomes. The process of making seeds and pollen -- meiosis -- has a step when half of the chromosomes go into one cell and half in another. Because there is an odd number, the process never finishes and you get no seeds.

to demonstrate how this doesn't work, lets look as a simple example.
Species 1 has two chromosomes [A and B]. It has two copies of each chromosome in all of its cells (one from each parent), and just one copy in its sex cells

Species 1 Normal Cells [AA BB] and sex cells [A B]

Now, Species 2 has a different set up. It has twice the chromosome number
Its normal cells are [aaaa bbbb] and its sex cells are [aa bb]

this means that when you cross pollen from one with seed from the other, you get
[aaA bbB] or [AAa BBb]

When these crosses try to make seeds, its impossible to halve the triplet chromosomes.

True GM technology is used to do things such as, in olives taking the genes that cause oil production to occur, and copying them many times. This gives you more oil production.

Or, in tomatoes -- when you pick a tomato the cells of the skin start expressing a gene that makes the skin soften and break apart. This facilitates seed dispersal. GM deletes that gene, making the fruit bruise less, reducing need for packaging and quadrupling the shelf life.


Can I compare Shannon indices of metagenome gene data? I'm comparing 12 Metagenomes. I'm using HMM counts of a number of proteins known to exists as groups within certain operons. I have grouped the HMM counts for each type of operon and calculated the Shannon-Weaver index for each Metagenome.

My question is: Can I compare these Indices? Is there a better test to use than Mann Whitney U test? I would like to do this on the ungrouped data, but I have many zeroes for some fields?

I'm not an expert on Shannon-Weaver Index, but according to wikipedia it is the same as exponentially transformed Renyi entropy. If it is the case, you can compare them since they are scale invariant summary statistics. If you want error bars, you can always try resampling methods such as bootstrapping. Hypothesis testing can also be done with bootstrapping, although the power of the statistical test may not be very strong and fail to reject the null.


Why does supercoiled DNA run faster? The DNA exists in linear and cirular forms. The latter form has interesting feature called Supercoiling. The more number of writhe makes it more supercoiled because of which it gets more compact. Hence the supercoiled DNA runs faster compared to other forms in a gel electrophoresis experiment.

But why does the circular DNA run slower than linear DNA? Isn't circularity supposed to make it compact?

To understand this, you have to understand how an agarose gel is able to effect the size separation of DNA in the first place.

The reason agarose gels work to separate DNA based on size is that the electric field produced the electrophoresis machine is imparting force on the DNA. The effect of the increasing charge for DNAs with increasing nucleotides is offset almost exactly by the increasing mass of those larger DNA molecules, so in the absence of the gel, all pieces of DNA would migrate through the apparatus at a constant rate.

The reason they don't is because of the mesh framework of the agarose gel. This is like a dense forest or a large number of sieves with random sized holes. There's small holes (of varying size) and in order for large pieces of DNA to work its way through the gel, it has to weave through these pores. Smaller pieces of DNA can go through smaller pores, so they take a faster, more direct path, while larger pieces have to make detours, and even when they find a pore they can fit through have to spend a bunch of time flopping around before they can stuff themselves through the pore.

So it's not strictly speaking "size" or "compactness" by which the agarose gel separates molecules, but instead it's the ability of the piece of DNA to navigate through the mesh of agarose molecules. While relaxed, circular  DNA is more compact than an extended linear DNA of the same nt length, that doesn't necessarily mean that it has an easier time working its way through the network.

For example, a linear piece of DNA can orient itself so it goes "end first" through the mesh. Once the end of the DNA goes through a pore, it's relatively easy to pull the rest of the DNA through the same pore, as compared to trying to bend the DNA and pull it "sideways" through the pore - you have to remember that on molecular scales, DNA is rather stiff. You can't kink it in half very easily, so a piece of DNA that has to go through the pore "sideways" takes much more space than one that can be threaded through end-wise, even if you bend it as much as possible into a hairpin.

With a relaxed circular DNA, there's no end, so it's always going through the pores "sideways" so it's limited to the larger pores. In addition, it's large and floppy, so it takes quite a while to go through the pores that are there. When you add supercoiling, you don't fix the issue with going through pores "sideways", but you do limit the flopping around it does, so once you do find a pore of a usable size, you get the rest of the DNA through faster. In fact, with enough supercoiling you reduce the time spent flopping around enough that it goes through the agarose even faster than the linear DNA, which - while it can fit through smaller pores - still spends a bunch of time flopping around instead of going through the pore that it's started to go through.


What are these little creatures living inside a silk web? They are found in Bangladesh. Some of my observations:

They are so small that their legs and appendages look transparent.
Their colour is brown and they have no wings.
My eye sight is not brilliant, but the don't look like spiders. Their head and mouthpart vaguely resemble that of the termite. When I tried to observe them closely, they looked bed-bug-shaped.
They are fragile: when I tried to grab them by pinching, they just squashed.
They seem like living in a big city made of silk strands. The can easily move in, out and within the structure which slightly bigger, potential predators could not.

Unfortunately my mobile camera is not good enough to capture a clear image of them. Click images for larger version.

From the comments above (in particular, "it's head and mouthpart vaguely resemble that of the termite") it is possible that what is here is a Webspinner colony (Order Embioptera); if so you either have one of the few species in which the male is wingless, or the colony was without adults of that sex when your question was asked.  Webspinners are distantly related to termites, but have little or no economic importance (some species have been accidentally spread by man).  The Wikipedia article (https://en.wikipedia.org/wiki/Embioptera) has some basic information on the group (including photographs of both sexes and of nymphs), and references for further information; identification of species from Bangladesh will be problematic, as Edward S. Ross (the expert on this group from the mid-1940s, and not fully replaced--he has retired) had reportedly collected enough undescribed species to more than double the known diversity.


Cell evolution: immortality vs reproduction Many sci fi movies produce interesting ideas and technologies that we seem to be able to realize in real life at some point. "Lucy" was not one of those movies.

But Morgan Freeman's speech in the movie on cell evolution did interest me.

The speech claimed that cells in harsher environments evolve towards immortality, while cells in favorable environments evolve toward reproduction.

Is this idea accurate?

You'll see that in many cases, when any sort of cell enters a zone of intolerance or zone of physical stress, the replication machinery gets put on the backburner (and thus replication). Expression of stress-response proteins like heat shock proteins is increased as a result (1). If a cell isn't within acceptable parameter to undergo division at G1 or G2 (anoxic environment, etc.), you'll find mechanisms like G0 phase or sporulation are preferred until the environment returns to something less stressful (2). I wouldn't say cells would rather be immortal, per se, but longevity or even apoptosis/entosis/etc. would be preferable to replication if nothing is going right (3, 4).

To be clear, when we're talking about evolution that's a tough one. Sure, some sort of stress-response transient signal could induce some lasting cell memory selecting toward a specific function. I simply don't have the data to quote you in that aspect, however.

Biology of the heat shock response and protein chaperones: budding yeast (Saccharomyces cerevisiae) as a model system.
Slonczewski, J., & Foster, J. (2011). Microbiology: An evolving science (2nd ed., p. 143). New York: W.W. Norton.
DNA damage-induced apoptosis
Cellular Stress Responses: Cell Survival and Cell Death

As a footnote, while replication does occur in sporulation, the replicated chromosome is destroyed in the process of forming the actual spore.


