Why are (some) cats attracted by bleach? (Sorry if this question is only partly biological)
I have noticed that several cats (including the one that keeps sleeping in my house), are fond of the odor of bleach (eau de Javel) and chlorine.

Among examples, chlorine is used in small quantities in tape water and the cat is fond of licking the faucet in acrobatic positions even if there is mineral freshwater nearby.
I was one day not careful enough using a bleach based gel cleaning product and some of it got on my hand. Even after cleaning my hands, they still had a bleach "perfume" and my cat cling to me and even cleaned my hands with his tongue for minutes.

Why is this so ? Are there other animals known to have this taste ?
Might it be in fact acquired through living with humans ?
Is this potentially detrimental to their physiology ?

I can't give a definite answer, and there's nothing in the literature about this specifically, but perhaps some relevant information and a suggested behavioural experiment will help.

Background
Firstly, I assume you are talking about sodium hypochlorite (which is usually what people mean by bleach)? If so, there are several compounds your cat could be reacting to. Chlorine is an obvious candidate, which is released as sodium hypochlorite decomposes in solution. Additionally, bleach can react with various organic materials to release a variety of volatile organic compounds (VOCs), which your cat might be able to smell. In addition to also releasing chlorine gas, the same suite of VOCs are released when the chlorine in chlorinated tap water reacts with organic contaminants (Odabasi, 2008). The VOCs include chloroform and carbon tetrachloride.

Next, cats are known to exhibit modified behaviour in response to a variety of compounds. Some are suspected pheromone components of cat urine, such as felinine (Hendriks et al, 1995) and its breakdown products, such as MMB (Miyazaki et. al, 2006).

Some cats also react to externally-produced compounds with a particular response called the 'catnip response', which involves rubbing the face on the ground or other objects, shaking the head, rolling, etc. (Tucker & Tucker, 1988). Not all cats exhibit the response, around 50-50% do, and susceptibility is genetic and heritable. Some sources eliciting the catnip response include:

nepetalactone released from catnip (Nepeta cataria)
actinidine released from valerian (Valeriana officinalis)
essential oil of Actinidia macrosperma (Zhao et al., 2006)
the compounds epinepetalactone, dihydronepetalactone, isodihydronepetalactone, neonepetalactone, iridomyrmecin, boschnialactone, onikulactone, boschniakine, actinidiolide and dihydroactinidiolide (Tucker & Tucker, 1988)

In general all the catnip response elicitors share a two-ring structure, which is not to my knowledge shared by any of the volatiles given off by bleach.

A possible experiment
So, two obvious possibilities (regarding what type of behavioural response is being elicited) are that either:

your cat is interpreting the volatile as a pheremone and therefore as some sort of sexual or territorial signal, or
it is showing the catnip response

As a first experiment, you could check whether your cat (and any others you can get hold of - in an ethical way) respond to bleach and/or to catnip. If the cats do not exhibit the catnip response to catnip, they aren't exhibiting it in response to bleach, and thus some other explanation is more likely.

As a second experiment, you could make a detailed observation of the precise behaviour shown in response to bleach. Compare it to that exhibited when the cats encounter catnip (depending on the outcome of the first experiment) and when they are oestrous (if female) or encounter an oestrous female (if male). You could also compare to the response to the urine of other (male and female, familiar and unfamiliar) cats.

An experiment you shouldn't do
If you wanted to find out which chemical your cat is responding to, you could allow your cat to sniff pure chlorine which hasn't encountered organic contaminants, as well as chloroform, and carbon tetrachloride. However, all three of those compounds are extremely dangerous and could easily kill you or your cat, so please don't.

I general, I would caution against exposing your cat to bleach, because it can induce serious health effects depending on dose and mode of exposure, ranging from asthma to third-degree burns to carcinogenesis. If they are attracted to it, that is a good reason to keep it away from them to prevent them ingesting it, which is more harmful than inhaling the fumes.

I can't comment on whether the behaviour is acquired as result of domestication, but that too could be tested by comparing the reaction of a large sample of wild cats (!).

References

Hendriks, Wouter H., Paul J. Moughan, Michael F. Tarttelin, and Anthony D. Woolhouse. “Felinine: a Urinary Amino Acid of Felidae.” Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 112, no. 4 (December 1995): 581–588.
Miyazaki, Masao, Tetsuro Yamashita, Yusuke Suzuki, Yoshihiro Saito, Satoshi Soeta, Hideharu Taira, and Akemi Suzuki. “A Major Urinary Protein of the Domestic Cat Regulates the Production of Felinine, a Putative Pheromone Precursor.” Chemistry & Biology 13, no. 10 (October 1, 2006): 1071–1079.
Odabasi, Mustafa. “Halogenated Volatile Organic Compounds from the Use of Chlorine-Bleach-Containing Household Products.” Environ. Sci. Technol. 42, no. 5 (2008): 1445–1451.
Tucker, Arthur, and Sharon Tucker. “Catnip and the Catnip Response.” Economic Botany 42, no. 2 (1988): 214–231.
Zhao, Yun-peng, Xiao-yun Wang, Zhi-can Wang, Yin Lu, Cheng-xin Fu, and Shao-yuan Chen. “Essential Oil of Actinidia Macrosperma, a Catnip Response Kiwi Endemic to China.” Journal of Zhejiang University. Science. B 7, no. 9 (September 2006): 708–712.


Loss of allelic variation per generation of full-sib mating If we take a male and female, cross them, and collect one son and one daughter to produce the next generation (and continually do this for many generations) - (full-sib mating design) how much genetic variance is lost per generation/how do we calculate this?

Assume all sites initially have allelic variation, and we imagine a diploid sexual species.

A classical result from the Wright-Fisher model of genetic drift is that at each generation the heterozygosity ($2x(1-x)$) is expected to decrease by $\frac{1}{2N}$ due to genetic drift. ($x$ is the frequency of one of the two alleles). In your example the expected loss of heterozygosity is $¼$. This same result has been derived from coalescent theory and a similar result is derived from the birth-death Moran model. The issue is that this model assume bi-allelic loci only.

Let's think of 1 tetra-alellic (4 alleles) locus and let's assume that the 4 alleles in our two original parents are all different. We can draw the 16 possible pairs of offsprings and see the probability to lose 0, 1 or 2 alleles in the next generation

lose 0 allele: ¼
lose 1 allele: ½
lose 2 alleles: ¼
lose more than 2 alleles: 0
Therefore, the expected number of lost alleles is $1$!

We can then do the same (calculate the probability mass function) for two parents with 3 alleles and then 2 alleles (with various frequencies). It is not very complicated. But it would be much better to have a general model to describe the loss of heterozygosity through time for more than 2 alleles. This paper probably gives this solution but I haven't read it yet. I will probably read it once and I will improve my answer then!


What is this insect or worm? I found it on the cedar siding of my home in Houston, Texas.

It was quite small, I'd estimate 1cm in length. I did not observe it move up or down the side of the house, but when I touched it gently and it did bend over.

Some species of Eupithecia perhaps. A type of moth, the larvae tend to resemble twigs. According to this relatively old text, Eupithecia miserulata is the most commonly distributed species in Texas, but I'm sure identifications stem largely from expertise and adult specimens, both of which I lack. The larvae for E. miserulata don't seem to visually match what you have, there.

In essence, though, it's a caterpillar that will turn into a moth.


What is the function of E-coli bacteria in our gut? So, I recently came up with this question. I  googled it, but couldn't understand the proper functions of E-coli bacteria. A little definition would be wonderful.

Nonpathogenic E.coli are a component of the gut microbiome of humans and many other organisms.

They are commensals, meaning that when they remain in the areas they have evolved to live in, and when they do not acquire virulence factors, they are benign. They live in our digestive tract and basically do nothing to harm us.

In fact, commensal microorganisms like E.coli can be considered part of the multicellular organisms innate immune system. They take up space on the exposed surfaces of internal organs such as the intestines and prevent the colonization of pathogenic strains of microorganisms.

Along with the endothelial cells and mucous, commensals form the barrier defenses that are the first line of protection against pathogenic organisms. Basically they are the good neighbors that don't cause problems and they don't leave space for bad neighbors to move in.

Problems can occur if they gain access to areas that are normally sterile. If the intestine is perforated and E.coli gain access to the thoracic cavity, they can become an opportunistic pathogen, as they will not be interacting with the host in a way that can control their proliferation. They can also come in contact with cells that are not expressing the necessary proteins to protect them from the E.coli.

You can also end up with the situation where a pathogenic bacteria or a bacteriophage carrying a virulence factor can transfer that virulence factor to the commensal E.Coli, turning them pathogenic.

But for the most part E.coli are there to take up space that could otherwise be colonized by harmful bacteria.


What is the explanation for the smaller number of tRNA than codons? Translation, or decoding, of the four-nucleotide language of DNA and
  mRNA into the 20–amino acid language of proteins requires tRNAs and
  enzymes called aminoacyl-tRNA synthetases. To participate in protein
  synthesis, a tRNA molecule must become chemically linked to a
  particular amino acid via a high-energy bond, forming an
  aminoacyl-tRNA; the anticodon in the tRNA then base-pairs with a codon
  in mRNA so that the activated amino acid can be added to the growing
  polypeptide chain.

  Some 30–40 different tRNAs have been identified in bacterial cells
  and as many as 50–100 in animal and plant cells. Thus the number of
  tRNAs in most cells is more than the number of amino acids used in
  protein synthesis (20) and also differs from the number of amino acid
  codons in the genetic code (61). Consequently, many amino acids have
  more than one tRNA to which they can attach ; in addition, many tRNAs
  can pair with more than one codon.

If perfect Watson-Crick base pairing were demanded between codons and anticodons, cells would have to contain exactly 61 different tRNA species, one for each codon that specifies an amino acid. As noted above, however, many cells contain fewer than 61 tRNAs.

What is the explanation for the smaller number of tRNA than  codons codons?

