What's the biggest obligate anaerobic organism discovered till now? Beside many anaerobic single cell organisms, there are some annelid worms that are obligate anaerobic at least in their early development stages. Probably, due to low concentration levels in nature, some of the other respiration methods (like uranium or iron reduction) can limit the maximum size an organism will grow. Given the lower energy level extracted compared to the oxygen respiration, what size limits enforces the sulfate, sulfur or methanogenesis respiration? What's the biggest discovered organism, extinct or alive, that is obligate anaerobic?

There are three worms which have been found in the sediment of the mediterranean seafloor, which not only live without oxygen but also do not tolerate the exposure to oxygen. They belong to the metazoans, for more details see either the report (reference 1) or the original article (reference 2). They reach a size og about 1mm.

References:

Scientists discover first multicellular life that doesn't need
oxygen
The first metazoa living in permanently anoxic conditions


Why are there seven entries for Pimpinella dioica in the Catalogue of Life? And six for Haliclona digitata, and five for Ichneumon varius. A couple of the duplicate entries are synonyms for other species, which is understandable, but most are the "accepted name". Shouldn't there just be one Pimpinella dioica? By my count there are 3068 species with two or more "accepted name" entries in the 2014 database. Where do these duplicate entries originate? Do they serve a purpose or are they errors?

Probably a question for catalogueoflife.org forums, but they don't seem to have any discussion area, so seeing if anyone here can answer.

While any large database may have errors that can lead to multiple entries (sensu har-wradim's answer), I think most of the multiple entries detail the taxonomic history associated with that species. Your link to the sponge Haliclona digitata provides a clear example. First, dismiss the H. digitata (Schmidt, 1862) entry. As clearly stated, it is a synonym for a different species of sponge, Tedania anhelans.

The remaining entries are all links to various homonyms of H. digitata. Skimming through the World Porifera Database entries (via the "Online resource" links), provides the necessary information. Lendenfeld's use of Chalinorhaphis is the original description. It is the senior homonym, meaning the specific epithet (digitata) has precedence over junior names. The junior names include Adocia digitata (Baer) and Gellius digitatus (Koltun). It was probably Tanita & Hoshino that transfered digitata to the genus Haliclona but I cannot verify this without seeing the article.

The taxonomic history can also be tracked for Ichneumon varius, but the linked databases don't hvae as much detail as the Porifera database for H. digitata. Still, it suggests that the description by Pontoppidan in 1763 is the senior homonym, and the subsequent uses by Cuvier, Gmelin and Muller are junior homonyms.

This is also what I think har-wradim is alluding to for Pimpinella dioica. Unfortunately, the Umbellifer database seems to have little detail in this regard.

The Catalogue of Life provides a convenient mechanims to begin a thorough search for the taxonomic history of a species.


can recessive alleles produce codominance? Maybe I'm confused by the term "codominance", but I wondering if codominance only occurs with two dominant alleles.

Can two recessive alleles produce codominance in an individual?

Likewise, can two recessive alleles produce incomplete dominance?

An allele is not dominant or recessive by itself. It is dominant or recessive compared to another allele. Therefore, if you consider one locus (position on a sequence) that has two alleles (bi-allelic locus), you cannot have two dominant or two recessive alleles. It is like saying that two things are darker. In reality you can either say that one is darker than the other one or that the color is as dark as the other one. So either one allele is dominant (or partially dominant) and the other is necessarily recessive (or partially recessive) or the two alleles are codominant.

Think of a gene that influence a phenotypic trait such as tail length for example. This locus is bi-allelic (two different alleles (=variant of a gene) exist (=segregate) at this locus). We'll call the two alleles $A$ and $B$. An individual that homozygous $AA$ has trait value $M_{AA}$. The homozygotes $AB$ have trait value $M_{AB}$ and individuals $BB$ have trait values $M_{BB}$. Viewing this in a table it gives:

$$
\begin{array}{c|lcr}
\text{Genotype} & \text{Tail length} \\
\hline
\text{AA} & M_{AA}\\
\text{AB} & M_{AB}\\
\text{BB} & M_{BB}\\
\end{array}
$$

The following table gives the tail length of the different genotypes under the different types of interactions (dominance, partial dominance and co-dominance).

$$
\begin{array}{c|lcr}
\text{Interaction} & \text{AA} & \text{AB} & \text{BB} \\
\hline
\text{A is dominant and B is recessive} & M_{AA} & M_{AA} = M_{AB} & M_{BB} \\
\\
\\ & & M_{AA} > M_{AB} > M_{BB}\\
\text{Partial Dominance} & M_{AA} & \text{or} & M_{BB}
\\ & & M_{AA} < M_{AB} < M_{BB} \\
\\
\text{Codominance} & M_{AA} & M_{AB} = \frac{M_{AA} + M_{BB}}{2} & M_{BB} \\
\end{array}
$$

Because, in the codominance case $M_{AB}$ is necessarily between the values of $M_{AA}$ and $M_{BB}$ ($M_{AA} > M_{AB} > M_{BB}$ or $M_{AA} < M_{AB} < M_{BB}$), one can consider codominance as being a special case of partial dominance where neither $A$ or $B$ dominates because they both contribute as much to the determination of the tail length.

Various definitions may exist for such concepts as well as for overdominance (also sometimes called heterozygous advantage) or stabilizing selection for examples. Those definitions differ in the sense that they sometimes apply to the value of the quantitative trait, to the fitness value (which is another quantitative trait) or to genetic polymorphism.


Why are local field potentials generally band-pass filtered? I was wondering what the rationale was behind low-pass or band-pass filtering in local field potential measurements?

It seems to me that we could potentially filter out potentially valuable information by filtering procedures.

Is there a physical limitation for this that would not allow to measure, say, the responses in a frequency range of 0 to 5 kHz?

There is no physical limitation whatsoever on the frequency band you wish to record, other than the hardware limitations on the sampling rate.

Often electrophysiological recordings suffer from noise (mainly in the high-frequencies) and drifts in the baseline (low-frequency range).

In the end, you wish to filter out as much noise as possible, without throwing away the baby with the bathwater. In effect, prior knowledge about the frequency range of the responses of interest are vital. Anything outside that range can, and likely should be filtered out.

For example, FFT analysis of EEGs mainly focuses on bands limited to the frequency range of 1 to 50 Hz. The mains frequency is 50 or 60 Hz, often imposing sinusoidal noise when the room is not shielded. Hence, what reason would there be not to use a low-pass filter with a cutoff around 50 Hz to get rid of it?

Lastly, offline filtering methods are aplenty. My personal preference nowadays is, is to collect the raw data and filter offline. That way you have the baby and the water, and you can focus, with trial and error, on where the baby is and where the water.


What on Earth is this? Found in a field near Braga, Portugal in October 2018.

OK, It does not look like a fungus. just going by the single close up photo - I'm pretty sure it is an abandoned bumblebee nest (or that of some similar social insect).  These bees often nest out of sight under logs or under the ground. Below is a link that may help you with a positive identification. I hope this provides at least a hint. Maybe you can fill in the blanks from your knowledge of your local fauna in Portugal.

http://www.bumblebee.org/lifeCcolDev.htm


General undergraduate zoology textbook recommendation? I am very interested in zoology,and I want to study zoology in my spare time.
Any undergraduate level zoology text book recommendation?

I used Zoology by Miller and Harley in my undergraduate years and I found it to be an engaging, informative text book.


How much energy does a small spider expend per day just waiting for its web to vibrate? Roughly speaking, a small, complex electronic circuit or IC might sit in "sleep mode" using a current of roughly 1 µA (e.g. 1, 2), thereby using roughly $3\times 10^{-6}$ Watts, and that converts to roundly $2.5\times 10^{-6}$ kcal/hour or $62\times 10^{-6}$ kcal/day.

I suppose you could call that 62 micro-kcal/day or 62 milliCalories/day.

One day I noticed a small spider in my home, sitting in its small web, and kept an eye on it. After several weeks of watching I hadn't seen it catch anything. I slightly perturbed the web and it reacted. It was still alive.

Question: I'm curious to know roughly how much energy a small spider needs to sit and wait. Might this be termed roughly the spiders Basal metabolic rate? It could be for any small spider that spends much of its time waiting for prey. As long as an approximate size or mass is available then it could be expressed as kcal/day/kg or some similar unit.

I have read about Kleiber's law in this answer, but I don't think it is meant to extend down to small spiders.

note: I'm just asking for the energy expended during resting periods. Of course during a day the spider may do web maintenance, catch or eat prey, but it's the resting rate of energy consumption, on a daily basis, that I'm asking about.

Short answer
Approximately 240 J on a daily basis.

Background
Ballesteros et al. (2018) modeled basal metabolic rates of insects. They reckoned that endotherms, like insects, basically use energy directly correlated to the number of cells, which is linearly correlated to their body mass. They checked their model with experimental data from Chown et al. (2007) (Fig. 1).

Acknowledging that arachnids aren't insects, but that both are arthropods, let's take an average-sized web making spider, like the black widow, weighing in at 1 g. This yields a basal metabolic rate of 10 J/h, or 240 J/day. However, and given the linear correlation between energy expenditure and mass, a dwarf spider weighing in at 1 mg expends 1000 times less, and a Goliath bird eater approaching 200 g will expend 200 times more.

To convert the unit for the Black widow to a Watt scale, we get 1 J/s that corresponds to 1 W, so 1 J/h corresponds to about 0.3 mW.

Fig. 1. Base metabolic rate for insects. Data from more than 300 species were extracted from Chown et al. (2007). source: Ballesteros et al (2007)

References
- Ballesteros et al., Sci Rep (2018)
- Chown et al., BES (2007); 21(2): 282-90


what makes our body warm? I would think that there would so many chemical reactions going inside our body,friction produced by blood in veins, subcutaneous and visceral fat acting as heat insulators.

I was wondering to what extent different factors play a role in protecting our
body against cold.for example say blood circulation might be responsible for
creating 70% of the body heat and also a person with high blood pressure may produce more heat in his body.

also, perhaps fever or any other disease would be an exception to the normal
heat creating process in our body.just like the gonads or testes which are
cooler than the rest of the body.

In summary, cellular respiration and thermogenin.

