What are the evolutionary niches differentiating an apple from a pear? So, as far as I understand (basic) evolutionary theories, diversity is generated by "niching." That is, if there is an environmental factor that hasn't been fully used by any species to "profit" off, there will be a tendency to fill up that "niche" and thus speciation occurs (not in one day of course).

I was standing in the kitchen earlier and was wondering: what is the niche that an apple fills in respect to a pear end vice versa? If I'm not mistaken they are form the same family and thus share a common ancestor (albeit I don't know if it is a "recent" ancestor).

Is it a geographical thing or do they genuinely vie for the same thing in a different way? (e.g. a pear aims to be eaten by animals that have small teeth and thus want a softer fruit, while an apple aims to be eaten by the bigger animals, that like a heartier bite).

note: I know that this question might be too speculative and too localised to be any good, but hey, some of you might just know this!

I wouldn't be suprised if no one has hard data on this. In any case there is more than one answer to this question.

Niches are defined more than one way.

In the narrowest definition, the niche might be defined as the ability of the different trees to grow in different terrains or be eaten by different animals in the same environment.  I can't comment on that, but in most environments, there is in practice little difference between the two.  The classic example of this is Darwin's finches - where a single species eventually becomes many, each specializing in a specific kind of lifestyle (what they eat/where they net) on the islands of the Galapagos where they were situated.

In the broadest definition of niche, they do have a different niche because they are different species, and their differences allow them to be eaten by different people.  In their highly domesticated environs, apples and pears each have a niche defined by the fact that they are both stocked in the produce sections for people to eat as they choose.

Its worth mentioning that Darwin determined that different organisms can inhabit the same niche.  In his case he saw that on different islands of the Galapagos he saw that the finches had evolved into different species, each of which took up the role that a different bird might have back home.  so its possible that apples and pears may have substantially the same niche in their respective evolutionary histories.


Divalent cation binding to calmodulin I have carried out a native PAGE with 4 reaction mixtures. To each I had added an equal volume of EDTA (1 µl/1mM) to sequester any divalent ions and an equal volume of calmodulin (5 µl/0.5 mg/ml). I added 2 µl of calcium (2 mM), magnesium (2 mM) and manganese (2 mM) ions respectively to three reaction mixtures and had a control that was made up to an equal volume with Tris-HCl. All reaction mixtures were made up to 10 µl with Tris-HCl. Here I ran into a problem with the waterbaths and the reactions couldn't be incubated at 37 degrees Celsius.

After I added the loading buffer to each, I added the 4 reaction mixtures to the polyacrylamide gel and electrophoresed for 45 minutes at 150 V. After this I placed the gel in Coomassie Blue stain for 20 minutes.

After the destaining process, I reviewed the gel to find that the calmodulin in the 4 lanes had migrated the same distance. I had expected the EDTA control to have migrated the furthest on the gel, with Ca2+ and Mn2+ migrating similar distances due to their similar ionic radii; making it a good substitute for the binding to the calmodulin. I was unsure of how far the Mg2+ would travel as I thought it would have a lower affinity to the calmodulin due to its binding to the N-terminus rather than the C-terminus. However, I was wondering if this was negligible in the absence of Ca2+, although now I can't be sure due to the results of the gel.

I was wondering what errors in the experimental design or process could have resulted in this? And if the experiment was run correctly, what results would be expected?

The first image is the result I was expecting. The second is the results from my gel electrophoresis.

The change in gel migration distance is due to the conformational changes due to the binding of the ion, and have nothing (detectable) to do with the ionic radius of the ion.

The left image shows calmodulin with no ligand bound, and the right image shows it with calcium and peptide bound to it.

As you can clearly see, the unbound calmodulin is significantly thinner, and therefore can migrate faster through the gel. The change in charge on the protein due to cation binding in native PAGE may also affect the result.

Since the calmodulin conformational change is enhanced by both a peptide and calcium cations, as well as its phosphorylation state, it would be reasonable to investigate the contributions of these factors to your result. Reading the original paper again to see what you missed the first time may also be helpful.


What makes a 'sense'? Is fatigue (tiredness) a sense? I have watched to new episode of Scishow on that scientists added 3 new senses (Thermoception, Proprioception and Equilibrioception) to our 5 sense list, and was wondering what makes a 'sense'?

Wiki definition:

  A sense is a physiological capacity of organisms that provides data
  for perception.

Does that mean fatigue (feeling tired) is a sense too?

To me, the defining characteristic of a sense is that it assimilates information from the external environment for your body to use if necessary. This is also the way the textbooks I've taught from treat it.  Thermoception senses external temperature, your body evaluates and, if need be, you take action. Equilibroception senses gravity to help you evaluate your orientation with respect to the Earth.

Proprioception is a hard one to categorize. Some of what is classified as such seem to rely on only internal sensors such as how much a muscle is stretched. Other aspects of proprioception rely on muscle tension which would indeed be affected by gravity and qualify proprioception as a sense by this definition.

I would say fatigue is not a sense because it is based on internal messages. How about a "sense of hunger"? I'd again say no, hunger is also the result of internal messages. Your sense of smell can lead to hunger but the information gathered was odor, not hunger.


How Mitochondria differs from Prokaryotes(probably regarding energy production)? In other words, what evolutionary advantage is offered by mitochondria to eukaryotes(probably regarding energy production), which prokaryotes themselves cannot evolve or do?(here I am assuming that mitochondria evolved from prokaryotes)

I seemingly found some answers in the below article. Will love to hear the opinion of others regarding the same.

http://blogs.discovermagazine.com/notrocketscience/2010/10/20/the-origin-of-complex-life-it-was-all-about-energy/#.WYXsH4h97b0

If you mean "why do we have mitochondria instead of our cells doing the work themselves"
Then I can think of several answers.

First, oxidative phosphorylation must take place within an organelle, and requires specialized cellular machinery to occur.

So either a prokaryote can wait a couple million years to evolve these structures, or it can ask its friend to do it, and HE is specially evolved to do just that.

Like the way you hire a plumber when your toilet gets clogged, instead of going to plumber school yourself.

Also, oxidative phosphorylation has to do with oxygen.

Oxygen, when busted apart, can form unstable molecules called free radicals that are essentially bleach.

These molecules zoom around smashing up anything they touch including DNA.

So the host cell says "better you than me!"
Remember how I said you need an organelle for oxidative phosphorylation?

This is why. So all the "bleach" gets contained.

Two very good reasons why we evolved to rely on a separate organism instead of just making our own breathing organelle.


Density of neurons/cells in the mouse brain Could someone point out some relevant papers or resources (an online DB maybe?) describing the density of neurons (or, more in general, of cells) in different areas of the mouse brain?

The newest and most accurate method (far more accurate than older extrapolating/manual counting methods (Stereology) and yielding some surprising results) to estimate number/density of neurons/cells in brains is Isotropic Fractionator to my knowledge. Using this keyword you find some recent papers, comparing different brain areas (cerebral cortex, cerebellum,...) among rodents:

  Combining our estimates of total cell number and percentage of NeuN-containing nuclei in each brain region, we find that adult rat cortex contains ∼80 million cells, 40% of which (∼30 million) are neurons. In comparison, rat cerebellum contains more than twice as many cells (∼170 million), >80% of which are neurons (Table 1, top). Therefore, the adult rat brain contains almost five times as many neurons in the cerebellum (∼140 million) than in the cerebral cortex. When all of the brain regions are taken into consideration, the cerebellum thus accounts for more than one-half of the cells and ∼70% of all of the neurons of the entire rat brain (Table 1, bottom). Overall, we estimate that of all of the cells in the adult rat brain, 60%, or 200.13 ± 21.17 million, are neurons. Glial cells, therefore, contrary to common belief, are not the most numerous cell type in the rat brain.

Isotropic Fractionator: A Simple, Rapid Method for the Quantification of Total Cell and Neuron Numbers in the Brain
Cellular scaling rules for rodent brains
The Human Brain in Numbers: A Linearly Scaled-up Primate Brain


What are respirasomes? I have read wikipedia but don't understand it well. Do we mean Complex I, II,III and IV when we say respirasomes?

What the article is saying, is that there are several respirasomes, each of which consists of multiple other mitochondrial complexes or cytochromes. The article makes an example of three commonly observed respirasomes when it says:

  The most common supercomplexes observed are Complex I/III, Complex
  I/III/IV, and Complex III/IV.

So, the short answer to your question is that a respirasome refers to a set of multiple cytochromes, whose combined action leads to respiration.

This paper goes into more detail, and reiterates that the term "respirasome" is used to describe multiple cytochrome supercomplexes.


How does collaboration on reconstructing metabolic networks work? I am a researcher in psychology and I am trying to come up with a framework/platform in which psychological phenomena can be studied from a dynamical systems / computational perspective in collaboration with many labs. To be more concrete, the question is how to organize knowledge about psychological variables and how they are coupled by functional relationships on different time-scales that may be a function of additional variables.

My hope was to learn from disciplines that already work with a dynamical systems/computational framework for a long time. The first interesting analogy I came across were metabolic networks. I read this review about their reconstruction and while many things are different, the task is very similar to ours in that a given network of entities and functional relationships is continuously refined by the scientific community.

I saw that there are many data bases with genes, pathways, annotated graphs etc. but my main question is:

How is the scientific process of refining such a metabolic network organized? Are there platforms for this? Is there anything in place to quantify the uncertainty associated with parts of the network or to resolve disagreements? Are there any standards for implementations? Or is each group simply creating their own version based on previous literature and then publishing their new network in a paper?

I realize that this is a rather broad question and I apologize if I posted this in the wrong stackexchange forum. But I didn't know where else it would fit. I'd appreciate a lot if someone could give me some basic insights about how this field works or if someone has some pointers to relevant reading material.

A bit of a preface:

A lot of this large scale collaboration (which I would maybe rather describe as the work of a whole [sub]field over a given time frame) often ends up in some sort of database. Really, there A LOT of those in modern biology - and often with minor but sometimes important differences. One of those would be the level of curation: are results gathered automatically from other sources, or always manually checked before being added? Another thing about databases is that (with certain exceptions of course) they often are only relevant for specific sub field, in some cases this can mean that only one lab maintains a website with a databases that is used by a few others, but that's it.
What I'm trying to get to is that there isn't really a 'one size fits all' solution and that especially the size of your field will impact which kind of solutions are both feasible and actually useful.