Th reason for this is that for the third base of the tRNA non-Watson-Crick pairing is allowed. This phenomenon is called "Wobble base pairing". See the figure (from here) for illustration (from here):

If you have a look at the codon table for amino acids, than the variation in the code for one amino acid mostly happens on the third position (from here):

This allows a smaller number of tRNA than 64, as there is some flexibility. The third base can be represented like this (taken from this answer):

In the table Cricks predictions are compared to the pairings found in experiments.


Does antidromic conduction occur in the brain under normal conditions? So I am reading a book on neuroscience and they mentioned in passing that the action potential is capable of travelling in either direction along the axon (orthodromic vs antidromic), The wikipedia antidromic article states that the effect is often used to confirm connections in laboratory experiments.

What I'm now wondering is if the phenomenon has been observed with normally behaving neurons in situ (as normal as a neuron under experimental observation can be anyway) and therefore possibly needs to be factored in when modelling neurons in software or is it safe/justified to treat the information as only flowing in one direction (orthodromic)?

Under physiological conditions, action potentials are generally assumed to travel one-way. Action potentials are generated in the dendritic region, and travel from the soma to the axon terminal. Because voltage-gated sodium channels are inactivated after having been active during action potential generation, the action potential cannot travel backwards because the tail-end of the action potential is basically temporarily shut down (Fig. 1). The duration of inactivation of sodium channels determines how fast a neuron can fire, i.e., it determines the refractory period of neurons (Purves et al., 2001).

Fig. 1. Action potential conduction and refractoriness. Source: Zoology.

When neural tissue is artificially electrically stimulated, however, action potentials can be generated anywhere along the neuron. When an axon is activated somehwere in the middle with an electrical stimulus, an action potential will travel both ways, i.e. normally to the axon terminal, but also antiodromically to the cell body.

However, it has been noted in vivo that some neurons do show antidromic action potentials under physiological conditions (Jansen et al., 1996). For modeling purposes I would not bother too much about this, though, because antidromic action potentials are generally only observed under artificial conditions.

References
- Jansen et al., J Neurophysiol; 76(6): 4206-9
- Purves et al., ed. Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates; 2001


What kind of tortoise is this? Can you help me to ID this tortoise? It was walking around near to my house and then my mom found it, so we'd like to know more info. Its Straight Carapace Length is about 5+ inches. Found it in mid-Mexico (Guanajuato state). Most part of the year we have a warm weather.

The front end of the plastron (the flat 'ventral' part of the shell) is hinged, so that the turtle can enclose itself almost completely, a characteristic of box turtles.

  Box turtles are turtles of the genus Terrapene native to North America (United States and Mexico). They are also known as box tortoises, although box turtles are terrestrial members of the American pond turtle family (Emydidae), and not members of the tortoise family (Testudinidae). The twelve taxa which are distinguished in the genus are distributed over four species. They are largely characterized by having a domed shell, which is hinged at the bottom, allowing the animal to close its shell tightly to escape predators.

Your turtle certainly has a domed shell. There is a lot of wear and tear on the shell, but not so much on the plastron. Box turtles can live 100 years.

From the lack of coloration on the top part of the shell and the paucity of markings on the plastron, I think it is either a Three-toed Box Turtle (Terrapene carolina triunguis), or a Mexican Box Turtle. The Mexican box turtle can grow slightly larger than the Three-toed box turtle. I can't really tell them apart. Boxturtles.com might help.

  Their appearance is similar to that of the Three-toed Box Turtle.

The three-toes refers to the hind feet (which can also have four toes, to make matters worse.)

  Three-toed box turtles have a domed shell which grows to an average 4.5 to 5 inches in length. The record shell length for this subspecies is 7 inches. The highest part of its carapace or upper shell is more posteriorly positioned than in the other subspecies. The dorsal and limb coloration is commonly completely absent, although some dark blotches are common in adult turtles. These areas more often being a uniform olive green or tan color.

From another site:

  Shy and quiet are the traits of a Three-toed Box Turtle, both in its personality and in its coloring. Unlike the bold patterning and color seen on other eastern box turtles, the color of this species is quite subdued. Occasionally there will be a Three-toed that is more brightly colored, but for the most part they are a fairly uniform olive-brown to brown or horn color.

See also Reptiles & Amphibians


What is the physiological difference between snorting/swallowing cocaine I know that mucosa inside the nose absorbs cocaine molecules when snorting cocaine, but what difference is there compared to swallowing?

Also more cocaine administration equals more cocaine molecules in the brain equals more inhibition of repute equals more serotonin–norepinephrine–dopamine in the synaptic clefts equals more work for receptors equals more intense effect, right?  What about the duration of a particular molecule which inhibits reuptake? How long this particular molecule stands there?

You can easily google for this question and find plenty of disreputable sources, but this is another case where Wikipedia does an okay job.  There are some misleading and erroneous sentences, but this one basically sums it up:

  Compared to ingestion, the faster absorption of insufflated cocaine results in quicker attainment of maximum drug effects.

Mainly, take a look at this 1981 article.  The researchers gave participants cocaine, measured drug activity, and did then did a great review of the literature.  They found that, like plenty of other drugs, ingesting cocaine results in a slower but longer-lasting effect.

Your stomach is not an efficient route of absorption for things besides water, alcohol, and aspirin; besides, it's highly acidic.


Forum on synthetic biology and hypothetical biology? I am interested in synthetic biology, but not a scientist, and would like some advice on where to look for an online forum on synthetic biology and creating fictional species and animals or if someone could suggest the best website to set such a forum up on.

The current research into synthetic biology with biobricks and all the complicated discussion of biochemistry and genetics is too advanced for myself and not what I am interested in. I have fictional ideas of how to create new organisms and symbiotic organisms that are designed and grown for humans to wear and utilise and would like to bounce ideas off other people who may be in to the same area - the potential application of synthetic biology in the far future.
Thank you for any suggestions.

Your best bet might be the sub forum on reddit specialized in synthetic biology. Have a look here

Happy science!


Are different eye colors indicative of chimerism? If an animal or person has different colored eyes, does that mean they are a chimera?

You will find this wiki entry [1] informative.

While chimerism is one possible explanation, it is certainly not the only one.

[1] https://en.wikipedia.org/wiki/Heterochromia_iridum


Large Alpine Hymenopteran Seen in the White Mountains I was hiking in the White Mountains in New Hampshire, USA, and at the peak of Mount Eisenhower saw a number of large bee-like insects. They appeared to be nesting in a rock cairn, and were strikingly large---length was about 1.5" (~40mm). Weather was clear, sunny, about 65 degrees Fahrenheit. Time of year was early July. Environment was alpine tundra, a few hundred feet above the treeline. Besides the habitat and large size, they seemed like fairly typical bees (I'm saying bees because they were almost certainly hymenopterans, but didn't have the typical "narrow waist" of wasps). The abdomen was the longest part of the body. Behavior-wise, they flew in and out of the cairn, and often rested on the ground (or on backpacks, water bottles, etc). Does anyone know what species this may have been?
(I'm sorry I don't have any photos; even if species is impossible to determine without them I'd be happy for any information on possible family or genus)

Looks like some sort of cimbicid sawfly. Thanks @ArthurJFrost !


How do ribosomes contribute to their own synthesis? In other words, what products synthesized by ribosomes are actual parts of ribosomes (if any)?   How are they involved in their own synthesis otherwise? What is the cycle/chain of products starting with the proteins synthesized by ribosomes and actually ending with the synthesis of a ribosome?

The most important parts of the ribosome are not made by other ribosomes - 5 rRNA (ribosomal RNA) of the ribosome actually do most of the direct work of creating the protein and are made by RNA polymerase ( a protein, but not the ribosome).

Then there are 92 ribosomal proteins, which as a rule bind to ribosomal RNA to support their structure and keep everything going.  These are all made by ribosomes.  They are thought to have appeared later in the evolution of the ribosome though I imagine that it would not be possible to constitute a working ribosome without each one of them.

these numbers are for the eukaryotic ribosome, the prokaryotic ribosome has 3 rRNA and 52 ribosomal protein components.

http://en.wikipedia.org/wiki/Ribosome


High concentration of primer in PCR Why is it that higher concentration of primers than the DNA template in PCR will favor the annealing of a template to a primer?

Using high concentration of primers ensures that after denaturation template DNA binds to primers instead of binding to each other. Also higher primer concentration enhanced product yield, as primers act as limiting factor for annealing.

(Reference: https://academic.oup.com/nar/article/24/5/985/1047654)


How many coronavirus particles are in the body at the peak? How many coronavirus (or other common virus) particles are in the body at the peak? How far it multiplies? Are there billions, trillions or other number of them?

This measure changes dramatically between viruses and infected individual but there are some estimates that have been done.

Bar-On, Flamholz, Phillips & Milo, Apr 2020, eLife
From MERS and SARS (similiar to the current coronavirus) we know that from each infected cell emerge around 10^3 virions and it takes them 10 hours from the infection of the cell. We cannot deduce that every 10 hours the magnitude of virions in the body increases by 3 because:

Not all virions infect a new cell
Some virions infect the same cell and the burst size depends greatly on the cell
Not all virions are viable or able to infect

Another paper from Sender et al. (Nov, 2020) that is still in preprint (this is a long time for Coronavirus related articles) estimates the number of virions in peak infection at 10e9-10e11.
This estimate was done by analyzing data from Rhesus macaques (a monkey).
Concentration of virions per tissue weight was multiplied by the tissue weight to get total amount of virions.
On the relevance of Coronavirus information
Since our knowledge of Coronavirus advances and changes all the time it is important to note the date and source of information. Also, to advance science many papers published preprint articles regarding Coronavirus. This articles are published before peer-review and should be taken with a grain of salt as every peer-reviewd paper gets many revisions before published to the public.


Could Cyanobacteria farms help dilute pollutants in the atmosphere If I understand correctly, roughly ~2.8 billion years ago cyanobacteria started pumping large amounts of oxygen into the atmosphere.

Using modern industrial processes could this be emulated by making cyanobacteria farms to help slow down the climate problem?

