Is the information in the brain stored in the connections rather than neurons? Can I imagine the difference between the model of the grandma neuron and the model of interconnected neuron network so that the information isn't primarily stored in the neurons (respectively in their states) but in the connections between them.

Is the information in the Brain stored in the connections rather than
  in the neurons ?

It depends on what information you are referring to.

The brain does not just store one type of information,the model of a grandmother cell and the model of an interconnected neuron network are 2 subsystems of a greater system working together perhaps in a competitive or complementary arrangement. The purpose of this system is to extract information from the environment and identify it again for the organisms benefit. 1.

So let's say we see something that will benefit us in the future or that we might want to avoid. This is a simplification, but as you see that something, neurons in your neocortex light up specifically in region V1 in the back of your head, they arrive there after a lot of computations along the way from your retina, but also project to other parts of your brain where they are perhaps processed consciously,they fire in an orderly fashion, in a map, this bouncing around of electrical signals represents your conscious, and unconscious processing of the image, so the information exists as a network of electrical signals. 2.

During recollection, ( there are different types of memories so the structure in charge could be the neocortex,basal ganglia, hippocampus or even a muscle)3. this same map ( or a smaller subset ) gets replayed. The mechanism(s) by which this information is first encoded and later retrieved is still not entirely understood, but it involves a map and a getaway or switchboard.4. This switchboard ties together different percepts ( a smaller network of electrical signals), so in a way the information is represented at the switchboard level, if you disable this switchboard, you can't make new memories or lose previous ones.

A grandmother cell in the scheme of what I just explained, is the result of another subsystem that helps recognize something. Once you successfully encode a percept ( thing we want to remember seeing) you might want to associate it with something ( good,bad,delicious,etc), at the top of a series of associations lies a grandmother cell, which in turn is a handy evolutionary way of signaling back to other systems when some previous information has been experienced. So in this way the information of whether a subset of relationships in between networks of electrical signals has been experienced and encoded lies here.

References/Sources:

The idea of grandmother cells and object recognition in general is summarized in the Object Recognition chapter of ( Cognitive Neuroscience,Gazzinga-3rd ed 222-225) along with the problems a grandmother cell introduces in object recognition (ie if you lose the grandmother cell you would lose all the information about your grandmother)
Koch( Quest for Consciousness-2004) chapters on vision provide a very readable account of how the information goes from retina to v1. Vision Science (Palmer) is a more thorough account.
The chapter on learning and memory (Cognitive Neuroscience) gives an overview.
(Gluck -2001-Gateway to memory) presents different models of this arrangement.


Structure coordinates in PDB file How the atoms-residues-amino acids structure information prioritized? Specifically, I am trying to understand how the first atom is identified since it does not seem to correspond to the first amino acid in the sequence. I assume it's based on the structure but is it bottom to top, left to right and such. Thank you.

The atom numbered 1 in a PDB file is the most N-terminal atom visualized by the structure determination — the most N-terminal amino acid, the co-ordinates of which are presented.
If the X-ray diffraction (or whatever technique used) does resolve the first amino acid, then it will, in fact, be the first amino acid. The following is an arbitrary example from 4LI3 (chain X):
ATOM      1  N   MET X   1     100.329 111.822  35.431  1.00 66.81           N
ATOM      2  CA  MET X   1     100.845 110.803  34.526  1.00 67.85           C
ATOM      3  C   MET X   1     101.961 111.361  33.646  1.00 71.14           C
ATOM      4  O   MET X   1     102.979 111.840  34.153  1.00 77.28           O
ATOM      5  CB  MET X   1      99.722 110.256  33.648  1.00 61.70           C
ATOM      6  CG  MET X   1      98.581 109.621  34.412  1.00 66.53           C
ATOM      7  SD  MET X   1      97.327 108.947  33.300  1.00 82.23           S
ATOM      8  CE  MET X   1      96.071 108.440  34.463  1.00 69.80           C
ATOM      9  N   ALA X   2     101.754 111.288  32.331  1.00 67.01           N

If the X-ray diffraction does not resolve the first amino acid, or if the structure is of a fragment of the protein that does not contain the first amino acid, then the co-ordinates of the first amino acid are not listed in the file and ATOM 1 is from the most N-terminal amino acid. The following is an arbitrary example from 1BTE (chain A), starting at amino acid 7:
ATOM      1  N   GLU A   7      15.888  47.505  13.150  1.00 34.63           N
ATOM      2  CA  GLU A   7      14.455  47.789  12.947  1.00 33.53           C
ATOM      3  C   GLU A   7      13.538  46.900  13.794  1.00 29.91           C
ATOM      4  O   GLU A   7      12.342  46.832  13.476  1.00 30.54           O
ATOM      5  CB  GLU A   7      14.084  47.715  11.461  1.00 37.16           C
ATOM      6  CG  GLU A   7      14.284  46.356  10.821  1.00 41.38           C
ATOM      7  CD  GLU A   7      14.124  46.366   9.313  1.00 43.82           C
ATOM      8  OE1 GLU A   7      12.959  46.323   8.849  1.00 46.10           O
ATOM      9  OE2 GLU A   7      15.151  46.420   8.600  1.00 45.51           O

(Knowledge of the first amino acid is from nucleic acid sequencing.)


Is the lac operon repressed in the presence of both glucose and lactose? In the presence of both sugars (glucose and lactose) will there be repression of the lac operon completely?

I know that more glucose means less cAMP --> less CAP --> less positive regulation, and thus less lac operon, but does that mean there will be repression of the lac operon?

According to Molecular biology of the gene by James Watson, in presence of both glucose and lactose, the lac operon has a basal level of transcription. However, when only lactose is present, the operon has an activated level of transcription, due to the CAP mechanism.


Any benefit to low dose radiation? Is there any survival benefit in humans that can be obtained from chronic exposure to low dose radiation, or is any dose of radiation a potential harm?  Has any research been done into this?

This is an interesting - and highly debated question. Generally there are two completely different directions of thinking when talking about dangerous substances (this applies to dangerous chemicals as well):

The linear no-threshold model (LNT).
The hormesis model, in our case the model of radiation
hormesis.

Summarizing the models the LNT model says that every dose has a negative response, so there is nothing like a stimulating dose and exposure should be avoided at any means. This reflects the policy in the handling of radioactive substances. If you look at the figure below, the curves a + b (supra-linear and linear) reflect the LNT model (the figure comes from here):

The radiation hormesis model says that there is a dose range in which the radiation above the background level is not only not harmful, but beneficial. High doses are (in line with the LNT model) also considered harmful. This can be seen in the curves c (linear-quadratic) and d (hormesis) in the figure above. The benefits are thought to take place through the activation of repair mechanisms (which are only activated by radiation) which protect against changes in the genome and thus also protect, once activated, against changes which are caused by other agents and reasons. See reference 1 for more details about radiation hormesis.

There are a number of studies which observe this effects in the laboratory and this is also one of the major critic points: To my knowledge it is currently unknown if these effects can also be seen outside a controlled laboratory environment.

Other critique points are low study publications (which makes studies prone to statistical errors), using wrong models (cell culture) or too high doses. See references 2 and 3.

