Why is Homo sapiens not categorized as an invasive species? According to Invasive Species Advisory Committee (ISAC), the definition of the invasive species is “a species that is non-native to the ecosystem under consideration and whose introduction causes or is likely to cause economic or environmental harm or harm to human health.”

But considering the following facts, why is this species not categorized as an invasive species?
Homo sapiens:

is non-native to the most of the ecosystem which it is inhabiting, since it originated from a certain area of Africa and spread quite recently.
has often caused environmental problems by decreasing the local species after its introduction, as it is known that the number of species in the planet is drastically decreasing ever since the advent of Homo sapiens.
is likely to cause the same problem after introduced to new environment where homo sapiens hasn't inhabited yet.

http://www.invasivespeciesinfo.gov/docs/council/isacdef.pdf

Ignoring for the moment the question of politics, let's consider the various definitions of the term "invasive species" that are in use. Colautti and MacIsaac write in their discussion of invasive species terminology (1):

  The greatest confusion [among the discussed ecological terms]
  surrounds the common term ‘invasive’ and its various derivatives
  (Richardson et al., 2000a). Explicit or implicit definitions for
  ‘invasive’ include: (1) a synonym for ‘nonindigenous’ (e.g. Goodwin et
  al., 1999; Radford &Cousens, 2000); (2) an adjective for native or
  nonindigenous species (NIS) that have colonized natural areas (e.g.
  Burke & Grime, 1996); (3) discrimination of NIS established in
  cultivated habitats (as ‘noninvasive’) from those established in
  natural habitats (e.g. Reichard & Hamilton, 1997); (4) NIS that are
  widespread (e.g. van Clef & Stiles, 2001); or (5) widespread NIS that
  have adverse effects on the invaded habitat (e.g. Davis & Thompson,
  2000; Mack et al., 2000).

Note that except for #2, all the definitions require that the species is a nonindigenous (non-native) species in the area under consideration. Therefore, while humans may be considered to have been an invasive species for much of our species history, under most definitions of the term we no longer qualify because except in a few places (mainly the arctic, antarctic and marine environments, where human presence is minimal) we are now a native species.

See also http://www.smithsonianmag.com/science-nature/are-humans-an-invasive-species-42999965/?no-ist


What are the differences between a liposome and simple cell membrane I'm learning about chemical evolution and the transition from RNA to protocells to cells.  I understand that the protocells have a phospholipid structure called a liposome.

I recently saw a video showing CG animations of the workings of a cell and it seemed that the cell wall was much more complex than what it seems a liposome is.

I'm looking for information about the differences between a liposome and a basic cell wall (not sure of the difference for different types of cells -
 but I guess for prokaryote since that would have been first.)

By looking on wikipedia I found:

About liposome

  A liposome is a spherical vesicle having at least one lipid bilayer. The liposome can be used as a vehicle for administration of nutrients and pharmaceutical drugs. Liposomes can be prepared by disrupting biological membranes (such as by sonication).

  Liposomes are most often composed of phospholipids, especially
  phosphatidylcholine, but may also include other lipids, such as egg
  phosphatidylethanolamine, so long as they are compatible with lipid
  bilayer structure. A liposome design may employ surface ligands for
  attaching to unhealthy tissue.

About cell membrane

  The cell membrane (also known as the plasma membrane or cytoplasmic
  membrane) is a biological membrane that separates the interior of all
  cells from the outside environment.The cell membrane is selectively
  permeable to ions and organic molecules and controls the movement of
  substances in and out of cells. The basic function of the cell
  membrane is to protect the cell from its surroundings.

  It consists of the lipid bilayer with embedded proteins. Cell
  membranes are involved in a variety of cellular processes such as cell
  adhesion, ion conductivity and cell signalling and serve as the
  attachment surface for several extracellular structures, including the
  cell wall, glycocalyx, and intracellular cytoskeleton. Cell membranes
  can be artificially reassembled.

So the major difference seems to be the presence of "embedded proteins" inside the cell membrane.


Is there a Lyme disease vaccine? Each Spring, our local health unit begins its campaign of Lyme disease and tick-bite awareness. I was wondering if there has ever been a vaccine available, and if so, what antigen does it target?

According to Wikipedia in 1998 a vaccine was approved by the FDA. It was directed against the outer surface protein A (OspA) of B. burgdorferi, but was taken from the market in 2002 after a large number of recipients reported the development of autoimmune diseases. An investigation of the FDA and the CDC found no connection to these claims, but afterwards the sales went to the bottom until the vaccine was withdrawn from the market. An interesting article on this story (with a number of references) can be found here.

There are two new approaches to develop vaccine candidates. One is directed against the outer surface protein C ("An octavalent lyme disease vaccine induces antibodies that recognize all incorporated OspC type-specific sequences.", another against glycolipoproteins on the bacterias surface ("Synthesis of an experimental glycolipoprotein vaccine against Lyme disease."). As far as I see, none of these vaccine candidates is already licensed.

Another approach is to vaccinate the animal reservoir hosts, as this has been done successfully for rabies. Here either vaccinated baits ("Reservoir Targeted Vaccine for Lyme Borreliosis Induces a Yearlong, Neutralizing Antibody Response to OspA in White-Footed Mice") or recombinant vaccines ("An ecological approach to preventing human infection: Vaccinating wild mouse reservoirs intervenes in the Lyme disease cycle") were used with good results. Neither of these methods is already been used, as far as I see.


The antibiotic 'kanamycin' in the growing of culture E. coli I'm a first year student and I'm not sure if I understand correctly the role played by the antibiotic 'kanamycin' in the growing of culture E. coli (Rosetta).

Can anybody explain me why we use 'kanamycin' antibiotic and kanamycin resistance gene during that process?

According to this data sheet, the genotype of the strain RosettaTM(DE3)pLysS is F- ompT hsdS (r- m-) gal dcm (DE3) pLysSRARE (CamR).

This strain carries certain tRNA genes on the same plasmid as the LysS gene, and these tRNAs boost expression from genes containing rare (in E. coli) codons. The plasmid encodes chloramphenicol resistance (CamR).

If you have a protocol that suggests growing your strain under kanamycin selection then presumably you have an additional plasmid present which carries your gene of interest. Then, as the accepted answer says, you are selecting positively for the correct strain.

I don't know how stable the pLysSRARE plasmid is, but I would have expected that you should also maintain selection for chloramphenicol resistance.


What, if anything, would prevent flying fishes evolving to be capable of extended flight? This extraordinary video documents a flying fish gliding above the surface of the sea for nearly two minutes. Occasionally it uses its tail for added impetus.

It is possible to imagine a fish gliding like this for longer and longer. However it would still be gliding. Is there any physiological reason that these animals couldn't evolve to flap their 'wings' and even learn to soar?

Another consideration is why this should happen. As I understand it, the behaviour is an adaption for escape from predators.  They do not fly in order to catch prey. What prey might they hunt in the air in the ocean?

Questions

Is there any physiological/anatomical dead-end that would prevent flapping/soaring from evolving?
Is there any adaptive reason that flapping/soaring should evolve?

As AMR said, fish are tied to the water by their respiratory systems. Bats and gliding mammals and herptiles don't have that limitation. Fish have an advantage over mammals and herptiles in that they're generally streamlined. On the other hand, they're adapted to "flying" in a denser environment and might therefore be a little heavy for flight. Also, I wonder if the need to keep their skin moist might present a problem.

Nevertheless, flying fish are halfway there. Just imagine if lungfish - which can survive out of water for long periods - were adapted for gliding.

P.S. I posted this as a comment by mistake, then deleted the comment.


Can boiling water without high temperatures kill bacteria? If you use a vacuum chamber to reduce the pressure of water such that it can boil at around room temperature will it still have the same effect on reducing harmful bacteria as boiling at the usual 100C?

No, you do need to reach high temperates to kill the bacteria.

It's not about the evaporation, or the pressure that kills bacteria, rather it is the temperature that does. Higher temperatures have drastic effects on the molecular structures that occur within the bacteria, such as the denaturing of various proteins present inside the cell. As a result, if you wish to boil water to kill it, it must be done at an elevated temperature.

Wikipedia mentions that the optimum temperature for killing microbes is around 70°C,

  Boiling water is used as a method of making it potable by killing microbes that may be present. The sensitivity of different micro-organisms to heat varies, but if water is held at 70°C (158°F) for ten minutes, many organisms are killed, but some are more resistant to heat and require one minute at the boiling point of water.


What is name of the red eyed rabbit or hare, found in Himalayan region? Is it Rabbit or Hare?

The eyes are red in colour.

These animals are habitat of Himalaya.

The pictures are taken in Dowhill Park, Kurseong, West Bengal, India.

Perhaps a bit underwhelmingly, those are Himalayan Rabbits.
https://en.wikipedia.org/wiki/Himalayan_rabbit

The pure white fur and red eyes are usually a sign of albinos, but in this case it's actually a trait of the entire species.

  [They] can only produce eumelanin under a certain temperature and they cannot produce pheomelanin at all.


How should I feed and keep an ant queen? I have captured wandering ant queen. I guess she was just fertilised and was looking for a place to start a hive.
I'd like to create my own ant hive in artificial environment.

I unfortunately only have a small clean chemical bottle (1.5 CM in radius) to keep her in. I was wondering how much space would she need to feel safe.

I'm also not sure what should I feed her. Every morning, I have dropped few sugar crystals in the bottle. She shows much more individuality than an ant, because she has immediately started to collect them. It seems that she ate almost everything. I have also dropped few tiny drops of water in the bottle. Although it's hot and she ate the dry sugar she doesn't seem to drink it at all.

So what does she need? (well, except of natural forest which I don't have in my room)

First you need to identify your ant, for Czech Ants: http://www.antweb.org/taxonomicPage.do?rank=species&project=czechants&images=true

How should I feed and keep an ant queen?

Home for Pet Ant, Ant Farm:

There are lots of things you can use, for example, a clean transparent glass or plastic jar, or a fish tank of a size which you will decide is best for the ants you're keeping in it. As long as the container provides enough space, and the addition of any air holes small enough to prevent the ants escaping (much easier said than done); and also so you can observe your ants going about their daily activities, then it should be fine! Worker ants like to forage, so your set up needs to allow for the ants to do a spot of hunting for their food.