I also read somewhere that someone was able to genetically (or through other means) turn off the ability of a specific bacteria to reproduce causing it to produce a byproduct much more efficiently. Could this also help these "farms"?

Alternatively could we genetically strip the bacteria of all other functions other than procreating and photosynthesis? Making this bacteria live in a "bubble" would mean it wouldn't need a lot of defense mechanisms. This could make a single purpose bacteria that would be super efficient at doing this single task.

You have various questions here.

  If I understand correctly, roughly ~2.8 billion years ago cyanobacteria started pumping large amounts of oxygen into the atmosphere.

The great oxygenation event was not an instantaneous process and represents a change from one equilibrium (low oxygen) to another (20% oxygen). This abundance of oxygen and organic carbon means that there is "niche" for organisms that burn up pre-existing organic carbon and use oxygen as terminal electron accept. Fermenting organisms use the organic carbon as a feedstock, but don't have oxygen so the use highly reduced organic molecules as terminal electron acceptors (less energetic), making mixed acids (sweat bacteria) or ethanol (yeast).

  Using modern industrial processes could this be emulated by making cyanobacteria farms to help slow down the climate problem?

Cyanobacteria and other aerobic phototrophs convert carbon dioxide to oxygen and organic carbon they can use to make biomass. So if you had enough of these you'd need to get rid of the biomass. Responsible forestry for housing actually ticks this box (cf. vs. a mature forest, which is nearly at equilibrium where the biomass gets consumed by other organisms, else you'd had a faster growing topsoil).

  I also read somewhere that someone was able to genetically (or through other means) turn off the ability of a specific bacteria to reproduce causing it to produce a byproduct much more efficiently. Could this also help these "farms"?

It is a grand challenge of synthetic biology to stop growth. It is really hard to do as "cheat" (i.e. variant that can grow faster) will dominate. Biofuel research suffers from this as the fatty acid biosynthesis pathway is highly expensive energetically and cheats eventually win despite the most complicated safeguards.

  Alternatively could we genetically strip the bacteria of all other functions other than procreating and photosynthesis? Making this bacteria live in a "bubble" would mean it wouldn't need a lot of defense mechanisms. This could make a single purpose bacteria that would be super efficient at doing this single task.

The carbon will be a problem, so you'd need to make biomass or some value added compound.

Three additional points:

Green biotech

There are many "green biotech" companies out there and there is an increasing number of green chemistry awards going to biocatalysis (enzymes for a reaction) and in some cases synthetic biology processes (whole enginereered organisms for a product or intermediate). But the former field is slow at growing because it needs to compete against a century of homo/heterocatalyis (normal chemistry), while the latter needs a lot more technological innovation to improve the production chassis (e.g. cheats, slow reactions, iron-sulfur cluster over-expression and electron balance are common issues: hydrogenase is a classically cited example of a hard target with great potential).

Note that most green biotech uncouple the process and use the biomass from regular algae or plants to feed their engineered organisms, as it is easier and there are less containment issues.

Algal blooms

In the comments I mention, iron fertilisation of the oceans (a ship releasing a container size of nutrients across an oceanic crossing is make a substatial planktonic boom, which either increases fish levels or sinks and thus buries the carbon it converted into biomass). This is a curious case of huge scale and cheap algal farming. But we don't know all the details, yes we'd be turbocharging the oceans (which are barren relative to say a jungle), but we may favour toxin-releasing algae, jellyfish and imbalance fisheries and actually send to extinction others.

Bioreactor in the ISS

The Internation space station splits water to make oxygen, dumps all carbon waste outside (CO2 and ...) and has water and food shipped up. This is odd as you'd expect they would be the first to use algae to scrub CO2! However, things are changing: they are trialing an algal bioreactor, which on a larger scale will result in a near-closed loop system. However, there are many engineering and some biological issues that need to be faced.


What is the role of glycine in the running buffer for SDS-polyacrylamide gel electrophoresis We used pH6.8 in stacking and pH8.8 in resolving gel. In the class, the professor explained that the glycine change is like:

glycine+ <-------> +glycine- <------> glycine-

it is said that most of the form will be +glycine- and glycine-. Why? And why does it change the charge when it runs from the stacking gel to resolving gel? What is the role of glycine in the running buffer for SDS-polyacrylamide gel electrophoresis?

The pH of stacking and resolving gel are set in such a way that one is above and one is below the pI of gly (5.97).Therefore, Gly has two different charges in stacking and resolving gel. That is in stacking gel gly has no charge (which will allow the protein to stack according to size in this part of the gel rather than separating because of presence of gly in between the protein molecules, constraint in separation of proteins) but in resolving gel charge is negative since the pH is higher (constraint in movement of proteins no longer present so separation of protein based on size possible).

Hope this was helpful..


Replicator dynamics giving probabilities greater than 1? I have a linear replicator equation and I want to simulate its dynamics to find the resting point and hopefully the Nash equilibrium.

I defined strategies' payoff as  $ \vec f = C*\vec p+ \vec b$, where $C$ is a community matrix similar to the one in Lotka volterra models, $p$ is the vector of probabilities for each strategy and b is a vector of constants. From what I understand, this is very similar to the replicator dynamics for a linear model, except that I'm adding a constant.

However, when I iterate over $\vec p_{t+1} =  \vec p_t+ \vec p_t (\vec f- \sum\vec f \vec p_t) $,   $\vec p_{t+1}$ frequently gets values greater than one or smaller than zero, which from my understanding is not suppose to happen.

An example to show the issue:

$C = \begin{pmatrix} -1 && -1.1 && 0 \\ 1 && -1.0 && -1.1 \\ 0 && 1 && 0 \end{pmatrix}; \space \vec b= \begin{pmatrix} 0.7 \\ 0 \\ 0 \end{pmatrix}; \vec p_0 = \begin{pmatrix} 0.8 \\ 0.9 \\ 0.25 \end{pmatrix} $

In this situation,  the second element of $\vec p_1 $ equals 1.448550!

What could be causing this error? Am I calculating  the replicator dynamics wrong? Does adding a constant to fitness "breaks" the replicator dynamics? Is my understanding wrong and replicator dynamics can go above 1 or below 0?

This is happening because the fitness for your first strategy can be negative. In the case of the discrete replicator dynamics, the fitness cannot be negative. Otherwise, you can leave the simplex. Note that the continuous replicator dynamics doesn't have this restriction (the fitness can be negative).


How to confirm pure-breeding parents I was reading Genetic Analysis (Sanders, Bowman) and saw the following figure summarizing the 1909 work of Herman Nilsson-Ehle in describing the genetic control of kernel color in wheat:

How did Nilsson-Ehle determine that the original pure-breeding parents were in fact homozygous for each allele?

If they are "pure-breeding", that means that they are homozygous.  If they were heterozygous, the offspring would not all have the same color as the parents.  But tree-breeding" means they all do.


Has there been any observation of species adapting the evolution process? I am very interested in the evolution of the evolution process itself. There are of course a lot of things that influence how evolution will work, but for this question, I am interested in things that are only related to the evolution process. Examples could be increase chance of mutations in newborns, change in reproduction age, and similar. I am specifically interested in observation where the evolution process itself has adapted to a change in the environment.

Bacteria such as E. coli are known to increase their mutation rate (by switching to a more error prone polymerase among other things) when under stress. This can mean being placed in a medium where it's not adapted to grow (http://www.micab.umn.edu/courses/8002/Rosenberg.pdf) or when treated with antibiotics (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1088971/?tool=pmcentrez).


Are there neurons that can sense light shining in your ears? I know someone who bought earphones that shine light in you ears. According to what he was told, there are neurons that sense light and then make you feel wide awake when activated, which seemed like snake oil to me. Apparently the pineal gland may be able to sense light and it does secrete melatonin - a sleep regulating hormone. I'm still sceptical though as its stuck in the middle of your brain. Would shining lights in your ears be able to have any effect on how awake you feel?

There is no known mechanism for light detection through the ears in humans, as far as I know. It is certainly true that the pineal gland is part of the system that regulates the circadian rhythm (briefly, the daily sleep-wake cycle). However, while the pineal gland in birds and other non-mammalian vertebrates is directly sensitive to light, the mammalian pineal gland is not (see, for review, Doyle and Menaker, 2007 and Csernus, 2006).

In all animals, the circadian rhythm is regulated by a photoperiod cue and therefore requires light detection. In mammals, the light sensors are found exclusively in the retina, the sensory portion of the eye. There are two classes of light detecting cells in the retina. First, rod and cone photoreceptors mediate vision in the usual sense of the word. These cells contain proteins called opsins that absorb photons of light and thereby excite the photoreceptors that contain them, informing the brain that light was detected.

A second class of photosenstive cells in the retina are called intrinsically photosensitive retinal ganglion cells (ipRGCs) (see Do and Yau, 2010 for review). These cells mediate "non-image-forming" vision and are an important part of the circadian rhythm pathway. They also contain an opsin called melanopsin which is a photosensitive pigment. This is not to be confused with melatonin, which is the sleep hormone released by the pineal gland. The ipRGCs in the retina send the photoperiod cue to a brain area called the suprachiasmatic nucleus (SCN). The SCN then signals to the pineal gland.

If we are generous and assume that these light-emitting headphones are the result of misunderstandings, we can guess that the confusion arises from (1) the fact that some animals have a directly photosensitive pineal gland, but not mammals and (2) that the pineal gland secretes melatonin but not the photosensitive pigment melanopsin.

Update: From a bit of research, it turns out that the company selling the headphones is not "confused" as I politely offered. I don't think this site is the appropriate forum to refute their research or claims. Suffice to say that the retina is the only part of the human brain shown to be photosensitive.


Why do marmosets have claws when most primates don't? What is the structure of their hands like? The majority of primates have really thick nails, though not as broad or flat as humans'. However, marmosets have 18 claws, and only their big toes have nails. What differences in evolutionary pressures caused this? And how does the structural relationship between marmosets' germinal matrices and their distal phalanxes differ from other primates, so they can grow claws?