Since our environment contains naturally radioactive substances as well as cosmic and UV radiation, we have developed pretty efficient mechanisms to deal with these problem. Additionally measurable effect of radiation on the activity repair mechanisms can be seen (and this is not debated at all), but the main question is if these effects can also have a beneficial effect. It is also not known, if all radiation ($\alpha, \beta$ and $\gamma$) have the same effect, or if some of these like $\alpha$-radiation is more dangerous.

So I think it may be possible that there is some positive effect, but until this is proven, I would rather be safe than sorry.

References:

Evidence for beneficial low level radiation effects and radiation
hormesis.
Uncertainties in studies of low statistical power
Health Risks from Exposure to Low Levels of Ionizing Radiation


What's the difference between evolution fitness and reproductive success? What's the difference biological fitness and reproductive success in the biological terminology?

The concepts are very similar but there are a few differences.

Firstly, fitness is usually applied to alleles or genotypes, reproductive success to individuals.

Secondly (and partially as a consequence of this), fitness is an average or idealised/expected property across a population; but actual reproductive success per individual is stochastic. Individuals possessing an allele with a relative fitness of "2" will on average have twice as many offpsring as their competitors, all else being equal, but individual reproductive success will vary as a consequence of other factors such as predation, parasitism, starvation etc.

Finally, absolute fitness relates to the proportional representation of a genotype in a population. Reproductive success relates to offspring per individual. For example, in a growing population a genotype could be simultaneously declining in proportion while it is increasing in absolute number, if other genotypes are increasing in number more rapidly.


What is the most recent non-primate ancestors of humans? If we go down the evolutionary tree of humans, (Homo sapiens, Homo erectus, ...), what will be the first non-primate ancestors?

According to the Tree of Life, tree shrews (Scandentia) are the sister group to Primates. So Scandentia are the most closely related extant mammals that are not Primates. Here's an image:


What are parental antagonism & parental conflict? I've been reading the chapter by Haig et al in The Genetics and Biology of Sexual Conflict. I think this chapter has them quite unclearly defined. Could anyone describe these two phenomenon more clearly than the chapter does? Real or hypothetical examples would be good to give clarification, and clarification of how they are distinct from sexual conflict and antagonism.

  "Parental Conflict will refer to phenotypic interactions in which
  matrigenes and patrigenes prefer different outcomes"

  "Parental Antagonism occurs when an allele has a relative advantage
  when inherited from one sex but a relative disadvantage when inherited
  from the other."

You may inherit a gene, which is actually detrimental to your (most efficient) functioning and hence has a cost (eg. gene for being small when food is available from tall trees). On the other hand, you may inherit a gene which has a benefit for you (gene for being tall with food available from tall trees).

Sexual Antagonism:

  What’s good for the goose may not be good for the gander. Thistwist on
  an old proverb captures the notion of sexual antagonism.Traits that
  confer high fitness on geese (females) may confer lowfitness on
  ganders (males), and vice versa.

In sexually dimorphic species (like all common complex life), the evolution of males is usually decoupled from females. This is not as bad as it seems, as females and males may have different patterns of selection, different phenotypes of mutations all at the same time dodging pleiotropic effects. Hence mutations benefiting one sex will sometimes be deleterious to the other (i.e. their fitness effects are ‘sexually antagonistic’)

Sexual Conflict:

Males and females have divergent interests in reproduction that are rooted in anisogamy and lead to distinct roles, due to sexual antagonism. Sexual conflict occurs between the same or different genes,  when there are different optima for a trait expressed in both sexes (intralocus conflict) or when there is conflict over the outcome of a male–female interaction (interlocus conflict).

Intralocus sexual conflicts are potentially very common. Researchers have found a strong positive genetic correlation between male and female fitness at the larval stage in the fruit fly (when interests of the males and females are essentially the same -> survive and grow), but a strong negative genetic correlation between adult male and female reproductive success (when the sexes are expected to have different genetic interests). This is possibly due to sexual antagonism.

Interlocus conflicts occur when there is conflict over the outcome of male–female interactions, so that the optimal outcome is different for the two sexes,as occurs in yellow dung fly mating behaviour. In a rare instance, wikipedia does a good job of explaining the example:

  In the yellow dung fly Scathophaga stercoraria, females can be injured
  in the battles between males suitors. Males are selected to evolve
  traits for competitive ability that would increase their reproductive
  success, but females would evolve a set of antagonistic adaptations to
  reduce their chances of being injured in battles between the males.
  Therefore, there is an interlocus sexual conflict in males and females
  that could possibly lead to an "unresolvable evolutionary chase" when
  a novel trait in males increases their competitive ability while
  harming the females

[5,6]

.

Parental Antagonism:

An allele in a gene is said to be parentally antagonistic if it has an inclusive fitness benefit when derived from one parent (say the mother), but an fitness cost when derived from the other parent (in this case the father)

There are many different theories out there, but the gist of it is essentially some process creating an asymmetry between the genes that you inherit from your father and mother (patriGENIC and matriGENIC), that causes differential expression of alleles (silencing the other copy) [2]

Parental Conflict:

  When parent-offspring relations in sexually reproducing species are
  viewed from the standpoint of the offspring as well as the parent,
  conflict is seen to be an expected feature of such relations. In
  particular, parent and offspring are expected to disagree over how
  long the period of parental investment should last, over the amount of
  parental investment that should be given, and over the altruistic and
  egoistic tendencies of the offspring as these tendencies affect other
  relatives. In addition, under certain conditions parents and offspring
  are expected to disagree over the preferred sex of the potential
  offspring. In general, parent-offspring conflict is expected to
  increase during the period of parental care, and offspring are
  expected to employ psychological weapons in order to compete with
  their parents. [7]

Reading:

[1] Haig, David. "Parental antagonism, relatedness asymmetries, and genomic imprinting." Proceedings of the Royal Society of London. Series B: Biological Sciences 264.1388 (1997): 1657-1662.

[2] Patten, M. M., et al. "The evolution of genomic imprinting: theories, predictions and empirical tests." Heredity 113.2 (2014): 119-128.

[3] Patten, Manus M., and David Haig. "Maintenance or loss of genetic variation under sexual and parental antagonism at a sex‐linked locus." Evolution 63.11 (2009): 2888-2895.

[4] Normark, Benjamin B. "Perspective: maternal kin groups and the origins of asymmetric genetic systems—genomic imprinting, haplodiploidy, and parthenogenesis." Evolution 60.4 (2006): 631-642.

[5] Connallon, Tim, and Andrew G. Clark. "Evolutionary inevitability of sexual antagonism." Proceedings of the Royal Society of London B: Biological Sciences 281.1776 (2014): 20132123.

[6] Chapman, Tracey, et al. "Sexual conflict." Trends in Ecology & Evolution 18.1 (2003): 41-47.

[7] Trivers, Robert L. "Parent-offspring conflict." American zoologist 14.1 (1974): 249-264.


What animal classes has also "Like Humans" XY Chromosomes for Males and XX for Females? Are other mammals. birds, reptiles, or even insects same to humans in that the male organisms have XY Chromoson at the end and female XX?

Thanks for the ansver

In mammals, Y chromosome determines the sex. SRY gene present on Y chromosome is responsible for sex determination. And, in absence of this gene results in female sex. Non-human mammals use several genes on the Y chromosome.