It is possible to make your own type of "Ant Farm" by using lengths of wood or plastic which have 2 grooves cut into them, like the frame used in double glazing. As long as you can place the frame onto a sturdy base to prevent it from falling over; or you can use plaster and other materials such as aerated concrete blocks, better known as Ytong nests. Two panes of clear glass or plastic can be placed into the grooves and sealed. Use the silicone sealant that is used around baths or sold where you buy glass fish tanks, but do remember to let it set and dry out well, as this will allow any chemicals to disperse harmlessly into the air before you add any ants. Also make sure that you can safely access your ant home, so you can put food in etc. You can also check out this youtube video or Wikihow.

Always try to cover your ants when not observing them to exclude light, as for most of their lives ants live in underground nests or places well away from daylight. This does not mean that they won't tolerate light; but they prefer to be in total darkness if possible, and queens rarely come out from their nests in the wild.

Feed the ANT:

If you are using a  gel-filled ant farms, it  contains all the water and nutrients your ants need for survival. Make sure to keep your kit sealed so the gel does not dry out.

In sand-filled ant farms, you need to add a few drops of water and small bits of food every few days. Ants also love a special treat of water with sugar dissolved in it, but this can’t take the place of fresh water for drinking. You can provide them with a bit of honey at times, and they will probably drink some of that. A small section of meal-worm can help provide her with a protein boost. Again, feeding them until the first workers arrive is not necessary as they do not forage during this period naturally.

Moreover, Interesting Links:

http://askabiologist.asu.edu/collecting-queen-ants

http://ant-farm-stores-review.toptenreviews.com/what-you-need-to-know-about-ant-farms.html

www.tarheelants.com/

Also, try "Ants can be pets" group on Facebook.


Why is mRNA needed in the Protein translation? The original question was to predict the basic requirements for information storage. Then the discussion moved to why is it necessary to include mRNA in the protein translation process. Why can't there be a similar chemical molecule like tRNA which can directly read from DNA and exclude the mRNA intermediate. Also is the current translation process optimal in the sense that can there be a system which does not need mRNA or a similar intermediate altogether. Or is the presence of an intermediate a necessary requirement.

One reason is that an intermediate like mRNA allows for higher amounts of protein expression. You can have multiple mRNA molecules that are translated simultaneously. If you read directly from DNA you can have at most two translations in parallel.

I'm not sure about this, but I would imagine that having to unwind the DNA double strand every time for translation could be a drawback to directly reading from DNA as well. The mRNA is also subject to various forms of regulation, which might be an advantage as well for the added intermediary.


Summarising ChIP-seq and controls needed As part of my study I have to present on a method of discerning binding sites of proteins to DNA, for which I have looked at ChIP-seq. This is a brief overview of what I have so far, and was wondering if there are any particularly glaring omissions that I have made so far.

  Cells treated with formaldehyde to cross-link proteins such as transcription >factors (i.e. HIF) covalently to DNA and incubated for 2-30 minutes. After >incubation glycine is added to terminate the cross linking and dissipate the >formaldehyde.

  Cells are lysed, and sonication (application of sound waves to agitate a >sample) is used to fragment the DNA into sizes between 200-1000 base pairs.

  HIF–DNA complexes are selectively immunoprecipitated by using antibodies >specific to the HIF protein of interest, complexed with a matrix of either >agrose or superparamagnetic beads.

  HIF-DNA-antibody-matrix complexes are isolated through the use of either a >centrifuge or magnetic field (depending on the matrix employed). Several >washings take place to further purify the sample.

  Cross-linking of the protein to the DNA is reversed by way of heating, >separating the DNA and protein-antibody-matrix complex. Proteinase K is used to >digest proteins, leaving only the DNA.

  Oligonucleotide adaptors (primers) are then added to the small stretches of DNA >that were bound to the HIF to enable rapid simultaneous sequencing.

  DNA sequences are then mapped to the reference genome to determine the binding loci.

I would also like to discuss controls that are used in these procedures. So far I have found limited mention of negative controls, positive and negative control loci, non-template control and positive control antibody, but am having trouble discerning what any of this actually is referring to.

I would seriously appreciate any help available on this topic!

Good experiment! ChIP-seq is good for a whole genome look at transcription factor binding. KEY POINT:  The data generated are only as good as the antibody. Considerable effort needs to taken to prove antibody is specific for only the protein of interest.  It is for this reason, that some TFs still haven't been characterized by ChIP-seq.

As far as controls for your experiment:

The breaking of DNA from sonication isn't uniform from experiment to experiment, and sonication will preferentially break at some regions of open chromatin more often.
Controls for this:

Isolate DNA from cells that have been x-linked and fragmented under same conditions but don't use antibodies to IP.  This is "Input" DNA.
You can conduct a "mock" ChIP using a control AB that reacts with some non important non-nuclear protein, such as IgG.

Then sequence these samples to same depth as the Immunoprecipitated DNA.

Here is a good paper that is a little dated, but still relevent: Go to Control Sample Section

Here is a link to the guidelines for ChIP-seq for ENCODE PDF

Last but not least, if you are working on a much smaller scale, don't forget about things like DNA footprinting and EMSA to identify the ACTUAL binding site.


Are there genes in humans from the common ancestor of all organisms? How long ago can human genes be traced? Are there any genes that go back unchanged to the beginning of life on Earth? And if so, how many?

I very much agree with bitwise's answer. I just want to point out that even in terms of nucleotide sequence there are some extremely conserved genes.

The most highly conserved are ribosomal RNA genes. The image below shows the conservation of 16S rRNAs from archaea, bacteria, and eukaryotes (eukaryotes do not have 16S in their cellular genome but the gene is present in the DNA of mitochondria and chloroplasts). Residues in red are conserved across all domains of life (image source):

A very nice study from 2008 [1] identified tRNA genes as the next most conserved and ABC transporter nucleotide binding domains (NBDs) after that. The alignment below (taken from the paper) shows the conservation of NBDs from various species. Note that they include eukaryotes, archaea and bacteria:
[2]

If you look at orthologous genes in general, without specifying a specific level of sequence identity, then you can find various genes (notably those coding for the enzymes of the glycolysis pathway as mentioned in the comments) that are conserved across most, if not all, cellular life.

So, to answer your question probably yes. At least, there are genes in humans today that can be found in all or almost all other life forms. Whether there were present in LUCA we cannot know for sure, it does seem likely however given how widespread they are today.

Reference

Isenbarger T.A. et al, The most conserved genome segments for life detection on Earth and other planets, Orig Life Evol Biosph. 2008 Dec;38(6):517-33.


Can a miRNA be upregulated and downregulated in the same disease I am computational guy and hence apologies if the question is silly.

Can the same miRNA show upregulation and downregulation in the same disease? (Not in the same experiment, though). For e.g. can there be a instance of miRNA hsa-miR-21 being upregulated in a disease glioblastoma in 1 study and in another study there is an occurrence of hsa-miR-21 being down-regulated in glioblastoma. Is this possible?

As an example, I found:
hsa-miR-345 -> overexpression in pancreatic cancer (PMID: 16966691) and,
hsa-miR-345 -> downregulation in pancreatic cancer (PMID: 17149698)

Any pointers would be appreciated.

Since diseases are frequently complex, it is not surprising to find specific genes (both miRNA coding genes or protein coding genes) being deferentially regulated when different studies of similar-sounding-diseases are compared. In other words, things like glioblastoma or Pacreatic Cancer should be treated as labels describing grossly similar disease states (i.e. excessive proliferation of glia and pancreatic cells, respectively), rather than as labels of specific cellular state associated with a particular gene expression pattern.


Multiple transcripts matching same gene in de novo assembled RNA-seq data, but FPKM values vary? I have a data set of de novo assembled RNA-seq datasets across different sample types.

When BLASTing, many of the matches of the individual transcripts match to the same gene on the reference genome. However, each individual transcript has its own unique FPKM value.

I'm confused, firstly, as to how you can have multiple sequences from the same gene with different FPKM values — and of course, I'm also wondering what would be a suitable approach for the subsequent analysis. Should I just add the FPKM values together for the sequences with the same matches?

If the quantification is done at the transcript level, each identified transcript of a given gene will have a different number of reads attributed to it, hence a different RPKM value.

For the subsequent analysis, you can continue at the transcript level.

I think you cannot sum the FPKM values directly, because they are inversely proportional to the transcript lengths ("K" stands for "by kilobase"). If you want to do the subsequent analysis at the gene level and use FPKM values, you would have to multiply the FPKM values of the transcripts by the corresponding transcript lengths before summing. Then you will have to divide this sum by the gene length, or something like that.


What does the nucleus look like in S phase of Meiosis? I was watching an animation video about Meiosis and this is what the video shows (pics attached.)
It shows that before synthesis, each chromosome exists as single chromatid and then after replication, it has a sister chromatid. I am confused because germ cells are diploid, so shouldn't the S phase look like this?
It should start with 23 chromosomes (46 different DNA's) and then replicated to 46 chromosomes (92 different DNA) which then get assorted into 4 different cells?

In terms of chromosome number
During meiosis, the meiocyte is a diploid cell ( 46 chromosomes for human). So during the S-phase , the meiocyte would contain 46 chromosomes.
At the end of meiosis I, the divided meiocyte contains 23 chromosomes so it's called the reductional division
At the end of meiosis II each cell contains 23 chromosomes.
In terms of chromatid number and number of DNA molecules
Meiocyte in S phase contains 2 chromatid in each chromosome, so the number of DNA molecules is doubled (if you consider that each chromatid is composed of a pair of DNA strands like in Watson Crick Model, then each chromosome of S phase contains 4 strands... So 46×4 strands of DNA is present. Often each helix / duplex is considered one DNA molecule , so in that case you have 46×2 molecules. So you have to be careful with the terminology mentioned.
After meiosis I there are 23 chromosomes in each divided cell with 2 chromatids in each chromosome...So there are 23×2 DNA molecules.
After meiosis II there are 23 chromosomes with 1 chromatid...So they contain only 23 DNA molecules.