Now to answer your actually state question (as far as I can):

Most known biochemical pathways (including the metabolic ones) are described in the KEGG database. Initially this project was started by a single lab (and is still run by that group as far as I can tell), but of course it contains a lot of published information from other sources (I couldn't find information on how they update the networks in the database, you may have to read the papers for this). The database can also be accessed remotely, so it allows people to use the same network for a given reaction, and by incorporating sequence data it also has information on which organisms even contain the given enzymes in the network.
One thing the database does not contain is information about dynamics in the network. In this case I think most groups will generate and publish their own models (e.g. based on ODE's).


Can prawns and lobsters live out of water for more than six hours? I live in Telangana which is a state of India.I like eating Non-vegetarian food.People of our state eat pond fish more comparing to other aquafood.In many places near me,I've seen people cutting alive fishes in to pieces with their big knives.I won't feel good to see this.So,usually I bring the pond fishes home and keep them aside for atleast 40 minutes with no water in contact to them.In these 40 minutes I prepare other ingredients needed for the recipe.After these 40 minutes,generally as there is no response from those fishes I start cutting them into pieces.In the same way I don't know how much time it will take for prawns and lobsters to die without water.Do they live more than six hours without water?

This question is not related to the experiments carried out by the biologists on lab creatures.They are great people.I encourage their experiments whether it involves humane killing or inhumane killing because their experiments on one creature may help millions of remaining creatures.

TL;DR version is they are gill breathers and need to be in a humid and moist environment to have a considerable longer life span outside sea water.

Dr. Cowan's on being asked the same question about lobster said:

  “Gills work best in seawater, but if lobsters are kept in containers of seawater with no aeration, they quickly use up the oxygen and suffocate,” she said. “That it why it is imperative to transport lobsters in containers with no standing water.” - New York Times

Many lobsters, shrimps and even crayfish & crabs are transported in boxes with a small amount of water in the bottom and they survive for several days like that. However the long term side effects of this are still to be discovered as most crustaceans transported this way get cooked.


Small worm living in some kind of cocoon, what are these animals? I am curious what animal is this. It is/lives inside some kind of cocoon, about 1 cm in length. They are attached to walls and to the ceiling, but sometimes they fall off. Inside the structure there is a small worm that can come out at both ends alternatingly. It can then hold on to the ground to move the cocoon around. They are said to feed on paper.

This little dude is not a Caddisfly, but a true moth,  Tinea pellionella, a case making clothing moth.  Confusing because they do resemble caddisfly larvae cocoons more so than those of their own family (Tineidae).  Sort blurb Here:

  "The brown-headed larva spins a silken case that is open at both ends. The case in the above image is covered with fine sand and debris, and superficially resembles a caddisfly case. The flattened case is about 10-11 mm long (3/8 to 1/2 inch). When crawling, the larva's head, thorax, and three pairs of legs protrude out of the case, and drag it along. According to Internet sources, the larva feeds on a variety of material, including hair, fur, silk, felt, feathers, woolen clothing, upholstered furniture and carpets. It apparently prefers darkness and soiled clothing, and is not fond of synthetic fabrics, such as nylon and polyesters."


Question about the quantity of orchid species and genera One flower which I am reminded of is the orchid and conjointly, the Orchidaceae family. I am surprised when discovering there is an abundance of species and genera, hence I would like to know the exact number. Moreover, what is the reason, is this a quality resulting from angiosperms?

The Plant List records 27,801 accepted species names in 899 genera within Orchidaceae. This estimate probably differs a bit between authorities. For example the Angiosperm Phylogeny website records 26,000 species in around 880 genera. Regardless it is I think the most speciose angiosperm family.

The explosive diversification of orchids, like the diversification of angiosperms, has been a big study point for evolutionary biologists. A lot of explanations center around the wide array of floral morphologies which you can find in the group, as well as (although not independently) the evolution of a whole range of pollination strategies. Other factors include evolving in a tropical environment and the evolution of CAM photosynthesis in the group. You can find more details in, for example Givnish et al. 2015


What's the difference between shotgun sequencing and clone based sequencing? In a lecture during  my undergraduate degree we were introduced to the race to complete the human genome. Celera were competing with Sanger and collaborators to sequence the human genome. Celera wanted to patent some sequences, whilst Sanger et al. wanted to keep their findings in the public domain. Celera knew they couldn't compete with Sanger et al. with conventional cloning techniques which required a lot of man-power, "so instead opted for shotgun sequencing".

To me it seems like both clone based sequencing and shotgun sequencing could have been used together, however the lecturers semantics were a bit vague (...okay, I wasn't paying close enough attention!) and I didn't ask for clarification at the time.

Whilst I appreciate this is a large topic, what are the main differences between Celera's shotgun sequencing and Sanger's clone based sequencing during the late 1990s? Are "shotgun cloning" and "clone based sequencing" actually mutually exclusive terms?

The v short answer is that in shotgun sequencing, the sequencer is fed a set of random sequences from the target.  This can be done for instance by mechanically shearing DNA and then building a set of shotgun sequencing jobs which are then compiled back together by a genome assembler (i.e. in whole genome sequencing projects) into a full sequence.

In clone based sequencing, the DNA to be sequenced is specifically sectioned off into sequence copied into of plasmids (BACs - bacterial artificial chromosome) to divide the sequencing job into sections- a divide and conquer strategy.  BACs can be 150 kb long just to give you an idea.

These are not mutually exclusive terms; clone-based sequencing projects usually use the large clone libraries to section the project into a set of shotgun sequencing projects.


Do the individual claws of a bear have names? The question seems pretty self-explanatory (if perhaps a little odd). Anatomical names or colloquial names are both appreciated, especially the latter if they exist.

I would be surprised if they do!

Bears have 5 clearly visible toes per paw. You could just name the claws based on the fingers it is on (thumb, index, middle, ring, pinky).


Peacock species identification A few weeks ago I encountered a peacock while driving to a friend's house in Central KY, USA. I don't believe I've ever seen a peacock in KY, and when attempting to ID [just through Google searches], I could only find restaurants & musical artists that contain "peacock" in their name.

Can someone help me ID this bird? And, are peacocks wild in KY? Have they always been, and are just rare? Aside from species ID, any insights about this bird and its prevalence within KY would be most appreciated.

That is the male of the Indian peafowl species (Pavo cristatus), also called the blue peafowl or common peafowl.  The male is called a peacock and the female a peahen, collectively peafowl, although often "peacocks" is used instead of peafowl.  The hen does not have the impressive tail of the peacock (although she does have a similar crest on the head).

They are not native to Kentucky, or anywhere else in the Americas, but have been widely introduced (because of their appearance).  There are only 3 species of peafowl, the green peafowl being similar and native to southeast Asia, and the Congo peafowl being much more subdued and native to Africa.


Which hormones can cross the blood brain barrier? Can hormones such as testosterone, aldosterone and estrogen cross the blood brain barrier?
I looked on Wikipedia and there no mention of it in the testosterone article. Through Googling around I also didn't find a list of which hormones can cross the barrier.

Yes, both steroid and peptidic hormones can enter the brain, the obvious proof being that the brain responds to changing blood concentration of hormones.

The situation is different for steroid hormones (such as estrogen, testosterone, cortisol etc) which are small and lipophilic, and peptidic hormones (such as insulin, ghrelin, prolactin etc) which are big and hydrophilic.

The blood-brain barrier (BBB) is selectively permeable to steroid hormones: some of them (such as the gonadal steroids) can readily pass the BBB, while others (such as corticosteroids) pass only in small concentrations. This may however be modulated by hormone carrier proteins in the plasma.

See: Transport of Steroid Hormones through the Rat Blood-Brain Barrier - Pardridge et al., JCI, 1979

When speaking of peptidic hormones, the classic hypothesis is that hormones pass through the areas where the BBB is "leaky", i.e. where capillaries are fenestrated.
These include circumventricular organs such as the median eminence (where the terminals of many neuroendocrine neurons are located), or the organum vasculosum of the lamina terminalis (OVLT), important for reproduction and osmoregulation. The chorioid plexus is also often mentioned as a site for hormone entrance and/or sensing.

However, how exactly hormones enter the brain is still very unclear.
Our lab published a paper on this topic recently:
Rapid sensing of circulating ghrelin by hypothalamic appetite-modifying neurons - Schaeffer et al., PNAS, 2013


What are the classical adaptations of amphibians? My question is about amphibians in humid or underwater environments. What biological adaptations can found in them, further what purposes do they serve?

"Amphibian" means "living both in water and on land" (see here). Here is a small list of classic adaptations in amphibians:

Eyes and nostril are positioned to poke out of the water while the rest of the body is immersed
Ears don't let any water gets in
Skin is very thin and allow direct gazeous and water exchange
Paws are webbed to move into water
Larvae of most amphibian species start their life in the water


Fst genetic distance: Autosomal vs. mtDNA As far as I'm aware, mtDNA is only inherited from the mother. Hence, if I compute Fst from autosomal SNPs, then I'll get the actual genetic distance between two human populations.

If I compute the genetic distance Fst between two human populations based on mtDNA sequences, then it alone can't be used to draw conclusions on their genetic distance.

For example, an admixed population will score relatively low Fst value with its maternal ancestral population (assuming the admixture was caused by unisex migration) when computing based on mtDNA sequences. However, the Fst distance based on autosomal SNPs will be relatively higher (depending on proportion of admixture).

Is this correct?

Yes, you are correct.

$F_{ST}$ can vary among specific genetic regions considered. If for example there is a strong influx of females from population A to population B, then the mtDNA and the X chromosome (excluding the pseudo-autosomal region) would show much smaller $F_{ST}$ between the two populations than the Y-chromosome would.

Many other non-demographic processes can affect $F_{ST}$. Background selection (Charlesworth et al., 1993; Matthey-Doret and Whitlock, BioRKiv, 2018), selective sweep (e.g. Chen et al., 2010), heterozygote disadvantage (Ingvarsson and Whitlock, 2000), negative epistasis and other processes can affect $F_{ST}$ as well and cause $F_{ST}$ to differ among genetic regions. Even mutation rate variation (Whitlock and McCauley, 2001) can affect $F_{ST}$ (if the mutation rate for the loci considered is not ridiculously small compared to the migration rate).