Why do mosquitoes appear to be repelled by magnets? A few days ago, I was playing with magnets and thought of placing one near a live mosquito (I had it held between my two fingers so it had no chance of escaping). When near the magnet, it twitched and flew away! I tried the same with semi-alive mosquitoes, but nothing really happened.
I googled about this and learnt that mosquitoes have got to do something with magnets, but I'm still confused. Could anyone tell me why mosquitoes get repelled by magnetic fields?
PS. I'm no biology student, so please go easy on me, thank you ahead of time!
Source (PDF)
EDIT: Strickman et. al. (2000) says:

we found that some specimens had a significant magnetic remanence
Could this possibly be the reason why mosquitoes may get repelled by magnetic fields?

That paper also states:

the mosquitoes were able to detect the magnetic fields but sensed a magnetic pattern that was impossible in nature.

Reference:
Strickman, D., Timberlake, B., Estrada-Franco, J., Weissman, M., Fenimore, P. W., & Novak, R. J. (2000). Effects of magnetic fields on mosquitoes. Journal of the American Mosquito Control Association-Mosquito News, 16(2), 131-137.

According to the research cited by the OP (Strickman et al. 2000), mosquitoes alter their behavior in the presence of a magnetic field, and the measured changes in behavior are statistically significant. The authors of the study found that the external surfaces of mosquitoes attract ferromagnetic particles from the air. They speculate that changing their orientation to the earth's magnetic field helps mosquitoes navigate while approaching a potential host.
Reference Cited
Strickman, D., Timberlake, B., Estrada-Franco, J, Weissman, M, Fenimore, PW, and R.J. Novak. 2000. Effects of magnetic fields on mosquitoes. Journal of the American Mosquito Control Association 16(2):131-137.


Does eating bananas help digestion? I don't know what I am asking is silly or not, but I have always heard that eating a banana after a meal helps in digestion.

Some people says before food while others say after.

Is it a fact or some silly myth?

Bananas seem to contain lots of dietary fiber that help move consumed food through the intestines (popular article) thereby promoting digestion. Whether one should eat bananas before or after dinner is probably a debatable subject (Yahoo forum).


What is the response vector in the fMRI GLM model? In fMRI, univariate analysis typically makes use of the general linear model (GLM), where the relation between experimental condition and BOLD activity is estimated with a linear regression model for each voxel separately ("mass univariate model"). However, I found it surprisingly hard to find out what the response vector $Y$ contains. I am aware that it is some measure of the blood oxygenation level dependent signal (BOLD signal) - but what is measured exactly, i.e. what are the units? Is it the oxy/deoxy ratio, or is it another property?

Short answer

The units aren't important, and are typically normalized.

Longer answer

The name "BOLD" is actually very instructive: Blood Oxygenation Level Dependent contrast (or signal). BOLD is not directly measuring anything like oxygenated/deoxygenated ratio, or we would probably call it something more similar to that: oxy/deoxy ratio.

Instead, "BOLD" is just the MRI image you get when you set up the scanner properties in a way that happens to be influenced by the oxygenation level of blood. Oxygenation level is far from the only contributor to the BOLD signal, but experimentally you try to factor out any influences that are time-varying but not interesting, and you ignore baseline levels that don't change.

fMRI works because the transverse relaxation time T2 of water in blood depends on oxygenation of the blood. From the original paper showing BOLD contrast in a rat brain Ogawa et al. 1990:

  At the 7-T field strength used in this study, T2 varies from 50 msec at 100% oxygenation to 4 msec at 0% oxygenation. The venous blood signal becomes very weak when the T2 value becomes comparable to or shorter than the echo time of the signal acquisition. At 60% oxygenation level, the estimated T2 value is 18 msec, similar to the echo time used in this report.

In other words, if you produce gradient-echo images with an echo time of 18 ms, the images you get show very different signal levels at 100% vs 60% oxygenation. Depending on the strength of your magnet, you can tune this time to go after the differences you want to see.

There is no straightforward way to compare images recorded in different conditions (i.e., different scanners, different parameters) on any useful scale of measurement. Instead, people typically report relative values, either in time or space. For this reason, you often see BOLD signals expressed as a % change or in terms of standard deviation (i.e., z-scores).

Ultimately, for fitting a general linear model it doesn't matter: you can freely scale a dependent variable without changing the structure of the model fit, all you influence is the interpretation of the magnitudes of the intercept and coefficients.

References

Ogawa, S., Lee, T. M., Kay, A. R., & Tank, D. W. (1990). Brain magnetic resonance imaging with contrast dependent on blood oxygenation. Proceedings of the National Academy of Sciences, 87(24), 9868-9872.


How old is the oldest intact DNA? DNA fragments are known from bone fragments from the Mesozoic, but these don't count. I'm guessing the oldest DNA is recovered from permafrost, but how old exactly?

Well, the oldest intact DNA found is actually 419 million years old, and it belongs to (not surprisingly) bacteria. Samples were extracted from surface-sterilized salt of different geological ages (23, 121, 419 million years of age, MYA).

But as you mentioned, these are fragments. Studies on the half-life of DNA suggest that even under ideal circumstances, DNA sequences older than 1.5 million years will be too short to be readable.

The oldest genome known to date, though, is 700,000 years old, and was recovered from samples from a horse leg bone. You were correct, the leg was in permafrost. That's a considerable jump from mastodon and polar bear fossils which were about 50,000 and 110,000 years old.


How do the brain and nerves create electrical pulses? The information between the brain and peripheral nerves is sent via electrical pulses or signals, How then does a non-metallic human cell manage to conduct an electrical
signal?

This is quite a big question! I'll try to outline the basic view.

First, let's review how neurons signal between each other. The canonical way for a neuron to send a signal to a downstream neuron is by generating an action potential, the "electrical impulse" you have heard of. This action potential causes the release of neurotransmitter at a point where the two cells are very close to each other called a synapse. The downstream postsynaptic cell receives the neurotransmitter signal and converts it into a small electrical signal. If enough of these small electrical signals happen in a short time, they sum together and are likely to initiate an action potential in the second cell and the cycle repeats all along the circuit.

How is the electrical signal generated? The basics of how this works was worked out most famously by Hodgkin and Huxley in 1952. The short story is that the plasma membrane is selectively permeable to ions. Let's build the concept from the ground up.