What is violet color? We have 3 color receptors in our eye, so assuming the above picture is precise we are checking for 3 wavelengths: 450nm, 540nm and 700nm.

Pink for example has an RGB value of

R (700nm): 1
G (540nm): 0
B (450nm): 1

Violet has an RGB value of

R (700nm): 0.5
G (540nm): 0
B (450nm): 1

However Violet has a wavelength of 400nm which is lower than the Blue receptor. So how can it activate the red receptor when red is clearly not active at that frequency?

Does that mean Ultraviolet appears blue to the human eye? Why is it constantly painted as violet in all frequency graphs?

The question was first duscissed here (https://physics.stackexchange.com/questions/486560/what-frequency-is-pink-color) but did not receive the answer I need.

this is a chart of the light activation of the light sensitive cells in the human eye.

see that little blip up on the tail end of the red cone, that minor ranges means the extreme blue end of the spectrum activates blue cones but also has a chance to activate red cones. That is why you can sometimes see magenta tinges in bluest of blue light. There is also a sensitive issue as blue cones are the least sensitive of our cones so it requires a stronger blue light source to activate it than the equivalent light on other cones, since red is more sensitive a strong blue and a weak red source will blend to about equal as far as our eyes are concerned so at the bluest end of the spectrum, where the blue activation is at its weakest it does not take much to activate the blue and red "blip" equally meaning all sources at that extreme end blend into magenta.

Also magenta itself is not actually part of the spectrum, it can be produced in two ways, the first I discussed above, hitting the far end of that little blip perfectly. The second and most common requires light from two disparate and different parts of the spectrum in other words not a single wavelength. It is blue light and red light without green light, it is not a real color but an artifact of how our eyes see light. Your cones can't tell how they are activated just that they are. Yellow and cyan (and every other common human color)on the other hand can be produced by a single wavelength, which may or may not activate multiple types of cones.
You can find more information here


What does fitness really mean? Fitness is certainly the most important concept in the theory of evolution. My question does not have to do with practical measures of fitness but with the theoretical definition of it.

I am a bit lost with the concept of fitness. Below I give some possible definitions of fitness and I am hoping to get critics for these definitions. The broad question is What is the definition of fitness?

In the following, to make things easier I will consider only one bi-allelic locus. For simplicity, I will assume a panmictic population of infinite size evenly distributed into age classes.

1) Let the variable $M$ be the mean time of a generation in the species of interest. Measure the allele frequency $p(t)$ and measure the frequency $p(t+M)$. By comparing the two you get the ratio of fitness of the two different genotypes. Obviously it does not work if we have sexual reproduction or diploid selection.

2) Genotype the individuals and wait until they die by counting the number of offspring they had and take the mean per genotype ($W_{AA}$, $W_{Aa}$, $W_{aa}$). This method would not work if they have different lifespan. One individual might make two babies in 8 years and the other would make two babies in 2 years but they would have he same fitness.

3) Do the same that at 2) but don't wait until they die, wait 1 month, Or 2 years?, or $M$?, or $2\cdot M$?, or...? What is the right decision? The more you wait, the closest you will be to the long term effect of natural selection. The less you wait, the more probable you will suffer of genetic drift.

4) Fitness is just a measure of natural selection that is not perfectly accurate because it is measured at short-term. In some circumstances, our measure on this short term is representative (Wright-Fisher equation) enough of what will happen on the long term.

The concept of fitness is very general. An adequate definition of fitness is hard to specify in the same way that a definition of "species" is hard to give. To be useful, scientific or technical definition of such broad concepets will often need to be so narrow that more than one is needed. A uselessly broad definition of fitness might be:

"Fitness is modeled as a utility function, where higher fitness is indicated by a higher score"

Here every important detail about whatever's fitness is being tested, how that fitness is measured, and the environment in which that fitness is determined are simply wadded up together and transformed into a different question that is no easier to answer.

The hypothetical problems you raise with various definitions are not (in essence) problems with the definitions, but problems with the definitions not being applicable to the domain in which such problems matter. You have to define your criteria for success, and then these constraints can be translated into a "fitness" function that allows the desired predictions.

Some issues that might matter are:

Are predictions about populations, or individuals.
Are predictions about dynamic fitness (snapshot at some time) or long-run steady state fitness.
Are predictions about quantitative values (like heights) or discrete values (like sex).
How do you want to present error in your predictions - p value, sensitivity/specificity, confidence interval, etc.

I'm sure this is not the kind of answer you were looking for, but I think part of your question revolves around a confusion that there is "one" technical definition for fitness. Part of the process of learning is comparing different presentations of the same concept, and realizing where they are different. A full walk over all the different ways one could evaluate and apply fitness would be a book, not a short answer. Perhaps some other people can provide good links to more detailed information.

I just found a blog posting, by Dr. John S. Wilkins, which says some of the same things. His perspective comes with a good pedigree; his PhD work was on trying to define "species" and he has authored a couple of books on the subject.


Is Hydrogen gas present in biogas, and does it spontaneously ignite? Is Hydrogen gas present in biogas? As it is highly inflammable, may it ignite the other gases like methane?

The constitution of the biogas depends greatly on its source and the fermenting microbe. But in general, it does contain hydrogen about 0-1%. Even if it did contain large amounts, the mixture would be inflammable, but it would not burst into flames without any external igniter, which could be any small fluctuation of heat if the mixture is too unstable. But in general, an inflammable gas doesn't start burning on its own.


Exercise causes number of cell divisions to approach Hayflick limit faster? And hence shorten life expectancy? A world class athlete spends a lot of time performing intense exercises.  Correct me if I'm wrong, but I assume that these intense exercises causes significant damage to the athlete's cells, but with proper nutrition, they are able replenish these cells with stronger ones.   This process of destroying and re-creating cells causes cell divisions to approach the Hayflick limit faster, and hence shorten the athlete's life expectancy.

I also heard that caloric intake causes the number of cell divisions to approach the Hayflick limit faster.  World class athletes generally consume substantially more calories than the average individual, which also contributes to a shorter life expectancy.

So for this reason, is the life expectancy of world class athletes generally shorter than the average individual? And what about casual athletes?

Edit
If world class athletes live longer lives than the average individual, why is this so despite performing activities that expedite the deterioration of telemeres, and hence, approach the Hayflick limit faster?

Following damage to muscle (e.g., as a result of strenuous activity) the injured fibers are removed (by immune cells) and then replaced by new myofibers (individual muscle cells that join to create new muscle tissue). This is why for a few days after exercise your muscles can be sore - it is the tissues being initially cleared of damaged cells and repaired.

Muscles, like other tissues, have resident stem cell populations ("satellite cells") that are used to replace damaged cells.

Stem cells have potentially indefinite replicative potential, as they express telomerase and thus do not have a traditional Hayflick limit.

Volonte D, Liu Y, Galbiati F. The modulation of caveolin-1 expression controls satellite cell activation during muscle repair. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 2005 Feb;19(2):237–9.


Visual and clear example of the idea that "animal doesn't need to understand the evolutionary function of its actions" This is a question about education. I am trying to come up with a very visual and clear example, to explain a particular concept in evolution.

The concept I am trying to explain is,

  the fact that an animal does not need to understand why it's doing something in order for that behaviour to be selected

(by "why" I mean, the evolutionary/functional role of that behaviour, the reason why it increases the animal's fitness).

Students who don't yet intuitively understand evolution, sometimes mistakenly think that in the theory of evolution, animals need to understand why their behaviour is leading to offspring in order to do that behaviour. (they might say: "the bee looks for flowers because it wants to feed his children", although bees (probably) don't actually make this computation, but simply act on stimuli).

(Note by the way that this is not simply about anthropomorphization: e.g. humans also don't need to understand what sex is for, in order to produce offspring).

What I'm looking for is an example of an animal, and a behaviour that is characteristic for that animal, that very clearly shows this principle:

It should be clear and intuitive, that the animal doesn't understand "why" it's doing what it's doing, because to reason about this would clearly be too complicated for the animal (I don't think the bee example really satisfies this).
It should be visual, and memorable.

Use human behavior, they're human, do they understand why they like salty foods or why thiols smell bad to them. These behaviors still work even when you have no idea why you are doing them.

Using humans circumvents the problem of them not understanding animal behavior, which they already have to do to grasp your explanation for animal behavior. Using any other animal requires them to understand that animals mind which an entry level student will not, however as humans they can assess their own knowledge directly.


What causes a 'stuffy' or 'runny' nose when you have a cold? When humans get the common cold, a common symptom is a stuffy or runny nose. Is that the body's immune response or is that the virus's doing?

It's mainly caused by swelling of large veins and by an increase in vascular permeability that leads to an accumulation of fluids in the nasal mucosa. These effects are mediated, at least in part, by bradykinin and histamine, and can be counteracted by epinephrine. These mediators are part of the immune response to the viral particles.

You can read more about it here:

http://www.cardiff.ac.uk/biosi/subsites/cold/commoncold.html
Chernick-Mellins basic mechanisms of pediatric respiratory disease
By Gabriel G. Haddad, Steven H. Abman, Victor Chernick (page 520)


Allosteric regulation: why involve extra molecules Why are molecules such as allolactose (for lac repressor) or 2,3-BPG (for haemoglobin) used for allosteric regulation rather than the actual molecules involved in biochemical pathways, such as lactose and 1,3-BPG? The formation of such "extra" regulators requires energy – what is the advantage of such organisation?

It's an interesting question, and there are a lot of potential explanations.

I can at least hypothesize a little bit for the case of 2,3-BPG and 1,3-BPG. I think the key point is that it's not obvious to me why sensing the 1,3-BPG concentration would be useful. This concentration actually has to be maintained in a pretty tight range for glycolysis to function (note that the entire lower portion of glycolysis is very close to thermodynamic equilibrium). The reason that I think 2,3-DPG is a useful regulatory molecule is precisely because its levels can be regulated independently of the function of glycolysis. The activity of the enzymes in the 1,3-BPG -> 2,3-BPG -> 3PG shunt can controlled independently of the control of normal glycolysis and can be regulated by whatever physiological parameter you want 2,3-DPG concentration to represent.