Platypus and Drosophila also uses XY sex determination system, but in different way. Like in platypus, combination of genes present on XY chromosome are used to determine sex characteristics. And in drosophila, two X chromosome gives female characteristics, and Y chromosome determines maleness.

Reference:
https://en.wikipedia.org/wiki/XY_sex-determination_system


Book Recommendation: Complex Traits and Complex Genetic Architecture I am looking for a book (or any good source of information) that offers an in-depth discussion and models about the evolution and analysis of complex traits and complex genetic architecture. Do you have any suggestions?

I'd define complex traits as those traits whose variance in the population is explained by quite a lot of various genetic loci and environmental factors.

Suggestions:

Evolutionary Genetics : Concepts and Case Studies: Concepts and Case Studies

Edited by Lexington Charles W. Fox Department of Entomology University of Kentucky, Faculty of Life Sciences University of Manchester Jason B. Wolf Lecturer

The mathematical theory of selection, recombination, and mutation

by R Bürger (as suggested by @rg255 in the comments)

Lynch and Walsh's Genetics and Analysis of Quantitative Traits

(as suggested by @kmm in the comments)

PS: Do tell us if you found a better one.


Are there human cells, apart from red blood cells and platelets, without a nucleus? I know that blood platelets and erythrocytes do not have a nucleus. Are there more cells in the human body without a nucleus, such as pancreas, cartilage, or lung cells?

Wanted to give a one line answer some day!!

Lens fiber cells and keratinocytes.


What is the species name of this moth? This insect was found in India. It looks like a hawk moth to me, but I still can't get the exact name for this species.

I believe that it is the vine hawk moth (Choerocampa rosetta).

https://www.whatsthatbug.com/2010/11/20/vine-hawk-moth/


Ultra Pasteurization and Pasteurization What is the effect of pasteurization and ultra-pasteurization on proteins, enzymes, and nutrients found in milk and other dairy products?

This is an interesting question and it is rather hard to find reliable information. According to a review which also did a meta analysis of all available articles, pasteurization (and also ultra pasteurization) affects the vitamins to some degree.

According to the analysis, vitamin B1, B2, B6, B12, C, E and folate decreased. The author notes however, that with the exception of vitamin B2, where milk is an important dietary source, the other vitamins are not included in very high concentrations. See the first paper for all details.

These findings are supported by another review (see reference 2), which shows some values in table 4:

This study finds proteins and amino acids not affected to a measurable degree, but data on protein behaviour is missing. My guess is that a part of the proteins are denaturated, but not all of them. There is some research which analyzes the effect of thermal treatment on milk in connection with other processes like the yoghurt or cheese production (have a look at reference 3). I haven't found any data on the proteins in milk which is directed to human consumption.

References:

A systematic review and meta-analysis of the effects of
pasteurization on milk vitamins, and evidence for raw milk
consumption and other health-related outcomes.
Which Milk is Fresh?
The Effect of UHT and VAT Thermal Processing Systems on Whey Protein
Denaturation and Gel Strength of yoghurt


Determine similarity in percentages between species A and B, A and C, and B and C The chart above is a graphic that shows the amino acid sequence differences between different organisms for a protein keratin.
The question I am required to answer begins as, "Keratin is made up of about 450 amino acids. Determine the similarity in percentages between species A and B, A and C, and B and C. Explain how amino acid sequences can be used in determining how closely related two species are."
My initial solution to finding the percentages is dividing the respective differences in the chart above by 450. Then, subtract that number by 100, and hence, find the similarity percentage. For example, for species A and B, I would divide 4 by 450, resulting in 0.89%. I would next subtract this percentage from 100%, resulting in 99.11% similarity. Is this the correct procedure?
My initial solution to explaining how amino acid sequences can be used to determine how closely related two species are is as follows: The larger the difference in amino acid sequences between two species, the less closely related two species are. Is this explanation correct as well?

Step number one is correct, but note that there are several similarity (or alternatively distance) measures. What you choose is the simplest and most intuitive one and it a good one without any other assumption or explanation given.
Step number two is also correct, if the similarity is a good proxy for when the last common ancestor between two species is in time, which in this case should be.


Is osmosis diffusion of water? My textbook says this:

Osmosis is the diffusion of water.

Wikipedia says this:

The diffusion model of osmosis is rendered untenable by the fact that osmosis can drive water across a membrane toward a higher concentration of water.

It's my understanding that diffusion is passive transport, and it moves material from a highly concentrated area of that material to an area where it is in lower concentration. By this definition, it looks like Wikipedia is correct. But if for example, a cell is put in saltwater, water from within the cell would go out. Is this diffusion now? Which definition is correct?
I would just go with the Wikipedia definition because it actively describes its own definition as a refinement of the textbook definition, but the paragraph above in the article is a bit confusing to me.

Yes, In most cases, osmosis is the diffusion of water. To my understanding, what I think Wikipedia is trying to do is to assert the fact that osmosis is also be the movement of water from a region of lower water potential to a region of higher water potential. These kinds of contradictions, as much as scientists try to avoid them, still come to play because science is very complicated. Just when we start accepting a theory, it gets discarded by another theory.


Is there any documented case in which floating substances led to the introduction of a new species? Floating substances in the marine or freshwater environment often carry hitch hiking organisms. It is argued that many species may use this dispersal vector to reach new habitats, however to my knowledge there is no hard evidence / no documented case. This may be because of the difficulty to associate an established species with a certain vector of introduction.

By floating substances I refer to natural floating substances such as detached algae, trees or pumice and those of anthropogenic origin such as litter items, detached buoys, etc. (in whatever aquatic environment: sea, lakes, rivers)

Any help to find a reference / documented case study is very welcome!

There is a number of reported cases of marine species reaching new locations through "hitchhiking" in recent times. However, it seems harder to find reports of species actually becoming established in a new location through this.

The following articles describe examples of species transported with ocean debris:

In an early study on the dispersal of plastic pellets (3), it was suggested that pellets encrusted with the bryozoan Membranipora tuberculata was transported to New Zealand across the Tasman Sea from Australia. Barring one exception, this was the first time the species was observed in New Zealand waters.

Appendix A of a later article by the same author (1) contains 13 examples of species transported by sea (not necessarily through debris, or invasive), including the previous example. Of it, the author writes that

  Later, L. M. Stevens (1992, unpublished data) was to report that [Membranipora tuberculata]
  was abundant on both eastern and western shores around northernmost
  New Zealand.

Thus, this is possibly a case of a species transported on floating debris and subsequently becoming established in a new habitat.

Jose Derraik also deals with the topic in a review (4):

  Plastics floating at sea may acquire a fauna of various encrusting
  organisms such as bacteria, diatoms, algae, barnacles, hydroids and
  tunicates (Carpenter et al., 1972; Carpenter and Smith, 1972; Minchin,
  1996; Clark, 1997). The bryozoan Membranipora tuberculata, for
  instance, is believed to have crossed the Tasman Sea, from Australia
  to New Zealand, encrusted on plastic pellets (Gregory, 1978). The same
  species together with another bryozoan (Electra tenella) were found on
  plastics washed ashore on the Florida coast, USA, and they seem to be
  increasingtheir abundance in the region by driftingon plastic debris
  from the Caribbean area (Winston, 1982; Winston et al., 1997). Minchin
  (1996) also describes barnacles that crossed the North Atlantic Ocean
  attached to plastic debris. Drift plastics can therefore increase the
  range of certain marine organisms or introduce species into an
  environment where they were previously absent (Winston, 1982).