Since marmosets and tamarins are considered the most primitive primates, we can't assume that evolutionary pressure led to the development of claws. Rather, it's accepted that claws disappeared as primates adapted to an arboreal lifestyle. So the question is really "Why did marmosets not completely lose their claws?"

The clues to the answer lie in their unusually large incisors and disgestive system. The marmoset occupies an evolutionary niche where they rely heavily (20-70% of total diet) on exudates (sap, resin, etc.) from trees. Their claws, and incisors allow them to claw/chew holes in the bark to get at the exudates, while a specially adapted large intestine allows them to digest this food. The advantage of exudates is they are not seasonal, offering the marmoset a relatively stable year-round food supply.

Other primates enjoyed the evolutionary benefits of tool use by losing their claws and gaining opposable thumbs (which marmosets don't have). I've come across no papers that describe a different phlange structure for marmosets and other primates, and there doesn't necessarily need to be one.

Most of this information came from the University of Wisconsin's Primate Research Center:

http://pin.primate.wisc.edu/factsheets/entry/common_marmoset

Edited to add (since I can't comment): One way to deduce how different features evolved is to look at phylogenetic trees. There are many out there, but I pulled this one from J.R. Roede et al. Redox Biology 1 (2013) 387-393.

If you look at this simple tree, you'll see that marmosets diverged from humans on a time frame where it's possible they kept their claws instead of reacquiring this trait (it would be unusual, but not impossible, for this to happen). One thing you can do is dive deeper into the phylogeny, square this up with how primate hands evolved, and see if the split of marmosets from the rest of the primates happened when nails began to evolve.


State of extracted DNA A well-known and commonly-done experiment is to extract DNA from strawberries or other fruit by first mashing the fruit of choice, adding the mush to a mixture of water, salt, and detergent, and then adding isopropanol. DNA then precipitates out.
How intact is the DNA obtained from this experiment? Does the experiment introduce breaks or other forms of DNA damage? Is the DNA intact enough to be sequenced and for one to be able to identify what organism it came from?

Yes, normal DNA extraction protocols fragment genomic DNA.  In my experience, extracted DNA tends to have a size distribution on the order of 10 - 20 kilobase pairs (kbp), independent of the protocol and source organism (assuming a chromosome size >> 20 kbp).  This seems to be corroborated by what I can find online -- see the gel below from Successful tips of DNA extraction and PCR of plants for beginners

Figure 1. Agarose gel electrophoresis of DNA samples extracted from horticultural plants. M, molecular weight marker. Modified from Kasajima et al. (2013)

as well as this gel from ThermoFisher

Genomic DNA purified with the Genomic DNA Purification Kit
Agarose gel (0.7%) electrophoresis analysis of undigested (odd lane numbers) and EcoRI digested (even lane numbers) DNA samples.
M – Lambda DNA/HindIII Marker [top band is 23130 bp]
1, 2 – human blood
3, 4 – human lymphocytes
5, 6 – human placenta
7, 8 – mouse liver
9, 10 – Hedera helix
11, 12 – Haemophilus influenzae
13, 14 – E.coli ER2267
15, 16 – Bacillus subtilis

The consistent size of extracted genomic DNA across organisms is a physical constraint rather than a genetic one.  When unwound and unprotected by the cell and nuclear envelopes, chromosomes are subject to the shearing forces of pipetting and vortexing.  Consider a mile-long length of high-test fishing line.  Coiled in the box or around a reel, the line is strong and stable.  If you laid the line out end-to-end, however, there would be many places along its length where the line gets snagged, knotted, and torn.
As hinted by canadianer, DNA fragmentation is necessary for most sequencing methods (specifically whole-genome shotgun sequencing, not sequencing of specific PCR amplicons).  As an example, Illumina sequencing platforms generally require libraries with fragment size distributions between 300 and 600 bp, and fragments larger than 1000 bp are sequenced inefficiently.  So, after DNA extraction, additional steps are required to further reduce the average DNA fragment size prior to sequencing adapter ligation.  The most common method of genomic DNA fragmentation for short-read sequencing is sonication, though enzymatic methods are also used in some kits.
Recently, long-read sequencing technologies have been developed to overcome the difficulty of assembling short reads.  Nanopore platforms can sequence DNA fragments that are 100s of kbp long.  To prepare these extremely long libraries, special care must be taken to not shear the DNA during extraction.  The Journal of Visualized Experiments provides a good guide on how to extract and process high-molecular-weight DNA:
Gong, L., Wong, C. H., Idol, J., Ngan, C. Y., Wei, C. L. Ultra-long Read Sequencing for Whole Genomic DNA Analysis. J. Vis. Exp. (145), e58954, doi:10.3791/58954 (2019).


How do cells relocate transmembrane proteins from one side of the cell to the other? Is it possible? Is there a process by which cells can relocate proteins residing on the cell membrane in areas of low demand to that of a high demand location somewhere else in on the cell? What's that process called?

Through protein catabolism, cells can break down the proteins into their individual amino acids and then reuse these resources to build new proteins in needed locations. This process seems inefficient if the cell simply needs to move a transmembrane protein (for example integrin or cadherin) from one side of the cell to the other.

I hope the question is clear. I haven't taken a biology course since early high school (8 years ago) so if there's something i need to clarify let me know!

The breakdown and reassembly of proteins is a ubiquitous process within cells, and yes this is expensive but transport is expensive, too, and recycling has the added benefit of dealing with proteins that become misfolded or otherwise damaged as well as allowing for transcription and translation to regulate overall protein levels. The Toyoma & Hetzer 2013 review (see references below) cites estimates of the median protein half-life in a non-dividing mammalian cell to be about 43 hours, though they discuss some exceptions that do last much longer.

However, it is possible to relocate transmembrane proteins via vesicles.

Essentially the same way proteins are put in the plasma membrane in the first place, but in reverse. Endocytosis is often taught as a way that cells (often macrophages are used as an example) take in materials from the outside world, but it is just as applicable to internalizing chunks of membrane. Nature has an entire 'web focus' on entocytosis reviews.

One situation where this happens is in synaptic plasticity; receptors can be internalized or trafficked to the membrane to decrease or increase the potency of that synapse, respectively (see Carroll et al., 2001), but similar processes occur all over (and some proteins constantly cycle back and forth; see Trowbridge et al. 1993 for a more general review, though a bit dated).

However, to your specific question, I don't know specifically of examples where transmembrane proteins are literally cycled from one side of the cytosol to the other. There may be examples I am not aware of, but my understanding is that it is more typical to think of a "store" of certain proteins in endosomes, from which they can be trafficked to the membrane and reinserted via exocytosis. Probabilistically, some will be transported from one place to another, but not so much in a stepwise fashion.

Toyama, B. H., & Hetzer, M. W. (2013). Protein homeostasis: live long, won't prosper. Nature Reviews Molecular Cell Biology, 14(1), 55.

Carroll, R. C., Beattie, E. C., von Zastrow, M., & Malenka, R. C. (2001). Role of AMPA receptor endocytosis in synaptic plasticity. Nature Reviews Neuroscience, 2(5), 315.

Trowbridge, I. S., Collawn, J. F., & Hopkins, C. R. (1993). Signal-dependent membrane protein trafficking in the endocytic pathway. Annual review of cell biology, 9(1), 129-161.


What are the rules for plasmid names? What are best practices for naming newly created plasmids?

For example, a common format is pABC123. What is the exact specification? Must there be 3 letters?

What databases of plasmid names exist? How much care is taken to avoid name collisions?

So there are no rules per say (although I wish there were). But there are commonalities among plasmid names and they can help people identify them:

Include the empty backbone name in your plasmid name. This simple piece of information can often convey many important details. Once you know the backbone a plasmid is based on, you can usually derive: a) the bacterial antibiotic resistance, b) the promoter that drives the insert, and c) any other selection markers (for use in other cell types, e.g. eukaryotic cells).

Include information about the insert in your plasmid name. This is often a 3-6 letter representation of the gene (or DNA sequence).

Often researchers will add a lower case letter to the beginning of their insert abbreviation to specify what species it is. Example: ‘h’ is for Human (homo sapiens), ‘m’ is for mouse (mus musculus), ‘r’ is for rat (rattus rattus or rattus norvegicus), etc.

Add any tags or fusions that are on your insert. Typically you would list any tag or fusion protein in the order they appear in the plasmid and their relative position to the insert. Example, if you have a Flag tag on the N-terminal of your insert, you would list it first.

e.g.   pBACKBONE-Flag-hGene

If there was also an EGFP fused to the C-terminal of your insert you would list it after the insert.

pBACKBONE-Flag-hGene-EGFP

If your insert contains a mutation or modifcation, this should be included in the plasmid name.  Mutations are generally listed as the amino acid change and not a nucleotide change. The proper way to denote an amino acid mutation is to list the one letter abbreviation of the wild type amino acid immediately followed by its position (number) relative to the start Methionine (Met) followed by the one letter abbreviation of the mutated amino acid currently at that position.

Check for more information at Addgene.com they are the largest plasmid repository in the world.

By collisions I'm guessing you mean naming your plasmid something that is already "taken." This is a benefit of submitting to a repository, they will ensure this doesn't happen.if your planning on filing a patent, your parent attorney will do it.


Were there any flying dinosaurs? I've seen some articles which came in contradiction with each other.

The first article was talking about flying dinosaurs, dinosaurs with feathers and so on.

A couple of other articles are talking about misconceptions about dinosaurs one of them being that there are no flying dinosaurs but just flying reptiles (from scholastic.com and livescience.com).

So, which one is right?
Also if possible please provide a source for argument.

I cannot find the first article again.

Birds are both flying dinosaurs and flying reptiles. Yes, that's potentially confusing.