One other thing to note is that typical red blood cell concentrations of 2,3-BPG are actually many orders of magnitude higher than 1,3-BPG. The very low concentrations of 1,3-BPG are a necessary consequence of the thermodynamics of glycolysis as mentnioned above -- if 1,3-BPG concentrations are too high, the GAPDH reaction will become unfavorable. Thus it may be that the typical concentration of 1,3-BPG is too low to be an effective regulator of anything (because it would have to bind very strongly). But I think this is a less important point than asking the question of "what does the concentration of my regulator represent".

There may be biochemical reasons at work in other cases -- for instance, some molecules may just bind better to the protein that you want to regulate, and that's why they're chosen by evolution. I think this is a case when it will be hard to come up with a blanket explanation -- it's better to look at each case, consider what signal biology is trying to measure, and look at the relevant constraints.

I don't know the answer for 1,6-FBP and 2,6-FBP, and note that in other species, 1,6-FBP does appear to be the major regulatory molecule. You could argue that by having 2,6-FBP be the regulator, there are more enzymes whose activity you can control and thus somehow you have more fine-tuned regulation </hand waving>.


What is a gene transcript, how is it different from an allele? Within human genetics,

My current understanding of a transcript for a particular gene is that it's the exact nucleotide sequence and position of a particular instance of said gene in some individual.

My current understanding of an allele is that it's a less granular breakdown of the instances of a gene in a population.  That is to say, one allele for a particular gene likely covers many (millions of?) unique transcripts for that particular gene, and groups them together due to their tendency to all have a similar phenotypic expression.

Is this correct?

I thought a transcript was the RNA sequence produced from transcription. The RNA copy of an allele that gets spliced and translocated to the cytoplasm for translation. Not sure if Wikipedia references are allowed here, but they seem to agree with my understanding.

An allele is a specific copy of a gene, i.e. you have two copies (alleles) of gene X; allele X1 comes from your mum, allele X2 from your dad.

I haven't heard of the less granular breakdown description of genes, so that might just be a different way of looking at it.


Oscillatory electrical system using a chain of neurons Many daily activities that we perform are result of inbuilt oscillatory circuits in our body. For example walking, breathing, heart beat, blinking, etc. The coding and decoding of stored memory also happen via controlled oscillations. The link http://en.wikipedia.org/wiki/Neural_oscillation contains information about neural oscillations. It says in here that a single neuron, an ensemble of neurons and activity of brain may exhibit synchronised oscillations. It is also said that these oscillatory circuits can control all the parameters of oscillations i.e. frequency, phase and amplitude.While above are true for neurons as a part of bigger systems, my question is related to study of isolated neurons.
There are many instances of studies of artificial neural circuitary created on a customized substrate(Micro Electrode Array) by masking techniques. Also there are loads of ongoing research to study the simple neural circuits in temporal and spatial domain by electrical interfacing of semiconductor and nerve cells using Field Effect Transistor(FET).

I want to know if these kind of oscillations are unique to some special kinds of neuron? Is the control of oscillation parameter possible in every neurons and isolated neurons? Can a neuron or any other cell exhibit change in action potential independently? Do other cells except neuron and pacemaker cells exhibit oscillation? Can a single neuron exhibit memory?
Can a simple circuit like below generate oscillations?
Suppose I culture the neurons on a substrate in a controlled way such that one neuron is connected to only one other neuron in a linear fashion and the last neuron is connected to first. Assuming we supply the ions if there is loss, can a clock pulse of varying frequencies be generated, where the frequency is the function of the no. of intermediate neurons and their length.

It would be a great help if somebody can provide information about softwares to simulate simple neural circuits (If available).

Short answer
A single pacemaker neuron can generate oscillatory behavior.

Background
Given our exchange in the comments, I will focus on single neurons with intrinsic oscillatory behavior. For example, thalamocortical relay neurons and inferior olive neurons have intrinsic oscillatory properties, mainly through the interaction of a hyperpolarization-activated cation current (Ih) and a low-threshold activated Ca2+ current (IT) (McCormick & Huguenard, 1992, and Fig. 1).

Fig. 1 Model for an oscillatory inferior olive neuron. Source: Bal & McCormick (1997)

Rhythmic burst firing is created through generation of a low-threshold Ca2+ current (IT), which activates fast action potentials mediated by Na+, K+, and Ca2+ currents (INa, IK, and ICa, respectively). Entry of Ca2+ in the cell during fast action-potential firing and low-threshold Ca2+ spiking result in after-hyperpolarization through activation of a Ca2+-activated K+ current. This afterhyperpolarization activates Ih. Combined activation of Ih and decrease of a Ca2+ activated K+ current (IK,Ca) results in depolarization of neuron, which activates another low-threshold Ca2+ spike. In this manner, Ih modulates frequency of oscillation. In addition, tonic activation of Ih also contributes to average membrane potential, and therefore to presence, strength, and frequency of oscillation
in these neurons.

Regarding the series of sub-questions - these are quite varied. Perhaps it is better to generate another one or two focused, well-formulated questions on this. For now, I will answer them curtly below. Further, the papers I linked contain a wealth of information, and the McCormick & Huguenard (1992) paper is a detailed modeling study. Both papers are awesome and the authors are three of my all-time favorites so far.

I want to know if these kind of oscillations are unique to some special kinds of neuron?
Answer: Yes quite unique, because Ih channels are quite unique (they have been called "funny currents") and they are not present in every cell.

Is the control of oscillation parameter possible in every neurons and isolated neurons?
Answer: No, as the molecular machinery such as Ih channels may be lacking in most other cells.

Can a neuron or any other cell exhibit change in action potential independently?
Answer: That depends whether the cells are coupled through synapses or other means.

Do other cells except neuron and pacemaker cells exhibit oscillation?
Answer: Yes, some cells start to oscillate, for example in the degenerated retina (modeling work only) and there are non-neural cells that when cultured spontaneously start to oscillate.

Can a single neuron exhibit memory?
Answer: Yes, through long-term potentiation or depression.

References
- Bal & McCormick, J Neurophysiol (1997); 77:3145-56
- McCormick & Huguenard, J Neurophysiol (1992), 68(4): 1384-1400


Can recessive alleles be expressed? Say I have a disease that is autosomal recessive. If one was heterozygous for this trait, could the recessive gene still be expressed?

I know sickle cell anemia has a heterozygous advantage so it must be possible but what are the conditions for this to happen and also to what degree?

EDIT: This isn't asking how a gene is recessive or dominant in a molecular level.

Short answer

The concepts dominance, additivity, epistasis, recessivity and others are all specific to a given phenotype. Here you are getting confused because you are considering two different phenotypes at once.

Slightly longer answer

By definition, if an allele is recessive, then in the heterozygote state, the phenotype of interest is just like the homozygous dominant. An important point in the above sentence is "the phenotype of interest". A given locus may show a pattern of simple dominance-recessivity for a given phenotype but may show a completely different pattern for another phenotypic trait.

Let's consider your example of sickle cell anemia. For the phenotype which is the disease, sickle cell anemia has a simple dominance-recessivity relationship. However, for the phenotypic trait which is fitness (yes, in quantitative genetics, fitness is often modelled as a simple phenotypic trait), sickle-cell anemia shows (environment dependent) heterozygote advantage. Also, the fitnesses of the two homozygotes differ greatly.

Note that, in reality, very few loci show cases of perfect recessivity dominance.

EDIT

You are considering two (or even three) phenotypes.

First Phenotype: Fitness

Fitness shows overdominance (with highly unequal fitness for both homozygotes).

Second phenotype: Disease

Double mutant are sick, the others aren't. Perfect dominance-recessivity (although if I am not mistaken heterozygotes individuals have some restriction when it comes to scuba diving if I am not mistaken)

Third phenotype: Shape of hemoglobin

If the heterozygote hemoglobin is shaped just like the healthy homozygote, then there is dominance-recessivity. If the shape differs (which might be causing malaria resistance, I don't know), then there is some partial dominance going on.


Why are not all species hermaphrodites? If a hermaphrodite animal (like slug, snail, etc) finds a partner they can mate immediately.

If another animal with "normal" reproduction (lets say a mouse) finds a partner they can only mate if they are opposite genders.

So it seems logical that the hermaphrodite way of reproduction is more successful than the "normal" way.

But it is not, as far as I know all higher developed species are using, the standard way of reproduction (male and female).

Why? What are the disadvantages of hermaphroditism?

Firstly I'll clarify that you are talking about simultaneous hermaphrodites rather than sequential hermaphrodites (1st one sex, then the other e.g. the limpet Patella vulgata).

It is perhaps easiest to address the question by countering it and asking why dioecy (2 sex systems/2 gonochoric types e.g. male and female) is better? As you have pointed out there are obvious advantages to being a hermaphroditic species such as more chance of mating - more likely to provide an advantage at very low population densities where interactions are infrequent.

There are two key disadvantages of hermaphroditism which I will briefly cover but have been discussed in this paper and probably other costs.

The first is energy costs. Maintaining the capacity to produce male and female gametes will be more costly than maintaining one. This gives the hermaphrodite a fitness disadvantage because energy is rarely an infinite resource. Therefore at higher population densities, when mating opportunities are not rare, the gonochoric individuals will have a higher fitness because they have more energy. Monogamy is also analogous to rare encounters but true monogamy is rare (1 partner for life).

The second disadvantage of hermaphroditism is self fertilisation. This will cause an increase in homozygosity and lead to inbreeding depression (reduced fitness).

So you are right to some extent...

  the hermaphrodite way of reproduction is more successful than the
  "normal" way.

...but the conditions which give rise to an hermaphroditic advantage are restricting. Overall, the above costs, combined with the obvious complexity of evolving the ability to produce male and female gametes, the ability to both fertilise and be fertilised, pregnancy and birth, and mating systems, mean that it is often more beneficial to be a dioecious species. Thus dioecy evolves.