Most of the energy in our body comes from cellular respiration. Cellular respiration is how ATP, the major source of cellular energy, is made from glucose. Cellular respiration generates heat mo matter what because not all of the energy from glucose is converted to ATP.

In certain cells, a protein known as thermogenin allows the protons in the cellular respiration to flow from the inner membrane to the matrix (the protons are in the inner membrane of the mitochondria as the electrons from glucose were used to pump them). This generates heat. In regular cellular respiration, the proton gradient is used to make ATP, but now, it juet generates heat.

Also, ATP can be hydrolyzed directly in brown fat cells and muscle cells to produce heat along with inorganic phosphate and ADP.


Why do ladybugs have a different number of points on their backs Everytime I see a ladybug I ask myself this question.
Why does every ladybug have a different amount of points on its back? Is it because of its age? Or because of its genes? Is it inheritable?

The spots on the back of Ladybugs over the surface is defense mechanism to avoid predators. The spots come in different shapes and different numbers. Some say that those dots tell us their age. Since some ladybugs have 24 spots which means its age would be 24 years and that is not at all possible. So this is a popular misconception running around us.

But the real truth about the number of spots on the ladybugs' back is:

  The number of spots on a ladybug does have significance. The spots and other markings do help you identify the species of ladybug. Some species have no spots at all. The record-holder for most spots is the 24-spot ladybug ( Subcoccinella 24-punctata), which has 24 spots, of course. Ladybugs aren't always red with black spots, either. The twice-stabbed ladybug ( Chilocorus stigma) is black with two red spots.

So now we know that the number of spots on the back of Ladybugs will help us to identify what species it belongs to. To give an insight into different species of them you can refer to this Identifying Ladybugs.

The above image shows different species of Ladybugs where you can see the varying number of spots in each bugs' back. More information can be found here Stripes on Ladybugs.


replenishment of wild salmon I understand fish from salmon farms are inferior, so I am wondering if it would be better to 'seed' the original waterways with wild caught roe/milt?  I am sure it is complicated, but so is salmon farming!

The process you propose is called 'stocking', and has been carried out for many different fish species for many years. The practice is, as you suggest, complicated, and more than a little contentious.

In the specific case of Atlantic salmon, Young et al. (2014) provide a non-technical overview of the conservation, population-genetic, and infectious-disease factors at play in stocking decisions. In general, fish raised in hatcheries are often wild-caught, which decreases the wild population, and once they are released, they sometimes have lower survival rates and reproductive success than truly-wild fish. If fish are raised in captivity for multiple generations, they can show evolutionary adaptations for captivity, and once released, captive-adapted fish can introduce harmful genes to the wild population. Similarly, captive-reared fish may be at an increased risk of communicable disease, and may introduce diseases to wild fish after their release.

A further complication from stocking is the impact of the stocked species on the local ecosystem. Many commonly-stocked species are non-native in the areas where they are released, and have negative impacts on the native species in that area. For example, brown trout have been introduced to many waterways in New Zealand, and they are predators of many native species, and compete for food with others. The New Zealand government has trialled an eradication of brown trout from some high-value conservation waterways in order to minimise the ecological damage caused by trout.


What is meant by re-absorption? It is said that PCT, DCT, Henle’s Loop reabsorb the filtrate. Does that mean they absorb the filtrate again? If it is actually reabsorbed to medulla then why it is said that PCT, DCT or Henle’s loop reabsorb the filtrate?

In the glomerulus of the nephron we have filtration occuring. The subsequent formation of an ultra-filtrate travels down the tubulus from Bowmans space; during this journey, the filtrate will be exposed to various transporters and forces such as solvent drags and diffusion gradients, which leads to the (re)absorption of this filtrate. Reabsorption occurs also in medullary tubules and later collecting ducts, until the filtrate (by now urine) reaches the calyces. (Note that secretion - that tubular cells permit the transportation of various electrolytes for instance to the tubulary lumen - also occurs in the nephron, giving it three ways to manipulate the its luminal contents: filtration, reabsorption and secretion)


Can estimating the likelihood of protein sequences adopting functional enzyme folds show life is too complex for evolutionary timescales? An acquaintance provided me with this article1. I can't understand for sure what it is about.

My acquaintance said that it proves that time for generation of even the simplest proteins is on a larger timescale than evolution history (billions of years).

I'm asking you, is that a valid conclusion to be made from this paper? What is in this article that might drive someone to that conclusion?

Axe,D.D. (2004) Estimating the prevalence of protein sequences adopting functional enzyme folds. J. Mol. Biol., 341, 1295–315. http://www.ncbi.nlm.nih.gov/pubmed/15321723

I think your acquaintance is trying to fit real science to some of his personal beliefs (that are obviously wrong).

If you read the article you'll see that it's not about evolution at all, but about protein folding and what proportion of possible sequences gives a working protein. It turns out random sequences are not that likely to fold, which leads to some conclusions about the probable mutational pathways to folded proteins.

The argument of your friend is sort of analogous to the infinite random monkey theorem. If you put a monkey behind a typewriter and wait long enough, eventually he'll write the complete works of Shakespeare. This doesn't mean we waited billions of years for this monkey to type it up, because the world doesn't work like that. There was just a guy with a brain.

In case of the proteins, evolution doesn't work by generating newly (random) 300 residue proteins that work 1 time in a billion. Probably in one generation a copy of the protein is made with the same function, and during many generations the function of this protein drifts towards a new function, while all the intermediate proteins stay folded because they're not that different.


What's the worst that can happen from too much sleep deprivation? Can you die? It is well known that sleep deprivation causes considerable discomfort in humans (and has even used as a form of torture), but nevertheless there have been people who went through protracted sleep deprivation, apparently with no long term consequence.

I've noticed that sleep deprivation seems to trigger an intense sense of "this is bad for me" - yet given the apparent lack of ill effects (beyond the obvious) I cannot say whether this is merely anxiety over discomfort, as opposed to a genuine perception of physiological damage.

What if you were to go without sleep for as long as possible, despite the discomfort? Is it possible to commit suicide in this way (and what would be the cause of death)? Would you fail because you eventually ignore whatever stimulus was preventing sleep, and sleep anyway? Would artificially counteracting the temporary debilitating physiological effects (such as loss of body temperature) allow you to survive sleep deprivation of arbitrary length?

The short answer is: Yes.

Fatal familial insomnia is a genetically passed down disease that at some random point in a carriers life will suddenly stop them from sleeping, ever, they die within 7 to 18 months

I know you did not ask about the disease, but it shows (even without illegal war tests) that it will kill you eventually, even in humans.

I believe in humans without the disease a complete lack of sleep may kill them within weeks, but who knows? maybe it was the drug.


Plasticity between excitatory and inhibitory neurons? All that I've learned about synaptic plasticity only concern the synapses between excitatory neurons. For example, all pyramidal neurons (excitatory) in the cortex have plastic synapses between them, but as far as I know there are no plastic synapses between pyramidal neurons and their inhibitory interneurons.

So I am curious, are there any plastic synapses between inhibitory and excitatory neurons?

Various forms of plasticity has been reported for inhibitory-excitatory synapses as well. See below figure from [Woodlin et al. 2003].

Holmgren CD, Zilberter Y (2001) Coincident spiking activity induces long-term changes in inhibition of neocortical pyramidal cells. J Neurosci 21: 8270–7
Woodin MA, Ganguly K, Poo MM (2003) Coincident pre- and postsynaptic activity modifies GABAergic synapses by postsynaptic changes in Cl- transporter activity. Neuron 39: 807–20


What is this insect from Brasil? SE Brazil Atlantic rainforest Oct 2017. I'm assuming this is an early stage of an insect. It was crawling around a tree in the moss and was about 6-7mm.

This is, indeed, a nymph (what you called a young stage), but not from a cicada as you suspected: it's a nymph from a leafhopper, which are hemipterans from the Family Cicadellidae (cicadas are also hemipterans, but they belong to the Family Cicadidae). More specifically, this seems to be a sharpshooter, which are leafhoppers from the Tribe Proconiini.

Narrowing down to the Genus is more complicated, but I'd guess it is Oncometopia. Here is an image of Oncometopia orbona for comparison:

This other image (also Oncometopia orbona) is even more similar to yours:


Gametes of two different species I always wondered why gametes from two different species dont fuse together to form an offspring. eg a donkey (sperm) and a female dog (egg)

I know this is not possible but I'm just curious.

The biological environment in every cell and tissue of your body is an extremely complex, tightly controlled system. There are tens of thousands of genes in a typical eukaryotic genome, and depending on tissue types and environmental conditions, these genes are turned on and off in a very controlled manner. There is regulation at every point in the flow of genetic information: nucleosome disruption to expose DNA; RNA transcription from the DNA; protein translation from the RNA; and in some cases, additional modifications of proteins or intermediate mRNAs. At early stages in development, regulation of RNA and protein levels is even more crucial than, say, when an organism is fully developed and healthy.

All living organisms share some basic building blocks--DNA, RNA, and proteins work pretty much the same in all of life (there are a few rare variations of the genetic code but the basic premise is identical). However, the way that specific genes, transcripts, and proteins work together to sustain life varies widely between different organisms.

For a very rough analogy, imagine you want to bake a batch of cookies. Then consider the three following scenarios.

You look at two different recipes for chocolate chip cookies. They will have some slight differences, but they will share a lot in common. If you put the ingredients for both recipes in one bowl, it's likely you can still come up with some pretty good chocolate chip cookies in the end.
You look at two different recipes: one for chocolate chip cookies, and one for chocolate muffins. There will be some big differences in these recipes, but combining all the ingredients and baking, you still might be able to come up with something edible (and maybe even tasty).
You look at two different recipes: one for chocolate chip cookies, and one for French onion soup. If you combine the ingredients from these recipes and try to cook or bake them, there is no way you will come up with something that anyone would want to eat.

The first example we can relate to two individuals of the same species mating. Of course there is natural variation in the population, but this doesn't typically lead to lethality during development. The second example we can relate to individuals of two related species (such as a horse and a donkey). Sometimes these matings can produce viable offspring, although these offspring are often sterile. The third example we can relate to individuals of two very divergent species (such as donkey and dog in your original question). The biological systems inside donkeys are just so different from those inside dogs that this mating cannot produce a viable offspring.