For an introduction into the common misunderstandings of how $F_{ST}$ works, Whitlock and McCauley (2001) is a must read!

  Just to complete this answer, would Fst computed from autosomal SNPs be fully representative of the genetic distance between two populations? Say for the influx of females from A to B, will the autosomal Fst correctly show that the admixed population is between A and B (depends on mixture proportion)?

The difficulty here is in the phrasings fully representative of the genetic distance and correctly show. There is no correct (true) genetic distance among populations, there is only the statistics of genetic distance that one wants to define and those statistics are affected by various processes.

Would an influx of female among populations affect $F_{ST}$ at autosomal loci? Yes. Would this effect be the same than at mtDNA? Not exactly, no. Is the entire parsing of genetic variation among population represented by $F_{ST}$? No, $F_{ST}$ is just a summary statistic (just like a mean or a variance is).

If there is a specific statistic (such as the effective migration rate, the effective population size or the location of loci involved in local adaptation for examples) that you are trying to infer from these $F_{ST}$ calculations, then maybe you should ask whether computing $F_{ST}$ by a specific method would allow you to make good inference of a specific statistic of interest.


I found this strange tooth in Galveston, Texas. What does it belong to? I found this on May 7, 2017, on Bolivar Peninsula in Galveston, Texas. What's not visible are the treelike rings inside the tooth and what looks like a tiny interior porous center. It looks like it was considerably larger but broken off.

We're all taking bets on what it is!

This is a cow tooth. Your image matches above image.
https://www.flickr.com/photos/61377404@N08/12300347505


Getting some concept of cancer genetics I have two groups of patients : Responders to chemotherapy and non-responders to chemotherapy. I treat this as a dichotomous outcome we can call response to chemotherapy.

For a fixed set of cancer driver genes, I have calculated cancer cell fraction (ccf) for each group.

Does anyone know of any interaction or relation of response to chemotherapy and ccf?

Assuming that my comment is trivial, I think that there is some literature on this question. I'm assuming that the ccf in question is for the relevant tissue type for the cancer.

You might also consider cross-posting to SE Medical Sciences, where people are more familiar with these subjects.

Of course, naively one would expect that a larger ccf would yield a larger possible population of cancer cells to provide "escape" mutations or resistance to chemo, so high ccf should then be negatively predictive. As an extreme example, a highly metastatic cancer will have a high ccf over the whole body, and will be more resistant to chemo just because that's a highly advanced disease.

However, as usual things are a little more complex. The ccf itself has subpopulations. The following I got by just googling around a little bit. For some of the fundamental thinking on this, see this old paper. In this paper, the author puts emphasis for example on the fraction of cancer cells in each stage of the cell cycle; this results in what the author calls "clonogenic" and "nonclonogenic" populations that respectively yield new clones of cancer cells or do not yield new clones. Probably that terminology is somewhat outdated, but it gives a sense of the problem; related are "tumor stem cells". For a more modern treatment, you can look at this.

For a med school lecture treatment, see here to learn a little bit more. For an example of a recent prediction study which uses omic data to predict chemo response, which might be helpful in reformulating your study, see here.

In other words, not all tumor cells are created equal, some are more likely to resist chemo than others. However, overall I would expect that there is probably some kind of relationship between ccf and response to chemo, because they are both related to the mediator variable "number of clonogenic cancer cells"; it's just a somewhat oversimplified model compared to the actual biology, so it looks like the publications in question don't tend to focus on it.


How many plants arise from a polyembryonic seed? When I asked this question to my teacher she said that she doesn't know. So I wanted to know? Is there any use of polyembrony in plants?

In plants due to programmed cell death only one plant arises.

Here is a good article

  The enigma of plant monozygotic polyembryony is that only one embryo in a polyembryonic seed usually survives while the others are eliminated at an early stage.


Why do the host cells containing iC3b fragment not undergo phagocytosis? As far as I understand, in complement system C3b gets deposited on pathogen surface but it can also be deposited on host cells. Host cells have some negative regulatory system such as membrane cofactor of proteolysis MCP, decay associating factor DAF etc which either removes C3b or cleave it using factor I to iC3b which can not form a C3 convertase or C5 convertase so no production of membrane attack complex on host cells.

However, phagocytes contain complement receptors CR2, CR3 etc that specifically recognise iC3b and engulfs the cells bearing it. While it is very useful for pathogens bearing iC3b (In those cases where pathogens contain sialic acid residue which attracts factor I and prevents forming MAC on those pathogens) wouldn't it be very dangerous for host cells?

So if there is receptors against iC3b on phagocytes then what is the point of host cells converting C3b into iC3b, they get killed one way or another anyway

There's a relatively new concept of self-associated molecular patterns (SAMPs), which much like DAMPs and PAMPs, help immune cells make a decision in a slurry of signals. There's at least a fair article on SAMPs here, and to go even further, the suggestion that tumor-associated SAMPs can dampen immune clearance of cancer cells.

In my head a few things are going on:

(1) The opsonins are potentially binding to everything. Of course, there are surfaces like ECM that don't have any receptors or patterns that you don't want getting damaged, and there's at least some evidence that complement clearance by factors I and H (paywall) may contribute to ablating that effect.

(2) The actual targets for the immune system are expressing patterns that specialized pattern recognition receptors on your phagocytes and so forth can recognize.

(3) Self cells are expressing receptors and patterns that tell the very same cells there's no threat, either through direct inhibition or degradation of kill signals.

Remember that when self cells are damaged, the expression of DAMPs help macrophages and the like come clear them away, so there's obviously a way for self cells to control that effect.


Why can't the brain and red blood cells use fuels other than glucose? The question is rather straight forward: I have always been curious as to why, but cannot find an explanation online.

I can imagine that the mechanism is different for each, but why does brain tissue and red blood cells use specifically and only glucose for energy metabolism?

In the case of red blood cells: human erythrocytes (red blood cells) have no mitochondria. Since the mitochondria are the cellular site for oxidative metabolism of fatty acids, erythrocytes cannot oxidise fatty acids to release energy. The erythrocytes also cannot fully oxidise glucose (to carbon dioxide and water) because this is also a mitochondrial process, so they have to rely upon anaerobic glycolysis. The end product of anaerobic glycolysis is pyruvate, and erythrocytes reduce this to lactate (to recycle the NADH that is produced during glycolysis) and then export this lactate into the blood for further metabolism by the liver.


Concentration calculation of Factor VIII for Elisa I have the following problem. I'm trying to get the concentration calculation for an Excel sheet that will calculate values from an Elisa plate.

The basis is a standard curve with the following values:

Std: PreDil factor 1: 40
PreDil factor 2: 55
---> Total Predilution = 2200
Concentration: 2123  µg/ml

Dilution  1:20      1:40    1:80

Std 1     1,3910    0,6360  0,2850

Std 2     1,4020    0,6360  0,3140

Std 3     1,3500    0,6250  0,2880

Std 4     1,4470    0,6810  0,2900

The sample values are the following:

Predilution: 15

Dilution 1:20   1:40   1:80

Sample   0,4060 0,1940 0,0760

According to the program that has been in use earlier, the concentration shall become 4,786 µg/ml. How do I calculate this in the best way? Unfortunately, I can't seem to get the right answer.

To add more context to the question. I work on a project to move an old program that calculated the concentrations to a new excel sheet. Unfortunately, I do not perform these analyses myself as I work on another part of the lab.

However, the question is based on how to get the concentration value of the undiluted sample. The standard used have an undiluted concentration of 2123 µg/ml. It is pre-diluted in two steps, first 1/40 and then 1/50 giving a total dilution of 1/2200.

The Standard is then analysed for three different doses 1/20, 1/40 and 1/80. Two times at the beginning of the run, and two times in the end.

The Sample is pre-diluted 1/15 to then be analysed for the same three doses as the standard.

What I have done now is that I used the Parallel Line model to try to calculate the concentration. Unfortunately, I don´t get the same answer as the earlier calculation program (Which is 4,786), and I have been able to figure out is that the problem is that I get a slight shift in the relative potency. Unfortunately, I can´t find where the problem lies.

Hopefully, this clears it up a small bit.

My answer: 4.79 µg/ml

(All values below are µg/ml)

Calibration data

Determine the mean of the four absorbance values at each dilution.

The calibration curve is then a plot of concentration (x-axis) against mean absorbance. Note that the actual concentration in the assay is (2123/2200)/dilution where dilution is 20, 40 or 80. If you chart this you will see that the data fit well to a straight line.

Use the Excel SLOPE and INTERCEPT functions to derive the parameters of the trendline. (I get SLOPE = 30.59; INTERCEPT = -0.8225)

The equation for converting an observed absorbance value to a concentration is:

concentration = (absorbance - INTERCEPT)/SLOPE

Sample data

For the sample measurements the only one that is valid is that for the 20x dilution because the other absorbances lie outside the range of the calibration data (see note below).

Using 0.406 as the absorbance value in the equation above gives a value of 0.01596 for the concentration in the assay well. This sample was diluted 20-fold for the assay, and the source for that dilution was derived from a 15-fold ‘pre-dilution’ so the original concentration of the sample is 300x the assay value which is 4.788 µg/ml.

Note

I don't know the nature of the discrepancy between your calculations and the target value, but if you try to incorporate the 40x and 80x dilutions for the sample you will get higher values for the sample concentration. Presumably the assay becomes non-linear at low concentrations.


Why are hens so different from other birds? Hens lay many eggs during their lifetime (at least, I don't know of one which can lay more eggs) and they can't fly. Compared to other domestic animals it seems to me they are the least capable of defending themselves or escape if it comes to be left alone in open wild. What is their evolutionary story?

Domestic organisms are bred to serve specific purposes for humans. Sheep are bred to produce wool; Cows are bred to provide meat and milk for human consumption; dogs are bred for service and companionship. Since domestic animal do need to survive in the wild in order to reproduce (ignoring feral animals, which is an interesting topic by itself), most of the other aspects of that animal relevant to its survival tend to be minimized.