EDIT: Question Raised by @Single_Digit

  I have been pondering this question for a while and I get what RG255
  is saying. I'm just not sure I entirely buy it. Take earthworms, for
  example. They are simultaneous true hermaphrodites (as far as I
  understand). The anatomy doesn't have to be that complex*. They simply
  have two genital openings (one for eggs and one for sperm) and they
  line up in a "69" (excuse the vulgarity) position. This should, in
  theory, minimize the inbreeding depression. However, it doesn't
  eliminate the maintenance of two sets of reproductive systems. But
  most organisms are not internally fertilized mammals with wildly
  complicated systems of internalized embryonic care. Most species lay a
  pile of eggs that a male squirts sperm on or squirt eggs while the
  male squirt sperm and then they hope for the best.

  I would think the advantages of simultaneous parenting (after all,
  many MANY species' males don't provide much in the way of child care)
  and its fitness advantage would vastly outweigh the burden of a second
  set of reproductive organs.

  With that said, I don't have a better explanation, but I find the
  question a very interesting one. The linked article is pay-walled,
  aside from the abstract, but I still disagree with some of its tenets.
  To me true hermaphroditism should be very common (I realize it isn't)
  in species that don't need two parents to raise offspring, but do
  benefit from some (as in one parent's) parental care. I recognize that
  it would do little to help species that merely dump gametes and leave
  because specialization of one reproductive system would likely do the
  job better and both genders equally contribute under that type of
  system.

  So, RG255 convince me! Clearly there are good reasons, since gender
  (or asexual repr) is the norm, but I need more/better evidence.

  Yes I realize they would need separate internal anatomies for each type of gamete, but still...

My response:

  You have presented one example of hermaphroditism and used that as
  evidence that all species should be hermaphrodites. Earthworms are
  small slow creatures living in soil, I don't imagine they have high
  rates of encounter, and therefore low rates of encountering the
  opposite sex, therefore hermaphroditism would be favoured as discussed
  above.

  Further, you say most species are external fertilisers (do you
  have a reference for this?) and therefore it is not costly be a
  hermaphrodite. I don't see your logic there, the cost is not
  necessarily to do with the cost of bearing child, producing &
  maintaining the gonads and gametes is also a costly process. I would
  argue that this is extremely complex. This is not just on a
  morphological level but also physiological: in non-hermaphroditic
  species the sexes have very different, and often, conflicting gene
  expression and hormone production patterns. Hermaphrodites would not
  be able to optimize to the fulfilling both the male and female roles.

  Finally, you pointed out that the worms do not inbreed. Inbreeding
  avoidance does not have to be the cause of the hermaphroditism
  persisting, if the environment/other factors favour hermaphroditism. I
  never said that both were simultaneously necessary.

  I hope this
  clarifies it for you, if not please expand as to why, I am on here
  because I want to help people understand biology properly!

Further response from @single_digit:

  Well fair enough about my external fertilizers comment. I don't have a
  reference, but I was thinking all multicellular life and I'd have to
  imagine that when you factor in plants, that external fertilization is
  relatively the norm (as is hermaphrodism (dioecy) for the plants). As
  to earthworms, I disagree about your description of them. Their
  densities are actually pretty high, so I'd wager they encounter each
  other frequently, so I'm not sure where that leaves them in terms of
  pressures for hermaphroditism. Your point on the physiologic/hormonal
  issues of maintaining the systems is one I haven't previously
  considered. I honestly don't have any clue as to how daunting (or
  simple) that is, but I'd imagine that the sophistication of the
  systems would play a pretty key role. Makes me wonder how much this
  has been researched in true hermaprhodites. I suppose the main thing I
  keep coming back to is the overwhelming disadvantage gender has in
  terms of potential to create offspring. Males in many (most?) species
  essentially act as little more than sperm donors, thus half the
  individuals have effectively zero fitness. That just seems like an
  overwhelming advantage for hermaphrodites.

My Response

  Why do you consider half of the individuals to have zero fitness?
  Fitness is widely accepted as the number of offspring a parent
  produces because this is directly related to number of copies of their
  genes passed to the next generation. Sperm donor type males achieve
  increased fitness by mating as do females - with out the male they
  would never be fertilized. The key disadvantage of dioecy is the
  halved (assuming equal sex ratio) frequency of potential encounters
  that could lead to mating. The general disadvantages of
  hermaphroditism are inbreeding depression and high cost & complexity.

Single_digit:

  Zero fitness isn't exactly correct, but if we look at parental care as
  conveying a survival advantage for K selected species, and huge
  numbers of offspring conveying an advantage for r-selected species
  (obviously the type of env affects this) does a deadbeat dad really
  optimize for either of these? Passing on genes is fine, but if
  offspring survival is low, does it matter? Does it simply boil down to
  the maintenance of two repr systems plus decreased fitness from
  inbreeding vs the increased reproductive success from extra child
  care? Or is there more?

My response:

  r/K selection theory has generally been disregarded in the
  evolutionary biology community due to the substantial evidence against
  it so it is unhelpful to think of selection in this way. As long as
  the 2 sexes strategy is more successful at passing on genes than a
  hermaphroditic strategy it will (should) prevail. Dioecy will be more
  successful if the hermaphroditism introduces to much cost through
  production and maintenance of sexual organs/gamete and inbreeding
  whilst not attaining substantial gains from higher potential mating
  frequency.

@Single_Digit

  Interesting about r/K selection. I hadn't heard that. Do you have any
  links? I'd be curious to learn more there. I incorrectly earlier made
  a comment about dioecy where I meant monecy. But this seems to beg the
  question, why is monecy/hermaphroditism so much more prevalent in
  plants? Obviously there are different survival pressures, but I'd
  think the same basic principles would apply as in animals, but the
  condition seems to be far more common than in animals.

My Response

  I seem to remeber there being a reason in plants, don't
  have time to look it up right now. The work about r/K selection was
  Reznick/Stearns/Charlesworth. Reznicks is the most recent and more
  overview type paper - best place to start:
  http://www2.hawaii.edu/~taylor/z652/Reznicketal.pdf


How is the number of mitochondria in a cell regulated? How does the cell regulate the number of mitochondria in a cell? What happens when there are too many or too few?

The concept you refer is recognized as mitochondrial biogenesis and it is regulated by AMPK which senses the cellular energy demand. If you have few mitochondria in the cell, the electron transport chain works suboptminally generating less ATP. When the AMP/ATP ratio is high (low ATP) AMPK is activated, and turns on the catabolic pathways required to produce more ATP, included mitochondrial biogenesis.


What does it mean to share similarities among living organisms "both horizontally and vertically"? I came across the following lines in a textbook (NCERT biology for class 11).

  Systematic and monumental description of life forms, brought in, out of necessity, detailed systems of identification, nomenclature and classification. The biggest spin off of such studies was the recognition of the sharing of similarities among living organisms both horizontally and vertically

What does "both horizontally and vertically" mean?

Ben Bolker's comment is correct; the next sentence in the passage helps to clarify (bold added):

  The biggest spin off
  of such studies was the recognition of the sharing of similarities among
  living organisms both horizontally and vertically. That all present day
  living organisms are related to each other and also to all organisms
  that ever lived on this earth, was a revelation which humbled man and
  led to cultural movements for conservation of biodiversity.

The relationship between species in the present day are the horizontal relationships; one can define species horizontally by looking at and grouping organisms existing today (or at any other time "slice"). You can compare species horizontally by, say, looking at the skull of a human and the skull of a chimpanzee.

The relationship between species today and species that have existed in the past are the vertical relationships. For example, you could look at the skull of a modern horse and compare it to the skull of Mesohippus.

I've included a couple sources below that use this distinction, though I'm not sure where it originates.

I'd say the "horizontal" terminology comes up more frequently and may be more familiar, for example in reference to horizontal gene transfer one is talking about genetic material moving between species living at the same time. "Vertical gene transfer" can also be defined as the transmission of genetic information from parent to offspring, but more typically you would just call it inheritance.

Alvarez-Venegas, R., Sadder, M., Tikhonov, A., & Avramova, Z. (2006). Origin of the bacterial SET domain genes: vertical or horizontal?. Molecular biology and evolution, 24(2), 482-497.

Stamos, D. N. (2002). Species, languages, and the horizontal/vertical distinction. Biology and Philosophy, 17(2), 171-198.


Why don't bacteria eat food leftovers? I have thrown a dirty spoon after eating some pasta into one of my desk drawers (doesn't do me much honor). It stayed there for around a year. My house is warm and I think there is enough humidity for bacteria to multiply, however I have found it today with seemly same amount of food on it when I left it.

I assume given enough time all food should get converted into bacteria (bacteria would eat and multiply until food is there and stop when it is all consumed). Is this assumption incorrect?

Why didn't bacteria decomposed the food on my spoon?

EDIT: This question has nothing to do with fried McDonald foods and is referring to bacteria consuming 'ordinary' food, plus I am asking if food should disappear completely while the other question is about it being decomposed,  answers are completely different.

First, your assumption is wrong. Bacteria multiplication is not limited by food availability only, it is one of many constraints.

Oxygen availability, water availability and the absence of toxins also play a role. You can easily start a thriving bacterial colony somewhere, but once one of these conditions changes sufficiently, the colony can die off. And it can be the growth itself which changes the conditions. A classic example is found in wine fermenting. The yeast there multiplies freely until it has produced so much alcohol as a waste product that it dies off. This is why wine is always in the 12 to 18% ABV range, anything above is "fortified wine" where the concentration was increased after the yeast's death. Yeast are not bacteria, but bacterial colonies' growth is limited in similar ways.

Second, even if the assumption were true, the spoon wouldn't be clean. Bacteria converting food in waste doesn't result in nothing, nor does it result in something gaseous which would literally disappear into thin air. OK, part of their byproducts are likely to be some gas. But you certainly get lots of bacterial bodies (alive, later dead) and also lots of waste product. Together, it forms some kind of sticky organic goo (frequently a biofilm).