The toolbox

Imagine a sphere of plasma membrane that represents a simple neuron. For starters, we assume that this membrane is bare lipid with no membrane-associated proteins. Because of the hydrophobicity of the bilayer, charged particles cannot diffuse through the membrane.
The cell is bathed, inside and outside, in a solution containing many ions (charged atoms), including sodium (Na+), potassium (K+), chloride (Cl-), and calcium (Ca2+). As we noted above, these ions cannot go through the membrane without "help".
Now we add an ion pump protein into the membrane which will pump sodium ions out and potassium ions in. This particular pump, the Na-K ATPase, creates an excess of sodium ions outside the cell and an excess of potassium ions inside.
Now we add a potassium ion channel to the membrane. This protein creates a pore in the membrane that only allows potassium ions through. This particular protein's pore is always open. Now things start getting exciting...
What do the potassium ions do now that they can go through the membrane? Ions will move based on the forces created by their electrochemical gradients. The pump created a chemical gradient by putting excess K+ inside, so the K+ ions start to flow out through the ion channels. But K+ ions are positively charged, so when they flow out, positive charge starts building up outside and negative charge builds up inside. This electrical gradient opposes the chemical gradient, tending to pull the K+ ions into the cell while the chemical gradients pulls K+ ions out. The influx and efflux reach an equilibrium at the Nernst potential, where the electrical and chemical forces equal out. For physiological concentrations of K+ ions, the K+ equilibrium potential is about -80mV or -90mV. This means that K+ ions will flow until the outside of the cell is 80-90mV more positive than the inside of the cell. We started at 0mV, so K+ ions mostly flow out.
We now have a membrane potential, a difference in electrical potential between the inside and the outside of the cell at about -80mV (usually closer to -70mV or -60mV in "real life"). In particular, this membrane potential is the resting potential that exists when the cell is not active. We can simplify for now and think of the resting potential as being set by a resting permeability of the membrane to potassium ions, but not to sodium ions. We call this membrane polarized, and thus depolarization is when the membrane potential becomes more positive, and hyperpolarization is when the membrane potential becomes more negative.
Now, we add to the membrane a voltage-gated sodium channel, an ion channel that passes only sodium ions but is usually closed. The voltage-gating means that this ion channel is sensitive to the membrane potential. At the resting potential, the pore is closed and the membrane is still impermeable to sodium ions. When the membrane potential becomes slightly more positive, the channels opens and sodium ions can flow. This channel is also inactivating, so that when it opens it only opens for a short period of time, letting in a limited amount of sodium.
What way will sodium flow when we open this channel? Because of the negative resting potential (-70mV) and the excess of sodium ions outside due to the pump, both the electrical and chemical gradient will drive sodium ions into the cell. The sodium equilibrium potential is usually around +60mV.
To complete the machinery for generating an action potential, we also add a voltage-gated potassium channel to the membrane. It works just like the voltage-gated sodium channel that is also closed at rest and opens when the membrane potential becomes more positive. This channel opens a bit more slowly than the sodium channel does, but it does not inactivate.

Generating an action potential

Ok, so how do these parts come together to create an electrical impulse?

The cell sits at its resting membrane potential, with all of its voltage-gated channels closed. It receives a signal from an upstream cell that causes a slight depolarization. The action potential will initiate when the membrane potential hits the threshold potential.
At the threshold potential, the voltage-gated sodium channels open letting sodium ions flow into the cell. The sodium flux pulls the membrane from the resting potential (-70mV) towards the sodium equilibrium potential (+60mV). These values are far apart, so the driving force is large and the membrane depolarizes rapidly. This is the action potential upstroke.
The depolarization also activates the (slightly slower) voltage-gated potassium channels. The potassium ions flow out and drive the depolarized membrane (about +20mV at the action potential peak) back towards the potassium equilibrium potential (-80mV). At the same time, the sodium channels are inactivating so that sodium is no longer depolarizing the membrane. The repolarization rate is usually slower than the depolarization rate. This is the action potential downstroke.
The whole process of the action potential depolarization/repolarization cycle takes about 2-3 milliseconds in an "average" neuron. Once the cell reaches resting potentials again, the membrane is basically reset. The voltage-gated channels are turned off. The ion pump moves the potassium ions that flowed out and the sodium ions that flowed in. That patch of membrane is ready to fire another action potential!

As a final note, I'll mention that the voltage-gated sodium channel provides a mechanism for the action potential to propagate down the axon. The action potential is initiated in one location of the cell, and creates a depolarization. This depolarization causes the voltage-gated sodium channels in neighbouring regions of the membrane to open and generate an action potential cycle of their own. This is how an action potential travel down axons (and sometimes dendrites too).


What is the point of being selection-free? I'm reading "Highly efficient endogenous human gene correction using designed zinc finger nucleases" by Urnov et al. They propose a way to use zinc finger proteins for gene therapy. They repeatedly claim their method is "selection free" and it seems they are claiming that as an advantage to their method.

Why would selection free be an advantage? Wouldn't you have to select for the transformed cells anyway to be relevant in a clinical setting?

Urnov et al. are trying to effect gene therapy - where a mutation causing a genetic form of severe combined immunideficiency (SCID) (also known as the bubble boy syndrome). Affected SCID patients can have little to no immunity to infection what so ever.  SCID in this case is caused by a single site mutation in the IL2R-gamma gene.

Their method is to use a DNA binding protein (containing zinc finger domains that bind the DNA) which attracts a DNA repair enzyme.

The result is that 18% of the cells have the SCID gene repaired.  This would have been a trivial result if they had applied selection, which generally refers to any method which eliminates cells which were not affected (in this case having their DNA repaired) by a transformation like their treatment.  They claim that 18% of all the cells were repaired (I assume this is in a cell culture).  This implies that if their treatment were applied to living tissue, 18% of the cells would be repaired in situ, which should be enough to restore immune function.

While its possible to apply a selection method to gene therapy, it would be far better if you did not.  Cancer chemotherapy for instance is a selection based treatment for instance, relying on toxins which kill fast dividing or growing cells preferentially, leaving the slower growing tissues relatively viable.   Still its quite toxic and disruptive to the patient.


How do we know that our genetic similarities to other species is actually due to common ancestry? I know all about how the fossil record shows more human-like species coming about over time, and how modern testing proves we have genetic similarities with other animals.

All that says is we have similar genetic blueprints to animals in the past and present. How do we know these similarities are caused by having a common ancestor?

We don't know, and we never will. Science doesn't work that way. But evolution is the simplest hypothesis that is both falsifiable and consistent with lots of experimental data. Therefore it is the currently accepted scientific theory.

I would agree that genetic similarities between current species does not in itself suggest that they evolved from a common ancestor. But knowing the genome sequence of various species let's you do much more than simply measure pairwise similarity between species. The structure of genetic variation (losses, duplications, inversions, mutations ... ) also fits with evolutionary models. And crucially, genome sequences confirm predictions made by the evolutionary theory --- evolution is not just a post-hoc explanation of data, it has actually been tested many times over, and has never been falsified.

A good example is the sequencing of the human and chimpanzee genomes. We knew long before any genome was sequenced that humans have 23 chromosomes (23 pairs), while chimpanzees have 24. If the theory of evolution is correct and we do have a common ancestor, then that ancestor should have 24 chromosomes, like the chimps do, and it must be that in humans, one chromosome is a fusion of two ancestral chromosomes$^*$. This is a strong, testable prediction: if we don't find this arrangement of chromosomes, then evolution is proven wrong! In the 1980's, the sought fusion chromosome was found using high-resolution cytogenetic banding: it's chromosome 2. Modern genome sequencing later localized the precise fusion point on the human chromosome.

Also, the fossil record provides a timeline, not just a bunch of more or less similar organisms. In general, we don't find old fossils of modern-day animals (including ourselves), but we do find old fossils of species that no longer exist today. And when piecing together the findings, it looks like there is a sequence of gradual changes over time. That's a pretty good clue. What hypothesis might fit this data?

If you are suspicious about the theory of evolution --- which is fine, you should think critically about everything in science! --- then you must look for an alternative hypothesis which is falsifiable and fits the data. (Note that "god made everything" is not a falsifiable hypothesis, since it makes no testable predictions, and therefore not relevant to science.) If you come up with anything, let us know!

$^*$ As pointed out in comments, a priori one could imagine other rearrangements between the ancestor genome and the chimpanzee/human genomes that give the same result, but I believe this is the simplest hypothesis.