So one could just as easily point out that there is no other animal that produces as much wool as a sheep, and yet producing copious amounts of wool isn't particularly useful to the animal itself (i.e. other than the fact that humans will tend to select good wool producers for breeding). So sheep are not particularly good at surviving in the wild, and yet they are incredibly successful as a species and are widely distributed, thanks to humans.

In short, domestic hens evolved to produce many eggs in their lifetime because over the past millennia since humans have started keeping them as livestock, humans tended to preferentially breed those individuals which produced more eggs and to eat those individuals which did not. Chickens tended to be kept in pens and guarded by humans or other animals, so the ability to defend themselves or flee from danger was not important to their survival, and in fact, those that did attack their handlers or escape were probably less likely to be bred.

This process is known as selective breeding or artificial selection.


Are there predators evolved to eat puffer fish? Puffer fish is known for having a anti-predation defense mechanism of having toxin-exuding spikes.

Are there predators which evolved specifically to prey on puffer fish? (presumably, by evolving immunity to the toxin)?

I know that sharks eat them, but I doubt sharks evolved to be immune specifically to puffer fish toxin, since their evolutionary development preceded puffer fish's.

Wikipedia has some revealing information here:

  Not all puffers are necessarily poisonous; Takifugu oblongus, for example, is a fugu puffer that is not poisonous, and toxin level varies wildly even in fish that are. A puffer's neurotoxin is not necessarily as toxic to other animals as it is to humans, and puffers are eaten routinely by some species of fish, such as lizardfish and tiger sharks. Also, Japanese fish farmers have grown nonpoisonous puffers by controlling their diet.

It seems that susceptibility to tetrodotoxin varies a lot from one animal to another, and so some natural variation might allow a reasonable amount of predation to occur.  I also wonder whether the variation in the amount of toxin in the fish implies that the fish are often depleted.

There are cases of animals who have evolved a resistance to Tetrodotoxin, but for the most part its may the predators you are thinking of.  The toxin is synthesized by a symbiotic bacteria and is found not only in fugu but also blue-ringed octopus, rough-skinned newts and some sea slugs.  These animals probably all began with enough intrinsically low sensitivity to the toxin to take on the symbiont and probably evolved to be completely insensitive.  To find a predator that would have co-evolved a similar resistance you would look for a predator that particularly favors the envenomed animal.  In the case of the rough skinned newt, its suspected that the common garter snake is an example of such co-evolution. Others may be out there to discover - its probably difficult to watch marine animals to know what their typical predators are.


Accuracy of a particular genetics test I am a newbie in biology and I am simply trying to discover the field of genomics.

Consider the question - Are genetic tests accurate?

I don't believe they are as the genes may not provide the complete information or maybe there are other genes responsible for a particular trait but they may not be known at the point when the test is conducted. This may not be the right answer though — I simply wish to understand from people here as to what they can say about the accuracy of these tests. If they are not accurate, can you explain why that is the case?

Like the comment said this question is very broad but Im going to try and clear some things up for you. A "genetic test" is just simply a test that tells you whether or not you have a certain genotype. Yes, it is often times used to tell if a person has a disease or not, but that doesnt always have to be the case. I may just want to know, for example, if a mouse I have carriers a certain transgene. The reason why genetic tests are good at determining if someone has a disease is because many diseases are simple, or at least have a well-defined genotype. Sure, you can make a genetic test for a complex disease like obesity if you want, but no one does this because as you pointed out in your question there are sometimes more than one gene involved, so a genetic test for that would not be very good.

But for genetic tests of diseases of a known genotype, they are very accurate. Of course you have some false positives and false negatives. Look up the terms selectivity and sensitivity. If you have a sensitive test you will catch a lot of people with the disease but also many false positives. If you have a selective test you will not have many false positives but you may miss people who actually have the disease. Its a trade-off. Testing someone twice will clear things up usually.

And then there are cases where you have a disease with a known genotype but still have an inaccurate genetic test on rare occasions. Heres a paper about a disease known as Spinal Muscular Atrophy. There is a genetic test that works 95% of the time but sometimes it does not match up with the phenotype. In the paper they find a mutation that explains why the genetic test does not match the phenotype. Two things are interesting about the paper. One, the genetic test is not wrong, its just that the phenotype is not what you'd expect. And two, not all people who have a discordant genetic test have this mutation. So whats going on in these patients and why their test doesnt match their phenotype is anyone's guess.

The first point is especially important so I will repeat it. The genetic test was not wrong, the phenotype just did not match it as expected. Genotype and phenotype are not always correlated, and mistakes can happen when you assume they are.


Help me identify this spider from my garden Found this in my garden today in Sydney, Australia (specifically Lane Cove). Can you tell me what it is?

I believe it is a Garden Orb Weaver spider. The Australian garden orb weaver, Eriophora transmarina, has a strikingly similar body


distribution of some injected materials/medicines through blood vessels Fastest distribution of some injected materials/medicines & with no risk of any kind can be achieved by injecting it into - artery or vein?

It depends on what your target tissue is, as @another 'Homo sapien' stated.

If you want to get something to the hand, for instance, injecting it into the brachial artery will get it there "faster" than injecting it into the cephalic vein.

However,

  Fastest distribution of some injected materials/medicines & with no risk of any kind

does not exist. There are risks with any invasive proceedure, and invading arteries is riskier than invading veins. Unless the risk outweighs the benefit, substances which cannot be administered orally are given intravenously. Arterial lines are usually used for purposes other than injecting substances.

Arterial Line Placement


Do all transmembrane proteins contain channels or tunnels? In my book, there is written something like this.
The integral proteins pass into the lipid bilayer to different depths and establish hydrophobic bonds with lipid molecules. Some of the integral proteins run throughout the lipid bilayer. They are called tunnel proteins OR transmembrane proteins.
My question is do all the transmembrane proteins have to have channel or tunnel for transport of materials?

Transmembrane proteins don't all have tunnels.

  Do all the transmembrane proteins have to have channel or tunnel for transport of materials?

Calling transmembrane proteins tunnel proteins is very misleading. There are a wide range of functions carried out by transmembrane proteins. I'd say the most famous example that don't include a tunnel are the GPCRs that have 7 transmembrane segments. These are used for passing information across a membrane by acting as a receptor to a molecule on one side causing a conformational change which causes an action on the other side of the membrane.

How many transmembrane proteins do have tunnels?

Here is a link to all the GO annotation held by UniProt on transmembrane proteins. There are 10s of millions of results including, but certainly not limited to tunnels and channels.

In the human proteome, there are 831 transmembrane proteins tagged with G-PCR (7TM proteins without a tunnel).
The "Transport" keyword, which probably has some sort of tunnel, is present in 1106 transmembrane proteins.
In total there are around 5200 human transmembrane proteins in the human proteome.


Why is there no toxic effect on the bulbuls feeding on Cascabella thevetia (oleander) nectar? I have a huge Cascabella thevetia by my house and I know that its sap and fruits are extremely poisonous.However I have seen red vented bulbuls and wasps feed on its nectar.Also this confirms it but doesnt specify nectar infact it says plant parts...The same source says the poison affects vertebrates and the birds are definitely vertebrates.So why it doesnt affect them?

The toxicity of Cascabela thevetia is due to the presence of cardiac glycosides such as thevetins A and B. Although these compounds are highly toxic for humans and several domestic animals, other vertebrates are much less sensitive to them.

This review article discusses various aspects of oleander toxicity, and the authors draw attention to species-specific differences in toxicity.

  In addition to dogs and cats, Szabuniewicz et al., (1972) also examined oleander toxicity in monkeys, goats, mice, rats and chickens. Dogs, cats, goats and monkeys were found to be very sensitive to the cardioactive glycosides extracted from dried oleander leaves. In contrast, the rodent and avian species were observed to be insensitive to oleander cardioactive glycosides.

They go on to suggest that differences in the toxin target molecule, the cardiac Na⁺,K⁺ ATPase, is the most likely explanation for this:

  Akera et al., (1979) postulated that the low affinity between cardiac glycosides and rat cardiac Na⁺,K⁺ ATPases could be due to stearic constraints in substrate (glycoside) binding. In this scenario, quaternary conformation of the OL-subunit glycoside binding sites physically precludes the simultaneous binding of all three glycoside structural components. Species-specific quaternary conformation of Na⁺,K⁺ ATPases coupled with subtle differences in glycoside composition (e.g. various sugar moieties attached to the steroid backbone) could, thus, conceivably account for the observed species-specific responses to cardiac glycosides, including those found in oleander.

We have a tendency to assume that susceptibility to the toxic effects of plant materials is universal, but the toxicity of onions and chocolate for domestic animals are clear examples that this is wrong. The variation in sensitivity to the toxins in oleander is a good example coming from the other direction.

Shannon D. Langford & Paul J. Boor (1996). "Oleander toxicity: an examination of human and animal toxic exposures". Toxicology. 109 (1): 1–13. PMID 8619248. doi:10.1016/0300-483X(95)03296-R.


What is the difference between a dermatome and a sensory neurone? I read that a dermatome is an area of skin supplied by a single spinal nerve but that this is sensory information? Why do spinal nerves supply the skin? I thought it was the other way round- sensory information is carried by a sensory neurone to the spinal cord.
Please could someone explain this in simple English because I am really confused.

This is just a confusion of English.
"Supplied" is a bit of a weird term to use, I agree, due to the direction of information flow, but feel free to substitute in just "connected to". It seems pretty common to use this word, for example Wikipedia says:

A dermatome is an area of skin that is mainly supplied by afferent nerve fibres from the dorsal root of any given spinal nerve

and I see similar phrases elsewhere (not sure which is your original source). Afferent nerve fibers, as you describe, are those carrying information into the central nervous system from the periphery, so yes, the information is coming in from the skin.
If you interpret it instead as the spinal nerve providing the connection rather than information flow, then it makes a bit more sense to say "supplied". I suspect the phrasing is borrowed from blood supply since nerves and major vessels tend to develop and travel together. I also suspect the phrasing comes from anatomy, which is sometimes not particularly interested in function which can lead to some confusing results. You'll also see similar phrasing in standard English in other contexts, like roads, even when movements of goods or people are two-way. Merriam-Webster also provides a definition addressing exactly this circumstance:

to furnish (organs, tissues, or cells) with a vital element (such as blood or nerve fibers)

So yes, a given spinal nerve is "supplying a single dermatome with nerve fibers", even if the information ultimately moves the other direction.