Admittedly this is a rough analogy, but hopefully is sheds some light on the issue.


Is it true that the human brain has not evolved in 100 000 years? I read that the human brain has not evolved in 100 000 years and that's why there are no genes for intelligence.

tl;dr
Here are the two claims you make

human brain has not evolved in 100 000 years

Wrong!

there are no genes for intelligence.

Wrong!
The claim there are no genes for intelligence. is unclear though (see below) but if rephrased in the most intuitive correct way, then the claim is wrong!
Are there genes for intelligence?

[..] there are no genes for intelligence.

The claim there are no genes for intelligence is unclear. Does that mean there is no genetic variance in the human population for intelligence? To understand why the claim "gene for something" makes no sense, please have a look at this post
Make sure to read this post..... Done? Now you understand why the concept of heritability is key. So let's rephrase the question so that it makes sense and can be answered
Is Intelligence heritable?
Well, the issue here is to define the term 'intelligence' in a way that is non-arbitrary and yet match our intuition of what we like to call intelligent. A number of studies have investigated the heritability of intelligence, often using different definitions / metrics for intelligence.
All these studies agree on one point. Yes, intelligence is heritable! How heritable it is varies a lot from one study to another (because those studies vary in the population studied and in the definition of intelligence). See the wikipedia article on Heritability of IQ for more layman information.
Has the human brain evolved in the past 100 000 years?
First you need to understand how evolution is defined. Here is a commonly used definition

Evolution is a change of allele frequency through time in a population

Have a look at the post What is meant by individuals do not evolve, populations do? to understand what this definition mean.
Well... first. Everything evolve. You can't stop evolution from happening on any phenotypic trait or on any genomic region. So, of course it evolves. But let's not stop there.
There is still one issue with this question. The saying brain characteristics rather vague. But I'll deal with it as I can.
Is the brain still evolving - phenotypic evidence
Spoting changes in brain structure through time is not easy, as brains don't preserve well. Over such a short period of time (100,000 years) it will be even harder to detect much difference on gross metrics we can use such as cranial cavity.
We can compare the volumes of cranial cavity. Neanderthals interbred with humans (see this loosely related post) with Homo sapiens and Nanderthals had a cranial cavity that is bigger than Homo sapiens, so this gene flow would very likely affect H. sapiens cranial cavity.
Is the brain still evolving - genetic evidence
Consider for example Evans et al. 2005 showing that the allele coding for micro-encephaly at the gene MCPH1 is currently increasing in frequency in the human population.
This article from NewScientist also reports the findings of Evans et al. 2005 in layman terms.
Is the brain still evolving - current selection pressures
You should have a look at the post Is intelligence declining due to the lack of selection pressure? and eventually on the wikipedia article for the Flynn Effect.


How did genome duplication in jawed vertebrates allow gene specialization? I am currently reading from Chapter 15 in Principles of Life, 2nd Edition:

  Many gene duplications affect only one or a few genes at a time, but in some cases entire genomes may be duplicated. When all the genes are duplicated, there are massive opportunities for new functions to evolve. That is exactly what seems to have happened during the course of vertebrate evolution. The genomes of the jawed vertebrates have four diploid sets of many major genes, which leads biologists to conclude that two genome-wide duplication events occurred in the ancestor of these species. These duplications allowed considerable specialization of individual vertebrate genes, many of which are now highly tissue-specific in their expression.

My question is: how exactly does duplicating a genome enable specialization of genes? In other words, after vertebrates underwent genome duplication, how did one copy of the genome become "highly tissue-specific"?

With a single copy gene, mutations may affect some vital function and are therefore often deleterious and negatively selected. Immediately after a duplication event, there is a level of redundancy in gene function and mutations in one copy giving rise to novel phenotypes are more easily tolerated since the ancestral function is retained by the paralogous gene.

Some reading material, if you feel so inclined:

Wikipedia:

Functional Divergence

  Functional divergence is the process by which genes, after gene duplication, shift in function from an ancestral function. Functional divergence can result in either subfunctionalization, where a paralog specializes one of several ancestral functions, or neofunctionalization, where a totally new functional capability evolves.

Neofunctionalization

  Following the gene duplication event there are two identical copies of the ancestral gene performing exactly the same function. This redundancy allows one the copies to take on a new function.

Subfunctionalization

  Specialization is a unique model of subfunctionalization, in which paralogs divide into various areas of specialty rather than function. In this model both gene copies perform exactly the same ancestral function. For instance, while the ancestral gene may have performed its function in all tissues, developmental stage, and environmental conditions, the paralogous genes become specialists, dividing themselves among different tissues, developmental stages, and environmental conditions.

Kryuchkova-Mostacci N, Robinson-Rechavi M. 2016. Tissue-Specificity of Gene Expression Diverges Slowly between Orthologs, and Rapidly between Paralogs. PLoS Comput Biol 12:e1005274.

  The most widely accepted model is that orthologs diverge slower, and that the generation of paralogs through duplication leads to strong divergence and even change of function.

Soria PS, McGary KL, Rokas A. 2014. Functional divergence for every paralog. Mol Biol Evol 31:984-992.

  Because genes can be constrained by selection at more than one phenotypic level, the relaxation of constraints following gene duplication allows for functional divergence (FD) along multiple phenotypic axes.


Does reversion of resistant strains to wild-type only occur when no more drug pressure is exerted We always read that wild-type reversion of a resistant strain occurs when no more drug pressure is exerted. Could resistance reversion also occur under drug pressure, but from a drug other  than the one to which the virus is resistant.

To illustrate my question, let’s assume an HIV strain resistant to a specific anti-retroviral drug class (e.g. NNRTI drugs). Would NNRTI-resistance reversion to wild-type HIV occur under the pressure of another drug regimen (e.g. PI drugs) or does resistance reversion only occur when no more drug pressure at all is exerted?

I am not an expert on HIV but I am answering based on general principles.

This is a typical example of selection of individuals/populations with different fitness.

Reversion to wild-type (WT) would happen if the WT has higher fitness in that environment. Assuming that WT is the fittest under drug-free conditions, it is not difficult to understand that the WT population will outgrow other mutants.

For your question — "would a drug resistant HIV population revert to WT under treatment with other drugs", the simple answer would be no.

Explanation

HIV generally acquires resistance against different drugs quickly because it has a high mutation rate. In your example case, the HIV population that is resistant to the new drug will outgrow other populations if we assume that the selection is strong. There would not be any reversal to WT because WT would also be unfit in the new environment. If the selection is weak then the population genetic diversity would depend on the relative fitness of different genotypes.

There may also be pleiotropic effects: mutations that provide resistance against one drug can also possibly provide resistance against other drugs. This is well known in case of bacteria and there are many reports for HIV too (Rhee et al, 2010, Other Google Scholar Hits).


How can rooted and unrooted (phylogenetic) trees be distinguished from one another I understand that rooted and unrooted phylogenetic trees are similar in structure

But how can they be easily identified as one or the other?

Is it simply based on the presence or lack of a named root (the root is identified as a particular ancestor) or outgroup?

In case of a drawn figure, either look for the a short stem to the left, or for an explicitly labelled outgroup. Trees derived from phylogenetic analyses are normally unrooted by default, you need to root them by either making an arbitrary (but hopefully informed) decision or by adding an outgroup.


Can Bacteria Repair Dephosphorylated Plasmids? I have been trying to insert a short sequence of DNA into a plasmid. I wanted to make two different versions, with the insert at different locations. I chose HinDIII and SalI sites approximately opposite each other on the plasmid and designed oligos with HinDIII or SalI sites, and of course extra bases on the ends to allow proper cutting.

I cut the plasmids and oligos and dephosphorylated the vector to help prevent empty vector ligations. I mixed the plasmid and oligos and ligated, then transformed into bacteria, all standard stuff.

The HinDIII version worked the first time, with few colonies on the empty vector control plate, and more colonies on the plates that received oligos during the ligation. I confirmed insertion by using the BpmI cut site the oligos just happened to carry.

However, the SalI version has failed every time I tried it. The empty vector control and all other plates are a just a carpet of cells. There are very few individual colonies, and the ones that exist don't look right, too small. I haven't even tried a miniprep, too likely to get an empty vector back. I did do a nontransformed control, where the cells were not given any DNA and were just directly plated. Those cells died, indicating it's not an issue with my ampicillin.

My hypothesis is that unligated empty vector outnumbers the correctly ligated plasmids, and that cells that pick up a copy of the unligated DNA somehow repair the cut, even though it's dephosphorylated. This is made more likely because I only used a single digest, so the plasmid has matching sticky ends, however the HinDIII version used the same strategy. I have been including a 1 hour 37 C SOC media incubation, which could allow the bacteria more time to carry out this repair. If I skip the incubation, maybe that would prevent unwanted repair.

I am testing this hypothesis with some additional controls, including transforming bacteria with empty vector that hasn't been treated with ligase to make sure the ligation reaction isn't the problem, as well as using the previously ligated DNA without the SOC incubation. I will report that data as it becomes available. I am short on competent cells, so I can't do much else right now.

Also, what do you think about treating the ligated DNA with klenow to blunt any remaining sticky ends before transformation?

EDIT: I have the data for the transformations that skipped the ligation and SOC media incubation. Skipping the incubation did not change anything, neither did skipping the ligation. All plates continue to show a carpet of cells.

As per WYSIWYG's suggestion, I tried the digest and dephosphorylation again with SalI and ran a gel. The gel showed that SalI was less than ideal at cutting this plasmid.

As you can see, the most intense band is the bottom band, which is most likely supercoiled DNA, with the linear DNA I want appearing in the middle, and open circle DNA coming in third. I very carefully cut the middle band out and did a gel extraction. When I ligated this the control plate had 1 colony. Unfortunately, the experimental plates had between 2 and 6 colonies each. I am running minipreps on those now, will just have to see what I get.

This explains why the previous attempts produced so many colonies on the control plates, most of the DNA was uncut, so no amount of dephosphorylation would help it.