To understand the apparent contradiction, you have to understand how modern classification of organisms works (phylogenetic systematics). Under the old (Linnean) classification system, Reptilia (reptiles) was an order and Aves (birds) was a separate order. Phylogenetic systematics, which has completely replaced the Linnean system, views all organisms as interrelated in a nested set of monophyletic groups (clades). It's like a set of venn diagrams, where all organisms fall into a giant circle and then successively smaller circles classify more and more specific groups.

The clade Reptilia includes snakes, lizards, crocodiles, and lots of extinct groups, including dinosaurs. So all dinosaurs are reptiles. The clade Dinosauria includes all the extinct dinosaurs (Stegosaurus, Triceratops, sauropods, etc.), including theropod dinosaurs, which include well known dinosaurs like Tyrannosaurus and Allosaurus. Based on a mountain on anatomical evidence, including lots of transitional fossils, living birds are a sub-group of theropod dinosaurs.

So all birds (Aves) are theropod dinosaurs (Dinosauria: Theropoda). All dinosaurs are reptiles. Therefore, birds are dinosaurs and reptiles. They are just more closely related to dinosaurs than to other reptiles.

The tricky part is that most people have an intuitive idea of what "reptiles" and "dinosaurs" are. To a systematist, whose job it is to classify organisms, these terms don't mean the same thing as they do to most people. Systematists think about groups like Reptilia and Dinosauria and how those groups are related to one another. So they have no problem saying that birds are dinosaurs and reptiles, because birds are nested within both of those groups.

A few words about pterosaurs

Along with birds and bats, pterosaurs are the other clade of vertebrates capable of powered, flapping flight. Pterosaurs fall within Reptilia (and Diapsida and Archosauria) along with Dinosauria, which includes birds. There are a lot of other extinct lineages in the tree that are not shown, e.g., ornithodirans that are not dinosaurs and not pterosaurs. Pterosaurs and birds share anatomical features that all reptiles, diapsids, archosaurs, and ornithodirans have, which is how we know that they are more closely related to each other than to other groups, like crocodiles. But their flight structures evolved independently and are anatomically distinct fro one another. So pterosaurs are flying reptiles but not flying dinosaurs.

These images might help you understand the above explanation.


What are the appendeges behind a crane fly's wings? I noticed that crane flies have strange appendages behind their wings. The appendages look like a pair of antenna or a pair of vestigial wings. In the following picture I marked these appendages with arrows.

The specimen in the picture sat on my window this morning. I looked through the genera on Wikipedia, that is, on the images if there were any. All crane fly species seem to have these appendages.

While the appendages are clearly visible in most images I couldn't find a description of them. I've never seen anything like them and would like to know:

What's the name of these appendages?
What are they good for? Are they vestigial wings, antenna, or some sort of counter weight to stabilize the flight?

They are the halteres. These structures help the flies to perceive body rotation and maintain balance.


Can conventional PCR amplify DNA from different organisms from a specimen in a single step? I've understood so far that in conventional PCR, the most abundant DNA/genotype present in the speciment at the beginning of the reaction is selected and esponentially amplified. So that cPCR are likely to miss mixed infections.

But I had 1 case in which when I sequenced the PCR product I got in BLAST 100% similarity for 3 different species at the same time. Is this suggestive of a mixed infection?

If you had a 100% BLAST hit for 3 species from a single amplicon sequence then it only means that region of DNA is conserved in the three species so you have at least one of those species present not necessarily all three.

If you had three different amplicon sequences and each one matched one species to a total of three, then you have all three species present.


What are the units of Phylogenetic Independent Contrasts (PICs) PICs are a popular phylogenetic comparative method and I was wondering what units the actual contrasts are in. I want to say they are unitless but I am not entirely sure.

From what I understand, the answer is; it depends. As you point out in the comment to Remi.b, contrasts are standardized by branch lengths (which are assumed to be proportional to "evolutionary time") before they are analysed (to obtain standardized independent contrasts). However, branch lengths can be come from a number of different sources (divergence times, genetic similarity etc), can be based on different evolutionary models, and can also be transformed (log etc). Therefore, you cannot say what the units of standardized independent contrasts are in general. They would probably not be dimensionless though, since branch lenghts are seldomly (if ever?) expressed in the same units as the raw contrasts. Units such as log(kg)/year or kg/log(year) are more likely. Ultimately, in the usual case, the point of standardizing is to assure that all contrasts receive equal weight in the the analysis, and the creation of suitable branch lengths can be a trial-and-error process, where you e.g. study the relationship between standardized contrasts and the standard deviation of contrasts to see if they have been adequately standardized.

I guess you could describe the process as:

calculate contrasts
calculate standardized contrasts (using branch lengths)
when the contrasts are appropriately standardized, you have obtained phylogenetically independent contrasts.

Here are a couple of relevant quotes from Garland et al., 1992:

  ...independent contrasts must be adequately standardized so that they will receive equal weighting in subsequent correlation or regression analyses.

also

  Second, the statistical adequacy of any proposed branch lengths should be viewed as an empirical issue (cf. Grafen, 1989, 1992; Harvey and Pagel, 1991; Pagel and Harvey, 1992). Third, different transformations -
  and indeed entirely different branch
  lengths, based on different information -
  can be used for different characters. The
  use of different branch lengths for different characters would be analogous to using different transformations for the two variables in an ordinary correlation or regression.

finally

  Standardized independent contrasts essentially indicate minimum average "rates" (or, in Bookstein's [1988] terminology, "reduced speeds") of character change occurring along two branches deriving from a
  common ancestor (Garland, 1992). Because
  they are standardized, they do not indicate
  absolute amounts of change. For example,
  a large contrast (absolute difference) between two species at the tips of a phylogeny may yield a small standardized contrast if the branch lengths of that contrast
  are long.


What is an irreversible reaction? There are reactions with large Delta G negative values. Why these reactions are irreversible? As in: out of 10 steps of Glycolysis, 3 are irreversible steps. I need an explanation for why they are irreversible.

The term "irreversible" means that the reverse reaction occurs so rarely that it is considered negligible. This means that you do not have to consider equilibrium, as you have to for reversible reactions. Instead, you can assume that all of the reactants will eventually become product.

As you stated, this is true for reactions that have a very negative Gibbs free energy.  Remember the formulation of the Gibbs free energy in terms of the equilibrium constant:
$$
\Delta G^o =  -RTln(K)
$$

This can be rewritten as follows:
$$
K = e^{-\Delta G^o/RT}
$$

As $\Delta G^o$ gets very negative, you can see that $K$ gets very positive.

The equlibrium constant has two definitions that are both useful. First, it is the ratio of the products to the reactants. Therefore as $K$ gets very positive, the equilibrium ratio of products to reactants approaches infinity, implying that all of the reactants will be consumed.

More useful is the definition of the equilibrium constant as the ratio of the rates of the forward and reverse reaction. From this definition we can see that as $K$ gets very large, the ratio of the rates of the forward and reverse reaction approaches infinity. This means that the rate of the reverse reaction becomes negligible compared to the rate of the forward reaction. This is exactly what it means to be irreversible.

Note that it is possible to make (what I think is) a more convincing argument using the concept of activation energy, using Hammond's Postulate to describe the character of the transition state. If you'd like, I can write this out. However, I think the argument given above is more easily understood with a basic chemistry background.


What is the role of glucose in plasmid isolation? My understanding is that glucose is used in the resuspension solution to prevent cells from bursting by maintaining the appropriate osmotic pressure. Why do we even bother doing this? The cells are going to be lysed with the addition of the SDS+NaOH, and we have EDTA in the resuspension solution to chelate Mg, thus inactivating nucleases.

This is a common misconception: in fact, in the alkaline lysis method for plasmid isolation, the glucose does not act as an osmotic stabiliser.

Glucose is present in the resuspension buffer at 50 mM. This concentration is not high enough for osmotic protection of spheroplasts formed by lysozyme treatment: from memory, 0.5 M glucose is typically used for stabilisation. So why is the glucose included?

The original method for plasmid preparation by alkaline lysis was published by Birnboim and Doly in 1979. They explain that the method relies upon achieving a pH of between 12.0 and 12.5 after addition of NaOH so that linear dsDNA (sheared chromosomal DNA) is denatured but closed-circular DNA (plasmid) is not. They state in the paper that:

  further pH control is obtained by including glucose as a pH buffer.

According to this site glucose has a pKₐ of 12.3, which aligns nicely with the claim that it helps to keep the pH within the desired range.


Can someone tell me the species of this lizard? It's a green lizard with a silver tail, and it has pretty, bluish eyes. I saw it today, July 26th, trying to get some shade on a hot, sunny day (32 degrees) at around 18:00 in Austin, TX USA. It's been hot and dry here the past few weeks, but it rained a lot a few months back.

Austin has a humid subtropical climate. The city is characterized by hot summers and mild winter days and usually cool to cold winter nights. The geo coordinates are 30.4 (lat), -97.7 (long).

Oh, it was able to jump a good meter.

Thank you.

I know nothing about lizards, but this looks like a Carolina anole (Anolis carolinensis), also known as a green anole. Apparently they can change colour:


Why extract DNA from certain white blood cells instead of whole blood? In my lab, human DNA is extracted from whole-blood samples.

I don't actually do the extractions and I am not familiar with the specific protocol but I understand that platelets and red blood cells do not have nuclei and therefore do not have DNA so I presume that isolating the sample's white blood cells is part of the procedure.

I also understand that different types of white blood cells have multi-lobed nuclei but I do not know how that affects the DNA which can be extracted from them.

I've seen a few papers, such as this one: http://www.ncbi.nlm.nih.gov/pubmed/15113441, state that they extracted DNA from specific types of white blood cells; lymphocytes in this case. These papers to not focus on, or even address, immune function.

Why extract DNA from only one type of white blood cell?

Do lymphocytes contain DNA that is more representative of the patient's genome than other types of white blood cells?

Are certain types of white blood cells easier to isolate than others?

Is this just the standard DNA-from-blood extraction procedure or are there multiple options to choose between depending on your research goals?