Question about Autosomal Recessive Alleles I had a homework question that I could not figure out.

It states:

  A woman has cystic fibrosis in her family and did not want to have a
  child that suffered from the disease. She and her spouse went for
  genetic testing and counselling. She tested positive as a carrier and
  her spouse tested negative, and their first child was born with cystic
  fibrosis. Explain how this could happen.

This doesn't make sense because the punnet square would be:

$$
\begin{array}{c|c|c}
  & A  & A  \\
\hline
A & AA & AA \\
\hline
a & Aa & Aa
\end{array}
$$

This says there are no two recessive alleles which can cause  cystic fibrosis.

If really cystic fibrose is expressed only in homozygotes, then here are some possible explanations:

Mutation

very improbable

Autofecundation

very improbable

False Negative when testing the father

Because of the test False Negative Rate. @kmm made a very interesting comment below. He said that according to this article 75% of the mutations coding for disease correspond to one pattern (3 base pair deletion). The other 25% of the mutations coding for disease might not be detected in the standard test. If so, it is very likely that a the test conducting on the father was a false negative. It would be worth further investigate the test that are usually performed to confirm this.
Because of human error. The laboratory operator might accidentally switch two samples or accidentally introduce stranger DNA before PCR (assuming the test is performed through sequencing)
I have no idea concerning the probability for such thing to occur!

trisomy

The assumes that a trisomic that have two recessive allele coding for disease and on dominant allele coding for health yield to a individual expressing the disease!
The gene for cystic fibrose is on chromosom 7. Trisomy 7 is extremely rare if I'm not mistaken.

The father is not the father!

According to different studies between 5% and 20% of the people are not fathered by the man they think is their dad.
According to this source the frequency of the disease is 1/2500 in UK. Assuming Hardy-Weinberg equilibrium the frequency of the allele coding for disease should be $p=0.02$.
The probability that the baby comes from another man and that the baby express the disease is $$a \cdot \left(\frac{2\cdot p\cdot (1-p)}{4} + \frac{p^2}{2}\right)$$, where $a$ is the probability that the baby was fathered by another man (let's say 10%) and $p$ is the frequency of the allele coding for the disease (0.02). The division by 2 and 4 are due to the probability that the (real) father and the mother transmit both the alleles coding for the disease.  This probability equals $$0.1 \cdot \left(\frac{2\cdot 0.2\cdot (1-0.2)}{4} + \frac{0.2^2}{2}\right) = 0.01$$ This seems to be from far the most likely explanation! Note: this assumes that the mother is heterozygote (does not express the disease) otherwise, the probability would be 0.02.


X Linked Hardy Weinberg Equilibrium Problem In a given population under Hardy Weinberg equilibrium, 40.0% of men have hemophilia. What is the probability that a random man and random woman will have a daughter with haemophilia?

I think the answer is 16%, but the answer given is 9.6%. According to  Hardy-Weinberg principle, p2 + 2pq + q2 = 1. In order to inherit the disease, the mother must either be a carrier of have the disease, which occurs with probability 1-q2 = 0.72

Therefore, the odds of having a child with the disease is (0.84)(0.4). Since it asks for the probability of a girl, the total must be divided by two, so the answer is 0.168

Where am I wrong?

I make it 8%. Here is my reasoning.
The gene is X-linked.
40% mutant males, so freq(mutant allele) = p = 0.4, and freq(wt allele) = q = 0.6
To get a mutant female we have to have a mutant male parent, probability = 0.4
Of these matings one half will produce a female offspring so 0.4*0.5 = 0.2
i.e. 20% of matings derive from a mutant male and produce a female offspring.
Now look at the female mate:

probability(mutant) = p2 = 0.16
probability(carrier) = 2pq = 0.48
probability(wt) = q2 = 0.36

so our 20% of matings that have the potential to produce a mutant female offspring partition as:

mating with a mutant female: 0.2 x 0.16 = 0.032 mutant female offspring
mating with a carrier female: 0.2 x 0.48 = 0.096 of which:
0.048 mutant female offspring
0.048 carrier female offspring
mating with wt female: 0.2 x 0.36 = 0.072 carrier female offspring

(sanity check - 0.032 + 0.096 + 0.072 = 0.2)
Thus the probability of random mating producing a mutant female is 0.032 + 0.048 = 0.08 (8%)
Incidentally there is another way of thinking about this. Note that the H-W frequency of mutant females in the population is 16%. One of the assumptions of H-W is random mating. So the probability of a random mating producing a mutant female = p(female) * p(mutant if female) = 0.5 x 0.16 = 0.08
So - where have I gone wrong?


is it possible that there is no gene at a locus? "the location of a certain gene on a chromosome " is the definition I know for locus. ı just read that a gene is not necessarily present on a locus. how would that be possible?

Like you said in your question - "locus" means location.  A locus may be anywhere on a chromosome - an entire "gene" coding locus, a non-coding locus (junk DNA), a regulatory sequence locus (example - the promoter region of a gene), or just a single nucleotide locus (SNP) etc.  A "locus" is the location of interest on the chromosome.

Yes, it is also possible that any genetic "locus" may be absent if it has been lost by a "deletion".  A deletion is a type of mutation.  They might be a single nucleotide deletion or a very large deletion of thousands of nucleotides. Genetic deletions can happen in several natural ways (a DNA repair error for example), and by other mechanisms, but also through "man made" genetic manipulations.


Is it fine to state every learned behavior has an innate component ? ie. Behavior X is largely/ mostly laerned with an innate component For example human acquisition of language, can we say it is learned, but has an innate component -- because there is a particular structure of the tongue, and perhaps also a specific cognitive ability which is requisite to speaking/ learning a language.

The aforementioned requisites are ones which are reliant on genetics, thus can we say there are innate components to it, even though it is largely, based on experience, as stated in the assertion below.

"The behavior of language acquisition is based on experience, and subject to continual refinement and therefore can be classified as largely learned, however, due to the requisites it also has an innate component to it"

Think of a cake. Is a cake determined by its ingredients or by its preparation (mixing, baking, etc)? It's a meaningless question. The cake is determined by both.

Now think of two cakes. In principal, we can now begin to talk about the causes of their differences. For example, if they had identical ingredients but were prepared differently, then we could say that the differences in the resulting cakes were due to different preparation.

Humans are baked cakes. Quantitative genetics is a field which tries to estimate to which extend differences between organisms are due to genetic factors. Learned behaviors are consistently found to be heritable in quantitative genetics studies. For example, adult vocabulary size is substantially heritable. It is not that the words are literally transmitted to the offspring, but rather genes that influence the cognitive abilities, interests and personality of the individual. That vocabulary size is "heritable" means that a substantial portion of the differences between individuals' vocabulary sizes are due to genetic differences (although by no means only due to genetic differences).

In short, what I'm trying to get at, is that you can only talk about the relative contributions of genes and environment if you're talking about it in the context of differences between individuals. In that case, yes, learned behaviors have an innate component.


How can a sequence be downloaded from UCSC genome browser If I have genome coordinates is there a simple way to download the entire intervening sequence from the UCSC genome browser? I found some fancy way of using ftp but I can't figure it out.

Yes. Table browser allows you to do that.

In the dropdown box called output format select sequence and click the button named get output. You'll get the sequence.