One thing that does bother me, is that my gel extractions seem like they have had really poor yields. I typically start a digest with 4 ug of plasmid. After phenol:chloroform extraction and isopropanol precipitation, I'll usually recover 2 - 3 or more ug of DNA. After gel extraction, I'm lucky to get 300 ng of DNA. To make things weirder, the liquid that comes off the spin column in the final elution step will gel up, like a low density agarose gel. The only explanation I can come up with is that residual agarose in the spin column is somehow forcing its way through the membrane and into the elution buffer. The goo clogs pipette tips and makes life difficult.


Green Film Build up in Glass Water Bottle So I have this Large Water Jug that I fill only water with.
And this is the 2nd time there has been a layer of green film that builds up at the bottom of the bottle. I don't have any way of getting to the bottom to clean this.

I wanted to know.

What does this green film consist of?
What Chemicals or methods can I use to remove the film without having to manually scrub the bottle?

Thanks

ps. not sure if this was the correct place to ask this question.

What seems to be forming in reusable water bottles and water coolers is a biofilm. Since it is a complicated system, after maturation biofilm might be very hard to remove without scrubbing. There is a nice article about cleaning water coolers, which might give you some information.

If you look closer on the Google Scholar search results, you'll find that quite a bit of research has been conducted in the area of sanitation of water coolers and study of their flora. For example, consider the following paper from 1996: Analysis of the Virulence Characteristics of Bacteria Isolated from Bottled, Water Cooler, and Tap Water.

There is a very nice list (Table 1) of different bacteria isolated from water. But I would like to point your attention to following table from the paper:

Quote from methods section listing tested antibiotics:

  The
  natural and first generation antibiotics included:
  penicillin, ampicillin, erythromycin, kanamycin,
  streptomycin, tetracycline, chloramphenicol, and
  sulphonamide. The synthetic and later generation
  antibiotics included: gentamicin, cefoxitin,
  cefoperazone, oxacillin, piperacillin, imipenem,
  ciprofloxacin, and sulphonamideftrimethoprim

The green slime you observe, I think, is a combination of all those bacteria, plus some that were brought after the water was poured into the container. And it seems that all commercial sources that you didn't purify yourself, will have a variety of microorganisms growing. And around 5% of the total bacterial cell mass is resistant to common antibiotics.


Why do Major and Minor grooves exist in dna strands? I've been trying to find what causes the periodic appearance of major and minor grooves in DNA but have not yet been successful. Geometrical explanations would also be appreciated as I cannot understand any of the geometrical explanations I have come across so far. As far as my knowledge of DNA is concerned I know of all the high school basics (e.g complimentarity, bonding between the individual components of a nucleotide etc.)

It is all explained here in Wikipedia. You are referring to Watson-Crick base pairs in the B-DNA structure.


When does a chromatid become a chromosome? When chromosomes lie on the metaphase plate, they have the characteristic X shape. But these are actually two chromatids that are held together at the centromere. If separation fails and both chromatids are pulled in the same direction it leads to trisomy (three homologues chromosomes). So when exactly does a chromatid become a chromosome if it's not after successful separation?

If no centromere split occurs during anaphase and consequently chromatids are pulled to one daughter cell, the possible outcome is during telophase the chromatids uncoils into chromonema which in subsequent divisions become supernumerary chromosomes.


Do men and women have the same number of genes? As far as I know, humans have 23 pairs of chromosomes, each one which contains a particular amount of genes. But in the "last" pair, men have a XY pair chromosome, and women have a XX pair chromosome. Does the missing "leg" of the XY pair make men to have fewer genes than women, and if so, how many genes do each sex have?

It is true that the Y chromosome is shorter than the X chromosome and that there are more genes on the X chromosome.

  Do men have fewer genes?

One could (mis)understand three things in the expression "number of genes".

Number of gene copies (see Copy Number Variation)
Number of genes
Number of alleles

Thanks to @GerardoFurtado for correcting my semantic in the comments.

1. Number of gene copies

From the statement that there are fewer genes on the Y chromosome, one can conclude that men have fewer genes copies than woman.

This is the intuition the OP seemed to have.

2. Number of genes

Men also have an X chromosome. So men have the standard genes present on the X chromosome (but they only have a single copy of it while women have two copies; btw you might be interested in dosage compensation).

Because women do not have a Y chromosome and because there are a number of genes on the Y chromosome that are not present on the X chromosome, men have genes that female don't have at all. Therefore women have fewer genes than men.

3. Number of alleles

There is not much reason to expect that one gender would be more heterozygote than the other at autosomes (=non sexual chromosomes). Some may hypothesize that women may have more heterozygosity than men if there is stronger selection among sperm than among ovules or things like that but let's not get down this complicated path.

One one hand women have more gene copies and therefore might experience more heterozygosity, one the other hand, men have more genes and would therefore eventually carry more alleles. I don't know which side wins!

Did you mean number of genes per cell or per individual?

So far I assumed you were interested about the number of genes (or gene copies) per cells but if you want to compare whole individuals than it is a different story!

Men are on average taller and therefore have more cells. Therefore if you compare the body-wide number of gene copies, women will have fewer gene copy on average (Thanks to @JM97 comment).


What's the difference between the *types* of tissue dissociation enzymes? I'm trying to dissociate a tumor, and most protocols like NCI/NIH recommend a 10X triple enzyme digestion stock consisting of: collagenase type IV, DNase I type IV and hyaluronidase type V in HBSS. This goes all the way back to the 90s, and the recipe varies between papers (dispase, papain, neutral protease, elastases, etc.). The so-called official recipe that I've been tasked to use is composed of the above, however, mostly from Sigma-Aldrich (C5138, D5025, H6254)

I can't really find anything that says what the real differences are between these types of enzyme are, however. Or why for example type IV DNase works better than type II, and so forth. Is it perhaps that the recipe just happened to stick?

It’s years since I looked at a Sigma catalogue (before it became Sigma-Aldrich) but as I remember, these designations are arbitrary proprietary ones used by Sigma to distinguish different sources — the key point being that Sigma didn’t generally manufacture all of these themselves, but obtained the from third parties.

The other point to note is that these enzyme preparations were/are generally impure,  but to differing extents, so the type designations allowed you to re-order a particular preparation that worked, and also to specify the actual grade you used when you published so that other people could repeat your work. More expensive grades would, no doubt, also work in the sort of crude application you describe, but they would be a waste of money.

I thought the catalogues used to give you some information (organism/tissue at least), but, as I said, it’s been a long time (although be careful with your “way back to the ’90s”, young man).


Why do soap molecules not break down your skin cells when you wash your hands? Soap molecules are similar in structure to phospholipids and interact with the cell membrane.  They can clearly cause damage to the cell membrane.

If this is the case, why then, does soap not break down your skin every time you use it?  The skin cells, keratinocytes still have a membrane, so wouldn't soap attack our skin in the same way it does to plant cells and cause deterioration?

The outer most layer of the mammalian epidermis (cornified layer or stratum corneum) is composed of 15-20 layers of dead cells called corneocytes, which are basically dead keratinocytes filled with keratin intermediate filament cross-linked other proteins as well as some lipids. As keratinocytes differentiate into corneocytes (a process called cornification), the plasma membrane is replaced by what is called a conified envelope which is composed of cross-linked structural proteins and some lipids (more details in here).

Surfactants in soap do interact with components of the cornfield layer such as keratin but not in the same way they would with the lipid bilayer of a typical plasma membrane. Outcome of such interaction depends on the kind of soap as well as amount and duration of application among other factors, but even a normal soap, upon normal use on a normal skin, may cause some keratin denaturation. But the cornified layer is actually continually shed (process called desquamation) and replaced by keratinocytes that proliferate in the inner most layer of the epidermis.

You can find more details on effect of detergents on skin here and here. You can also find useful info on skin structure here and here.


Is this lizard protected or endangered? We think that it's a type of alligator lizard. It was found in the open space area near my home in Moss Beach California (about 10 miles south of San Francisco). Thank you!

It appears to be a California Alligator Lizard - Elgaria multicarinata (subspecies multicarinata), although another photo from the side would be helpful for a positive ID. This species seems to fit the range for the observation as well.

According to CaliforniaHerps.com, there are no associated conservation concerns for this particular species.

Elgaria multicarinata multicarinata conservation status


Is it unusual for populations of archaea to be found living inside trees? The NPR News article and podcast Getting Fire From A Tree Without Burning The Wood begins with

A scientist walks up to a cottonwood tree, sticks a hollow tube in the middle and then takes a lighter and flicks it. A jet of flame shoots out from the tube.
It seems like a magician's trick. Turns out, there's methane trapped in certain cottonwood trees. Methane is the gas in natural gas. It's also a powerful greenhouse gas.

and describes the discovery that quantities of methane have been observed to be produced within cottonwood trees.
There is a video of the methane tapped from a tree being set on fire.
The article continues:
"The wood in this particular species naturally has this condition called wetwood, where it's saturated within the trunk of the tree," says the lighter-flicking scientist, Oak Ridge environmental microbiologist Christopher Schadt.

This wetwood makes for a welcoming home for all sorts of microorganisms.
"You can't actually see a lot of the organisms because we can't grow a lot of these organisms," says Melissa Cregger, a staff scientist at Oak Ridge. "So we're able to identify them using their gene sequences."
Some of those organisms turned out to be species of archaea that are known methane producers. So it's not the trees themselves that are making the methane, it's the microbes living in the trees.

It's not clear to me if the use of "wetwood" refers to the natural condition of cottonwood trees, or if this is meant to refer to some kind of bacterial infection. For example, Mirriam-Webster defines wetwood as:

wood having a water-soaked or translucent appearance because of abnormally high water content sometimes due to bacteria and sometimes to physiological factors

Question: Is it unusual for populations of archaea to be found living inside trees? Is this something new and surprising or is this well documented?

The exact term — wetwood, is used only once in the original article (Yip et al., 2018).

Others have found that water content of heartwood tissue was the best
predictor of methane flux across multiple plant species (Machacova et
al., 2016; Wang et al., 2017), however this was not a strong predictor
of methanogen relative abundance in our analyses. It is possible that
within trees characterized by wetwood such as Populus deltoides,
other factors may become more important than water content above a
certain moisture threshold.

However, if you look at these lines from the introduction of the paper, it seems that wetwood just means wood that has a high water content. It definitely does not refer to a disease or infection.