So, about your spoon

it is entirely possible that it never got a thriving bacterial colony, because the conditions weren't right despite food availability
it is also possible that it got some kind of colony (pathogenic or not), and it died off before the food was consumed
in the case of a colony, it doesn't matter how much it got to consume before dying off. The spoon wouldn't have ended up clean under any circumstances, including the very unlikely "death by food going out" scenario
depending on the conditions in which the spoon is held, the colony which dominates the spoon can be bacterial, or fungal (mold, yeast), or you can end up with different species building their colonies in parallel. Still, the previous points hold under the "mold colony" or "multiple colonies" scenarios just as under the "single bacterial colony" scenario.


What is this species of green frog found in store-bought flowers in France? Today I found a frog in a big flower composition bought at a french shop (living in Grenoble, south of France).

It started snowing today, and I'd like to keep it until it's warmer outside.

So could someone tell me what species it is ? (To check what it eats and if it's legal to keep it)

Thanks !

(I'll edit with more pictures if it's needed and if she moves)

Edit :

This looks very much like a tree frog of which there are many similar looking species. Without knowing where your flowers came from or more characteristics about the specimen, it'll be difficult to provide an accurate answer*.

One possibility may be the European tree frog (Hyla arborea).

According to Wikipedia:

  Members of the H. arborea species complex are the only representatives of the widespread tree frog family (Hylidae) indigenous to mainland Europe.

which is supported by genetic work by Stöck et al. 20081

Description [source]:

Small (3.2-5 cm in length)
Slender body shape with long legs and smooth dorsal skin+
Usually green (but variable) with dark brown lateral stripe across eye caudally to groin and whitish ventral skin surface.
Gripping discs on toes

The range of this species also includes much of France:

 Image Source

+ Although the description states this species has smooth dorsal skin (possibly like the OP's specimen -- I can't tell for sure), many of the pictures I've seen seem to suggest that the dorsal skin of this species is actually rather granular. For example, see here.

*Feel free to update your post with additional info and perhaps a better response will be added.

 Citations:

 1 Stöck, M., Dubey, S., Klütsch, C., Litvinchuk, S.N., Scheidt, U. and Perrin, N., 2008. Mitochondrial and nuclear phylogeny of circum-Mediterranean tree frogs from the Hyla arborea group. Molecular Phylogenetics and Evolution, 49(3), p.1019.


Was there originally a non-ribosomal way of synthesizing proteins? Proteins are synthesized on ribosomes from mRNA copies of regions of the DNA. But ribosomes themselves are made up of proteins (and RNA). So how could the first ribosomes have arisen? Was there previously some other way of making proteins other than by ribosomes and mRNA?

(A quick answer to a question that will be likely closed being not well focused on the physics of all this)

First: the ribosome translates mRNA into the chain of amino acids that eventually will become a protein. The ribosome is a huge complex, made of both proteins and RNA. RNA can have enzymatic activity like a protein: the ribosome is a Ribozyme.

This chicken or the egg problem has puzzled biologists, chemists and biophysicists for a while. The structure itself of the ribosome was the "smocking gun" for the model we have today: the RNA world. In few words: because RNA can act as a protein and it is so similar to DNA, probably our DNA-world (i.e. information stored on the DNA, work done by proteins, RNA between the two) emerged from a fully RNA-world, where RNA was responsible for both protein activity and information storage.
How in detail all this happened by evolution, is probably the subject of several nobel prizes to come.


What do viruses do during incubation period? For example, there is an incubation period of around 1 to 3 days for common cold, and that of AIDS can range over to decades.

What do viruses do actually do during the incubation period?

What triggers them to turn active again?

during the incubation period the virus is typically increasing in numbers and spreading between cells. It takes a while for symptoms to become obvious because it takes time for enough damage to be built up in the tissue to become noticeable.
Take for instance the Rhinovirus which causes the common cold, once you become infected it is a day or so before enough damage has been caused to the tissue at at the back of the throat to give you a cough.

In addition some of the symptoms of infection are caused by your own immune system as a way of fighting the infection. For instance inflammation is often a sign of infection but is typically caused by the immune system to allow the movement of plasma and leukocytes into the infected tissue. As the immune system requires time to recognise and respond to a pathogen this leads to the delayed onset in symptoms.

AIDS is actually a syndrome caused by the HIV virus. the HIV lifecycle occurs CD4+ T-Cells, after infection occurs the immune system tries to cope by destroying the infected cells but over long time the infected population increases. The immune system becomes more and more compromised until the CD4+ cell count drops to a level where the patient is diagnosed with AIDS. At this point the immune system is compromised and the chance of a secondary infection by a different organism increases which the patient can no longer fight off. The actual cause of death for someone infected with HIV is rarely the HIV itself but is quite often a different agent.


Is C. elegans always observed with precisely 302 neurons? Are there ever individual viable exceptions? This answer mentions that the C. elegans hermaphrodite has exactly 302 distinct neurons. This has made it a very effective model for a variety of types of biological research, including neurology and cell differentiation. It is also currently the only organism with a completely mapped connectome.

But the word "always" made me wonder - has a viable specimen ever been verified to naturally have a number of neurons other than 302? Not as a result of an experiment, just naturally?

According to the highly respected WORMATLAS: A Database of Behavioral and Structural Anatomy of Caenorhabditis elegans, the number is invariable in this animal, one of the most studied in the world.

  There are 302 neurons in the nervous system of C. elegans; this number is invariant between animals. Each neuron has a unique combination of properties, such as morphology, connectivity and position, so that every neuron may be given a unique label. Groups of neurons that differ from each other only in position have been assigned to classes. There are 118 classes that have been made using these criteria, the class sizes ranging from 1 to 13. Thus C. elegans has a rich variety of neuron types in spite of having only a small total complement of neurons. (Emphasis mine)

From the above, you might guess that the number of synapses are not, however.

  The full list of synapses for hermaphrodite (including larval stages) and adult male are currently being reviewed and revised for the Wormwiring Project. All data comes from re/analysis of the sections for the hermaphrodite N2U, N2T, N2W and JSE animals, and male N2Y and n930 animals. The total counts of both electrical and chemical synapses are likely to be substantially higher than what was reported in the Mind of a Worm.

Would I be surprised if someone found a different number in a particular  specimen? No more so than when people are born with four kidneys, a parasitized twin, etc.

Edited to Add:

An article, Mutations that affect neural cell lineages and cell fates during the development of the nematode Caenorhabditis elegans has identified mutations with more or fewer neurons:

  Specifically, unc-83 and unc-84 mutations affect certain precursor cells that generate both neural and nonneural descendants; lin-22 and lin-26 mutants lead to the generation of supernumerary neural cells with a concomitant loss of nonneural cells; lin-4, lin-14, lin-28, and lin-29 mutants perturb global aspects of developmental timing, altering the time of appearance (or preventing the appearance) of both neural and nonneural cells...

However, access to the paper is restricted, and I don't know if these mutations were induced (most likely were.)

HT to @canadianer for the link that led to my link.


What are iPSC cells, and what are their applications? I also searched it on internet, and just basically know it's related to the Stem Cells, but there are too many resources, can anyone help me find out more about them, like their applications? They really interest me.

From this article: iPSC's or induced pluripotent stem cells are somatic cells that have been driven to acquire an induced pluripotent cell state.  Somatic cells can be any cell of the body except sperm cells, egg cells and undifferentiated stem cells. Investigators can induce these cells to 'return' to a stem cell like state by forcing the expression of key transcription factors, and by genome-wide remodeling of epigenetic marks.

There is an entire spectrum of different iPSC's that can be generated, but much is not yet known. Future applications include using them for regenerative medicine, drug discovery, etc.

Recently there were several articles published in nature:

Stem cells: A designer's guide to pluripotency
Genome-wide characterization of the routes to pluripotency

amongst others. Also you can check out http://www.stemformatics.org/ for more information on stem cells and research being done.


What Type of Mushroom is this? Recently in Eastern Pennsylvania, there has been lots of rain and heat (90's) for a couple weeks now, so lots of mushrooms are popping up.
A neighbor posted a picture of this fungus in a community group, and was wondering if it is edible.

I am no mycologist, but I think it looks like the false death cap, Amanita citrina var. alba.

I'm basing this mostly on color, size, and the universal veil remnants on the cap.  Here is a picture for comparison:

  Amanita citrina is now known to contain the toxin alpha-amanitin;
  however, if eaten in normal amounts it is considered the concentration
  is so low that it is unlikely to have any significant effect on a
  healthy adult. Of far greater risk is the possibility of confusion
  with one of the deadly Amanita species such as the Deathcap, Amanita
  phalloides, or the Destroying Angel, Amanita virosa. For this reason
  our advice is not to eat Amanita citrina, whether it is raw or cooked

Source: First-Nature


The mechanism of mechanoreception? I am interested in knowing the molecular mechanism behind mechanoreception/mechanotransduction (i.e. mechanism behind receptor potential generation on mechanical stimulation). I know that most mechanoreceptors (touch, stretch, pressure etc) respond to mechanical modification of plasma membrane or of some external projection embedded in plasma membrane. I want to know the molecular basis behind this mechanical transduction.

Also, the sensory hairs in lateral line sense organs of fishes, and equilibrium and auditory sensation in animals involve generation of receptor potential when the steriocilia( or any equivalent extracellular projection), externally embedded in gelatin, bends in specific ways, another example of mechanotransduction.
(I don't know if all these receptors function with slight modification of the same basic framework or all of them operate with distinguishable mechanisms. If the latter is true, I just want one example of how molecular mechanism might bring about mechanoreception.)

A mechanical stimulus can act on a tissue with elastic and viscoelastic properties in two ways [1, 2]:

distort the cellular membrane which leads to opening of ion channels.
create tension on the extracellular matrix or cytoskeleton, to which a ion channel is bound, thus leading to opening of the channel.

Stretch-activated ion channels opening leads to the formation of an action potential, if there is enough ionic flow to trigger depolarization [1, 3].