Finally, the book Marine Pollution: New Research (2) contains the following passage which ends with the observation that conclusive proof is difficult to obtain:

  Drift plastics are known to have introduced exotic marine species to
  several areas (Winston et al., 1997; Deraik, 2002). Winston et al.
  (1997) reported that the non-indegenous oyster Lopha cristagalli was
  fond on plastics wshed ashore in southern New Zealand, and that the
  exotic bryozoan Thalamoperella evelinae was found on plastics washed
  ashore in Florida. Barnes and Milnder (2005) fond the exotic barnacle
  Elminius modestus on plastic debris in the Shetland Islands (Atlantic
  Ocean). The bryozoaen Membranipora tuberculate is believed to have
  crossed the Tasman Sea from Australia to New Zealand rafting on
  plastic pellets (Gregory, 1978). M Tuberculate and the bryozan Electra
  tenella seem to be increasing their abundance on the Florida coast by
  drifting on plastic debris from the Caribbean sea (Winston, 1982
  Winston et al, 1997). Maso et al. (2003) (...) However, attributing a
  marine biological invasion to floating marine debris and not to other
  mechanisms is very difficult in most cases, and available data are
  generally insufficient.


Do ectotherms think slower when they are cold? Animals near the ectotherm side of the endotherm-ectotherm spectrum rely on external heat sources to regulate their body temperature. When they are cold, overal enzyme activity and metabolic rate is lower.

My question is if these animal tend to 'think' slower when cold?

To be honest, my knowledge of brain physiology is very sketchy, I'm not sure biochemical activity plays a large role vs. electrical and diffusion processes and the latter would be less temperature dependant. So I'm not sure we would expect ectotherms to 'think' slower.

OTOH, wikipedia on endotherms states ...

  Some ectotherms, including several species of fish and reptiles, have been shown to make use of regional endothermy, where muscle activity causes certain parts of the body to remain at higher temperatures than the rest of the body. This allows for better locomotion and use of the senses in cold environments.

The source for this claim is on google books, just not the relevant pages (Willmer, Pat; Stone, Graham; Johnston, Ian (2009). Environmental Physiology of Animals)

I'm also not sure how to define 'thinking' within this wide range of animals, I'll take any metric for  speed at cognitive tasks or reacting to external stimuli.

I would assume as the temperature decreases, even as an ectotherm organism that the neuro processes would decrease. From my experience in chemistry, the colder the temperature the slower the molecules vibrate. As a result, it would take a longer time for the sodium and calcium molecules to move from the end of the neurons to the synapses resulting in delayed thinking. If they are absorbing the energy necessary, then their neuro processes should be functioning normally.


Why don't bees sting hornets for defense? Why don't honeybees sting hornets for defense when their hive is attacked? It seems like a good weapon against bigger animals - why not against hornets?

Smithsonian mag says that the bee stings can't penetrate through the predator hornet's armor, which is simply a case of the hornet's armor being tougher than the blunt barb of the bee sting. https://www.smithsonianmag.com/smart-news/invasion-murder-hornets-180974809/
Here's a good research:"

To examine their behaviors of penetrating into different materials, we performed penetration–extraction tests and slow motion analyses of their insertion process. In comparison, the barbed stings of honey bees are relatively difficult to be withdrawn from fibrous tissues (e.g. skin), while the removal of paper wasp stings is easier due to their different structures and insertion skills. The similarities and differences of the two kinds of stings are summarized on the basis of the experiments and observations.

Some research suggests that bee stings have evolved to ward off vertebrates, physically and chemically. Wasps have more slender stings and perhaps that's why the hornets prefer bees nests.
Actually, a lot of insects have phenomenally hard keratin, beetles and the bulldog raspy cricket, as far as i know, even parasitoid wasps which have specialized stings evolved to cope specificially with insects are more common on caterpillars and spiders than strongly armored animals like big beetles.


What is the meaning of a selection regime in this context? "Our second approach was based on modeling adaptive regimes
across a phylogeny for each of the groups in our study using an OU
model. We especially focused on the lineage leading to humans, and
tested whether a shift in the selection regime was inferred on this
branch. Under the OU model, species evolve through various selection
regimes that map to branches on the phylogeny. The goal is to characterize the regimes across the tree, and to assess whether a shift in selection regime occurred on the branch connecting Homo to the
other primates."

taken from:
Nunn, Charles L., and David R. Samson. “Sleep in a Comparative Context: Investigating How Human Sleep Differs from Sleep in Other Primates.” Wiley Online Library, John Wiley & Sons, Ltd, 14 Feb. 2018, onlinelibrary.wiley.com/doi/abs/10.1002/ajpa.23427.

I'm an evolutionary biologist. When someone says "selection regime" they simply mean the general conditions (environmental, ecological, etc.) that could have produced a particular evolutionary outcome. For instance, in the example that you mention, they seem to imply that they are interested in knowing if these condtions (i.e. the "selection regime") in the branch that lead to the evolution of humans were somehow different than these of other primates. So, it is a hypothesis, in this case. Unless they state elsewhere in the paper what exactly is this "selection regime", they are simply referring to this idea.


How many people are required to maintain genetic diversity? Imagine humans were to colonize a distant planet and it was a single one-way trip. How many people would they need to bring?

Obviously 2 is the minimum, but that would result in a lot of inbreeding.

So what number is the minimum number of people you can have in an isolated community and still maintain a healthy diversity?

Actually it is a very important question for laboratory animals (and, I imagine, endangered species) and was calculated to be 25 couples.

With any number of animals (including humans), there is always some inbreeding happening, but you can reduce it with the number of breeding pairs and careful pairing. When you get to 25 pairs (50 animals) and have complete control over pairing, you can sustain the genetic diversity practically infinitely (especially if you take into account spontaneous mutations).

Of course, such control over who can have children with who (plus whether one is at all allowed to procreate and what will be the sex of their children!) would be questionable morally, so in case of populating a distant planet, we would need a larger group, to provide for sexual preferences, fertility problems etc.

Some information on laboratory outbred stocks.


Transposons, Viruses and RNA interference My textbook says that in RNAi, a complementary double stranded RNA sequence attaches to an mRNA and silences it using a protein machinery. I Googled and read about this so now I know what siRNA and RISC and microRNA are. But the next thing my book says is

  “the source of these complementary double stranded RNA
  sequence [obviously my textbook means siRNA] may be viruses and
  transposable elements.”

What does this mean? Do transposons make siRNA? I thought transposons were non-coding except when they travel via the retrotransposon mechanism.

Do viruses that infect eukaryotic cells donate their own RNA genetic material for the cell to use in RNAi? But I thought RNAi was a cellular defence against viruses, how can viruses help give the dsRNA that’s supposed to fight the viruses? A number of sites online simply state that siRNA is exogenous is origin; do they mean that it comes from viruses?

I would greatly appreciate it if someone could take the time to answer each of my questions one by one or even recommend a site that answers them all.