There are several reasons why a lab might choose to get DNA from lymphocytes instead of whole blood. Generating genomic DNA from whole blood is not necessarily the best idea, as all the excess protein (mainly hemoglobin from RBCs) needs to be gotten rid of at some point. By narrowing down your input to just include cells that have DNA, you lessen the amount of protein you need to extract in comparison to the total amount of DNA present.

Lymphocytes include T cells, B cells, and NK cells, and are relatively easy to quickly purify, especially in a lab with the requisite experience and reagents/equipment. They are by no means the only type of white blood cells from which one could purify DNA - peripheral blood mononuclear cells (PBMCs) can also be used, for example. They contain lymphocytes as well as other cell types like monocytes, macrophages, dendritic cells, etc. (In my experience they are even more straightforward to purify from whole blood than just lymphocytes, as it is essentially a single-step protocol with a few washes afterwards.) The end result is the same, though - DNA from lymphs should be the same as DNA from PBMCs, granulocytes, or neutrophils.

Any somatic nucleated cell in the body contains "representative" DNA, as except for in a few specialized cell types like T and B cells that undergo genomic rearrangement to form the T- and B-cell receptors, respectively, all cells from an individual contain the same genomic DNA sequence. Blood is relatively easy to come by from patients and clinical study participants, which is why it is often the source of DNA for studies instead of, say, skin punches or mouth swabs.


What causes skewed lanes in a DNA gel electrophoresis experiment? In gel electrophoresis, what causes effects like these (see column 11 in the first one, and column 6 in the second)?

(These images were samples that I took from an online activity we did for class)

These are sequencing gels (in the cases here even radioactive ones) - they are run a lot longer than ordinary agarose gels and they are made from polyacrylamide. Im my experience, the most likely cause for skewing of lanes (not only bands) are samples, which still contain too much salts from the PCR reactions. This can also happen to only a few bands as seen here. Overall these are still pretty nice and clean gels, I have seen much worse.

Other reasons which cause uneven gels are cases where the acrylamide is not mixed good enough (causing the gel to have different concentration and thus causing different running conditions), uneven warming (although this was usually preventing by the gel heating system) and leaky gels where the electric field was not completely even.


What does this Barbary Macaque facial expression mean? A girl pretended having a piece of food in her hand and pointed it to a Barbary Macaque in Gibraltar. As a response he made this facial expression to her. What does this mean?

It looks like it is trying too threat.

Source:

Individual differences in scanpaths correspond with serotonin transporter genotype and behavioral phenotype in rhesus monkeys (Macaca mulatta)


Animal gene in plants Usually only microbes, specifically bacteria are used to express genes of other species for various functions. But, it is possible to try and express an animal gene into a plant. Bacteria like Bacillus thuringiensis is used in many plants like cotton, to modify them to BT cotton with insecticidal properties. Can one use an animal gene to get those characteristics in the plant?

One example that I am aware of where an animal transgene was put into a plant was to produce the ZMapp, a chimeric, monoclonal antibody against the Ebola virus.

This is a wikipedia article on ZMapp, that gives you an idea of the process.

Other than this, I am not all that familiar with plant transgenics, other than Round Up resistance genes that were transfected from soil bacteria that developed a resistance to the active chemical in Round Up.

Hopefully other answers can provide you with more details, but these are the two examples that I know off the top of my head.


How many rounds of TCA Cycle would a complete oxidation of a triacyl(15-Carbon fatty acid)-glycerol, give? This was a trickier question on a previous test, and I'm still not sure why, but the answer was "at least four". I answered "more than 22" and got it marked wrong. I assume that each fatty acid chain would break down into 1 propionyl CoA and 6 Acetyl CoA, but I'm not completely sure how many rounds this would give us. Can anyone help me out here? Thanks!

I am not too sure but this is my logic:

There would be in total of 18 molecules of Acetyl-CoA which means 18 TCA cycles. Propionyl-CoA gets converted to Succinyl-CoA which is a TCA intermediate (at about half of the cycle). If you do consider this, the 3 molecules of propionyl-CoA would only give you 3 partial rounds (or lets assume 1.5 rounds) of TCA cycle. Still 19.5; less than 22. Even if you consider the metabolism of glycerol, then 1 molecule of glycerol will give you 1 molecule of pyruvate i.e. 1 TCA cycle. So, the total is still 20.5 rounds i.e. less than 22.

I don't know what the other options are but "more than 22" is certainly not correct.


As WYSIWYG touches on in the comments, usually dashes mean that there are gaps in the alignment as the result of an indel event. Dots are used to show specifically point mutations where the biochemical properties are mostly conserved, but the residue has changed.

From original question, not relevant to question as it stands.

You are right in that this isn't a proper alignment, however I'm not sure it is a bug. What you have appears to be the alignment of a nucleotide sequence that has gone horribly, horribly wrong.

As a first guess without any more details I would say it doesn't look like you have installed clustalw correctly or pointed your bioperl to it. From the documentation here are common problems:

  Make sure the clustalw executable is in your path so that
  which clustalw
  returns a clustalw executable on your system.
  Define an environmental variable CLUSTALDIR which is a
  directory which contains the 'clustalw' application:
  In bash:

  export CLUSTALDIR=/home/username/clustalw1.8

  In csh/tcsh:

  setenv CLUSTALDIR /home/username/clustalw1.8
  Include a definition of an environmental variable CLUSTALDIR in
  every script that will use this Clustalw wrapper module, e.g.:

  BEGIN { $ENV{CLUSTALDIR} = '/home/username/clustalw1.8/' }
  use Bio::Tools::Run::Alignment::Clustalw;

Unless you are doing massive amounts of sequence alignment, the clustalW2 webserver is quicker, more sensitive and way easier to use.


How exactly does heterozygous sickle trait help patients survive malaria Heterozygous sickle cell anaemia trait is known to increase the survival rate of carriers to malaria attacks. How does a recessive gene not expressed in the phenotype allow for such an advantage? Is the red blood cell of a recessive carrier structurally different from that of a non-carrier?

Sickle cell anemia is characterized by the formation of sickle shaped red blood cells rather than the usual biconcave ones. For a double recessive homozygous genotypic person, i.e. an infected person, this causes severe lack of oxygen diffusion into the RBCs because of defective haemoglobin production.
In case of a carrier, he/she carries the gene for the defective version of haemoglobin but does not show the symptoms for the disease.

The malarial agent, Plasmodium uses haemoglobin, or more specifically haem as its main nutrient source The defective sickle haemoglobin induces the expression of heme oxygenase-1 (HO-1) enzyme in hematopoietic cells (those which produce erythrocytes, for example marrow of long bones). Carbon monoxide (CO), a byproduct of heme catabolism by HO-1, prevents further accumulation of circulating free heme after the infection by Plasmodium. This decreases the pathogenicity of the organism and prevents the disease from occuring.  Moreover, sickle haemoglobin inhibits activation and/or expansion of T lymphocytes (specifically CD8+T cells), which recognize the antigens expressed by Plasmodium and hence do not attack it. This is an immunoregulatory effect that does not involve the heme oxygenase enzyme.
This leads to the carrier person having innate resistance to malaria (or at least Experimental Cerebral Malaria )

And no, the RBC itself is not structurally different. Though there might be some
sickle shaped RBCs in the blood, their number is very less. The major difference comes from the haemoglobin in the red blood cell.

Here is the original paper which explains the phenomenon in detail.


Can DNA base pairs go through each other? Consider the simplified version of the motion one DNA base pair held together by a hydrogen bond:

Use u and v to denote the displacements of the bases from their equilibrium position along the direction of the hydrogen bond that connects them,
Define y = u-v to measure the stretching distance between the bases in a pair of bases.
So, y = 0. u=v. No stretching. When y > 0. Stretching. When y < 0. Compression. u

I would like to say, that physically, it is not possible for u to go through v or vice versa. Meaning that the stretching distance measured by y has a lower bound. In other words and my question, does it make physical sense for two base pairs to go through each other?

The base pair you are describing is only stable if each base is part of a macromolecular polymer, a polynucleotide. Specifically the DNA strands need to be oriented in an anti parallel alignment, and there will be a chain, or string, of base pairs (imagine the rungs of a ladder).
Remember, individual hydrogen, or H-bonds, are one of the weakest molecular interactions that we can detect. So the scenario you propose, where one single base forms a Watson-Crick base pair with its complementary base, free in solution, is so unstable as to be undetectable.

Once the base pairs are formed in a DNA double helix (think of a flexible ladder where one end is fixed and the other end has been twisted through several clockwise revolutions) then there are many other energetic contributions that stabilize the base pairs. For example, the electrostatic repulsion of the anionic phosphates in the sugar-phosphate backbone drives the two strands apart.  The hydrophobic stacking interactions of the pi bonds of adjacent bases also makes a major contribution to the stability of the helix, and permits the H-bonds to be more stable in this context.

Finally, the fact that base pairs are only stable in polynucleotides means that if you melt a single base pair, the sugar phosphate backbones will topologically prevent any other melted base pair from "passing through" the first one.


Is it safe to publish a person's genome? I recently went through the process of having my genome analyzed by 23andme, and received my raw data.

Its very interesting to me, and I want to share it with the world.

Is it safe to publish the raw genome to a public site, or are there reasons I should keep this information private?

What could someone do with the raw genome of another person? Outside of privacy concerns, is there any potential for malicious concerns from someone with this information?

It is as safe as to publish your fingerprints. Right now, there is little that anyone can do with your genetic information but in the future, this will change.

One of the feared consequences it concerns what companies may do with that information. Can it be used against you? In some cases, it may.

For example, if you have a predisposition for a genetic disease, then an insurance company may find a way to refuse to insure you. As far I know, right now this is illegal, but you never know.


Interbreedability between current humans and his ancestors I want to know the first point of time in the past when genomes have diverged so far from modern human genomes so that they both (human and ancestors) are not interbreeadable anymore and can be seen as separate species.