If you don't think it works then this is the output that I am getting. (Fist few lines):

>hg19_gold_AL096773.6 range=chr1:115207623-115347729 5'pad=0 3'pad=0 strand=- repeatMasking=none
GATCTGCCAGCGTCCACCTCCCGAGGTGCCGGGATTGCAGACGGAGTCTG
GTTCACTCAGTGCTCAATGGTGCCCAGGCTGGAGTGCAGTGGCGTGATCT
CGGCTCGCTACAACCTCCACCTCCCAGCCGCCTGCCCTGGCCTCCCAAAG
TGCCGAGATTGCAGCCTCTGCCCAGCCGCCACCCCGTCTGGGAAGTGAGG
AGCATCTCTGCCTGGCCGCCCATCATCTGGGATGTGAGGAGCCCCTCTGC
CTGGCTGCCCAGTCTGGGAAGTGAGGAGCGCCTCTTCCCGGCCGCCATCC

Actually Table browser is quite useful as you can get different kinds of data for a given genomic region which include annotations, variation, transcription factor binding sites etc.


Why is sarcoma more prevalent and common in right heart? Ewing's sarcoma or Ewing sarcoma is a malignant small, round, blue cell tumor. It is a rare disease in which cancer cells are found in the bone or in soft tissue. It is more common in right heart than left heart? Why? Which one is more dangerous?

Ewing's sarcoma is a bone cancer. As such, it does not arise as a primary tumor in the heart.

Ewing's sarcoma does metastasize. Like any metastatic cancer, it seeds along it's venous return to the heart, "taking root" in suitable tissue.

Cardiac metastases of Ewing's sarcoma are exceedingly rare, with only a few reported cases. Since all blood returns to the right side of the heart first, then the lungs, this is where distant metastases of Ewing's sarcoma are found. The side doesn't matter; it's never good.

Primary heart tumors do occur, about 1/20th as often as metastatic tumors. Of these, myxomas are the most common. Of sarcomatous types, which are very rare, they can occur anywhere.

Ewing's Sarcoma
Metastatic Ewing's Sarcoma to the Right Ventricle
Primary Malignant Sarcomas of the Heart and Great Vessels in Adult Patients — A Single-Center Experience
Echocardiographic and pathologic characteristics of primary cardiac tumors: a study of 149 cases
Primary cardiac sarcomas: an immunohistochemical and grading study with long-term follow-up of 24 cases


Why do plants have green leaves and not red? I know plants are green due to chlorophyll.

Surely it would be more beneficial for plants to be red than green as by being green they reflect green light and do not absorb it even though green light has more energy than red light.

Is there no alternative to chlorophyll? Or is it something else?

Surely it would be even more beneficial for plants to be black instead of red or green, from an energy absorption point of view. And Solar cells are indeed pretty dark.

But, as Rory indicated, higher energy photons will only produce heat. This is because the chemical reactions powered by photosynthesis require only a certain amount of energy, and any excessive amount delivered by higher-energy photons cannot be simply used for another reaction1 but will yield heat. I don't know how much trouble that actually causes, but there is another point:

As explained, what determines the efficiency of solar energy conversion is not the energy per photon, but the amount of photons available. So you should take a look at the sunlight spectrum:

The Irradiance is an energy density, however we are interested in photon density, so you have to divide this curve by the energy per photon, which means multiply it by λ/(hc) (that is higher wavelengths need more photons to achieve the same Irradiance). If you compare that curve integrated over the high energy photons (say, λ < 580 nm) to the integration over the the low energy ones, you'll notice that despite the atmospheric losses (the red curve is what is left of the sunlight at sea level) there are a lot more "red" photons than "green" ones, so making leaves red would waste a lot of potentially converted energy2.

Of course, this is still no explanation why leaves are not simply black — absorbing all light is surely even more effective, no? I don't know enough about organic chemistry, but my guess would be that there are no organic substances with such a broad absorption spectrum and adding another kind of pigment might not pay off.3

1) Theoretically that is possible, but it's a highly non-linear process and thus too unlikely to be of real use (in plant medium at least)
2) Since water absorbs red light stronger than green and blue light deep sea plants are indeed better off being red, as Marta Cz-C mentioned.
3  And other alternatives, like the semiconductors used in Solar cells, are rather unlikely to be encountered in plants...

Additional reading, proposed by Dave Jarvis:

http://pcp.oxfordjournals.org/content/50/4/684.full
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691134/
http://www.life.illinois.edu/govindjee/photosynBook/Chapter11.pdf
https://www.heliospectra.com/sites/default/files/general/What%20light%20do%20plants%20need_5.pdf


What do you call clearly different sub-groups within a species? If you look at species of bees and ants, you can clearly see there are drastically different specialized ants, like queen ants and workers. They're both part of the same species, yet are still obviously different. What is the proper name for that phenomena?

In eusocial insects, especially ants and bees, these groups are called "castes" (see e.g. Hölldobler & Wilson, 1990. This is the same term that is used for social stratifications in some human societies e.g. in India.

One definition of caste is:

  ...the physical or the behavioural/physiological phenotype of a eusocial individual, or both.

(from Hölldobler & Wilson, see also antwiki.org)

Some division of labour as well as collective rearing of young can occur in prosocial animals as well, but there the term caste is not used.


Intermediate of Krebs cycle that can form Chlorophyll? This was a question in a test in my school today.

Q) Which intermediate of Krebs cycle further can form chlorophyll?

A) Oxaloacetic acid
B) Citric acid
C) Succinyl CoA
D) Fumarate

Given answer was (C).

How can Succinyl CoA form chlorophyll? All I could find was related to porphyrine ring. Can anyone explain it or recommend a good source?

The standard treatment of this topic is covered in Section 24.4.3 of Berg et al., available freely online:

Succinyl CoA is a precursor for porphyrin in mammalian cells by condensing with glycine to form δ-aminolevulinate as shown in this diagram from that book:

This reaction is catalyzed by mitochondrial δ-aminolevulinate synthase.

To quote from that reference:

  Two molecules of δ-aminolevulinate condense to form porphobilinogen, the next intermediate. Four molecules of porphobilinogen then condense head to tail to form a linear tetrapyrrole in a reaction catalyzed by porphobilinogen deaminase. The enzyme-bound linear tetrapyrrole then cyclizes to form uroporphyrinogen III, which has an asymmetric arrangement of side chains. This reaction requires a cosynthase. In the presence of synthase alone, uroporphyrinogen I, the nonphysiologic symmetric isomer, is produced.

This is illustrated in Fig. 24.35 of that section, which also shows that uroporphyrinogen I gives rise to protoporphyrin IX, the precursor of haem:

As regards the synthesis of plant chlorophyl (which also contains a porphyrin ring), the review quoted by March Ho contains the following statement:

  The porphyrin ring with its conjugated double bonds is assembled in the chloroplast from eight molecules of 5-aminolevulinic acid…

(5-aminolevulinic acid is the chemically preferred name for δ-aminolevulinic acid.)

However the review goes on to explain that although 5-aminolevulinic acid synthesized in plant mitochondria uses the same pathway as mammals, that produced in the chloroplast and used for the synthesis of haem that gives rise to chlorophyl uses a different pathway, termed the C5 pathway, in which — as March Ho stated — glutamate is the precursor:

I suspect that the person who set the question is an animal or biochemist who thought he would try a variant of the standard question “which intermediate is a precursor of haem”, and ventured into waters where he was out of his depth.