Transposons and viruses don't "make siRNA". However, an endonuclease called Dicer can process dsRNA from these sources to produce siRNA which is then loaded to the RNA-induced silencing complex (RISC) to suppress propagation of viruses and transposons. The following papers provide a good overview:

Buchon N, Vaury C. 2006. RNAi: a defensive RNA-silencing against viruses and transposable elements. Heredity 96:195-202.

van Rij RP, Andino R. 2006. The silent treatment: RNAi as a defense against virus infection in mammals. Trends Biotechnol 24:186-193.


Identification of a beetle found in a basement in Virginia, USA Beetle found in basement in Alexandria, VA, USA

Approximately 5cm (2 inches) in length.

That is a female Eastern Hercules beetle. Dynastes tityus https://bugguide.net/node/view/4462 Family Scarabaeidae, Subfamily Dynastinae. One of the largest of the beetles in the South-East U.S.


Is probability for double crossing over included in distance cM? [task] We got this task:

There are 3 genes (acb) on one chromosome (linked inheritance). Distance a-c = 12cM, a-b=16cM. Probability for double crossing-over (CO) is 0,6%. Find ratio of genotypes of descendants (AcB/acb X acb/acb).

I don't know whether the 0,6% for double CO is included in the 16% (16cM) probability.

I think it is not, so I got these ratios:
No CO and double CO: 42% AcB/acb, 42% acb/acb,
1x CO: 8% Acb/acb, 8% acB/acb

Centi-Morgan (cM) is based on observation not precise measurements. Now since double crossing-overs (and actually any arbitrary even number of crossing-overs) revert gene combination to the parental type, resulting lower recombinant frequency. So in your case since the chance (or the frequency if you wish) for double COs is 0.6%, you have to subtract this from parental genotypes and add it to the recombinants.


Can anyone identify this mystery caterpillar? I found this caterpillar in in El Cerrito, CA and was wondering what kind it is?

Best assumption, Gulf Fritillary Caterpillar (Agraulis vanillae). I could be wrong though.

  The larva is a caterpillar which grows to approximately 4 cm (1.6 in) in length. It is bright orange in color and covered in rows of black spines. The spines are soft to the touch and do not sting, but the larva is poisonous if eaten. Source: Wikipedia.


What gives things their colour? My 6 year old daughter asked me 2 biology-related questions yesterday and I tried my best to answer them with the aid of YouTube videos.  One of the questions (I may post the other one too) was

  How do we see colour?

I showed her a video on YouTube where it was explained that light hits an object and if that object is a tangerine then that object will absorb all colours except orange and will reflect orange and that's why we see it as being orange.  I then repeated this explanation and she said.

  But how do we see different colours?

I then showed her a video describing corneas, vitreous humours, lenses, optical nerves and so on.  I think I lost her.  I got a bit lost too.

Now I have two problems, which I'd like to ask to you all as questions

I do not know how to explain to a 6 year old how we are able to perceive colour.  Does anyone know how this can be explained?
I have never quite understood this idea that an object has a colour depending on the light that hits it.  Okay, I understand that in low light objects have a different colour because there is a not much light hitting it and that different objects absorb different wavelengths of light and therefore appear as different colours.  What I don't understand is that if I place a bar of gold a bar of silver side by side in the same lighting conditions they do have different colours, so therefore there must be something inherent in these object that give them different colours.  What is that something?

I do not know how to explain to a 6 year old how we are able to perceive colour. Does anyone know how this can be explained?

Well, depending on the depth you want to introduce her to, it can be difficult to explain to adults - much less children. You explained the basics well enough. Without going to the molecular mechanisms, here's a useful diagram:

Light will pass through the eye and Retina until it hits the Cones and Rods. That produces a reaction (which I'll address next) - which then causes signals to either resume or cease (Rods are, ironically, shut off by light - not turned on). These signals pass through Ganglion cells, through the Optic Nerve, and interpreted by the brain. When some cells are switched on, like a 3-Way traffic stop, they will prevent the information from other cells being transmitted.

A simple way of explaining it might be that inside our eyes are millions of teeny-tiny molecules that act like light-switches, and the brightness and color of light determine which of the "light-switches" are on or off.

If you want to go further into the actual mechanisms (or just have the background knowledge for future reference) the next diagram shows the mechanism itself (and the original in full-size since the one shown is squished if you prefer):

The big things to note above is the change from cis-Retinal to trans-Retinal which occurs after a Photon is absorbed. This causes signaling molecules to go a bit wild, open ion channels, and the depolarization of the membrane propagates the charge down the cell - much like a neuron.

  I have never quite understood this idea that an object has a colour depending on the light that hits it. Okay, I understand that in low light objects have a different colour because there is a not much light hitting it and that different objects absorb different wavelengths of light and therefore appear as different colours.

Well, let me stop you here. Low-light is a different situation than colored-light. Let's get the basics down:

Photons are absorbed by the electrons of the atoms that compose the molecules of an object. Whatever Wavelength of light is not absorbed by the electrons is reflected, and it's this Wavelength that we perceive as the color of the object as our Cones absorb the reflected light.

Photons can also be emitted when an electron moves to a lower-energy state. The Wavelength emitted by the electron is directly related to the difference between the High and Low energy states, as this diagram shows fairly well:

The emitted photons are the object's "Incandescence" - which is when an object produces a color of light by itself. The color you perceive is NOT going to change if the object emits incandescent light because the object is generating its own light. Neon signs are a great example: The gases being subjected to a current emit light, and will appear whatever color it's supposed to be whether or not it's a blue moon or sunset.

Photons which are reflected and not emitted - i.e. almost everything that doesn't have a power source - as I said above, are then absorbed by our Cones and our brain interprets the signals to produce a color.

The reason why objects that reflect light can change color is because not all environmental light is the same. Red objects will appear Black under Blue light because Blue light doesn't contain Red Wavelengths - there's nothing to reflect, so the object absorbs all of the available Wavelengths - the very definition of Black!

A lot of our color perception depends on ambient light, and most of the time - thanks to the Sun - that is a full-spectrum white light. Which brings me to answer the last bit of your question:

  What I don't understand is that if I place a bar of gold a bar of silver side by side in the same lighting conditions they do have different colours, so therefore there must be something inherent in these object that give them different colours. What is that something?

Yes, there definitely is something inherent in both objects. That is: Their electron configurations absorb different chunks of the spectrum, and accordingly reflect different chunks of the spectrum. Although that's still a bit simplistic, since metals have some unique properties that other Elements do not. Their electrons exist in more of an "ocean" than around central atoms, but that's a whole other question.

As a fun bit of Trivia to impress your daughter when she's old enough, it's always a fun fact to know that the color Yellow is completely constructed in your head.