Indeed, both mechanisms may be important depending on tree species
(e.g. those containing dry and dense vs wet and porous wood) and
ecosystem under study (e.g. wetland vs upland forest soils).

Based upon past work and our own informal observations of odors
associated with tree coring at these sites indicative of fermentative
environments, we hypothesized that an anaerobic community including
methanogenic archaea would dominate woody tissue, particularly in
heartwood tissue which is often water‐soaked.

Now coming to your question on whether it is unusual for populations of archaea to be found living inside trees.
Roots have been known to harbour microbes; plants establish this symbiotic relationship with the microbes for nitrogen fixation (See mycorrhiza and root nodules). So, it may not be very unusual that archaea interact with plants but it may possibly be unusual that they are living inside this part of the tree. Yip et al. (2018) highlight that although microbial composition of the wood has been studied in the past, these studies have been done ex situ. This means they are the first to study these microbes in situ.

Microbiological investigations of living wood have been conducted in
the past (Zeikus & Ward, 1974; Zeikus & Henning, 1975; Ward & Zeikus,
1980; Schink et al., 1981a,b, 1982), but these studies primarily
focused on ex situ wood incubations and the isolation of microbial
representatives, rather than overall community characterization across
tree conditions. For example, Zeikus & Ward (1974) demonstrated that
methane production occurred from extracted wood tissue from Populus
deltoides and were able to isolate pure cultures of a new species,
Methanobacterium arborphilicum (Zeikus & Henning, 1975), later
reclassified as Methanobrevibacter arboriphilus (Balch et al., 1979).

So, it seems that people have been working on this area since 1970s.
However, it also appears that there is not much research on archaea as a part of the plant microbiome (Taffner et al., 2018).

IMPORTANCE: Archaea are still an underdetected and little-studied part
of the plant microbiome. We provide first and novel insights into
Archaea as a functional component of the plant microbiome obtained by
metagenomic analyses. Archaea were found to have the potential to
interact with plants by (i) plant growth promotion through auxin
biosynthesis, (ii) nutrient supply, and (iii) protection against
abiotic stress.

So whether this is unusual or not depends on whom you are asking (hence a bit opinion based).


Questions concerning synaptic input and dendritic processing In the article How Spike Generation Mechanisms Determine the Neuronal
Response to Fluctuating Inputs, I read (p.11629)

I have four questions concerning some formulations:

What is "the membrane time constant" if this depends on the membrane resistance and capacitance which varies over the membrane? Maybe "local membrane time constant"? Or "mean membrane time constant"?
What do the authors probably mean with "instantaneous postsynaptic currents"? Occurring at the same time all over the dendritic tree?
What do they probably mean with "exponentially decaying synaptic currents"? The decaying of the PSPs while travelling down the dendritic tree?
What's the relation between "synaptic decay time constant" and "membrane time constant"?

(Having digested the paragraph a bit more, another - probably more accurate - reading of "instantaneous" came to my mind: "starting and ending abruptly with the abrupt opening and closing of the ion channel".)

Started writing a comment and realized it was an answer...

These guys are basically saying "take a uniform spherical neuron" the same way you would say in physics "take a uniform spherical cow." There isn't a dendrite mentioned in the whole paper.

By "the membrane time constant" they mean exactly that: one membrane time constant, effectively the somatic time constant. They aren't talking about dendritic trees: they are essentially saying assume a uniform spherical neuron that gets inputs on its soma.

Membrane time constant is associated with the rate of change of the membrane voltage; synaptic time constant is associated with the rate of change of the synaptic current (this is what they refer to when they talk about exponentially decaying synaptic currents). Real biological synaptic currents have a time course governed my neurotransmitter concentrations and the gating properties of postsynaptic receptors. Real biological postsynaptic potentials (voltages) are governed by both the time course of the synaptic current and the capacitive properties of the membrane (i.e., the membrane time constant).

Instead of considering synaptic time constants, you could simplify a synaptic event as an instantaneous current impulse: essentially the entire current all in one instant rather than over time. The presence of the membrane time constant helps with making this assumption somewhat reasonable, because the membrane time constant ends up filtering input currents anyways, whether they are impulses or have a synaptic time constant.

In a simulated environment, you can make computations simpler by just adding a little time to the membrane time constant to roughly simulate the effect of the membrane time constant + synaptic time constant. Again, this is for computational efficiency, like when you assume a cow is spherical, not for perfect biological accuracy.


What experiment for first time showed DNA is anti-parallel? Scientists how to prove DNA is anti-parallel?

The definitive proof came with the crystal structure of B-DNA (see Watson & Crick, 1953). Anti-parallel strands is the configuration that best explained the diffraction data while not violating chemistry (bond lengths and angles, no steric clashes, etc.).

The relevant sentence from the article is:

  the sequences of the atoms in the two chains run in opposite directions

I underlined this sentence in the following screenshot of the article:


Why is Portuguese man o' war considered a colony? The wikipedia entry on the Portuguese man o' war says:

  ... the Portuguese man o' war is ... not actually a single multicellular organism but a colonial organism made up of many highly specialized minute individuals called zooids. These zooids are attached to one another and physiologically integrated to the extent that they are incapable of independent survival. (emphasis added)

This is contradictory. If it's got multiple cells, and those cells are highly specialized to the point of being incapable of surviving on their own, then how does that differ from a multicellular organism? That last sentence seems like it describes the cells in my body.

In fact, the entry colonial organisms says:

  The difference between a multicellular organism and a colonial organism is that individual organisms from a colony can, if separated, survive on their own, while cells from a multicellular life form (e.g., cells from a brain) cannot. (emphasis added)

So, is the Portuguese man o' war a colony or a multicellular organism? And if it's a colony, can its zooids survive independently, the wikipedia text notwithstanding?

Physalia and Siphonophorans in general are multicellular Metazoans.

But the whole discussion is about modularity on the level of individuals: Siphonophorans are colonial organisms, which means they are composed of multiple individual polyps and medusae. This is in fact quite common among Hydrozoa, but in Siphonophora the degree of integrity and function division among the components is of extraordinary level.


Does any lifeforms can make a haploid cell from any other cell without meiosis? Like the title says, is it possible to produce haploid cells without meiosis?

The question is a bit unclear

  Can you produce haploid cells without meiosis?

The question is a bit unclear. for two reasons

What do you mean by "you". You mean can we do such thing with modern technology or do you mean does it ever happen or do you does it ever happen in human cells.
It is also unclear what from. Are you implicitly asking whether "you" (whatever 'you' mean in your sentence) can make a haploid cell from a diploid cell or form anything?

Answer

In this answer, I will assume that the question is

  Does any lifeforms can make a haploid cell from any other cell without meiosis?

The answer is yes. Many organisms have a long haploid stage during which many mitosis occur. Haploid cells undergoing mitosis results into two haploid cells.

You might want to read more about life-cycle (wikipedia), especially the sections on haplontic life-cycles and haplo-diplontic life cycles.


How does blue, yellow and orange coloured light affect photosynthesis? I've been conducting an experiment with different colored light and photosynthesis, and so far my hypothesis states that red light will grow the plant, green will slow or kill it, and white will grow it as normal.

I'm wondering what would happen with blue, yellow, and orange.

Thanks.

Your thought process should revolve around optimal spectrum for photosynthesis, since whether that happens sufficiently will determine the health of your plant. Just poking around, I found this document.

What light will be usable for photosynthesis depends on which version of light absorbing protein is being used to capture energy from photons.

This diagram would indicate that pure yellow would be pretty ineffective for any pigment. Blue is fine, as is darker orange/red for chlorophyll A and B.

Keep in mind that a lightbulb, unless a very special one, will still have lots of other spectrum bleed.  It won't be a pure single color (even though it may look like a single color to your eye).

Another source from Khan Academy.


Do squirrels and blue jays play a role in oak tree distribution? White oak (Quercas alba) acorns have lower tannin levels than red oak (Quercas rubra) acorns, therefore animals tend to eat the white oak acorns before red oak acorns.  Animals such as squirrels and blue jays will often catch red oak acorns for later consumption when the tannin levels have lessened or when food sources are scarce.  Since red oak acorns are more likely to be hauled off, cached, and forgotten about wouldn't this cause red oaks to be more widely dispersed than white oaks?  By this I mean that white oak trees would be spaced closer together than red oaks.

Source 1: https://www.allianceforthebay.org/2017/09/the-complicated-relationship-between-acorns-and-animals/

Source 2: https://link.springer.com/chapter/10.1007/978-1-4419-0378-5_6?no-access=true

In case anybody is curious this paper seems to answer this question.

  The obvious conclusion to follow from these summaries is that acorns
  of RO have a significant dispersal advantage. RO acorns are dispersed
  greater distances from their sources, cached more often in a wide
  variety of environments, and even show the ability, under some
  circumstances, to escape partial predation. Acorns of WO, in contrast,
  should show short dispersal distances and may be in fact adapted for
  rapid germination near or under parent trees.


Does the edge effect promote biodiversity? I define the edge effect as:

A term used to describe what occurs at habitat boundaries where two bordering communities influence one another.

My question is whether it generally leads to an increase or decrease in biodiversity (both evenness and richness) and why.

Also, what are the biogeographic factors that impact biodiversity relating to this edge effect?

I believe that species diversity would increase, as at such habitat boundaries species that inhabit the bordering habitats and those that can also be found in habitat boundaries would be present.

I do remember reading that light intensity increases due to the edge effect and thus also allows for shade-intolerant species to thrive, but I do not understand why.

EDGE EFFECT PROMOTES BIODIVERSITY.
EDGE EFFECT OCCURS IN ECOTYPE.
ECOTYPE IS THE TRANSISSION ZONE WHERE TWO COMMUNITIES MERGE.
HENCE SPECIES RICHNESS IS FAIRLY HIGHER THAN THAT OF THE SURROUNDING ECOSYSTEMS.
IF ANY OF THE SPECIES TENDS TO EXPLOIT THE RESOURCES OF THE ECOTYPE IT WHOULD HAVE TO MODIFY ITS CHARACTERISTICS BY THE PROCESS OF  ADAPTIVE RADIATION AND EVOLUTION .
HENCE NEW SPECIES EMERGES PROMOTING BIODIVERSITY.