References:

Wikipedia contributors, "Stretch-activated ion channel," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Stretch-activated_ion_channel&oldid=606349902 (accessed July 12, 2014).
Grigg P. Biophysical studies of mechanoreceptors. J. Appl. Physiol. 1986 Apr;60(4):1107-15. PubMed PMID: 2422151.
Wikipedia contributors, "Mechanotransduction," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Mechanotransduction&oldid=593605473 (accessed July 12, 2014).


How are epigenetic marks transmitted during cell division? As far as I know, this is one of the biggest questions in the epigenetic field: how are the epigenetic marks like histone modifications propagated through cell division? A lot is already known about DNA methylation (e.g. as in How does “inheritance of methylation” of DNA and/or histones work?), but very little about histone modifications. What is the current state of knowledge?

I can get the ball rolling..
Found a nice paper which looks at this phenomenon in yeast.
So as a primer, 8 histone proteins come together to make a spool of sorts which DNA wraps around:

Histone proteins have many sequence variants, and each one of them can be covalently modified with methyl, acyl, phospho, SUMO, adp and many other sorts of chemical groups via a chemical bond.  Although its not yet clear exactly how it works its clear that these modifications can change the behavior of the histones which prevent transcription of the gene when they have the chromosomal DNA all wrapped up.
So as to the question a pattern of inheritance of modified histone patterns is indeed seen and has epigenetic effects.  (that is, it modifies the genetic phenotype of daughter cells which retain the histone modifications of the parent cells).  In this paper, newly synthesized (and labelled) yeast histone can be found incorporated into certain segments of the genome, which demonstrates that large segments of the histones are carried forward from the parent cell.
They also found a particular case of histone epigenetic labeling carried forward through division:

Furthermore, if the heterochromatin-binding protein Sir3 is unavailable during DNA replication, histone H3-K4

So there's evidence that histone configurations are transmitted epigenetically, In this 2011 paper, the author support a 'conservative distribution model' and compare it to a 'semi-conservative' model:

The conservative distribution model proposes that newly synthesized histone molecules form nucleosomes that are randomly inserted among preexisting parental nucleosomes.
The semi-conservative distribution model proposes that a hybrid nucleosome that contains both newly synthesized and parental histone H3-H4 dimers is formed, which facilitates the transmission of epigenetic information within the basic nucleosome unit.

They go on to say that a conservative model of histone inheritance allows for strong epigenetic inheritance as the remaining parent histones will tend to attract similarly labelled histones as the new histones incorporate themselves among the parental histones on the daughter chromosome.
Its still being worked out though...


How do I know which molecular structure is glycine's "base state"? I was looking up the chemical structure of glycine, and I found the following two images:

and

.

My question is, what is the "base state", or the "natural state" of glycine? Under what scenarios does glycine become oxidized/reduced?

Also, I know that amino acids contain a carboxyl group, an amino group, a lone hydrogen atom, and a side chain. What is the formula for the amino group? Is it $\ce{-NH_2}$ or $\ce{-NH_3^+}$?

Short Answer: You need to define base state.

Background: The point to keep in mind here is that the base state (as you call it) is not constant. As @jeppenielsen points out in the comments, amino acids are zwitterions. According to Wikipedia:

  In chemistry, a zwitterion, formerly called a dipolar ion, is a neutral molecule with both positive and negative electrical charges. (In some cases multiple positive and negative charges may be present.) Zwitterions are sometimes called inner salts. Unlike simple amphoteric compounds that may only form either a cationic or anionic species, a zwitterion simultaneously has both ionic states.

In glycine, the center of positive charge is the -NH2 group while the center of negative charge is the -COOH group. At different pH (acidic, neutral or basic), the structure of the molecule keeps on changing as shown in the image below:

source

Structure of other amino acids also changes similarly. To know why this change occurs, just keep in mind that (in very simple terms) pH is inversely proportional to the concentration of H+ ions in a solution (higher the pH, lower the concentration of H+). The exact formula is $\ce{pH = - log[H_3O^+]}$ (yes, it means that a pH of 4 is 10 times more acidic than pH 5 and so on). Also, as pH changes, so does the formula for the amino group (see the diagram again).


Transcription factor binding site located in intron I have noticed that some TF binding sites are located in the introns of the genes.

I am puzzled about whether the TF only binds to DNA in the initiation stage of transcription and will detach during transcription. (I am thinking if the TF bind to the sense strand, it will block the PoLII for transcription, thus they should be removed.)

Many thanks in advance.

Even in a quiescent state, DNA is bound to a lot of proteins. It is not a lone double-helix of DNA with an occasional protein attaching here or there. Rather, it is tightly wrapped around histones, which themselves have other proteins attaching and detaching constantly. Repair enzymes are always whizzing about and fixing the random damage that occurs in DNA naturally, and transcription factors may be sitting on the DNA for a while and then diffusing away again without doing anything. There are probably more proteins around that I've forgotten.

As you can see, the nucleus, DNA and in general the cell interior are extremely crowded spaces, and for transcription to happen it takes more than just removing some TFs attached to intronic sequences. Histones need to be modified to repel each other and make space. Ultimately, all proteins will need to detach for a short time when RNA polymerase comes through. If they don't, polymerase will stall until they move away, or it may simply fall off, producing an incomplete RNA fragment which will be degraded quickly. Another polymerase will come along soon enough and produce a new transcript if the promotor is still in a permissive state.


Why aren't cat hybrids common? Why aren't hybrids of different species of felinae (say, hybrid of domestic cat with manul, cheetah, ocelot, puma or panther) widespread? Why were they not artifically created?

In order to form a hybrid, substantial genetic similarity between the organisms is required. To understand why, the successful formation of a zygote from the gametes of the two parents (i.e. fertilisation) in higher animals like mammals requires that the genomes of the organisms be reasonably similar (or homologous; see for instance human fertilisation). This is because successful development of the fetus appears to require that a very specific combination of genes and proteins be present and in the right relative ratios (it's helpful to remember that the genome is a highly analogue computer (see here also), not just a set of instructions to build an organism) - think of the significant effects of simply having an extra copy of one chromosome in Down syndrome, or the fact that triploidy or quadruploidy are often tickets to the death of the human embryo (and so having half of your genome from two different animals could lead to an imbalance in the proteins required to develop normally). I'll be addressing mainly the feasibility of obtaining a hybrid at all; of course in order to become widespread a hybrid would need to be fertile (although see the sterile mule) which would require even more genetic similarity, specifically in order that the chromosomes from each parent can interact, they have to be similar enough that the proteins regulating this process will recognize them as homologous, and enable a process like chromosomal crossover to take place during the meiosis occurring in gametogenesis.

To answer your question about felinae and panthera first, several panthera genomes have been sequenced, and (see here) the tiger for instance has only 95.6% similarity with the domestic cat and diverged 10.8 MYA. For comparison, human and gorilla have 94.8% similarity and diverged 8.8 MYA, so that puts into perspective why you wouldn't expect a tiger-cat hybrid, or for that matter any felinae-panthera hybrids. Those dates are from the linked paper. (Edit: It appears from wikipedia as referred to by the OP above that there actually is a puma-leopard, i.e. felinae-panthera, hybrid which I wasn't aware of (although all of the reports are old, so there is no genetic evidence to prove that it was in fact a hybrid). I assume this may be an exception to the rule; what I was trying to show is why such hybrids are not necessarily to be expected, and as I said below, I'm more surprised about how many hybrids are possible. It does appear though that this particular hybrid is prone to dwarfism, which indicates that it probably does not have a particularly viable genetic makeup, and I think it was sterile).

With regards to your question about felinae hybrids, if you go to Timetree, then it will tell you that Panthera tigris and Felis catus (domestic cat) diverged 14.4 MYA, and by comparison Aciconyx jubatus (cheetah) and Felis catus diverged 9.4 MYA, so it seems reasonable to suppose that they can't hybridise. (But note that P. tigris and P. leo still diverged 6.4 MYA and they can hybridise: the relatedness of two organisms isn't the only thing at work, and a better measure is the genetic similarity; this paper mentions that hybridisation ability correlates both with genetic similarity and time since divergence). Interestingly, this paper actually indicates that the percentage alignment of the cheetah genome to the domestic cat genome is only 91.1% with 93.6% similarity to the tiger, indicating that the cheetah may be a specialised outgroup.

For a more familiar comparison to all of these, Canis lupus which is the ancestor of the domestic dog, dingo, and the gray wolf only arose around 700,000 YA according to wikipedia, although I do not know the exact sequence similarity. Domestic dogs (everything from chihuahuas to great Danes) only diverged 40,000 YA, so the different cats are only superficially similar by this comparison.

There's a diagram on wikipedia shown below which nicely illustrates the different hybrids within felinae (although some seem dubious), so you can see there are actually quite a lot, and although most of the cats involved haven't been fully sequenced, presumably some of these hybrids cross some of the boundaries which I've mentioned above. They do actually include a successful hybrid between a domestic cat and an ocelot (although I can't find another source for this, so it might not be possible), and a hybrid with a jaguarundi (which appears to be closely related to the cheetah) is described as dubious here. Unfortunately, I don't know if either of those cats has been completely sequenced. Ultimately predicting hybridization is a complicated field.

This image below shows a more detailed phylogeny of the cats to illustrate the evolutionary timescale:

And for a comparison to all of that, this image below (from here) shows the phylogeny of the dog (which you might be more familiar with in terms of hybridisation), and if you realise that the whole part of the tree in B from the bush dog down diverged 9-10 MYA (see here - comparable to the whole cat family) and that the bush dog despite its name is extremely dissimilar to modern dogs (for instance it only has 74 chromosomes compared to the domestic dog's 78), then this will illustrate that the evolution of the modern hybridisable dog family (in C in the image) is tightly packed into a much much shorter time than the entire cat branch. All of the names like D1 on the right are modern dogs.

With regards to your question about artificial creation, I think a point to remember is that a lot of these cats are rare/endangered and although such hybrids are still done, there is also criticism of such proceedings. Anyway, I think a good take-home point is that the cat family is actually very genetically old and diverse. I think it's more surprising how many cats can actually be hybridised.