The human eye only has Rho (Red), Gamma (Green), and Beta (Blue) color receptors which have the following absorption pattern (from photo.net):

What everybody sees as "Yellow" is actually when both the Green and Red receptors are activated at the Wavelength where they intercept above, which your brain interprets as "Yellow":

Because your brain does a lot of processing, despite having only three color receptors we can perceive millions of colors (and shades/tones). Now for a while everywhere you look you'll be utterly amazed at what's going on, and you rightfully should be. ;-)


How pricey does the media need to be for a typical bacterial culture experiment? I'm considering various lab supplies for a protocol we're going to be running, and have been struck by the remarkable difference in price for different quality levels of the same basic substance.
Sigma will sell you water, for example, for anything from \$15/L to \$500/L and even over \$10,000/L, depending on what level of purity is guaranteed. Obviously, one doesn't want to use inferior tools and guaranteed unreliable results, but also it would be foolish to use a reagent that's far pricer than one's actual tolerances.
Most of the actual protocols that I encounter, however, don't seem to actually specify what grade of purity they need, and I'm trying to figure out how to navigate the problem. Trial and error is definitely not a good option, since (a) it can waste a lot of time, and (b) good and bad results in a trial don't actually tell you what you need (a good result could be an unusually good batch of poor reagent; a bad result could be from an entirely different problem). Asking the authors is also not a great solution, for a number of similar reasons.
To make this concrete, let's consider a very simple and typical case that I am currently encountering. The protocol I'm setting up for right now cultures E. coli in LB media. Sigma will sell me LB media powder as "quality 100" L3152 for \$139/kg and "quality 200" L3522 for \$182/kg. Both say they are "good for E. coli".
Is there any reason not to pick the cheaper media? How should one decide how much quality their media needs to have for a typical bacterial culture experiment?

It looks like Merck have different levels of quality control for their products. MQ 100 being the lowest up to MQ 600 being the highest. From what I can see the MQ200 product here has defined composition (of salt, tryptone and yeast extract in g/L) whereas the cheaper MQ100 product does not appear to have its composition ensured.
I am sure your cultures will grow in cheaper media but perhaps you would theoretically lose out on some replicability and perhaps if you were doing metabolically focussed experiments you would want to be certain of your media composition.
As for water, I have always used distilled water which is then autoclaved after you add the media with no problems.


What's a good reference for learning about recombinant proteins? I'm looking for books and articles that can bring me up to speed on the design, expression, and purification of mammalian proteins in recombinant systems, both in E. coli and in more complex systems like CHO or Sf9 cells. I have a weak but functional background in general molecular biology.

i would start by searching PubMed literature database for relevant articles using this query:

"protein"[Title/Abstract] and "expression"[Title/Abstract] and "purification"[Title/Abstract] and "recombinant"[Title/Abstract] and "mammalian"[Title/Abstract] and ("E. coli"[Title/Abstract] or "CHO"[Title/Abstract] or "Sf9"[Title/Abstract])

which returns 116 articles (including 7 reviews).


Phenoptosis, behavior evolved for good of species? I was reading this and felt like the argument is being made that organisms die for the good of species. Isn't this nonsense?

This especially bugged me:

  "'Age-induced, soft, or slow phenoptosis'" is the slow deterioration and death of an organism due to accumulated stresses over long periods of time. In short, it has been proposed that aging, heart disease, cancer, and other age related ailments are means of phenoptosis. "'Death caused by aging clears the population of ancestors and frees space for progeny carrying new useful traits.'"

Per the selfish nature of genes, it might be okay if it was only your offspring you are dying for, but even that only when you know you can't reproduce further. And the above argument says that old age death is exactly that.

I don't really have an opinion on whether or not this is the main or even a reason for the evolution of senescence and death, but it is certainly not nonsense.

Death can indeed be good for a species. Diversity is always good and the death of the elders allows phenotypes that have been selected for more recently to take hold in the gene pool. If the young need to compete with the old, this will make it harder for them to grow and reproduce. In situations with a limited food supply, having to support old individuals who can no longer forage/hunt for themselves will be a strain on the species/society/pod or whatever it is we are looking at.

Therefore, genotypes that encourage the death of elders who are past the age of reproduction could be selected for. This does not contravene the selfish gene hypothesis at all, these individuals have already reproduced, the selfish gene no longer 'cares' about them. The main idea of the selfish gene hypothesis is that the genes themselves 'want' to be passed on, not that the genes 'want' to save themselves. Once their host has reproduced, they loose interest so to speak.

The selfish gene theory is just a conceptual tool, it should not be taken literally. It does not suggest that genes are actually selfish or in charge of their own evolution in any way. It is just a useful approach to take when studying evolution and was instrumental in our understanding that the gene (the nucleotide actually) and not the individual is the smallest unit of selection.

Anyway, in the strictest sense, the statement in your question is absolutely compatible with the selfish gene hypothesis. If you can no longer pass your genes along, you are useless and just a drain on the species, why should you keep living?


Photosynthesis production of oxygen If you are to increase the intensity of light indefinitely, would you expect the production of oxygen to continue to increase?

No — there are both theoretical limitations and experimentally proven ones.

Chemistry in cells is subject to the same laws as chemistry in general. For photosynthesis to take place, certain molecules (e.g. ADP and NADP+) have to be present to transport the energy harvested to the place where carbohydrates are synthesized from this energy. The transport rate of molecules is limited by the rate of diffusion (see Brownian motion) within a fluid at roughly room temperature (where photosynthesis takes place). This limits the amount of energy that can be processed within a defined volume of plant tissue.

There are further limiting issues. Above certain light intensities, some parts of the plant cell suffer heating and destructive effects, which also limit photosynthesis.

See an abstract on this topic

There are also measured limits. Most plants with leaves exhibit stagnant photosynthesis rates at light with $$600 \frac{μmol}{m^2 \cdot s} $$
or higher.


"Twig-with-leaf"-like insect in central Mexico What's that?! I have googled around and found insects that looks like a twig, and others that look like a leaf, but this one looks deceptively like a leaf at the end of a twig (I swear it's a real living thing despite the appearances: it has legs and moves around!). As you can see from my hand on the photo it is also fairly big (well, at least for my European standards...).

Location: Morelia, Mexico (about 2000m high, in the tropics)
Time: October (humid season), in the morning

That is a Mexican/Texas unicorn mantis, which is of the species Phyllovates chlorophaea.


Is their goli in plant cell? We know that plant cells have dictyosomes instead of golgi but in my book it was written that plant cells have golgi apparatus?

From wikipedia > Golgi apparatus

  The Golgi apparatus, also known as the Golgi complex, Golgi body, or simply the Golgi, is an organelle found in most eukaryotic cells.

and further

  In plants, Golgi stacks are not concentrated at the centrosomal region and do not form Golgi ribbons. Organization of the plant Golgi depends on actin cables and not microtubules. The common feature among Golgi is that they are adjacent to endoplasmic reticulum (ER) exit sites.

and also

  The [trans Golgi network] may act as an early endosome in yeast and plants.

The dictyosome is a part of the Golgi apparatus. There is no english wikipedia for dictyosome but here is the french one


Is a pampa an example of ecological succession? I'm not very sure if a pampa is an example of an ecological succession.
The reason of my doubt is due I've remember hearing that a Pampa is formed when a Valley which has had a river on it, no longer has it due the river changed its course and left the place without water.
But is it okay for this reason to imply that the Pampa (biome) is the result of an ecological succession?. The wikipedia entry doesn't give much details.
But it constrains the term for only the lands located in Brazil and Uruguay. It does not give any indication why some other places such as in Bolivia and Peru also use the term. Given these, could it be confused with a Mediterranean forest or with a Chaparral?.
Are those of the same origin?. Can someone help me here?. I'm confused about these.