Selection on linked loci in a diploid population Let’s consider two linked loci $A$ and $B$ that are both bi-allelic. In consequence, we have four different possible haplotypes $A_1B_1$, $A_1B_2$, $A_2B_1$, $A_2B_2$, which frequencies are $X_1$, $X_2$, $X_3$, $X_4$ respectively. Let the linkage disequilibrium $D$ be defined as:

$$D=X_1X_4 - X_2X_3$$

The change in haplotype frequencies through time is given by:

$$\delta X_1 = \frac{X_1(w_1 - \bar w) - Drw_{14}}{\bar w}$$

$$\delta X_2 = \frac{X_2(w_2 - \bar w) - Drw_{14}}{\bar w}$$

$$\delta X_3 = \frac{X_3(w_3 - \bar w) - Drw_{14}}{\bar w}$$

$$\delta X_4 = \frac{X_4(w_4 - \bar w) - Drw_{14}}{\bar w}$$

, where

$r$ is the recombination rate between the loci $A$ and $B$
$\bar w$ is the mean fitness (sum of the fitnesses of each haplotype weighted by their relative frequencies)
$w_{14}$ is the fitness of the (diploid) individual that has the 1st and the 4th haplotypes
$w_i = X_1w_{i1} + X_2w_{i2} + X_3w_{i3} + X_4w_{i4}$

The change in allele frequency of locus $A$ is $x$ and $1-x$. The change of allele frequency of locus $B$ is $y$ and $1-y$. Those changes are given by the addition of haplotypes frequencies:

$$\delta x = \delta X_1 + \delta X_2$$

and

$$\delta y = \delta X_1 + \delta X_3$$

Question

I don’t fully understand these formulae! Could you please help me making sense of them. Especially of the presence of the expression $-Drw_{14}$.

source

These equations describe how the haplotype frequencies will change over time due to a combination of recombination and natural selection.

Before I proceed, I need to change your four $\delta X_i$ formulas above. Lewontin and Kojima (1960) writes the equations as:

$$\Delta X_i = \frac{X_i(w_i - \bar w) \pm Drw_{14}}{\bar w}$$

where the minus sign is used for $i = 1,4$ and the plus sign is used for $i=2,3$. (See also this chapter by Sergey Gavrilets.) Decreasing the frequency of a haplotype through recombination will necessarily increase the frequency of a different haplotype (adjusted by selection).

$D$ is the measure of linkage disequilibrium. It ranges from $-0.25$ to $0.25$ and indicates how much the haplotype frequencies deviate from an expectation of no linkage ($D=0$, the loci are independent).

First, assume no natural selection. That is, $w_i = 1$ and therefore ${\bar w} = 1$. When fitness is equal, the equations reduce down to

$$\Delta X_i = \pm Dr$$

Some recombination will occur between the linked loci proportional to the distance between them. In a large randomly mating population with no selection, $D$ will eventually decay to zero.  The larger the value of $r$, the quicker that decay will occur. Eventually, the haplotype frequencies will appear as if they are not linked. (See this figure.).

For example, assume that $A$ and $B$ are linked, with these four haplotype frequencies:

$$A_1B_1 = 0.5$$
$$A_1B_2 = 0.38$$
$$A_2B_1 = 0.05$$
$$A_2B_2 = 0.07$$

In the absence of natural selection and assuming that $r=0.1$, then $\Delta X_i = \pm 0.0016$, again with plus or minus depending on the value of $i$. This is the rate the frequencies will change each generation.  As $r$ decreases, the rate of decay decreases.

Differential fitness among the haplotypes will also affect the rate of decay. The fitness interactions among loci on the same chromosomes and between homologs can get rather complex depending heterozygote advantage, epistasis, etc. (see Lewontin 1964 for several fitness models).

The equation $w_i = X_1w_{i1} + X_2w_{i2} + X_3w_{i3} + X_4w_{i4}$ is the average fitness of the each haplotype in combination with all the other possible haplotypes. For example, for $w_1$, you're calculating the average fitness of four genotypes: $A_1B_1/A_1B_1$, $A_1B_1/A_1B_2$, $A_1B_1/A_2B_1$, and $A_1B_1/A_12B_2$.

I am uncertain why $w_{14}$ is used in the second term of the numerator. I thought it might be because that combination is heterozygous at both loci so recombination generates all four possible haplotypes. However, both Lewontin and Kojima (1960) and Lewontin (1964) use $w_{11}$. It may also be that a relative fitness component is necessary for comparison so the fitness of any one of the genotypes could be used there. I don't know.

Regrdless, as a simple example to illustrate the effects of selection, assume $r=0.1$, $\bar w = 0.5$, and $w_{14} = 1$ (heterozygote advantage, given maximum relative fitness). For $w_1 = 0.9$ then $\Delta X_1 = 0.397$. Selection strongly favors this haplotype in all genotypic combinations so it will increase in frequency.  For $w_1 = 0.3$ then $\Delta X_1 = -0.203$. The haplotype is selected against and decreases much more rapidly, relative to no selection at all.  The same idea would apply for the other haplotypes.

References

Lewontin, R.C. 1964. The interaction of selection and linkage. I. General considerations; heterotic models. Genetics 49: 49-67.

Lewontin, R.C. and K.-I. Kojima. 1960. The evolutionary dynamics of complex polymorphisms. Evolution 14: 458-472.


Simulating DNA sequences in R with a given value of $\theta = 4N_{e}\mu$ This might not be the most appropriate site to be asking such a question, but perhaps someone has a solution.

My question is: is there an R package or function for simulation of DNA sequences of a given basepair length generated according to a prespecified value of the population mutation rate $\theta = 4N_{e}\mu$, where $N_{e}$ is the effective population size and $\mu$ is the per-generation mutation rate

I have real sequence data from GenBank, but I would also like to simulate some random DNA sequences according to a coalescent process.

Essentially the function would output the generated aligned DNA sequences as a FASTA file.

I have been rather unsuccessful in tracking down a suitable package, as most only output generated phylogenies.

There are a number of tools but I don't know any that comes with an R library. They are usually all called from the command line. I don't either of any that produce FASTA file. SimBit (my own software) can produce vcf files which can easily be converted into FASTA with PGDspider.

However, if your simulations are so easy, you might not need these individual-based softwares. Just write the code yourself. It might only be take a few tens of lines. Here is a simple example

freq = 0.1 # initial frequency
N = 1000   # Constant population size
mu = 1e-7  # mutation rate

for (generation in 1:nbGenerations)
{
   # Drift
   freq = rbinom(1,N,freq) / N

   # Mutations
   oneWayMutations   = rbinom(1,N*freq,mu) / N
   otherWayMutations = rbinom(1,N*(1-freq),mu) / N
   freq = freq - oneWayMutations + otherWayMutations
}

If you need something more complex (such as several loci), then you should probably use one of the existing individual-based software. See the post Sequence evolution simulation tool


What is this blue insect? I found this insect in my garden

It's the first time I see this insect, so I'm wondering what it is.

It has blueish, purplish reflections, a head like an ant or wasp but it's the size of a thumb (4-5cm)

I am located in Hungary if it can help identify it

I am pretty sure that this is an oil beetle (also known as blister beetle) of the family Meloidae. In this special case this is probably the violet oil beetle (Meloe violaceus), although this does not completely coincide with the size you mention. The slightly different color is probably caused by the different lighting.

See the image from this Wikipedia for comparision:

Be careful with them, as they can secrete a poisonous substance making blisters on the skin (hence there name) when they feel attacked. For more information see also here.


What is the difference between Founder effect and Bottleneck effect? Both are examples of genetic drift in which there is a change in the allele frequency when the population size becomes small.
What is the difference between the two?

Genetic drift is an EVOLUTIONARY PROCESS

Source: Wikipedia > Genetic Drift

  Genetic drift (also known as allelic drift or the Sewall Wright effect2 after biologist Sewall Wright) is the change in the frequency of a gene variant (allele) in a population due to random sampling of organisms.

I think that these terms are used without a perfect semantic. An obvious case

A population bottleneck is a DEMOGRAPHIC EVENT

Source: Wikipedia > Population Bottleneck

  A population bottleneck [..] is a sharp reduction in the size of a population due to environmental events (such as earthquakes, floods, fires, disease, or droughts) or human activities (such as genocide)

A founder effect is an EVOLUTIONARY PROCESS THAT RESULTS FROM A FOUNDING EVENT

Source: Provine 2004

  The “founder” principle, as introduced by Mayr in 1942, was an auxiliary mechanism (less important than random drift) for producing reduced variability in an isolated population started by a few individuals or even by a single fertilized female. Mayr saw a distinction between the “founder” effect and random drift. The founders were not a random sampling of the main population, but, once isolated as a small population, would undergo random drift

In other words, a founder effect does NOT refer to the ppulation bottleneck causing by a founding event. A founder effect refers to the increase in genetic drift (loss of genetic diversity is expected) caused by a founding event. A founding event is the event by which few individuals (eventually only one) quit a large population to settle down a new small populations. As such, a founder event is a type of population bottleneck. I think that one could further extrapolate the term "founder effect" to any increase in genetic drift caused by a population bottleneck.

Do all authors use the same definitions?

I have not done a good literature review to answer this question but I would not be surprised if different authors, use slightly different definitions.

For example, some authors (e.g. Peery at al 2012, Raymond and O'Brien 1993, Duarte et al. 1992) have used the term "genetic bottleneck" instead of "population bottleneck". Wikipedia indicates that these two terms are synonyms. However I could not find any paper that formally define the term genetic bottleneck but all the papers using this term seem to be specifically interested into the genetic signature of population bottleneck. As such, the semantic relationship between population bottleneck and genetic bottleneck could be the same as between founding event and founder effect. Genetic bottleneck could be defined as the increase of genetic drift that is caused by population bottleneck.