How can predicting protein folding speed up drug discovery? I'm asking this as a layperson without much knowledge in biology, so please correct me if my understanding is wrong.
Recently DeepMind's AlphaFold managed to predict protein structure from acid amino sequence with stunning accuracy. We are being told that this could "pave ways toward advances in drug discovery."
But I fail to see how it can happen. From my understanding the combination of protein structure is infinite, and if we tweak a protein structure that works good to fight against a virus, it will either work better or worse, but the key point is we don't know until we try. So essentially this is still a hit-and-miss thing, depending purely on dumb luck.
So how can the fast, accurate prediction of protein folding help in drug discovery?

Firstly protein structures are not infinite. Most proteins adopt specific structure.
Drugs carry out their function by binding to its target protein. Structure prediction helps drug discovery process in two ways -

it allows identification of pockets in target proteins (where drugs can bind) whose structures are not yet solved using experimental methods
it allows in silico experimentation i.e. you can take a large number of molecules and simulate whether they will bind to a specific location in your target

I would suggest going through these reviews to get a better overview of the importance of fast and accurate structure determination in drug discovery :

Verinde and Hol, 1994, Structure
Montfort and Workman, 2017, Essays in Biochemistry


What limits our ability to grow enamel rods? From what I've understood from what I've read (which might be wrong), enamel rods extend away from the dentin in our teeth. As young people grow, the rods are thickened.

What are the technical limitations and/or problems/challenges of trying to extend/grow the rods/crystals while the teeth are in the mouth?

One issue I guess could be that the enamel is porous, and so chemicals could affect the other parts of the teeth.

But one example of trying to improve the quality of tooth enamel is Novamin, which some manufacturers have claimed creates a glass on the tooth. But I don't understand what that means.

Chandra's Textbook of Dental and Oral Histology and Embryology with MCQs p40-42 explains the complexity of enamel, and provides diagrams and images of real enamel.

What I didn't know before was that the hydroxyapatite is in the form of very small crystallites packed inside the key-like structure of the rods. The rods are packed together with a cement-like material. The rods themselves are segmented.

This small design and lack of vital parts suggest to me that bioglasses like Novamin would at least not recreate the natural enamel structure.

What isn't so easy to guess is whether crystallites from the components of the bioglass are formed on the existing crystallites, and if so, whether this can continue indefinitely, and with what qualities.


Fst Differences Between Mature Trees and Seeds For a single co-dominant locus in two populations of blue oak, I am given genotype frequency data (genotypes are AA, AB, BB) for adult trees (at least 150 years old) in both populations (pop 1 and pop 2) and from sampling of seedlings taken in fragmented woodland from the same populations (pop 1 and pop2) very recently. I am asked to detect any difference in Fst among adults and seedlings, and propose a hypothesis explaining how any difference observed could have come about.

To tackle this question, I calculated the Fst value between Pop1 and Pop2 using the adult's genotypic frequencies and then Fst between Pop1 and Pop2 for seedlings using the respective genotypic frequencies given for the seedlings.

The Fst values for the adult's was 0.004 and the seedling' was 0.113.

Clearly there is genetic differentiation between population 1 and 2 in seeds, but not much in adult trees.

I'm mostly stuck on the explanation for why this would happen. My gut response was that there is some selection against certain adult genotypes in population 2 in that they are unable to produce seeds? Or maybe that adults in population 2 are mating non randomly and therefore produce seeds that do not match the genotypes of the adult population?

I will assume the claim Clearly there is genetic differentiation between population 1 and 2 in seeds, but not much in adult trees. is correct and that you have done your stats correctly.

A complete analysis of the situation depends of how you calculated Fst. Did you use Weir-Cockerham Fst or standard Nei's formulation? How did you average (with or without weights) over population and loci? But without going to these details, here is an extreme scenario that explain why you could observe such patterns.

Imagine, the migration rate from any population and to any population is 0.5. In such case, in absence of selection you would not expect any divergence between populations. However, if genotypes AA and AB both have seed survival probability of 0 in pop2 (but not in pop1), then pop2 will be fixed for A2A2 at the adult stage even though when looking at the seeds you cannot see any evidence of divergence.


Is it more likely that the very first living organisms had a linear genome? Is it right to assume that the first living organisms on earth had a linear genome? I base this on the fact that linear macromolecules are clearly much more common in nature that circular ones. To be honest, I can't even think of any naturally-occurring circular macromolecules that aren't already a part of current living organisms.

Were the very first living organisms more likely to have linear genomes? If so, when during evolutionary time did circular chromosomes originate?

It is hard to give an answer to this question that is not just speculation.  We can be reasonably confident that the most recent common ancestor of bacteria and archaea had circular genomes.  However, we currently have no way to get any conclusive evidence earlier than that.  3 billion year old DNA doesn't fossilize.  So it's just speculation what DNA looked like back then.

On the other hand, my understanding is that most experts think that RNA genomes predated DNA genomes.  These RNA genomes would be linear.


What information do bipolar cells encode? Short version: I don't see what information on-centre bipolar cells are actually capturing.

Longer:

Actually, the question could be extended to on-centre retinal cells as well, but I'll focus on bipolar cells for now.

On-centre cells will fire when a spot of light hits the centre of their receptive fields and doesn't touch their surround, off-centres are the reverse (light in the centre is inhibitory, surround is excitatory).

Here's an over-simplified illustration that I made, red is hyperpolarized (excited), blue is hypopolarized (inhibited). Let's pretend that horizontal cell effects have already happened, and ignoring overlapping receptive fields for simplicity.

So my question is, if off-centre cells would be useful to highlight contrasts like edges (as I understand it, though eventually edges get detected further down in the complex cells), what are on-centre bipolar cells used for?

From my perspective it looks like they'd be good for single points in light which are small enough to hit the small number of rods that encompass the centre of a receptive field but not hit the surround. But when would this ever be the case? The centre of a receptive field would be incredibly tiny given the large number of rods in say the fovea (though, granted, maybe on-centre cells become more important in the periphery?).

One source:
http://thebrain.mcgill.ca/flash/a/a_02/a_02_cl/a_02_cl_vis/a_02_cl_vis.html

Recent nature neuroscience review on bipolar cells says that bipolar cells are classified into 13 (12 cone bipolar + 1 rod bipolar) different types.

Depending on the polarity of their light response, bipolar cells can be grouped into ON and OFF cells.

Answering your question, what are on bipolar cells used for ? ON bipolar cells predominantly depolarize at light-onset and stratify in the Inner Plexiform layer (ON).

Considering rod - rod bipolar path way: Eyes are sensitive to very low light level. Imagine you are seeing a star during night. As the number of photon reaching retinal layer will be very small. It reaches order of few rod photo receptors (receptive field) & then converge to rod bipolar cell for efficient signal processing. It makes vision at dim light really interesting and promising.

In case with central surround organization, It is one of the classical stimulus study which has been explored further in detail with various complex stimuli.
I recommend you to go through The Neuronal Organization of the Retina for more details.

I am absolute beginner in visual neuroscience field. Please correct me if am wrong.

-Sathish


Does preservation in ethanol alter leaf litter mass? I have benthic samples that were collected with an Ekman dredge from some small ponds.  The samples contain quite a bit of coarse particulate organic matter (CPOM, basically dead leaves).  I would like to quantify the amount of CPOM in the samples but they were preserved with 70% ethanol in the field.

Is there any evidence that ethanol preservation alters benthic CPOM mass?

It's very likely that you should have at least minor changes in mass.

The reason is because ethanol can extract a number of substances from leaves (e.g. tannins, pigments, etc.).

However, you could still easily double check on your own.

You could still figure out the mass of the CPOM even without knowing the answer to this answer directly.

Drain and collect the EtOH.
Determine mass of separated CPOM.
Determine the excess mass present due to any leaching/dissolving from the CPOM by using density = mass / volume (or ρ=M/V) with your collected volume of ethanol.

EtOH has a density of 0.789 g/mL  at 20°C. 70% EtOH has a density of 0.885 g/ml at 20°C.
Determine the volume of the collected EtOH.
Determine the mass you'd expect of "pure" 70% EtOH given your volume (m = ρV )
Determine the mass of the collected EtOH
Subtract the expected mass from your calculated measured mass. The difference (if any) would represent mass leached/dissolved from the CPOM.


I found these skulls in a old bottle in the woods. Can you tell me what they are? Can you help me identify these skulls I found in an old bottle in the woods?

Its a Shrew skull.

Hainault Forest Website

Photographs by © Brian Ecott


What is this apple's abnormality? The apple pictured is a of the Gala variety,typically striped.The stripes swirl around a brown protrusion. The protrusion is flexible,in the way a leaf is flexible. The flesh underneath is not discolored or soft. The apple is not misshapen,the seeds are not un-developed or underdeveloped. What is this brown protrusion called and what causes it?

I take it that the question is about the mis-shapenness of the apple, that the stick we see in the dip is the core. The morphology (shape) of fruits such as apple and pear are very sensitive to how well the fruit was pollinated. As we know there can be a variable number of seeds in an apple, but the important fact determining shape is that there should be viable seed develop in each of the five seed pockets resulting in balanced development of the fruit. If the pollination is poor and only a few embryo seeds are fertilized, then the development of the surrounding flesh will favour the pockets that contain viable seed, resulting in possibly mis-shapen fruit. Once you have wondered enough and decide to eat, cut open carefully and on the small side you should see that the seeds are either too few, non-existent or failed to develop.


Are humans an eusocial species? In the evolution of sociality among animals, different degrees are acknowledged. Some species present overlapping generations, some division of labor, and the minority present reproductive division. Those that present the three traces above are called "eusocial" (e.g. some wasps, some bees, all ants and termites, and an african mole).

Maybe our own species could be eusocial? After all, homosexuality is present in virtually every culture studied by anthropologists. Some say it may bring an advantage to the group via group selection (not having kids of their own, they could study plants, medicine, weapons, and so on). What do you think? Are we an eusocial species?

The question of homosexuality and its role in nepotism is interesting.

According to this wiki article, less than 10% of the population is homosexual. If you consider that homosexuality makes human eusocial because homosexual do not reproduce but help their brothers and sisters to reproduce, then you would have to consider any species where a few percentage of the population produce some kind of altruism to be eusocial. Given that all phenotypic traits theoretically have social impacts, then I would bet that you might call eusocial a lot of species.