This is a difficult question to answer. I would say that is uncommon (though not improper) to think of questions of ecological succession at the biome scale. In this case, the pampa is probably a good example of a climax community (if we exclude human-caused changes). After the rivers changed course there would have been a lot of bare substrate. Over time different plant species would establish and then  be replaced by other plant species. After thousands of years you would get to the somewhat stable state of the pampa biome. It is important to note that this biome is maintained by fire and grazing (Vignolio et al 2003). Fire/grazing prevent trees and shrubs from establishing in high densities and maintains the open grasslands of the pampa. In general, every place in the world that has natural life would be the result of ecological succession. Succession is a process that happens as life establishes and ecological communities change.
As for why other places are also called pampas, the word "pampa" apparently comes from a Quechua word for plains, that was then adopted into Spanish. Since Peru and Bolivia both have Quechua speaking populations, it seems reasonable that this work was applied to plains areas in those countries.
Edit in response to comments
Comment about biome scale
The reason behind the scale comment is that typically we observe succession for a given habitat. Part of this stems from the origin of the succession ideas, where Frederic Clements posited that climate was the major driving factor of successional trajectories (Clements 1916). This would actually fit well with the biome view of succession, however in order for this model to explain all the variation we see in the world (eg. why a tree grows in location X but not location Y 4 metres away), you devolve into splitting the world into infinitesimally small micro-climates. Henry Gleason proposed a more individualistic model, which suggested that climate was just one influence, and that each plant species responds to a myriad of different environmental cues (Gleason 1927). The sum of these responses results in the community at a given location. This seems to fit better with our current understanding of succession but is not without problems. In a Gleasonian model, any variation can be expected to result in a different community. Since it would be strange for the pampas region to be homogeneous over 1.2 million km2, there are likely distinct communities within the biome, each developing as a result of factors like soil moisture, soil chemistry, climate, wind exposure, and herbivore use. One can still talk about succession at a biome scale, but at that scale we would be thinking about what factors lead the pampas region to become a grassland, rather than what factors lead grass X, tree Y and forb Z to coexist next to each other.
Factors maintaining grassland type ecosystems are fairly uniform globally. You need some sort of event that will kill woody vegetation but not kill grasses and forbs. Fire and grazing are natural examples (Briggs et al. 2002), but mowing would also maintain grassland (Fidelis et al. 2012). Earthquakes are unlikely to maintain grassland as trees and shrubs are likely to survive earthquakes.
Comment about global pampas
Yes, and no. There are other wet grasslands in the world that would have similar moisture regimes and productivity levels seen in the pampas of South America. However, these are likely not called pampas. Temperate grasslands in Canada and the US are typically called prairies or plains, while the same kind of system is called a steppe in Eurasia. Ecologically they are very similar in function, though they may have very different species present. Perelman, Burkart, and Leon (2003) use prairie and steppe to refer to different sub-communities of the Pampa. Perhaps the closest analogue would be the Great Plains of North America. There is no other area called the Great Plains, but since the great plains are made up of prairie, steppe, and savannah (Oesterheld et al. 1999), there are many other areas globally that exhibit similar ecological function. This can get confusing, as there are cultural usages of these terms to refer to places, and there are ecological uses of these terms to refer to grassland sub-types.
I am not sure I understand how you are relating chaparral/Mediterranean forest to this. Both of those ecosystems will have much higher presence of trees and shrubs than pampas/prairie/steppes (Hanes 1971, Palahi 2008). Chaparrals tend to be dominated by evergreen drought tolerant shrubs, while Mediterranean forests will have more trees present. All of these systems are influenced naturally by fire and drought, so they are similar that way.
Sources
Briggs, John M., Alan K. Knapp, and Brent L. Brock. "Expansion of woody plants in tallgrass prairie: a fifteen-year study of fire and fire-grazing interactions." The American Midland Naturalist 147.2 (2002): 287-294.
Clements, Frederic Edward. Plant succession: an analysis of the development of vegetation. No. 242. Carnegie Institution of Washington, 1916.
Fidelis, Alessandra, et al. "Short‐term changes caused by fire and mowing in Brazilian Campos grasslands with different long‐term fire histories." Journal of Vegetation Science 23.3 (2012): 552-562.
Gleason, Henry Allan. "Further views on the succession‐concept." Ecology 8.3 (1927): 299-326.
Hanes, Ted L. "Succession after fire in the chaparral of southern California." Ecological monographs 41.1 (1971): 27-52.
Oesterheld, M., et al. "Grazing, fire, and climate effects on primary productivity of grasslands and savannas." Ecosystems of the world (1999): 287-306.
Palahi, M., et al. "Mediterranean forests under focus." International forestry review 10.4 (2008): 676-688.
Vignolio, Osvaldo R., et al. "Effects of fire frequency on survival, growth and fecundity of Paspalum quadrifarium (Lam.) in a grassland of the Flooding Pampa (Argentina)." Austral Ecology 28.3 (2003): 263-270.


Restriction enzyme digestion A circular plasmid of 10,000 base pairs (bp) is digested with two restriction enzymes, A and B.  This produces a 3000 bp and a 2000 bp bands when visualized on an agarose gel. When digested with one enzyme at a time, only one band is visible at 5000 bp.

If the first site for enzyme A (A1) is present at the 100th base, the order in which the remaining sites (A2, B1 and B2) are present is -

(A) 3100, 5100, 8100

(B) 8100, 3100, 5100

(C) 5100, 3100, 8100

(D) 8100, 5100,. 3100

NOTE: This is a Kishore Vaigyanik Protsahan Yojana 2014 exam (stream SX) Question. I really couldn't understand the diagram shown in the solution, and my teachers were of no help either. The diagram in the solution is:

Examine the effects of Enzyme A on its own.

Enzyme A performs two cuts that result in 2 fragments that are 5000bp long.
We know that the first cut is made at the 100th bp.  Therefore the second cut is made at the 5100th bp (A2).

You can stop there and determine that the answer is C.  C is the only answer that states A2 = 5100.


Do the antibodies in a patient suffering from Hashimoto's, attack the thyroid hormones or the thyroid gland (or both?)? If oral thyroid hormone supplement is administered, is the attack stopped or does it just create an excess of thyroid hormones so that even after a lot of it is destroyed by the antibodies, there is still enough for normal bodily functions?

Hashimoto's Thyroiditis is an autoimmune disorder where autoreactive attack on the actual thyroid tissue results in hypothyroidism. Pyzik et al., 2015, provides a good review of what we know about HT. The prevailing theory is that nonspecific infection can induce HLA expression on thyroid cells through the action of interferon gamma.

HLA is an antigen-presenting complex in humans that in our case is the major histocompatibility complex II or MHC-II you will see in texts (to avoid confusing names). Processed segments of protein are loaded onto the MHC-II, and displayed to the extracellular space where T cells positive for CD4 can recognize them. CD4+ T cells, upon recognition of MHC-II, are stimulated into T-helper or Th cells that are specific for the protein antigen they found on the MHC-II. The problem with MHC-II expressed by thyrocytes and the like is they can load either foreign or self peptides, so if it loads a part of thyroglobulin (Tg) on there and that's what the T cell recognizes, it's going to produce an immune response specific for Tg in a complex series of downstream events.