How increased potassium intake increases sodium excretion? "K+ antagonises the biological effects of Na+". I have been reading the same many times without any explanation. How actually (mechanism) K+ helps excretion of Na+?, their interactions? And eventually lowers blood pressure?

That's because cell membrane could have a protein, called Na/K pump who's able to regulate the level of Sodium/Calcium using the energy gained by the hydrolysis of a phosphate bond from ATP.


How many, and how severe, are known single gene polymorphisms for obesity? A fairly recent meta-analysis of studies examining the association between adult obesity and polymorphisms of the FTO gene (Peng et al., 2011). The paper looked at 59 studies and concluded that, "FTO may represent a low-penetrance susceptible gene for obesity risk", although the association was weaker (or non-existent) for some ethnic groups.

Are other polymorphic genes which are currently known to be more strongly associated with obesity risk than the FTO gene?

MC4R, TMEM18, GNPDA2, KCTD15, NEGR1, BDNF, ETV5, MTCH2, and SH2B1 have also been identified as being associated with adult onset obesity risk, however FTO currently appears to be the one with the strongest evidence. For example see Thorleifsson et al. (2009), Elks et al. (2010) and Willer (2009)


Is it possible for virus infected cells to continue to present a self-antigen on the MHC1? Forgive my ignorance, as I'm new to immunology, however it seems like there would be some amount of positive selective pressure for viruses to develop the ability to continue to present the host's self-antigen on the MHC1 of a newly infected cell, thereby disguising the infection from the body's immune system (or at least from the cytotoxic T cells).

Is this in theory possible? Or is there a reason it cannot occur.

Self antigen is presented throughout viral infections.  You seem to think that cytotoxic T lymphocytes respond to absence of self. That’s backward. CTL respond to their specific peptide target no matter how much self antigen there is. In a typical response, there may be 100,000 self peptide/MHC complexes and 100 viral peptide/MHC complexes, and that’s enough for a CTL response.

One trigger for NK cells is absence of self, so perhaps that’s the source of your confusion.


Where are all the seagull nests? Seagulls are common. I live on the shore of New Jersey (U.S.), but I have never seen a seagull nest. Where are they?

Breeding season

Chances to see nests will be higher during breeding season which normally occurs once a year. Eggs will be laid in early May but they will be built in the previous months.

Area

In densely populated urban areas gulls may build their nests on rooftops instead of ground nesting. In the case of New Jersey I found the following brochure:

https://www.nj.gov/dep/fgw/ensp/pdf/bnb_brochure.pdf

If you mean seagulls as in all Laridae, then you have two members of that family (black skimmer and least tern) in that brochure that actually use NJ's beaches and even have their own designated space for that.

Googling 'seagull rooftop nests' brings a decent amount of pictures of rooftop nests. 'Seagull nests' brings a lot of cliff-placed nests, rooftop and ground nests. I assume the choice depends mostly on food availability and predator population density. I remember in Spain a few years ago there was a big enough problem to appear on local TV news related to seagulls attacking people. They would nest on every roof and attack people that would go out on the balcony with a sandwich.

Sources:

Habitat Selection and Nesting Biology of Roof-Nesting Glaucous-Winged Gulls
Kees Vermeer, Damian Power and G. E. John Smith
Colonial Waterbirds
Vol. 11, No. 2 (1988), pp. 189-201 https://www.jstor.org/stable/1521000?seq=1


Is lumosity.com based on science? I always see these Lumosity ads on TV, and I personally feel they are just trying to "sell me something". I did some layman's research (wikipedia) and read that "Studies of Lumosity's effectiveness have shown mixed results".

Does anyone with knowledge on the topic of learning know if the "brain games" they post are simply games? I guess the proper question would be:

Can games like the ones Lumosity offers increase cognitive ability?

Zickefoose et al. did a study, and showed that while you might improve while playing the game, it called into question if you actually improved outside of just getting better at the game.

Redick et al. also reported that when they did a double blind study in brain games like Luminosity that you improved in the games, but they didn't see any transfer from game to every-day life.

Also see my previous answer on the topic: Cognitive Science Forum


Can experiments in ELISA kits be monitored via both fluorometry and photometry? In my bioanalytics course slides, the professor has written at one point that in a heterogenous immunoassay such as ELISA, we use fluorimetry to measure concentration of an analyte. In another slide it is mentioned that we use photometry to measure UV-vis absorption. I am confused... is it one or the other, or can we use both methods depending on whether the marker enzyme on the antibody is given a fluorescent or chromogenic substrate?

can we use both methods depending on whether the marker enzyme on the antibody is given a fluorescent or chromogenic substrate?

This is essentially correct.

You can have the same ELISA work on different methods of detection. The most common ELISA is colorimetric, and works by binding a secondary antibody conjugated to some enzyme to your primary antibody. Fluorescent ELISA platforms are less-widespread but only because the colorimetric ELISA is reputed and "gold standard."

Horseradish peroxidase (hrp) is a common conjugate system utilized in sandwich ELISAs, and by adding TMB solution to the reaction wells, the resulting reaction produces a diimine that turns the liquid in the well blue, and does so in proportion to the amount of analyte captured. You stop the reaction by adding an acid, which turns the well yellow, and you read the OD at 450nm (they also recommend you subtract the OD at 510nm to account for the light scattering of the microplate).

Figure 1. R&D Systems Quantikine assays, HRP-streptavidin detection. https://www.rndsystems.com/products/quantikine-hs-colorimetric-sandwich-elisas-high-sensitivity

On the other hand, we know that we can also conjugate the antibody with a fluorescent molecule if we wanted to, like FITC or PE. All we need to do is excite the molecule with an appropriate light source or laser to get a fluorescent emission, and read with an appropriate system to read those signals. The fluorescent intensity would then be proportional to the captured analyte, based on a standard curve just like any ELISA.

So the real answer is we can use one, the other, or both, just not at the same time.

Just be cognizant that different platforms can yield different results, so you have to validate your two platforms, and correlate the two to ensure reproducibility. Most labs just try to stick with one or the other, though.


Strange insect identification Tonight I have found this new friend flyng inside my home. First time ever I sea something like this here in the north East of Italy

That is an Oleander Hawk Moth, Daphnis nerii. Order Lepidoptera,family Sphigidae. https://en.wikipedia.org/wiki/Daphnis_nerii


Why is the current Ebola outbreak different from previous outbreaks? I don't know if this question has an answer at this time, but I would like to know if there is some biological reason why the current Ebola outbreak is so much more complicated and widespread than in the past. Traditionally it has been initially very virulent and has then has rapidly waned. I hope what I am saying is accurate, and if so why dont we see the same pattern now ?

This is too long for a comment, so I put this in here: The main reasons are sociological. From the data I have read so far, this outbreak (actually these are two independent outbreaks, one in West-Africa and another one -not connected- in the Democratic Republic of Congo) is not exceptionally deadly in terms of Ebola. The death rate is about 60% which is extremely high compared to other diseases, but Ebola had reached up to 90%...

I think the main differences are that this outbreak struck in a much more populated area which has a very poor health care system (if you can call it like this at all). Then it happened in a border region, I recall reports about a traditional funeral of a Ebola victim which infected visitors, some of them crossed the border afterwards.

Then it was completely underestimated in the beginning, because a lot of cases stayed unknown. This led to a wider spreading as people who got sick infected relatives and medical personnel subsequently. And although the reaction has been powered up a lot since then, it is still not adequate to contain the outbreak.

Former outbreaks happened in rural areas which where easier to contain with a smaller number of personal, which is not possible this time. If you want to read further about this, I recommend the blog of Tara C. Smith which has been doing research about Ebola for some time and also worked in crisis response teams.
Especially interesting are these two:

A historical perspective on Ebola response and prevention
Addressing more Ebola myths


What small insect is this? Lately, lots of these little bugs have been lurking in my house in Italy. Should I worry?

I'm curious to know what they are.
For reference, the 2 cent Euro is 18.75 mm in diameter.

It looks like a carpet beetle larvae(Anthrenus verbasci) to me. This seems to fit considering you found it in your house, which is one place they are fairly common. I would not be able to tell you if you should be worried, I am not a biologist.


Absorption of glucose in small intestine During the absorption of glucose in the small intestine, glucose enters the epithelium by Na+/glucose co-transporter by the concentration gradient of Na+. The gradient is generated by pumping 3Na+ out each time and the entrance of 2K+ by Na+/K+ pump. The K+ is then removed by the concentration gradient via the potassium channel protein.
My question is is it more favorable to use a Na+ channel protein to pump Na+ out of the cell to generate the concentration gradient? Or there are some biological significance for K+ to enter the cell and leave again repeatedly (e.g. maintain stable charge distribution in and out of the cells? Thank you.

Na+ channel proteins would not be able to generate a concentration gradient, as they are passive transporters, not pumps. They essentially can only facilitate diffusion of Na+ down a gradient. The Na+/K+ pump is ATP-driven, providing active transport needed to establish or maintain a concentration gradient.


Besides X. morgani praedicta, are there any species whose existence was predicted before they were discovered? The orchid A. sesquipedale has a spur so long that at the time of its discovery, no insect was known that could pollinate it.

This led Charles Darwin to predict the existence of an undiscovered moth based on the idea that the moth and the orchid had co-evolved. That moth, X. morgani praedicta, was subsequently discovered in 1903 – a triumph for early evolutionary biology.

Has it ever happened again that a species was predicted to exist before being discovered?

I'd imagine there would be numerous examples of this. One species I can think of is Monocercomonoides sp., before the discovery of which we didn't know any examples of eukaryotes that had completely lost their mitochondria, or the derived forms of these organelles, such as hydrogenosomes and mitosomes. A prediction wasn't necessarily coined by any particular person like in your example, although there might be some papers somewhere that make such a prediction, I'm sure many people hypothesised that it was probably possible for eukaryotes to completely lose mitochondria if their iron-sulfur cluster biogenesis pathway was replaced by a cytosolic system that could fulfil the same role but we didn't know of any that had.