Short answer
Considering only post-zygotic isolation and based on below discussion, I would tend to think that 20th century human could interbreed with our ancestors living a 1 to 2 millions years ago. I would give a range between 100k years and 8 MYA for safety.
Long answer
Concept of species
The post How could humans have interbred with Neanderthals if we're a different species? makes a good introduction to the difficulties behind the concept of species.
Pre-zygotic isolation
Anatomically speaking, it is probably possible to get a spermatozoid cell from a 20th century man start fusing with a Homo abilis ovule (and vice-versa). The potential pre-zygotic isolation will rather be caused by aesthetic appearance.
To the risk of sounding posh, I would say that Homo abilis hairy face does not exactly fall within my standards! I suspect it will be the same for many of us, humans of the 20th century. It is hard to really know how much time one needs to go back to consider that we don't disgust each other enough to refuse mating together. There are a few reasons why this is hard

Reconstruction (esp. facial reconstruction) is often too inaccurate to really allow to tell how ugly their faces were.
It is going to be super hard to tell what they would just about our faces today! I bet they'd laugh at our ridiculously small jaws!
It is hard to fully separate the environment from the person. In middle-age (in Europe at least) people would bath a few times in a life-time. Again I would consider this not in my standards!

But let's focus on post-zygotic isolation.
Post-zygotic isolation
Humanzee

The humanzee (Homo sapiens sapiens × Pan) (also known as the chuman or manpanzee) is a hypothetical chimpanzee/human hybrid. An unsuccessful attempt to breed such a hybrid was made by Ilya Ivanovich Ivanov in the 1920s. There have been occasional reports of human-chimpanzee hybridization, notably regarding a performing chimp named Oliver during the 1970s, but none of them have been confirmed. Similarly, the possibility of a chimpanzee–gorilla hybrid, known as a koolakamba, also remains unsubstantiated.

There is no evidence of humanzee but it is important to realize that the idea of such hybrid is not fully unthinkable. Human and chimpanzee share a common ancestor about 6 millions years. So, if a humanzee is consider eventually possible, I would quite definitely consider that a H. abilis (~1 MYA) or H.erectus (~2 MYA) and 20th century human could well interbreed if we were to live at the same time.
Sumatrans and bornean orangutans can hybridize (Malinson, 1984) despite that their lineages have split about 1.3 MYA!
So putting all of that together and follwing some vague intuition, I would personally tend to think that 20th century human could interbreed with our ancestors living a 1 to 2 millions years ago. I would give a range between 100k years and 8 MYA (MRCA with gorillas). But really, it is a rather vague intuition.
See also CrashCourse > How to Make A Humanzee


Do people with gout live longer? Antioxidants reduce damage to tissue (by scavenging the free radicals) and thus may reduce ageing.It is known that Uric acid is a very good antioxidant.

People with gout have excess accumulation of uric acid.

Considering the above information the authors of the book  "Why we get sick?" put up an interesting question : Do people with gout live longer ?

I would like to know if there are any studies done to answer the question.

In men, gout is associated with a higher risk of death from all causes. This would imply that their life expectancy is shorter. From a review by Kim et al. (1):

  Among men who did not have pre-existing coronary heart disease, the
  increased mortality risk is due primarily to an elevated risk of
  cardiovascular death, particularly from coronary heart disease. Also,
  an extension study of a large clinical trial among men with
  above-average risk for coronary heart disease found that a diagnosis
  of gout accompanied by an elevated uric acid level is associated with
  increased long-term (approximately 17 years) risk of all-cause
  mortality that arises largely from an increased risk of cardiovascular
  disease (CVD) mortality.

This does not rule out that some subset of people with gout (patients with less severe symptoms?) might benefit in some way from an antioxidant effect, but in general gout is obviously not good for life expectancy.


RNAi in nematode resistant plants Background : Certain plants have been genetically engineered to have sense-antisense gene of a parasitic nematode. The dsRNA produced by the plant then inactivates the mRNA produced in the nematode, who, then isn't able to synthesize the corresponding protein and dies as a result.

Question : How is the dsRNA from the plant transfered to the nematode's cell ? By transformation ?

The question is little bit unclear: is in vitro or in vivo introduction in question?

In vivo:

  As the nematode feeds on the plant during its parasitic phase, it
  consequently assures the introduction of dsRNA and/or siRNA molecules
  into the nematode’s digestive system.

in vitro introduction etc  ->

The status of RNAi-based transgenic research in plant nematology


Perplexing by the way of estimating the shared or different genes between humans and chimps We share 98.5% genes with chimps (it means we have 98.5% same DNA sequeces ),so there is about one percent difference .It means we can approximately differ from them by one base pair every hundred base pairs on average.

The following is my question.

A human receive 3 billion base pairs from each of parents ,and has six billions in total .Do the math by using one hundred to divide six billions and then it equals sixty millions.

Due to that, The person have ,on average ,sixty-million-nucleotide differences with a chimp.

However,the professor of the online courses I attended said it's thirty-million-letter differences.

Dose that mean it's counted on haploid?Why?

Also ,I'm not sure that about one percent difference is calculated on one base pair or one nucleotide every thousand base pairs or nucleotides .Because he mentioned the both.

This is the course ,my questions occur at 1:58

In another course , similar questions occur at 3:11

Even though I am not sure I understand your question completely, I want to try to explain to you the genetic difference between humans and chimpanzees. I will work through your questions:

We share 98.5% genes with chimps ,so there is about one percent difference .It means we can approximately differ from them by one base pair every hundred base pairs on average.

It is correct that humans and chimpanzees differ approximately every 100 nucleotides in their DNA sequence. This is does not mean that 98.5% of the genes are shared. It means that humans have about 98.5% (more precisely about 98.8%, The Chimpanzee Sequencing and Analysis Consortium, 2005) sequence identity with chimpanzees, disregarding indels. The main part of this difference (about 85% of the 30 - 35 Mio. different nucleotides) comes from fixed differences: a fixed difference is a position in the haploid genome in which every human has, say, a G and every chimpanzee has a T. Accordingly, the site is different between the two species for every individual of the respective species. The smaller part (about 15%) comes from sites that are either variable (SNP) in humans or variable in chimpanzees, or in both (there is even a small number of very old variants, i.e. shared alleles between humans and chimpanzees, e.g. see Azevedo et al., 2015). Note that the estimates get better the more individuals of the respective species are sequenced and compared.

A human receive 3 billion base pairs from each of parents ,and has six billions in total .Do the math by using one hundred to divide six billions and then it equals sixty millions.
Due to that, The person have ,on average ,sixty-million-nucleotide differences with a chimp.
However,the professor of the online courses I attended said it's thirty-million-letter differences.
Dose that mean it's counted on haploid?Why?

Yes, it is counted on the haploid genome. I would not make any sense to count it on the diploid genome. When looking at my last paragraph you might see why: Remember, we are looking at (i) fixed differences (both copies of a diploid human genome differ from both copies of a diploid chimpanzee genome) or (ii) at variable sites. Assume you find one site in one haploid genome that fulfills either (i) or (ii). If you then look at the same site in the other copy of the genome you already know that the position is either (i) or (ii). This means that it has already been counted as a difference. If you counted it again, in the worst case, over the complete genome, you would count everything twice. In general, you would strongly overestimate the absolute difference.

Also ,I'm not sure that about one percent difference is calculated on one base pair or one nucleotide every thousand base pairs or nucleotides .Because he mentioned the both.

I do not understand this. I had a brief look at the video and heard him talking of one nucleotide per thousand. He compares the sequence difference between human-chimpanzee (98.8% overlap, approx. 1 per 100, about 1.2% fixed differences and SNPS) and human-human (99.9% overlap, approx. 1 per 1000, 0.1% SNP), pairs. Note that in the last case we cannot look at fixed differences as there are no fixed differences between human populations. The 0.1% difference are the percentage of SNP in the human genome.


What evolutionary advantage do viruses have in host specificity? Warning: I have almost no knowledge of biology past the high school level.

Viruses generally have three components: the DNA, the virus protein coat, and an outer membrane "decorated" with these surface marker glycoproteins. I am thinking that a virus would want to infect as many hosts as possible, so that it would reproduce as much as possible, why would a virus just infect one group of organisms.

What evolutionary advantage do viruses have in host specificity?

It is true for any living creature, that it would be great for it if it could thrive in all environments. Any creature would do better if it had a greater ecological niche while remaining as competitive in each of these niches. However, competition, predation and other biotic and abiotic factors lead species to specialize in specific niches. Of course, some species are more generalist and some are more specialist but I won't go into these details.

When it comes to parasites, such as viruses, the story is the same. A host is an environment. Being less specific would be great but the immune system is no easy detail to get around. Viruses are often quite specific to a given species, just because it evolved to be efficient for a given host but tend not to be that efficient in other hosts.

Note that parasites are not only species specific but also often tissue specific and specific to the specifics genetics of the host (e.g. malaria).

Somewhat related posts:

Why do parasites sometimes kill their hosts?
Why aren't all infections immune-system resistant?

Thank you @DeNovo for helpful comment


Do intestinal flora have the same DNA as their host? Please bear with me, this is not my professional field and I might be mixing things up. In an explanation why seeds won't start growing in one's intestines, the explanation given was that foreign bodies are detected by the DNA they carry and get attacked and digested, separating all strands of amino acids so they can be reused by the host and no DNA mixture can occur.

I also heard that the immune system uses the same technique to detect intruders (and subsequently attack donor-organs).

I was wondering, when a baby gets weaned (starts eating regular food), where do these fauna come from? Does the baby produce them, or are they provided in the food and survive the defense system?

Could you suggest a good source for beginners. - Louis Somers

The interactions between the human body and its microbiome are quite complex. I am going to provide you with an answer that will be based on your comment that you would like an answer from a beginners perspective.

For simplicity sake I will keep the answer to humans as the host organism, though pretty much any multicellular organism can act as a host for microscopic organisms.

Note: A number or the references I use come from Janeway's Immunobiology. The links provided are to the 2001 edition that is on the NCBI bookshelf. The issue, however, is that over the past decade we have learned a great deal more about the immune system since then, and some of the things I refer to were not represented in that edition of the text.