What can the timing of human urination tell about the human's physical condition and circadian rhythms? I've noticed a peculiar phenomenon. A subject drinks 400 ml of water, then observes time until the urge to urinate is felt. The time is 15 minutes. The subject releases water. 14 minutes later another urge to urinate is felt. The subject releases water again.

I'm particularly interested in what kinds of biological systems are involved in timing of such events.
Does the time depend on how full the subject's stomach is? Does caffeine and other diuretics play a part?
Is it time of day (circadian rhythm) sensitive?
Does that predict anything about the suppression/release of diuretic hormones?

What I'm trying to understand is if the timing between human urges to urinate after water consumption can be used to make predictions about the human biological clock and the state of various systems within the body (for example the digestive system).

I will be conducting this experiment at different times of the day. My hypothesis is that at night, when diuretic hormones are suppressed, the timing would be longer for the same amount of water consumed. This is based on my limited research in the area.
Update: I did perform the same experiment at night, the time was 75 minutes for the same amount of water. The experiment was performed at the end of one of sleep cycles, which makes me think that 75 minutes was the duration of the subsequent sleep cycle.

I appreciate your input on the subject, along with any keywords that can help me advance my research in this area.
Thank you!

The fact that urine output (enuresis) and other kidney functions are circadian is well known, just search on pubmed 'circadian urine kidney'. This can be due both to the fact that liquid consumption is less during the night and to the fact that hormones regulating kidney function like aldosterone and plasma angiotensin II are circadian.


How many cells are in prophase on this onion root tip slide? In the following image, I have to identify the cells in the different phases (not counting the cells that are too faded to see), and it's fairly easy to identify metaphase, anaphase, and telophase, but I'm not sure I'm doing it right for prophase vs. interphase.

I try to see if there's a nucleolus or not, but sometimes it's difficult. When I counted, I got 7 cells in prophase. Is this close to what you guys see or am I way off?

Thanks!

Hard call on early prophase versus interphase, especially since these are not natural distinctions with discrete boundaries but are used to articulate a continous process.

I'd say you're pretty close, I count six for sure. That includes the one in the top row on the far left that is partially clipped in the photo. One iffy possibility is in the third row just left of the obvious anaphase on the left.

Unless your teacher is far more particular than I was with students, I think you're good to go.


Do human beings have pheromone receptors? What is the current consensus on whether or not humans have receptors that detect pheromones?

If there are purported receptors, in what anatomical areas are they located?  With what organ systems do they interact?

From what I have gathered, I would think that humans do have receptors that are able to detect pheromones.

For example, some studies that have indicated human responses to pheromones.  Of these pheromone responses, some have been traced to the olfactory mucosa and olfactory epithelium.

The trace amine-associated receptors (TAAR) for which humans have 7 genes (TAAR1, TAAR2, TAAR3, TAAR5, TAAR6, TAAR8, TAAR9) and 2 pseudogenes (TAAR4P, TAAR7P) are found in the olfactory epithelium whereas androstadienone receptors are found in the olfactory mucosa.  As suggested by the anatomical location, these receptors interact with the human sense of smell and the olfactory system

More information: http://en.wikipedia.org/wiki/Pheromone#Humans


How is instinct carried from one generation to another? How can non-structural information, specifically instinct (a fixed pattern of behavior that an organism reverts to as a response to certain stimuli), be passed on from generation to generation (such as an unborn baby's instinct to begin inhaling and exhaling amniotic fluid while still in the mother's womb to "practice" breathing, a sea turtle's inclination to enter the sea after hatching, etc.)?

Does DNA have anything to do with it? I can't imagine what else it could be, considering that the genome is the only thing an organism passes on to it's progeny.

This stuff is hard-wired into either the organism's nervous system, or endocrine signalling pathways (e.g., hormones), or possibly a combination of those two mechanisms.  In that sense, yes it is encoded in the genome, but not in a language that we can understand or interpret yet. Also, don't overlook all of the macromolecules that the female provides to the developing egg during oogenesis, your mother gave you lots of things besides a copy of her genome--you just don't have any of those macromolecules left now--but you wouldn't be here without them.


Could two women have a child through artificial insemination/genetic engineering? This is something I just thought of while looking up stuff about matriarchies.

I recall a comic series I heard of once, I think it was called 'Y, the last man'. In that story, all males (besides the main character, and one monkey he keeps as a pet) were wiped out by a plague or something, leaving the world's population entirely female. They of course start focusing on developing cloning technology to avoid the extinction of the human race.

But thinking about it, would it really be necessary for them to develope such a technology? Afterall, females can already incubate offspring, they just can't impregnate each other. But could it possible to extract the DNA from a woman's egg, and put it in another egg?

Note that I know nothing about artificial insemination or genetic engineering, so I don't know if that would work (I've only heard of people putting one animal's entire genome into an egg, not from two individuals). So I'd like a more expert opinion. Could you actually do that? Or the mechanism for mixing the DNA of two individuals more complicated than that?

Recently, researchers have been able to produce sperm and ova from germ cells.  It's not been proven yet that the two can produce a viable embryo, but probably the technique will be perfected eventually. [https://www.technologyreview.com/s/608452/a-new-way-to-reproduce/]


Where does tracrRNA comes from? I'm talking about CRISPR system. I know the crRNA is transcribed from the palindromic repeat and the "spacer" but I don't know where the tracrRNA comes from.

Usually the tracrRNA is a part of the CRISPR locus and is encoded in the the vicinity of the CRISPR array (e.g. upstream or downstream of the cas genes or the array).

http://www.genome-engineering.org/crispr/wp-content/uploads/2013/01/crispr_processing1.jpg


Why is gyrification advantageous? Standard 'Explanation':
I've seen countless neuroscience articles and experts explain that 'cortical gyrification is advantageous because it increases surface area which obviously increases your intelligence' (e.g. this wikipedia article).
Question(s):
But this explanation is woefully lacking, why does surface area matter at all? That implies  that somehow empty space is contributing to cognition (since the alternative is that space being filled with brain matter).
My best guess:
The only guesses I have are that perhaps it functions like skip layer connections in Residual ANNs. This section of the wiki page, says it is advantageous because 'it allows neurons to be closer together' which I guess kind of corroborates my idea?
Question(s):
But it is still far too vague and speculative. Why could these same wiring patterns not just emerge within a smooth-surfaced brain without wasting space? Also, does this imply that if you got more brain matter to fill in these spaces later your intelligence would decrease?