See paper: http://dx.doi.org/10.1016/j.cub.2016.03.053


Deletion errors with Phusion Polymerase? I was wondering if anyone has ever seen large deletions (~40-50 bp) occur when using phusion polymerase to clone a gene.  I have recently tried using Circular Polymerase Extension cloning to clone a 200 bp insert into a 6.5kb plasmid and obtained two separate clones with 40bp+ deletions in the center of the insert.

Phusion has a 5'->3' exonuclease activity, but I didn't think it could cut in the center of a sequence.  While our inserts were created with oligo synthesis, it is my understanding that such large deletions are rare with oligo synthesis. If you have heard of this happening please let me know.

In my own personal lab experience, I got some unexpected results using Phusion polymerase. However, I have not seen deletions, only insertions (ranging from single bases to 3 tandem copies of a primer sequence). This is not an answer to your deletion question, but it does suggest unusual things might happen.

I have seen deletions with T4 DNA polymerase during "blunting" reactions. According to the NEB website:

Q10: Is T4 DNA Polymerase active at room temperature?

A10: We suggest 12°C. The DNA ends "breathe" at higher temperatures allowing the exonuclease to remove nucleotides past blunt.


Core Biological concepts explained to a Computer Scientist? I am a computer scientist delving into Bioinformatics and I need to gain insight in biological phenomena. How would you explain three core concepts as:
Evolution, Selection and Variation, to a Computer Scientist? I am looking for something in the middle. I read Futuyma's book and was very useful, but I would like an explanation I can relate with my background, something to start building "bridges"...

Bibliography suggestions are welcome.

Evolution

Evolution is the accumulation of genetic mutations that results in phenotypic variation (physical characteristics) where surviving variations are more suited to the environment the organism lives in, thus allowing it to survive better and -- critically -- reproduce as-good-as or better-than its competing organisms.

In terms of computer science this would be like a starting with basic CPU design with all the absolute necessities. Now, let's pretend every generation of CPU after your first is going to be randomly designed by something called "Pressure OS". Pressure OS doesn't care if the CPUs it designs match the needs of the consumer. PrOS is unfeeling. An OS of pure logic. ALL it will do is make a bunch of random ones, note which ones sell the best, and make the best-selling ones to be the template for its next round of random designs.

  Selection and Variation

Selection is the process by which environmental pressures (low moisture, high heat, high altitude, available food, extreme pressures at the bottom of oceanic trenches, etc.) dictate how well each successive generation of organisms survive.

In our analogy, the Pressure OS is the cause of Selection. Some CPU designs aren't going to meet the needs of consumers (first-gen Atoms which could barely operate a toaster). Those ones won't be produced again. Others will be very successful (like the Pentium-4 Series which lasted for years) and will quickly outnumber the inferior ones.

Some designs, as odd as they are, will find success in areas outside enthusiast desktops or workstations. Like ARM designs which were never part of the desktop market, but found lots of success in phones and business devices.

Market requirements/environments, as met by the random variations produced by Pressure OS, created Variation in the types of CPUs available.

ARM Snapdragons could never, ever compete in the desktop enthusiast market. That's the realm of Sandy Bridges, Haswells, Semprons, and Phenoms. Then again, they're dramatically different designs -- which stem from common designs decades ago that have been heavily modified over the years -- that don't need to compete. Snapdragons and Semprons can co-exist because they fill different niches.

Now, when consumer needs change again -- if everybody gets tired of mobile phones, tablets, and desktops in favor of cone-shaped personal assistants which go in your ear -- then designs will change again under that new pressure. Eventually CPU one design will become the standard for that particular piece of hardware, and you could say that CPU variation had evolved to get there via selective pressure from consumers.

Biology operates in the exact same way, except the selection process is instigated by environmental pressures to produce organism variations that can successfully reproduce. It's also been going on for >3 Billion Years.


What makes animal to continually reproduce? I was reading about Trypophobia and reached to Surinam Toad's reproduction methods. Then I had this doubt-
Why would animals want to reproduce so much?
In case of humans we mostly have the offsprings nearby for entire life, so some of them may take care of us. But in case of many other animals after birth they have no connection with their parents.

So why do they always try to reproduce in large quantities in entire life time?
What they achieve in this?

Why organisms reproduce

If they didn't reproduce, they would die out.

More concretely, suppose an animal is born with a mutation that removes the desire to reproduce.  That animal will not have any offspring, so its genes will not be passed on to the next generation.  When that animal dies, that mutation will die with it.

Why some organisms reproduce a lot

Different animals or other organisms have differing strategies for reproduction, based on their ecology.  Some animals, like the Surinam toad, try to have a lot of offspring with relatively little "investment" (of energy, time, effort, etc.) in each one.  Many of the offspring will die, but enough will survive that the organism's genes can persist.  Other animals, like elephants, only have a few offspring but spend a lot of effort in making sure those few offspring survive.

You can read more about this in the Wikipedia article on life history theory.


Why is an allele dominant or recessive? Alleles refer to duplicate genes, where one allele can be dominant over the other. What makes an allele dominant or recessive, given that both code for a single protein?.

There are several hypotheses about the evolution of dominance. It is important first of all, to note that empirical observations show that beneficial alleles tend to be more dominant than detrimental alleles. Among the two main hypotheses to explain the evolution of dominance, one has been formulated by Ronald Fisher and one by Sewall Wright.

Fisher's hypothesis

According to Fisher's hypothesis, between two equally beneficial alleles, if one is more dominant than the other than it's heterozygote carrier will have higher fitness. In consequence, beneficial alleles evolve to become more dominant while detrimental alleles evolve to be recessive (so that they can hide from selection in heterozygotes).

Wright's hypothesis

According to Wright's hypothesis, beneficial alleles are more dominant because of the kinetic of biochemical reactions. The rate of a biochemical reaction is a function of the concentration in the substrates of interest. The function is called "Michaelis-Menten function" after the name of the authors. The Michaelis-Menten function looks like this:

Think about a knock-out mutation. Such mutation will decrease by half the concentration of protein the gene in question produce in heterozygotes. Imagine, the concentration of proteins in the wildtype homozygote was 3 (see above graph). The rate of reaction of this homozygote is therefore about 3. The heterozygote would have a concentration of 1.5 and the rate of the reaction is therefore about 2.5-2.75. Assuming that the rate of this biochemical reaction is directly related to fitness, then a the locus of interest, benefical alleles are necessarily dominant and detrimental alleles are necessarily recessive. Selection for dominance is not involved in Wirght's model.

Is Fisher's or Wright's hypothesis correct?

Current state of the art is to consider Wright's model to be correct and Fisher's model to be wrong. In reality, the truth probably lies somewhere in between these two extremes. Note also that some other alternative explanations may exist in the literature but Wright and Fisher original hypotheses are by far the most considered hypotheses for the evolution of dominance. During my undergrad, I remember a speaker (but I forgot his name, sorry!) who showed that some alleles actually have some domain that are directly responsible for decreasing the expression of the other allele on the sister chromosome suggesting that Fisher's hypothesis might sometime be a good explanation as well.


Is the suicide of a moribund individual to be considered group selection? When a moribund individual commits suicide (e.g., Refardt, Bergmiller & Kummerli, 2013; http://rspb.royalsocietypublishing.org/content/royprsb/280/1759/20123035.full.pdf), is this to be considered group selection?  It could be considered costly to the individual, since the individual commits suicide and, therefore, loses reproductive opportunity.  And it occurs to the benefit of the group, by saving resources for the group and sparing it susceptibility to infection.  Is this group selection or does group selection require an intentional formation of a group?  If not, what else is necessary for this to be an example of group selection?  (Thank you.)

It depends on what form of group selection you are talking about.
Group selection carries a lot of baggage and can refer to two very distinct concepts.  Concepts of group selection comes in two forms type 1, selection occurring on the group level, and type 2 selection on the group level that produces adaptations in said group or organism. The latter is the traditional usage of "group selection" the first(type 1) is now commonly (and confusingly) referred to as multi-level selection. (type 1 and type 2 are my terms I am using them to keep the two concepts identifiable)
Type 2 aka multi-level selection
Group selection (type 2) is simply selective pressures that occur above the individual level, kin selection could be seen as a form of this or it could not. It is still producing advantages and disadvantages to the genes and genes are still acting as the basic unit of evolution. Selection is occurring between groups with the differences between the groups being a product of the genes of the individuals within those groups. The genes are still favored or unfavored there is just many levels on which that the genes products can manifest. This models of group selection are basically just another form of gene based selection and adaptation it just adds another layer in which selection can occur.
Now few argue this form of group selection could not occur just that it would be swamped by normal gene based selection in most instances. There are genes known that are horribly detrimental to the individual and population in return for greatly favoring their own spread, the famous R2D2 gene in mice is an example.
Bacteria can be problematic in this as relatedness may not be a good measure of whether they share the same genes, and kin selection only requires shared genes. Could the behavior in bacteria be group selection in this case, yes, of course it could also be kin selection, the relatedness (Hamilton's original description) description of kin selection is really only useful in animals. In organisms with more lateral gene transfer they only need to share the gene in question, they could be completely unrelated in any other way. Indeed the paper even proposes this low but non-zero relatedness.
Now the big problem type 1
Type 1 is the traditional and first usage of the term group selection, but also the one only rarely proposed today, making it a very confusing term.
the big difference between kin selection and group selection (type 1) is that kin selection (or any form of selection including type 2) is about the selective advantage to the gene, an already well established principle, while many forms of group selection (type 1) propose a new "thing" on which selection occurs. what this thing is is never well defined but then neither were genes when natural selection was discovered.
To prove this form group selection and not kin selection you would have to show no selective advantage (or disadvantage) to the gene, basically you have to eliminate kin selection and other phenotypical expressions as a possibility. Proposed forms of group selection (type 2) can be shown to be products of normal gene based selection so you have to show this is not occurring. (thanks to Remi for this source). Intentional group formation in intelligent organisms (humans) is so far the only proposed mechanism in which this could work, and this would fall under memetics, which means it is occurring when related genetic differences are minor or non-existent.
Your paper does not show this form of selection, it does not even attempt to.
for a further breakdown of the diffrent forms of group selection I recommend this paper, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850877/


Are there public records of results with laetrile treatment against cancer? I'm looking for what the title says. This is based on the book by Edward Griffins. Is laetrile actually fatal because of its cyanide content? Or can it really help in this fight?