Energy input during ATP Dephosphorylation? What is the energy input needed to break the phosphor bond during ATP Dephosphorylation? How and when this will occur?

Many thanks for your answers.

Edit 1: I know how much free energy (∆G) is released with the hydrolysis of ATP, but I dont know how much energy is needed to start the hydrolysis of ATP.

Updated Question/s:
To break the phosphorus bond of ATP, must there be some input energy? What is the amount of this energy? Else how can break any bond of ATP without the supplement any energy?

It sounds like you are asking about the activation energy of the ATP hydrolysis reaction. This paper estimates the activation at 35--39 kcal / mol, depending on details of the reaction mechanism. So yes, energy is needed to break the phosphate bond; this ensures that ATP does break down spontaneously (which would make it a rather useless molecule for cells).

Note that this concerns ATP hydrolysis without enzymatic catalysis. Enzymes that break the phosphate bond of ATP to drive reactions lower this reaction energy substantially.


In the notch signaling pathway, what is Fringe activating? Take a look at the notch signaling pathway in human from KEGG : https://www.genome.jp/kegg-bin/show_pathway?hsa04330

I want to know what is Fringe activating. It is not pointing to another gene or protein, it is pointing to an interaction. What does that mean?

Usually, in such depictions where a species is pointing to a reaction or an interaction, the arrows mean that the species affects that reaction (for example, catalysis by an enzyme ). Generally pointy arrow heads denote positive effect (enhancing the reaction, for example an enzyme) and flat heads denote a negative interaction (repression). An arrow from one molecule to another can be used to depict a conversion (like glucose converting to glucose 6 phosphate).

There are no real standards on how to depict a pathway. So, it can be confusing.

In this case, Fringe actually alters Notch signalling (see below). So the arrow makes sense. However, the figure also has an arrow from Delta to Notch which can be interpreted as Delta getting converted to Notch. They also show an arrow from Notch to NICD which actually means a conversion. I would say that the depictions in this figure are inconsistent.

From NCBI Gene entry on Human homolog of Fringe, LFNG:

  This gene is a member of the glycosyltransferase 31 gene family.
  Members of this gene family, which also includes the MFNG (GeneID:
  4242) and RFNG (GeneID: 5986) genes, encode evolutionarily conserved
  glycosyltransferases that act in the Notch signaling pathway to define
  boundaries during embryonic development. While their genomic structure
  is distinct from other glycosyltransferases, these proteins have a
  fucose-specific beta-1,3-N-acetylglucosaminyltransferase activity that
  leads to elongation of O-linked fucose residues on Notch, which alters
  Notch signaling. The protein encoded by this gene is predicted to be a
  single-pass type II Golgi membrane protein but it may also be secreted
  and proteolytically processed like the related proteins in mouse and
  Drosophila (PMID: 9187150). Mutations in this gene have been
  associated with autosomal recessive spondylocostal dysostosis 3.
  [provided by RefSeq, May 2018]

From Shao et al (2002):

  Recent studies have demonstrated that O-fucose modifications play an
  essential role in Notch function. Reduction of O-fucosyltransferase
  expression in Drosophila using RNAi (11) or in mice by gene ablation2
  causes Notch-like phenotypes, suggesting that O-fucose modifications
  are essential for Notch function. In addition, we and others have
  shown that Notch activation is modulated by extension of O-fucose on
  Notch with the fucose-specific β1,3-N-acetylglucosaminyltransferase
  Fringe (for recent reviews, see Refs. 12 and 13). Fringe was first
  identified in Drosophila and shown to inhibit Notch's ability to
  respond to Serrate but to potentiate its ability to respond to Delta
  (14). Three Drosophila Fringe homologues have been identified in
  mammals: Lunatic fringe (Lfng), Manic fringe (Mfng), and Radical
  fringe (Rfng) (15). The β1,3-N-acetylglucosaminyltransferase activity
  of Fringe proteins is essential for their biological activity in
  Drosophila (16-18) and in cell-based Notch signaling assays (19), and
  the O-fucose residues are required for Fringe to modulate Notch
  activity (16, 19). Thus, Fringe mediates its effects on Notch
  signaling by the addition of GlcNAc to O-fucose moieties. Nonetheless,
  neither the specific role ofO-fucose in Notch function nor the
  mechanism of how a change in sugar structure alters Notch function is
  known.


Why do squirrels have twitchy bushy tails? Whenever I see a squirrel in the woods, it is always the big bushy tail flipping around that gets my attention first.  A pray animal with a big bushy flag calling attention to it's self seems to be counter survival, a big flag waving here I am, come eat me.

*Image from Wikisource

Video link, of tail twitching

Why do squirrels have twitchy bushy tails?

Edit to Clarify
Squirrels do not have a high reproduction rate, there are multiple difference between species but most seem to average about half a dozen young per year.. While a pair of rabbits can (though unlikely) create 1300 offspring in a year Wild rabbit and squirrels have similar coloring and predators.  There are of course multiple differences between rabbits and squirrels.  Given the difference in reproduction and a big wavy flag that says come eat me.  It seems that if there is a rabbit and a squirrel sitting on the forest floor eating breakfast, the one waving the flag is most likely to be seen and eaten.

Tree jumping.
The obvious answer is that having a balancing ballast is incredibly handy for some of the death defying jumps squirrels perform. The tail is needed for that.
A big bushy tail might be a good counter to predation.
You make the assumption that an inconspicuous tail would be bad for predation. I would challenge that assumption, but I am making an educated guess so feel free to debate this.
Tail flagging in ground squirrels is used to deter predators and communicate vigilance. Perhaps something similar occurs in tree-dwelling squirrels too.
Rabbits have a short white tail which isn't particularly camouflaged. It helps to confuse the predator allowing the rabbit to make sharp turns that the predator cannot anticipate.
In the case of this big bushy "twitchy" tail (which like rabbits, some squirrel tails have white tips, like in your picture), a predator probably cannot see the body and importantly cannot see or is distracted from the footing and pacing of the squirrel. If you've ever seen a dog chase a squirrel, the squirrel is easily able to outmanoeuvre the dog long enough to make it safely to a tree, probably because the dog can't predict the squirrel's trajectory due to the distracting and writhing tail.
Let's say a predator did get its jaws or claws near the squirrel and tried to take a chunk. There is a good chance all the predator will grasp is a bunch of tail fur. The squirrel will probably be sore but will live to tell the tail. (I couldn't resist)


Mechanisms of Flagella I know that dynein arms and microtubules are involved in the contraction of certain parts of the flagella to produce a wave motion, but I don't understand they are related to the 9+2 structure of the basal body.

How do flagella work in prokaryotes and eukaryotes?

Flagella in prokaryotets is very different from that of eukaryotes.

The main structural protein in a prokaryotic flagellum is flagellin. The flagellar motion is caused by a molecular motor similar to Mitochondrial ATP-synthase; molecular motion generated by the chemiosmotic energy.

Eukaryotic flagella or cilia are made of microtubules with dynein attached on to them and cause the movement by the energy generated by ATP hydrolysis.

See the wikipedia article. It is clear enough.


Is it possible to temporarily paralyze someone through the use of electric signals or focused ultrasound? I've been reading about how it is possible to send signals to the brain using focused ultrasound or electrical impulses. It is possible to make someone see a certain shape or color by stimulating different areas of the brain. I was wondering whether or not it would be possible to temporarily shut off a person's motor functions by for example, sending signals to the cerebellum or perhaps intercepting them before they can travel down the spinal chord.

Yes. Those weapons exist, they are called Electroshock weapon, the most famous of which is the taser.

Tasers spill much ink in the media. You have probably already seen their use (and misuse) in videos.


The replicator equation vs the Lotka-Volterra equation Background

The replicator equation with $n$ strategies is given by the differential equation:
\begin{equation}
  \dot x_{i} = x_{i} \left( \sum_{j=1}^{n} a_{ij}x_{j} - \phi \right)
  \qquad i = 1, \ldots, n
\end{equation}
where $x_i$ is the frequency of the strategy $i$, $A=[a_{ij}]$ is the payoff matrix, and $\phi$ is the average fitness of the population. Basically, what the replicator equation is saying is that the rate of increase of the strategy $i$ (i.e., $\dot x_i/ x_i$) is the difference between the fitness of $i$ (i.e., $\sum_{j=1}^{n} a_{ij}x_{j}$) and the average fitness $\phi$ of the whole population.

The Lotka-Volterra equation with $n-1$ species is:
\begin{equation}
  \dot y_{i} = y_{i} \left(r_{i} + \sum_{j=1}^{n-1} b_{ij}y_{j}\right) \qquad
  i=1, \ldots , n-1
\end{equation}
where $y_i$ is the abundance of species $i$, $r_i$ the intrinsic growth rate, and $b_{ij}$ describes how the species $i$ and $j$ interact (wiki entry on the Lotka-Volterra eqn).

According to Nowak's book Evolutionary Dynamics, these two equations are equivalent to each other (the same result appears in Hofbauer and Sigmund's Evolutionary Games and Population Dynamics). This is a neat result because it shows that results in ecology based on the Lotka-Volterra equation has a game theoretic interpretation and vice-versa.

Question

This would mean that the replicator equation for two strategies (e.g., the Hawk-Dove game) is equivalent to a single species interacting with itself under the Lotka-Volterra equation. How could that be? The replicator equation would describe the frequency of two strategies in the population, but the equivalent Lotka-Volterra equation would describe the evolution of a single and undifferentiated population. My problem is not so much with the proof of the equivalence between these two equations (Hofbauer and Sigmund give a proof of this equivalence in their book), but with the interpretation of the equivalence between the two eqns.

The key point is that the first equation is describing frequencies, i.e., $\sum_{i=1}^n x_i = 1$, so there are only $n-1$ degrees of freedom. For instance, if $n=2$ (as in Hawk-Dove), you can totally describe the state of the system with just $x_1$, because $x_2$ is just $x_2=1-x_1$. This constraint is enforced by adjusting $\phi$.

To convert the Lotka-Volterra model to the first equation, define $x_i\equiv y_i/\sum_j y_j$.