  Do intestinal fauna have the same DNA as their host?

The short answer to this question is no. Also, we generally identify microbes of this nature as flora instead of fauna, so you would say intestinal flora.

The human microbiome (microbiota), as it is often referred to, is made up of hundreds of trillions of microorganisms that live in the niche of our digestive tract, airways, urogenital tract, and skin. In fact, the estimate is that there are 10 times as many microbial cells that live on the human body than there are human cells that make up the body itself (1). The difference is that human cells are immense when compared to most of the microbial cells that colonize us (2).

The vast majority of the microorganisms that populate us are single-celled organisms, such as bacteria or fungi (yeasts). Each of these cells is its own entity, in other words is an independent living organism, and they have their own genome (the complete genetic material of an organism) that encodes for their own proteins.

There is a good reference tool, though maybe a little advanced from The University of Utah, The Human Microbiome. This interactive presentation gives a layman's overview. The American Museum of Natural History has also curated an exhibit called The Secret World Inside You.

To add a point for clarification, while the genetic codes of these microbes are different in different species and are different from that of the human host, the molecules that hold the information, namely DNA, are all made of the same nucleic acid building blocks (5). To use an analogy, it is like using the same letters but writing in two different languages. We may use mostly the same characters, but the way we arrange those letters to form words in Spanish or words in English create different meaning.

When these single-celled organisms reproduce, they copy their own DNA and they divide into two new cells, each receiving one copy of that DNA (6).

Since yeast and other fungi are evolutionarily closer ancestors to humans than are bacteria, some of their genes, the sections of DNA that are functional and encode for proteins and RNAs, have a very similar sequence to our own (referred to as having homology) and often perform similar or the same function (7). When this is the case, we say that the genes are evolutionarily conserved, but for the most part evolutionarily conserved genes will vary in sequence from organism to organism, and the variation will usually increase the farther back you go in order to find a common ancestor between the organisms.

The human body is made up of about 37.2 trillion cells, on average (8). Almost all of these cells, with the exception of Red Blood Cells, have a copy of the hosts genome (9). All of these cells arose from a single egg produced by the mother and fertilized by the father's sperm (10). The egg and the sperm contained half the genome necessary for the embryo to develop. The DNA from the mother and the DNA from the father come together when the nuclei fuse. So we have our own genome that came from our mother and father, and the microbes have their own genome which they inherited from the ancestral cells that gave rise to them.

That is a slightly simplified answer as there can be different ways that the DNA can be passed between the organisms, but for the most part, we have our own DNA and, even though they live on us and in us, the microbes have their own DNA.

  Your first paragraph.

I cannot tell you necessarily why seed that we swallow and digest do not germinate inside of us. It is likely that the seeds are not receiving the proper signals from the environment of our digestive track to initiate the genetic program to begin germination and development into a plant.

  I also heard that the immune system uses the same technique to detect intruders (and subsequently attack donor-organs).

The vertebrate immune system is a diverse, highly-tuned system of surveillance that monitors for pathogens or foreign bodies that are introduced into the body that may be dangerous to the survival of the organism (11).

For humans, the first set of defense are barrier defenses (12). The surface of our skin consists of several layers of dead, keratinized cells that form an impermeable barrier. As long as this layer is not breached, it does an excellent job of keeping yeast and bacteria outside, away from tissue that they could damage.

On the interior surfaces, our airways, gastrointestinal tract, and genitourinary tracts contain specialized cells that produce large amounts of mucus that will coat the surfaces of these tissue. Mucus serves multiple roles. First it keeps the tissue moist, so that it does not dehydrate. Next it keeps the microbes at a distance from our cells, so that they do not come in direct contact with our epithelial cells (The cells that make up the linings of our digestive tract, genitourinary tract, and airways). Third, it can trap microbes in it. The epithelium is able to "sweep" the mucus along and as a result it is able to clear bacteria out of the body (13).

Included in the barrier defenses are actually the microbial organisms themselves. The interaction between the host and an organism which is neither detrimental or actively beneficial is known as commensalism (13). Basically, all of these trillions of microorganisms that life on us do not hurt us. In return, they get an environment in which they can live. As a result of this, commensal organisms will grow on these surfaces, will take up all of the space, and will use up the nutrients that could be used by pathogenic organisms (organisms that are actively able to cause an infection) to establish an infection.

The next level of defense comes from the cells of the innate immune system (14). In innate immunity, specialized cells monitor the area they are in for Pathogen-Associated Molecular Patterns (PAMPs). PAMPs can be sugars that make up the cell walls of the microbe or proteins that get expressed on the surface of the organism, such as Flagellin, a protein only found in the flagella of certain pathogen. The innate immune cells have pattern recognition receptors (PRR) that have a general specificity for recognizing and responding to the PAMPs. Our cells even have PRRs for DNA and Double Stranded RNA's, however those are usually found in vesicles on the inside of the cell. These interactions are very general, however once PRRs bind to the PAMP, they are able to signal into the cytoplasm, which can lead to the production of proteins, among other possible responses.

Here you can think of PRRs like a motion detector in a security system; the dog, or your two year old, or an intruder are going to set off the alarm just the same. It is not specific. The motion sensor "knows" that something that it is supposed to recognize, i.e. a moving object larger than a mouse passed by and it triggered the response, but it cannot tell you which moving object triggered it, only that it was triggered.

The innate immune cells are also able to respond by "eating" the pathogen in a process called phagocytosis. Here, they break up the bacteria, yeast, or the remnants of other dead host cells or large pathogens, things like worms, and put the broken up pieces on protein molecules on their surface.

When innate immune cells do this, they are presenting molecules to specialized immune cells (adaptive immune cells (14)), B-Cells and T-Cells, that are highly specific as to what they will react to. These cells can also cause a lot of damage to the host, so they are tightly regulated. Think of the interactions as keys and locks. A protein from a bacteria should turn a few of these cells on, but a protein from the host should not fit the lock.

All of these immune cells also respond to diffused chemical signals called cytokines. These molecules are secreted by some cells and are received by receptors on the host cells. Sometimes the secretion is by another immune cell, sometimes it is from a non-immune system host cell, and sometimes these molecules can be secreted by the bacteria, fungi, or worms themselves.

Depending on the chemical signals that are secreted, and how the cells are interacting at the time of the message, and which cells are receiving the message, will determine the response to the message. It is contextual. Think of the phrase "You're killing me." If someone says it, while laughing, to a good friend who is telling jokes, it means one thing. If it is screamed as someone is being choked by an attacker, it means something very different.

To summarize, the immune cells are surveilling the environment and trying to pick up what is friend and what is foe and they try to respond accordingly.

Over time and coevolution, our microbiomes have developed ways of communicating with our immune system to let it know that these microbes do not mean any harm. They are able to "train" the immune cells using chemical signaling to temper the immune systems response to them (15), and this is how they are able to coexist within our body and with an immune system that is constantly on seek an destroy missions. Also because of the mucus, our microbiome usually isn't in direct contact with our cells, so it is a different kind of interaction than if an infecting pathogen were to breech the barriers and gain access to sterile areas where no bacteria or fungi should be found, and as a result, the immune system reacts differently.

As for organ and tissue rejections (16), the issue here is that each of our cells, except for Red Blood Cells, present molecules on their surface that identify it as being a cell that was made by the body itself. You can almost think of it as a sport's teams jersey. The immune cells can survey the proteins displayed on the surface of our cells and tell that they are ours instead of from a pathogen. The problem is that each person makes a different array of these proteins, so if I were to give you a kidney, the proteins that the cells from my kidney make and put on their surface for immune cells to look at will be different from yours. In this case, because the keys do not fit the locks, the immune system reacts to the donated organ as an intruder and begins to attack it. Immune cells are extremely lethal and will kill the donated organ if they are not suppressed. That is why transplant recipients need to have their immune systems suppressed in order to survive with the donated organ. You might ask "well what if we just took all these proteins off of the surface so that they don't get recognized?" Well, the problem is that we have another class of immune cells known as Natural Killer Cells that patrol the body looking for cells that are not presenting these proteins, so the immune system is pretty adept and finding and killing things that it does not recognize specifically as self.

  I was wondering, when a baby gets weaned (starts eating regular food), where do these fauna come from? Does the baby produce them, or are they provided in the food and survive the defense system?

To be honest, the majority of the microbiome is laid down during vaginal birth and breast feeding. Passing through the birth canal, microbes from the mother's vagina and feces are ingested by the newborn and this is their first real dose of microbiome, though some research is suggesting that the microbiome begins to form in the fetus before birth and is transferred through the placenta from the mother to the fetus.

Assuming we do not kill these bacteria with antibiotics, have other pathogenic bacteria take over the territory (yes, bacteria and fungi, like gangs, have turf wars; that is why we often find our antibiotics as compounds secreted by these organisms), or have a disease that wipes out the microbiome, and provide it with a health diet, then the microbiome pretty much is maintained by the microbial cells reproducing by cell division.

Also we will pick up these bacteria from the environment. We are constantly shedding enormous amounts of these cells into our environment. Babies touch things and put their hands in their mouths. This transfers good microbes as well as bad ones, and it is really just a natural part of the process. That is why the overuse of antibiotics and antibacterial soaps can cause unintended consequences. We are killing the good as well as the bad.

This reference, Your Changing Microbiome, again from The University of Utah is a good resource.

So to summarize, babies get the microbiome at birth through vaginal flora and maternal feces. They are also getting daily doses from the microbes that colonize the mother's skin when she nurses the child. Then these bacteria are also in the environment, so babies touch things, then they put their hands (or feet, the little contortionists) in their mouths and they get doses this way. Raw fruits and vegetables will also have microbes on them that will be taken in. As for the microbes, they have cell walls that allow them to live in environments that would be hostile if they did not have the cell walls. They also communicate with our immune system and "train" it not to kill them, and as long as nothing that we do, such as take antibiotics or get a disease, the microbiome will pretty much maintain itself through replication.