Short answer
The structural anatomy of the cerebral cortex is closely related to its functionality. The cortex is a thin sheet of only a few cell layers deep. Expansion of processing power requires enlargement of the surface area of this sheet, and simply increasing its volume doesn't help. As a consequence, gyri and sulci developed during evolution to accommodate this restriction.
Background
The human brain is characterized by a prominent and enlarged cortex, much larger than that of other primates. This is mainly due to the great expansion of the cerebral cortex during evolution. The underlying structures have, however, remained stable (Toro et al., 2008). The cerebral cortex houses the higher cognitive functions that separates us from other animals, allowing us to reason, talk, write books, develop culture and so on. As a result, to allow the development of these higher cognitive functions in man, it was the cortex that needed expansion, and not the deeper more ancient brain structures that govern more basic needs of life (breathing, heart beat etc.).
Because the cortex forms only a thin sheet a few cells thick that overlies the rest of the brain, a solution had to be found when the cortex was expanding in our early hominid ancestors, because the whole brain did not need inflation, just the cortex. Folding of the cortex increases the surface-to-volume ratio such that an expanding cortical surface fits onto a relatively stable base.
To take this a step further - why not increase volume in order to fit those extra neurons in? Since the volume of a ball increases by a third power with radius, why on earth would nature keep holding onto increasing the surface area, and not simply inflate the cortex by enhancing its thickness?
This has to do with the fact that the vertical architecture of the cortex has remained remarkably stable during evolution. In other words, evolution of a bigger cortical area to enhance higher cognitive processes has occurred in the most parsimonious way so typical for evolution: take an existing structure and enlarge it when there is need for more.
The cortex typically consists of a thin sheet covering the brain, and is not more than 3 mm thick. The neocortex represents the great majority of the cerebral cortex. It has six layers and contains between 10 and 14 billion neurons. The six layers of this part of the cortex are numbered with Roman numerals from superficial to deep (Fig. 1). Layer I is the molecular layer, which contains very few neurons; layer II the external granular layer; layer III the external pyramidal layer; layer IV the internal granular layer; layer V the internal pyramidal layer; and layer VI the multiform, or fusiform layer (Review of Clinical and Functional neuroscience, chapter 11).

Fig. 1. Cortical layers. source: Mental Construction.
Basically, layer IV receives most input from the periphery via the thalamus (visual, auditory, tactile inputs etc.), layer II/III takes care of horizontal projections for further processing, while layer V takes care of the output (motor output etc.). This basic architecture cannot be changed easily without changing the entire core workings of the cortex. As an analogy - to speed up computers in a parsimonious way, one can expand the number of processors quite easily. Coming up with a speedier processor is difficult these days, as evolution of single processor capabilities is pretty much at a dead end.
Thus, to increase the number of cortical neurons, the cortical surface must be enlarged. As the basis (subcortical structures) remain pretty much the same, creating folds (gyri and sulci) is the best way, and perhaps the only way to increase cortical surface area.
Reference
- Toro et al., Cerebral Cortex (2008); 18(10): 2352–7


If eating 100% fat 2 times more worth the energy I spend during the day, will I store body fat? So in theory, insulin hormone is the one that tells the body "eat more. don't burn body fat". Alongside with glucose blood level regulation and turning excessive glucose into liver (which later goes into muscles as glycogen or into fat cells). Fats are the only thing that do not provoke insulin secretion. 0 glycemic index.

So in theory, if I eat 2 or 3 times more worth the energy I spend during the day, I'll never store body fat because of 0 glycemic index?

Or will I still gain because such huge fat intake will make liver into making glucose from fats & proteins?

Surely u'll never find a sustainable product to eat that is 100% fat, but just a few examples are butter, lard, heavy cream. This is just a theoretical question, where the proteins/carbs intake is so low that it is not count.

Could you please clarify it since I got lost.

There are a couple of reasons why this approach doesn't work quite as well as you might hope.

First, insulin doesn't go away after a high-fat meal. This paper reports changes in serum insulin following pure-sugar and pure-fat meals. Although there is much less of an increase in insulin following the pure-fat versus the pure-sugar meal, you will notice in Figure 1 that the insulin levels following the pure-fat meals (panel A) are higher than the levels during a fast (panel B). So even if high insulin were the only signal for fat storage, your dream of eliminating insulin with a high-fat meal is not realistic.

Second, when a high-fat diet is designed for medical purposes, a good deal of care is required to avoid significant potential adverse effects. Adequate protein intake is still required, and amino acids from the protein can be converted to glucose. Furthermore, ketoacids are produced when fatty acids from ingested fat are in excess. (As noted in comments, humans do not convert fatty acids to glucose.) Although ketoacids can be excreted in the urine (admittedly, heading toward your goal of not storing all the calories you consume), the net metabolic effect on the body when you excrete ketoacids is increased acidification, which in turn can lead to difficulties with potassium regulation and thus, in severe cases, with heart function. In the extreme if this were continued for a long time, you may face a problem of life-threatening ketoacidosis as occurs in type-1 diabetics (low/no insulin) whose disease is not being managed.

That said, your basic idea is similar to the arguments for low-carbohydrate diets. How well they work and, if they do, through what mechanisms are still somewhat controversial, as I understand. Insofar as they work through excreting some of the ingested fat through urinary loss of ketoacids, however, the associated risks need to be considered.


Effect of alcohol on parasites I recently came across an article saying that fruit flies use alcohol to deter parasites. The researcher was quoted as saying there have not been any studies on the effect of human alcohol consumption on parasites. Is there any research being done on this? Another related question I have is whether the fruit flies can tolerate higher alcohol concentrations than mammals/humans.

Drosophila is seen as a highly alcohol tolerant species which is mainly dependent on the environment it lives in. So are flies, which are captured in the cellar of a wine yard more tolerant to alcohol than flies which are captured outside (see first reference).

The environment in which the flies grow up and live does not influence the activity of the alcohol dehydrogenase enzyme but seems to influence the expression (amount) of it. The more alcohol is present, the higher the expression is (see reference 2).

I haven't seen explicit data on the comparison between humans/mammals and drosophila, but since drosophila is seen as a good model organism to study alcoholism, I would think it is not too different. (see reference 3).

Micro-differentiation in a Natural Population of DROSOPHILA
MELANOGASTER to Alcohol in the Environment
Alcohol tolerance, ADH activity, and ecological niche of Drosophila
species
Functional Ethanol Tolerance in Drosophila


Recombination frequency, linked genes, and independent assortment Gene R is genetically linked to gene T with a recombination frequency of 0.3. Gene T and gene X assort independently from each other. Your colleague tells you that gene T and gene X reside on the same chromosome. How is this possible?

So I know that R and T are on the same chromosome. T and X assort independently, so they should be on different chromosome. And then due to recombination, X gene crosses over so that it's also on the same chromosome as T and R? Can someone please help me?

The comments pretty much answer the main concern here. But just to sum up:-

  "....T and X assort independently, so they should be on different
  chromosome...."

Not necessarily. They can be on the same chromosome at such a distance that there is usually atleast one chiasma formation between them, and will undergo independent assortment, i.e.  segregation of one gene among the gametes will be independent of the other. They will pretty much act and segregate like mendelian factors. Specifically, if the recombination frequency is 0.5 (50cM or map units' distance on the chromosome), they will assort independently.

  "....And then due to recombination, X gene crosses over so that it's also
  on the same chromosome as T and R...."

This part is a little bit unclear. I assume (correct me if I am wrong) is that you are assuming X,T,R to be alleles, which can be present on only one chromatid and hence recombination might change their distribution and positions relative to one another. But as the question states, they are genes (or specifically gene loci) which are present on both chromatids and their relative position is fixed. The recombination frequencies refer to the recombination of different alleles at this locus.


Satisfication with irrelevant things I am not sure if this question is better suited CogSci.SE so please tell me.

My question is why are we satisfied when we get things that aren't useful in any important way? For example, relating to Stack exchange, why are we satisfied and happy when we get badges because badges don't increase reputation or help you get privileges in Stack Exchange. Similar with Winter Bash. Why are we happy when we get hats? They are just for decorations. Is there a biological explanation for this?

What chemical leads to us getting that feeling of satisfaction?