It seems wiser to me to limit the definition of eusocial when an important part (maybe 98% minimum) of the population do not reproduce but help others to reproduce. One might also want to consider some other restrictions for a the use of the word "eusocial"

Therefore, using the argument of "reproductive division" I would rather not include Homo sapiens in the list of eusocial species. But it is nothing more than a question of definition. You're free to define your words the way you want and call human eusocial but make sure your interlocutor knows your definitions.

Now, let's say we place the limit to the definition of eusociality at 1%. When more than 1% of the population does not reproduce but help their kin to reproduce, then the species is eusocial. Then, humans would seem to fit in this definition at first sight. But do homosexual in our modern society really help their kin to reproduce? In other words, do siblings of homosexual reproduce more (or have offspring that have a high fitness)? This study investigated the question (as pointed out by @oreotrephes in the comments) and they indeed found some pattern but the difference in reproduction between relatives of homosexual and non-relative of homosexual is is quite weak. But if homosexual don't reproduce and don't help their kin reproducing then, humans is definitely not a eusocial species.

Finally I want to add that individuals from lots of different species have been found to perform homosexual behaviour (see this wiki article). If you want to consider human as eusocial because some homosexuality, then you will have to consider sheeps, labradors and pigeons to be eusocial as well!


Is this plant lantana camara? If not what is it? I was in a botanical garden recently and wasn't able to find the tag on this plant. The diameter of the entire flower tended to be around 5cm.

Google seems to suggest its lantana camara but I'm not 100% convinced yet.

When rubbed, its leaves produced a minty aroma

It is Lantana camara, you can check here: https://en.wikipedia.org/wiki/Lantana_camara


Can a hormone be absorbed into the body digestively? Obviously, to act most hormones must be present in the bloodstream. What happens if a hormone or hormone-containing food is consumed normally? Is there any way for the hormone to reach the bloodstream?

A related question is whether hormones are destroyed by digestive enzymes and chemicals, which include hydrochloric acid and bile salts. If hormones are destroyed by these chemicals then it may be impossible for them to enter the blood stream.

This entirely depends on the kind of hormone. Hormones can be chemically completely different things. For example, estrogen is a steroid hormone and is chemically very stable so that it can pass the stomach without being harmed by the acidic conditions (even without enteric coating. AFAIK enteric coating is only used in emergency contraceptives, not in regular ones. And for the emergency contraceptives it is used in order to reduce side effects such as vomiting). As such, estrogen in your food or drink will have an effect on your body and there are many studies suggesting that this is a reason for reduced fertility in men.

On the other hand, insulin is a peptide, which would be digested and its hormone function completely inactivated when swallowed.

There is even the notion, that the gas nitric oxide may have a hormone function. In that case, it could reach the blood stream even through inhalation.

In summary, whether or not a hormone can be active after ingestion entirely depends on the kind of hormone.


Ka/Ks (dN/dS) analysis module for Python? From this wiki article:

  In genetics, the Ka/Ks ratio (or ω, dN/dS), is the ratio of the number
  of Nonsynonymous substitutions per non-synonymous site (Ka) to the
  number of synonymous substitutions per synonymous site (Ks), which can
  be used as an indicator of selective pressure acting on a
  protein-coding gene.

Question:

Are there any modules/packages available in Python for doing Ka/Ks analysis? I wish to carry out whole gene Ka/Ks analysis and then maybe "codon level" Ka/Ks analysis (i.e. within gene via sliding window).

Do you know about BioPython?

Here, on another website, someone already asked this question and a pretty nice answer was provided by Brad Chapman. He gives already written functions to perform this kind of analysis (I personally haven't tried the codes).

In Perl there is Bio::Align::DNAStatistics. You might adapt it to Python.

This might be useful as well.

I think there are plenty of possibilities that are offered to you. You can go through some others by doing google search with the keywords synonymous, non-synonymous and BioPython.


Why is ATP hydrolysis to ADP, rather than ADP hydrolysis to AMP, used to drive biochemical reactions? ADP has two phosphate groups, and can be hydrolysed to AMP in a reaction which involves a similar free energy change to that of hydrolysing ATP to ADP.

Why is the latter reaction, rather than the former reaction, coupled to energetically unfavourable reactions to provide an overall reaction with a negative change in Gibbs Free Energy?

Summary

The original question was edited — with the approval of the poster — so that in brief it now asks:

  Why is ATP hydrolysis to ADP, rather than ADP hydrolysis to AMP, the
  normal way in which cells drive reactions which alone involve positive changes in Gibbs
  Free Energy?

The scope of this is wider than that originally assumed in the answer from @user1136, but he has also contributed to this answer by his comments, which I have incorporated into my revision.

To my knowledge there is no generally-accepted provable answer to this question (as opposed to listing advantages for the system as it works today). What I shall do is present a hypothesis that could explain this situation. The fundamental idea† of this is that:

  The contemporary use of ATP rather than ADP in energy transfer
  reactions evolved from a preference for NTPs, rather than NDPs, as the
  precursors of RNA synthesis. This preference was a result of the fact
  that the conversion of NTPs to NMPs and pyrophosphate could prevent
  the reversal of this (and other) synthetic processes in a way that conversions  liberating phosphate could not.

AMP, ADP and ATP: Standard Free Energies of Hydrolysis

There is general agreement that the values for ∆G°′ (standard free energy change at 37˚C) for the hydrolysis of the terminal phosphate bond of ATP (β-γ) and ADP (α-β) are similar. (The following are from J.L. Jain, et al.:

ATP → ADP + Pi  –7.3 kcal/mol
ADP → AMP + Pi  –7.3 kcal/mol

Hence, there is no intrinsic energetic difference that might explain the preferential use of ATP over ADP as an ‘energy donor’ in biochemical processes, i.e. it is not evident why e.g.:

  Glucose + ATP → Glucose 6-phosphate + ADP

and not

  Glucose + ADP → Glucose 6-phosphate + AMP

And, as @user1136 mentions, there are examples where the energy of the hydrolysis of ADP to AMP can be used to ‘drive’ other reactions. He mentions polynucleotide phosphorylase, to which I would add  adenylate kinase, as this is not a synthetic process and is pertinent to the energy metabolism of nucleotide phosphates:

  ADP + ADP ⇄ AMP + ATP

The introduction of AMP into the discussion raises the question of the value of the ∆G°′ for the following reaction:

ATP → AMP + PPi

Many texts quote a value only slightly greater (ignoring the minus sign) than those for phosphate release (the one cited quotes –7.7 kcal/mol), but a 1995 review of the situation in the Journal of Biochemistry suggests that the difference is actually greater: –10.9 kcal/mol, as opposed to –7.8 kcal/mol for the hydrolysis of ATP to ADP and Pi.

The relevance of this is considered in the next section.

Biosynthetic processes and ATP

It seems to me that the example of polynucleotide phosphorylase is especially pertinent because it is a biosynthetic process in which the nucleotide monophosphate is actually incorporated into the product.

  [AMP]n + ADP → [AMP]n+1 + Pi

However this ADP-driven non-template dependent synthesis of polynucleotides is not model for template-dependent RNA synthesis, one reason being that it can also operate in the reverse direction as a phosphorolytic 3ʹ to 5ʹ exoribonuclease reaction:

  [AMP]n+1 + Pi → [AMP]n + ADP

Irreversibility is an important feature of template-dependent synthesis of RNA¶, and it is thought that the key to this is that fact that ATP is the substrate and is cleaved between the α and β phosphates liberating pyrophosphate rather than monophosphate.

  [NMP]n + NTP → [NMP]n+1 + PPi

The reason generally proposed to explain why this reaction is irreversible is that in the cell pyrophosphatase hydrolyses the pyrophosphate to phosphate in an exothermic reaction. However the problem in evolutionary terms is that pyrophosphatases would have to evolve before this would work. However, if the ∆G°′ for pyrophosphate release has a greater absolute value than that for phosphate release, this in itself would affect the equilibrium of the reaction in a manner favourable to synthesis, albeit at the greater effective cost of an extra ATP. The later evolution of pyrophosphatases would have served to reinforce and enhance the irreversibility.

The Hypothesis

The hypothesis is that nucleoside tri-phosphates developed early in evolution to provide a means of making nucleic acid synthesis essentially irreversible by a mechanism that generated pyrophosphate. As the example of polynucleotide phosphorylase shows, nucleoside di-phosphates do not allow this.

A priori it would seem that there is no reason why ATP rather than ADP should be preferred for coupling biochemical reactions. However, if one accepts the argument that ATP synthesis was required for nucleic acid synthesis, there would seem no reason for having a set of reactions generating ADP for other purposes. The energy of hydrolysis of ATP to ADP in such reactions would, in any case, have to be utilized, otherwise it would represent a net loss. Why go any further?

It may have been that ATP was preceded in evolution by an an earlier ‘energy donor’. However I would suggest that once a mechanism evolved for synthesizing and using ATP (and other NTPs) for synthetic purposes, it was more efficient to use this for metabolic purposes, largely displacing any previous energy donor molecule.

† Footnote 1

I have touched on this very tangentially in my answer to a quite different question about ATP. The common idea, however, is that the purine and pyrimidine rings of NTPs serve no purpose in energy transfer, but are a relic of their requirement in RNA synthesis, where the NTPs are not merely providing energy, but are incorporated into the RNA product.

¶ Footnote 2

RNA and DNA synthesis are not the only synthetic processes in which this strategy for irreversibility is adopted. The tRNA amino-acylation reaction — essential for protein synthesis is as follows:

  Amino Acid + ATP → Aminoacyl-AMP + PPi

And the first step in glycogen synthesis is the formation of UDP-glucose:

  Glucose 1-phosphate + UTP → UDP-glucose + PPi


Difference between protein channels, protein carriers and protein pumps? I'm revising for my biology exam and I don't fully comprehend the difference between protein channels, carriers and pumps. I know that:

Protein channels do not require ATP (passive transport)
The difference between passive and active transport

My questions are:

Are protein carriers and pumps the same?
I read that protein carriers can perform both active and passive transport, is this true?
But protein pumps always require ATP?