Yes, there are several articles describing experimental data from animals and clinical trials in humans. The results clearly show that laetrile is not effective for cancer treatment, and the drive for laetrile as a cancer drug is widely considered to be a quack. See for example this NCI summary or this article.

Laetrile is a modified form of Amygdalin, a toxic plant product found in some seeds and nuts, for example bitter almonds. The compound contains a cyanide moiety and can cause cyanide poisoning. It was labeled "Vitamin B17" by Ernst Krebs in an attempt to get the compound classified as a nutritional supplement rather than a pharmaceutial (to escape FDA regulations), but this is misleading; it is not a vitamin.


Mechanics of going from DNA sequence to metabolic network My apologies for possibly a naive question. I'm a statistics type and have been asked to assist with analysis of metabolic pathways (and networks). However, I would like to have at least a layman's understanding of how metabolic pathways/networks relate to DNA sequences. Been doing the Google for a few days and, given the results, it's clear I am not formulating the query correctly since nothing seems to be clicking.

Something that helps me understand the mechanics behind going from a string of T,A,G, and C's to a network of substrates,enzymes, and products.

Thanks in advance for your patience.

The question is not too broad, just involves a fair bit of work to both do the research and compose a response. I'll do the latter, but in brief.

The strings of the four nucleotides encode genes. Sometimes these genes are broken into protein-coding portions (exons) and sometimes intervening, non-coding regions (introns). Bacteria, for example do not have introns within genes while most human genes do. The nucleotides in the protein-coding portion of the gene do just that - give instructions on how to synthesize the protein by directing which tRNAs the ribosome uses to translate the genetic code into a protein chain.

A useful phrase is protein sequence dictates protein structure and that structure dictates function. So, the proteins do things and many act as enzymes or modulators of enzyme activity. An enzyme catalyzes a biochemical reaction, lowering the activation energy to go from reactant(s) to product(s). One enzyme can be thought of as one unit within a metabolic network. A modulator might activate or deactivate an existing enzyme. A protein kinase is a good example of a modulator.

Next, string some of those enzymes together to build a pathway. A common example is glycolysis. Think of this as a chain where the output or product of enzyme A serves as input to enzyme B, whose product is the input to enzyme C, and so on. These pathways are two-way, but it is exceedingly difficult to travel from the final product all the way up such a pathway to the initial input within the confines of a biological system. Thus, the pathways in practical terms are thought of as one-way.

However, the pathways do not function in isolation. The final product may serve as input to one, two or more other pathways. Your pathway of choice may begin with the output of another process. Furthermore, pathways can branch: Glycolysis can proceed to glyceraldehyde 3-phosphate and pyruvate, or directly after glucose 6-phosphate formation can be shunted to the pentose phosphate pathway to yield reducing power and 5-carbon sugars (to be used in ATP, CoA, FAD, NAD+, DNA and RNA). Now, pathways leading to other pathways and branches and such make a network.

You and your colleagues might want to know if genes within a metabolic network are over- or under-represented in a test compared to control. Or, genes for a given network are not present in one species compared to several others. Or, one could estimate the flux through such a network given a set of measures.

Peruse examples at both KEGG and Reactome, expecially at KEGG where you can view pathways pertinent to your organism(s) of choice.


How to turn teosinte into corn? If I want to turn teosinte into corn, using ancient methods like the Native Americans did, then how much time it takes, and what do I have to do?

For the sake of the question, let's assume that time is not a problem for me. Say I live 10,000 years. But of course, I prefer to have maximum efficiency. If I can get the result in 3,000 years, that's better than 5,000 years.

Initially I didn't like this question very much, but I changed my mind when I realized that there is actually ongoing research to do exactly what you propose in order to study just how long it takes to get maize from teosinte.
John Doebley at the University of Wisconsin-Madison has a project ongoing to breed 30 generations of teosinte to be more "corn-like" on a single parameter, the length of the lateral branches.
The first challenge is to find a strain that isn't already contaminated by modern maize - that isn't completely possible, but he selected a strain that has minimal hybridization. You would have to do the same.
Second, you have to plant someplace isolated to further prevent hybridization. Dr. Doebley has a plot in Hawaii for this purpose.
Note that even though this scientist is only selecting over 30 generations, he doesn't anticipate that much of a change (i.e., he doesn't expect to have anything like corn when he is finished), and he is only selecting on a single parameter and furthermore, this parameter was chosen specifically for being easy to score, showing a lot of variation in the existing population, and influenced by a known single gene. Many more generations would be expected to get a product like modern corn. And even domesticated corn has changed significantly over thousands of years of agriculture.
For this answer, I simply reference the project site that I linked above, but in case that link goes dead, here is some literature that the project cited directly:

Beadle, G. W., 1977  The origin of Zea mays, pp. 615-635 in Origins of Agriculture, edited by C. E. Reed. Mouton, The Hague.
Beadle, G. W., 1978  Teosinte and the origin of maize, pp. 113-128 in Maize Breeding and Genetics, edited by D. B. Walden. John Wiley & Sons, New York, NY.
Doebley, J., A. Stec and C. Gustus, 1995  teosinte branched1 and the origin of maize: evidence for epistasis and the evolution of dominance. Genetics 141: 333-346.
Doebley, J., A. Stec and L. Hubbard, 1997  The evolution of apical dominance in maize. Nature 386: 485-488.
Doebley, J. F., A. Stec, J. Wendel and M. Edwards, 1990  Genetic and morphological analysis of a maize-teosinte F2 population: implications for the origin of maize. Proc. Natl. Acad. Sci. 87: 9888-9892.
Iltis, H., 1987  Maize evolution and agricultural origins, pp. 195-213 in Grass systematics and evolution, edited by T. Soderstrom, K. Hilu, C. Campbell, and M. Barkworth. Smithsonian Inst. Press, Washington, D. C.
Wang, R.-L., A. Stec, J. Hey, L. Lukens and J. Doebley, 1999  The limits of selection during maize domestication. Nature 398: 236-239.
Wilkes, H. G., 1967  Teosinte: the closest relative of maize. The Bussey Institute, Harvard University, Cambridge.
Wilkes, H. G., 1977  Hybridization of maize and teosinte in Mexico and Guatemala and the improvement of maize. Econ. Bot. 31: 254-293.


Why are flies not scared when landing on a monitor with changing graphics? I have been wondering why would insects in general, not be scared when important changes happen on your monitor where they have landed...

If you move even just a finger, they are scared to death and fly away, but anything on my monitor and they remain completely placid.

Flies see motion. When the monitor screen changes, the visible spectrum of the pixel is changing and nothing is moving.

  Flies have limited color vision. Each color has its own wave frequency, but flies have only two kinds of color receptor cells. This means they have trouble distinguishing between colors, for instance discerning between yellow and white. Insects cannot see the color red, which is the lowest color frequency humans can see. However, houseflies have the ability to see polarized light, but humans cannot differentiate between polarized and unpolarized light. Polarized light is light in which the waves travel only in one plane. [1]

Monitors have polarized film on them so you could test the color hypothesis by taking an old monitor you are willing to sacrifice and removing the polarized film. Then you could test if the flies jump when the screen changes. See here for removing the polarized film on the monitor, or if you have access, this article on A behavioural study of polarization vision in the fly, Musca domestica may hold the answer without needing to ruining a monitor.


Breathing in and out I was reading my textbook and it says that breathing involves inhaling and exhaling but it doesn't say whether they happen simultaneously or sequentially.

Also is my overall understanding of breathing competent?  When you breathe in air, air ends up in the lungs passing through the nasal passages (heated, moistened, cleaned) through the pharynx, through the glottis through the larynx, through the trachea and into the bronchi and then into the bronchioles. Once air gets to the lungs, Is their already carbon dioxide in the lungs waiting to be expelled or will carbon dioxide diffuse into the alveoli and into the lungs when oxygen diffuses into the blood. And after this the carbon dioxide will be expelled?

Inhalation and exhalation happen sequentially as Herman stated in the comments.

Yes, your general understanding of inhalation is correct. After the air gets into the lungs, the oxygen is diffused into the capillaries covering the alveoli. The now oxygenated blood travels back to the heart to be circulated throughout the body. As this blood enters capillaries in other regions in the body, the oxygen diffuses out of them and into the surrounding cells. Carbon dioxide (CO2) produced by the cells as a waste product then diffuses into the blood vessels. The CO2-rich blood is then circulated back to the heart to be pumped back to the lungs. This blood flows into the capillaries surrounding the alveoli, and diffuses out. The exchange of carbon dioxide and oxygen occurs simultaneously. So, as oxygen is diffused from the lungs into the bloodstream, CO2 in the bloodstream is diffused out into the lungs.

Here are diagrams to depict what is described above.


What species is this? What the fruit? The berries of the fruit are sweet. The tree is growing in Israel.

Looks like it is Phytolacca dioica.  I found this by searching your first image in a phone app called Pl@ntNet (PlantNet).  Looking at Wikipedia confirms the ID.

Interestingly, you said the fruit was sweet.  The North American relative Phytolacca americana is extremely poisonous.  A brief search suggests your species is possibly poisonous, with reports about the leaves more common than the fruit.


What is the name of this plant, from Bangladesh? This is a small plant from my backyard. I have found the flower closes in the evening.

This plant belong to Malvaceae, and the yellow flowers open towards morning to mid-day.
This plant is most-likely Sida rhombifolia or may be Malvastrum tricuspidatum .
From broad leaves it seems not Sida acuta
Check epicalyx ( made up of bracteoles)... is there is no epicalyx then Sida rhombifolia.
If epicalyx is 3, it is Malvastrum tricuspidatum
look also https://en.wikipedia.org/wiki/Sida_rhombifolia,
https://books.google.co.in/books?id=Roi0lwSXFnUC&lpg=PA258&ots=N7DNvrN4UL&dq=malvastrum%20tricuspidatum%203%20epicalyx&pg=PA258#v=onepage&q=malvastrum%20tricuspidatum%203%20epicalyx&f=false
Epicalyx of Malvastrum tricuspidatum :

C= Corolla (all petals), K= Calyx (all sepals), E= Epicalyx the bracteole

3 bracteoles