Dopamine is one of many neurotransmitters which modulate information passage between one brain area to another. Dopamine is thought to play important role in  pleasure, addiction,
and learning.Massive increase in the
amount of dopamine released in the brain during video game play, the releasing of dopamine
are in areas thought to control reward and learning.

Reference

Certain neural structures, called the reward system, are critically involved in mediating the effects of reinforcement. A reward is an appetitive stimulus given to a human or some other animal to alter its behavior. Rewards typically serve as reinforcers. A reinforcer is something that, when presented after a behavior, causes the probability of that behavior's occurrence to increase. Note that, just because something is labelled as a reward, it does not necessarily imply that it is a reinforcer. A reward can be defined as reinforcer only if its delivery increases the probability of a behavior.

The reason why we are happy when we get these decorative items is because they are things which we can possess. Reward system is responsible for this kind of behavior, when we gain or achieve something in life its usually gets rewarded in the form of a pleasure. Foraging ants and bees are provided with these reward systems and which in turn makes these animals to derive a pleasure out of their daily achievements. Whether in life, video game or stack exchange or anything, an achievement is something brain thinks relevant and rewards it with a pleasure in mind.
Considering badges in stack exchange, really badges are an analogy to reputation. When we have more badges usually our charisma increases like in the case of reputation. Also levels and scores in games,achievements in office, stack exchange badges and hats all fall under the same analogy. So when we have more badges we are meant to be more successful and brain will reward us to attain more badges and also people like hats too.

References
Digital Media: Transformations in Human Communication - Paul Messaris, Lee Humphreys
Cyber Junkie: Escape the Gaming and Internet Trap - Kevin Roberts


Doubly-compound leaf examples? I've got a project where we collect leaves, classify them, etc. There are some required classifications. One of the requirements is to get a doubly-compound leaf. What are some trees that are doubly-compound? Please help! I have Hickory, but that's just compound I think.

Edit: I did try googling, but it's hard for me to know what's available in my region.

From Comments: I live in Tennessee, U.S.

Albizia julibrissin (Persian silk tree) is doubly compound (AKA bipinnate) and has a conspicuous pink/white fluffy flower. This tree is an Asian native, but it's a commonly cultivated (and equally commonly escaped) plant in the U. S. You should be able to find it in numerous locations. Look in yards and along roads.

http://www.missouriplants.com/Pinkalt/Albizia_julibrissin_plant.jpg

For native species: Gleditsia triacanthos (honeylocust) is a fairly widespread (though uncommon) example of bipinnate leaves. Here is an image from Will Cook's wonderful website:


What does the 34/70 in Saccharomyces pastorianus Weihenstephan 34/70 stand for? I've searched everywhere.
No Wikipedia page.
No information on NCBI.
I searched all occurrences of 34/70 in some primary research articles!
The best I've found is this brewery forum where someone asked the same question.

And the user rockfish42  answered:

  No idea why they use that number, but it's the catalog number at
  Weihenstephan's hefebank.

I went to the Yeastbank website at Weihenstephan for some info. The keyword here is "Stamm," which is German for stem, clade, clan, or strain. So, I would take this to mean that the 34/70 is an isolate (#70) of strain 34. Two of 34/70's strengths, according to the link above are it makes clean beer and gives a pleasant taste profile due to its low yeast-like aroma in the finished beer. I can attest to that firsthand, having had on numerous occasions the pleasure of partaking of Weihenstephaner beer in its home city of Freising.


What does hypolithial mean I'm writing a thesis in biology and my supervisor asked me to find literature about beetles living under rocks - specifically she wants me to find something about hypolithial diversity. However Google doesn't even recognize the word 'hypolithial' so I'm kind of stranded without any references on where to start searching.

I know that hypo lithia comes from ancient greek and means below stones, but nobody mentioned it like that in the literature.

Has anybody heard of this term or knows a similar one which I could use for my research?

Google for sublithic or hypolithic.

You'll find lots of things like (https://link.springer.com/referenceworkentry/10.1007%2F978-3-642-11274-4_767) with further references and links


Examples of environmentally influenced gene-expression in humans? In discussions of the relevant importance of genetic and environmental influences on the development of the individual, it's often stated that the genetic and environmental influences interact.
An example that is often given is a certain kind of rabbit (usually white), carrying a particular gene for fur color. When the proper allele is present, AND the rabbit is exposed to cold, it will a dark spot on its fur. When the allele is present, the dark spot does not develop without the cold, and when the rabbit has the opposite allele, the spot will not develop even with cold exposure.

This is fine, but when I want to explain genes and environment to people, it has two pedagogical flaws:
(1) it's about rabbits
(2) it's about a trait people don't really care about

Is there a human example of this phenomenon?
That is, a phenotype which requires BOTH a certain genetic background and particular environmental influences in order to be expressed?

I think your question is interesting, though the use of "expression" is misleading in context of your rabbit example.

Examples of environmentally influenced gene-expression in humans?
...
That is, a phenotype which requires BOTH a certain genetic background and particular environmental influences in order to be expressed?

In the example you give, the color-changing phenotype is not due to changes in gene expression but rather a conformational change in a tyrosinase variant at low temperatures that leads to decoupling of an inhibitor from the enzyme.  This is not to say that there aren't any changes in expression with changes in temperature -- only that the phenomenon you describe is ultimately a change in enzyme activity and not the induction of a specific allele.  See Kidson and Fabian, 1981 [1] --

It is proposed that at the normal body temperature of 37 degree C, tyrosinase from Himalayan skin is strongly bound to an inhibitor. At lower body temperatures, the affinity of the enzyme for the inhibitor decreases, thus allowing the synthesis of melanin to increase. This change in affinity of the enzyme for the inhibitor could be regulated by temperature-induced conformational changes in either the enzyme or the inhibitor or both.

Note that this study was conducted in "Himalayan" mice, not rabbits, though the authors do reference an earlier rabbit study [2] --

These results are in support of Danneel's visual observations ('41) that "ferment" activity of Himalayan rabbit skin is absent at temperatures above 25 degree C.

the full text of which can be found, in German, on Google Books.

Concerning a human example of allele-environment interactions, look no further! The same temperature-sensitive tyrosinase mutation has been reported in people with oculocutaneous albinism (OCA) [3], albeit with a slightly different phenotype.  From the abstract:

In this paper, we report a new type of OCA that results from a tyrosinase allele producing a temperature-sensitive enzyme. The proband had white hair in the warmer areas (scalp and axilla) and progressively darker hair in the cooler areas (extremities) of her body. Melanocyte and melanosome architecture were normal. Quantitative hairbulb tyrosinase (dopa oxidase) assay demonstrated a loss of activity above 35-37 degrees C. Plasma pheomelanin and urine eumelanin intermediates were reduced and correlated with hair melanin content. This is the first temperature-sensitive tyrosinase mutation to be reported in humans and is analogous to the Siamese mutation in the cat and the Himalayan mutation in the mouse.

References

Kidson SH, Fabian BC. The effect of temperature on tyrosinase activity in Himalayan mouse skin. J Exp Zool. 1981 Jan;215(1):91-7.
Frisch KV, Goldschmidt R, Ruhland W, Winterstein H. Ergebnisse der Biologie. Eighteenth Volume.
King RA, Townsend D, Oetting W, et al. Temperature-sensitive tyrosinase associated with peripheral pigmentation in oculocutaneous albinism. J Clin Invest. 1991;87(3):1046-1053.