No, carriers are not the same as pumps. Carriers may or may not carry out active transport and pumps always use energy. Carriers, for example, can make use of the concentration gradient of a certain ion built up by pumps to transport other molecules actively against their gradient. For example, the glucose transporter uses the sodium gradient to transport glucose against the concentration gradient into the cell, while getting the energy by co-transporting sodium into the cell along the gradient. The sodium import yields energy. That in turn is caused by the Na+ K+-ATPase, which builds up the sodium gradient using ATP. The glucose transporter is called a symporter, because it co-transports sodium into the cell. An antiporter transports another particle in the opposite direction.
Yes, true. The glucose transporter as explained above is an example of active carrier-mediated transport. Other carriers just mediate passive diffusion of, for example, large molecules that don't fit through channels and won't readily cross the cell membrane.
Yes, pumps always use energy under physiological conditions. The energy source is always ATP.

Will add references shortly.


Structure of fitness landscapes in the NK model The NK model of rugged fitness landscapes consists of $N$ sites where fitness contribution of each site depends on its state $\{0,1\}$ and is epistatically affected by $K$ other sites. When defining the model, Kauffman & Weinberger (1989) stressed that:

The actual structure of [fitness] landscapes, although knowable is currently unknown

They then go on to assume either epistatic interactions are with adjacent sites in a linear ordering or at random, and that fitnesses are assigned to each of the $2^{K + 1}$ epistatic combinations at each site uniformly at random in $[0,1]$. Although it is definitely possible to justify this random generation, it tends to produce a very structured fitness landscapes, that although rugged (for high $K$), has a very regular distribution of local fitness optima. As a computer scientist, this assumption of an arbitrary random distribution over possible NK landscapes seems very misguided. I would be more comfortable with a worst-case analysis on a "reasonable" (hopefully as determined by experiment) subset of possible NK landscapes.
What is known about the typical structure of NK landscapes in biological domains? Also, are there examples of biological papers that do a worst case instead of an arbitrary random analysis on some non-trivial subset of landscapes? The only example I am familiar with is the gadgets used by Weinberger (1996) to show that the unconstrained model is NP-hard, but that is a trivial subset (all possible landscapes) and not of biological interest.

References
Kauffman, S. and Weinberger, E. (1989) The NK Model of rugged fitness landscapes and its application to the maturation of the immune response. Journal of Theoretical Biology, 141(2): 211-245
Weinberger, E. (1996). NP-completeness of Kauffman's N-k model, a Tuneable Rugged Fitness Landscape. Santa Fe Institute Working Paper, 96-02-003.

Very little is known about the structure of fitness landscapes.
H.A. Orr (2005; also Whitlock et al., 1995; Kryazhimskiy et al., 2009) explains that most experimental results do not actually attempt to measure the fitness landscape, but instead report just the average fitness versus time and average number of acquired adaptations versus time. This can't be used to discern epistatic interactions, or any combinatorial structure of the landscape. In general, the theory of adaptive walks has developed without reference to real data and even the most refined theories can only correspond in vague qualitative ways (see Kryazhimskiy et al., 2009 for the best example I know).
Szendro et al. (2013) surveyed the few recent experiments that conducted a methodical examination of all mutations in a subset of loci of model organisms, but most studies (6 out of 12) were able to empirically realize only small fitness landscapes of just 4 to 5 loci (so 16 to 32 vertexes), with the largest full fitness landscape having length 6 with all 64 vertexes examined (Hall et al., 2010), and the largest number of vertexes in a single study being 418 out of the possible 512 in a length 9 landscape (O’Maille et al., 2008). These are extremely small landscapes, and thus don't have much power in distinguishing proposed theoretical models.
After extensive searching, I have not been able to find examples of theorists doing worst case analysis of fitness landscapes. The closest to worst-case analysis is Orr-Gillespie theory (Gillespie, 1991; Orr, 2002; 2006; Kryazhimskiy et al., 2009) that assumes that the wild-type is still very fit after an environmental change, and so beneficial mutations are extremely rate. This allows the authors to introduce extreme value theory and consider just the asymptotic properties of distribution tails thus allowing a more general treatment with fewer parameters; in some cases leading to a full classification of adaptive trajectories (Kryazhimskiy et al., 2009). This approach is easier to relate to experiment, but unfortunately completely ignores the combinatorial structure (beyond first-order) of the fitness landscape and always just samples the next potential mutant from the tail of a distribution without taking into account how it is progressing in the landscape. Although Orr (2006) introduced the basics of fitness landscape structure, the structure was much simpler than the NK model; he used Perelson & Macken's (1995) block model with each block as completely unstructured beyond first-order.

References
Gillespie, J.H. (1991). The causes of molecular evolution. Oxford University Press.
Hall, D. W., Agan, M., & Pope, S. C. (2010). Fitness epistasis among 6 biosynthetic loci in the budding yeast Saccharomyces cerevisiae. Journal of Heredity, 101: S75-S84.
Kryazhimskiy, S., Tkacik, G., & Plotkin, J.B. (2009). The dynamics of adaptation on correlated fitness landscapes. Proc. Natl. Acad. Sci. USA 106(44): 18638-18643.
O’Maille, P. E., Malone, A., Dellas, N., Hess, B. A., Smentek, L., Sheehan, I., Greenhagen, B.T., Chappell, J., Manning, G., & Noel, J.P. (2008). Quantitative exploration of the catalytic landscape separating divergent plant sesquiterpene synthases. Nature Chemical Biology, 4(10): 617-623.
Orr, H.A. (2002). The population genetics of adaptation: the adaptation of DNA sequences. Evilution 56: 1317-1330.
Orr, H.A. (2005). The genetic theory of adaptation: a brief history. Nature Reviews Genetics 6(2): 119-127.
Orr, H.A. (2006). The population genetics of adaptation on correlated fitness landscapes: the block model. Evolution 60(6): 1113-1124.
Perelson, A.S., & Macken, C.A. (1995). Protein evolution of partially correlated landscapes. Proc. Natl. Acad. Sci. USA 92:9657-9661.
Szendro, I. G., Schenk, M. F., Franke, J., Krug, J., & de Visser, J. A. G. (2013). Quantitative analyses of empirical fitness landscapes. Journal of Statistical Mechanics: Theory and Experiment 2013(01): P01005.
Whitlock, M.C., Phillips, P.C., Moore, F.B.-G., & Tonsor, S.J. (1995). Multiple fitness peaks and epistasis. Annu. Rev. Ecol. Syst. 26: 601-629.


Question on kilobase - packaging of genomic material in viruses I have been looking up some information of SARS. Wikipedia says it is 29.7kb in length while 1kb is around 300nm. However, the microscope image on wiki shows the virus size <100nm. It doesn't make sense mathematically so that think I missed some knowledge. I hope this question qualifies to be posted on stackexchange. Thanks in advance.

This value is only true for linear DNA. However, DNA in cells is not linear, it is folded, which makes it ways more compact (otherwise the DNA in our own cells would be around 2 meters long).

See the figure from reference 1 for a schematic view how this works in higher cells:

The table below (from reference 2, either klick on the picture or the link below for a bigger version) shows how the length of a piece of DNA is influenced by packaging:

There is another caveat in this question, Corona viruses (as the SARS virus) are singlestranded RNA viruses. The RNA of viruses contains packaging signal sequences, where special proteins bind, before the virus is assembled around the bound genetic information. See reference 3 for a general overview and reference 4 for the packaging of the SARS virus in special.

DNA Packaging: Nucleosomes and Chromatin
DNA, chromatin and genome numbers
Genome packaging in viruses.
Assembly of severe acute respiratory syndrome coronavirus RNA
packaging signal into virus-like particles is nucleocapsid
dependent.


Probability of number of boys and girls being born on a single day I am new to genetics, I have the following question at hand :

If four babies are born on a single day, what are the chances that
$A>$ Number of boys and girls will be equal.
$B>$ All $4$ will be girls.
$C>$ At least one baby will be  a girl.
$D>$ Which combination of boys and girls is most likely?

My solution:
Let $X$ be the number of boys .
$X$ follows $Binomial (4,{1\over 2})$ , since the probability of a child being a boy is half.
So the answers are
$A>{3\over 8}$
$B>{1\over 16}$
$C>{15\over 16}$
$D> $ Equal number of boys and girls.
Is everything right ?

I know this is kind of tedious and only practical when you are considering no more than 10 children  (which I think is a lot to parent), but anyway, I like to solve these problems with a binomial expansion.

So we have binomial probability so 2 options - either a boy (n) or a girl (g) at equal probability or 50% or 1/2.

(b + g)^n = a binomial expansion according to the coefficients of Pascal's triangle.
Where n = 4 children, then the row of Pascal's triangle is 4 in which the first row of pascal's triangle is technically row 0.

Equation: (b + g)^4 = 1(b)^4 + 4(b^3)(g) + 6(b^2)(g^2) + 4(b)(g^3) + 1(g^4)

Problem A)
So the probability that the number of boys and girls will be equal is

Probability((6(b^2)(g^2)), where (b^2)(g^2) means two boys and two girls, an equal number.
When b = 1/2, and g = 1/2, or well ... b + g = 1

6(b^2)(g^2) = 6[(1/2)^2 * (1 / 2)^2] = 6 * (1/2)^4 = 6 / 16 = 3/8

B) All four will be girls: Prob((1(g^4))

= 1(1/2)^4 = 1/16

C) At least one baby will be a girl:
That corresponds to 4(b^3)(g), 6(b^2)(g^2), 4(b)(g^3), and 1(g^4)

The probability that at least one will be a girl is

= (4 + 6 + 4 + 1) * (1/2)^4 = 15 / 16

D) Which combination of boys and girls is most likely?
That would be 6(b^2)(g^2), so when b = g = 1/2

Prob(most likely combination) = 6/16 = 3/8 or two boys and two girls.

Note that if you add up all the combinations, the result is 100% of all probabilities:

(b + g)^4 = 1(b)^4 + 4(b^3)(g) + 6(b^2)(g^2) + 4(b)(g^3) + 1(g^4)
When b = g = 1/2, then basically:

(1 / 16) + (4 / 16)+ (6 / 16) + (4 / 16) + (1 / 16) = 16 / 16 = 1 = 100%

You did it right. But I suppose this is another way to evaluate a binomial like this.