Being said, supplementation of thyroid hormone is a good treatment for hypothyroidism but it won't stop the attack on the actual gland. Thyroid hormones aren't often attacked by autoimmunity because they aren't protein antigens, and different subsets of cells respond to non-peptide antigens.


Are there any examples of how to apply evolutionary models? Apologies if this question it too open-ended; evolutionary biology is not my primary field.

I have been reading a lot about the use of statistical mechanics in analyzing evolutionary dynamics. As an example, consider this paper: http://www.pnas.org/content/102/27/9541.short.

The ideas are pretty straightforward. There is some genotype-fitness landscape and selection drives populations towards maximal fitness. However, genetic drift can pull these populations away from maximal fitness. These two concepts are analogous to minimization of internal energy and maximization of entropy in thermodynamics.

However, most of the papers that develop these models never properly explain how to apply them to observable phenomena. Is it because there is some disconnect between the parameters in the models and nature? For example, many of these models use the effective population size, which is unknown for most species.

I guess my main question is this: are there any demonstrations on how to use these toy models to predict something in nature, or are they simply for theoretical purposes.

Hypothesis testing in evolutionary biology

Pretty much any paper of empirical evolutionary biology tests hypothesis. If you go on google scholar and look for any empirical paper in the field of evolutionary biology such as "does sexual selection has antagonist effect to natural selection", "evolution of range limits", "evolution of mutational robustness" or "sensory drive speciation" you will find tons of papers that test hypotheses. Many of these hypotheses have been developed either in pure theory papers on in papers that mix some level of theory (no necessary need of complicated modelling) and empirical work. There is nothing in evolutionary biology that is different from the other field of biology or the other fields of science in our ability to test hypotheses.

A tiny bit of history

In the first half of the century most work in evolutionary biology was theoretic. Many hypotheses were left untested. Today, we perform lots of tests and the technics of molecular genetics (sequencing and stuff) help a lot to test hypotheses. Some papers, indeed uses metrics that are very hard to estimate, eventually too hard (too expensive) to be estimated today, it is true and it is an issue, an issue that all sciences know of. We sometimes have to wait for technical advancements before being able to test a hypothesis.

Concerning the paper you mention

From your description of the work they performed in the paper you linked (I haven't read this paper) it sounds like they are describing the concept of shifting balance theory, a process that has been first hypothesize by S. Wrigth in 1932. As said on the wiki article, there is little empirical evidence for shifting balance theory (but you may want to read this and that). The reason is that shifting balance theory is link to the concept of adaptive landscape. Adaptive landscape is what we call the relationship between fitness and phenotype or fitness and genotype. We have descriptions of fitness-phenotype relationship but we are only starting to offer good and complete descriptions fitness-phenotype-genotype relationship. Understanding the link between genotype and fitness is essential for testing shifting balance theory. Shifting balance theory is a logical consequence of the process of drift and selection, both of which are very well known (and well tested). Most of the issue is in the description of how rough is the fitness landscape to know whether shifting balance theory is indeed a thing that occurs in nature or whether it is very unlikely of such process to ever occur.


Identification of beetle: black with orange stripe and 2 orange dots I found the following beetle in a wooded area in Essen, Belgium. Does anybody know what species it is? Thanks in advance.

Looks very much like Nicrophorus investigator https://www.pinterest.com/pin/815362707508687290/


How does ubiquitin recognize misfolded proteins? Misfolded proteins are tagged by ubiquitin and then are destroyed by proteasomes. How does ubiquitin know which protein to tag?

Ubiquitin and the UPS

The ubiquitin proteasomal system (UPS) is a common method of regulation for many proteins in the cell. The modification is actually generated by E3 ubiquitin ligase, of which there are ~400-800 in the mammalian cell and the main source of specificity in the UPS (E2 ~40 and only 1 or 2 E1).

Ubiquitin gets its name from ubiquitous, meaning found everywhere. It's a 76 amino acid molecule that modifies proteins at lysine residues. Monoubiquitination can act as a signalling molecule whereas polyubiquitination leads to degradation. Ubiquitin is first activated via an ATP-dependent pathway to create a high energy thioester with E1. This is transthiolated to E2 and finally E3 allows the addition to the target protein. So really, your question is how E3 ubiquitin ligase recognises its target. 1

E3 ligases

There are 3 classes of E3 ligases, according to whether they contain a RING, U-box or HECT domain. These domains are responsible for either directly catalysing the addition of ubiquitin or simply facilitating another E3 ligase to do so. RING and RING-like domains are by far the most common (<600). Exactly how these domains mediate the transmission of ubiquitin is not clear, but it can be via an E3-Ub intermediate or directly from E2 to the target. The domains are relatively standardised, due to the fact they bind to E2 proteins, which contain less diversity than target proteins. However, it's the combination of the E2 and substrate binding domains that generates the selection. 2

Target recognition

So how does the target come into all of this? Each E3 ligase recognises a specific sequence on the target protein due to it's own conformation and signal sequence creating a unique interface full of intermolecular interactions- just like any protein recognises any other protein. However, although individual cases vary, the tight control primarily comes from post translational modifications on the target. Phosphorylation in particular is common in signalling and may allow E3 to bind, inducing degradation of the target. I'll use some examples to demonstrate this point, but note that every case will be different.

c-Cbl (E3) recognises activated receptor tyrosine kinases and ZAP 70/Syk kinases (target) by binding a phosphotyrosine sequence through its tyrosine kinase binding domain (containing SH2 domain). The phosphorylation is controlled by other cellular signals
Glycosylation
Proline hydroxylation
Sumoylation

Other regulations of the process that are linked but perhaps outside the scope of your question include E3 post translational modifications (eg. autoubiquitination), sequestration of E3 via binding partners (Cand1 and Roc1), pseudosubstrates and substrate competition. 7

Misfolded protein degradation

Making protein is a large investment for the cell and so there are several protective measures to prevent misfolding/aggregation. Whilst there are many different types, chaperones generally work by isolating the misfolded protein and undergoing a series of binding release steps, triggered by hydrolysis of ATP. The protein can still be released unfolded, and the cell will continually try to isolate it for refolding. However, certain chaperones form a complex with the proteasome, and can recruit other UPS components. The choice to give up on refolding appears to be a stochastic process, and will depend on the concentration of the appropriate chaperones. Misfolded proteins tend to have significant regions of exposed hydrophobic residues, and E3 ligases are therefore likely to recognise this less specifically than the degradation pathway described above.

Relevant sources include endoplasmic reticulum associated degradation and chaperones.

Summary

The answer to your question is that there is no standard recognition sequence in E3 to know which protein to target, the binding needs to be diverse in order to give the control the cell needs. That means it could be anything, but each E3 is likely to be relatively specific for its target, and is often controlled by other post translation modifications on the substrate. Misfolded proteins can be recognised and degraded due to the association of the UPS with chaperones.

If you're really interested, you can download this file and open it in something like PyMol to actually see the ligase ready to transfer ubiquitin.


What are Some Classical Examples of Local Adaptation? Question

Can you please give a list of classical (textbook) examples of local adaptations?

How to answer

Examples don't necessarily need to include what evidence supports this specific example of local adaptation. A simple description of the local adaptation (e.g. coat colour changes from black on dark soil to white on light soil) and an brief explanation of the reason (e.g. because being nicely camouflaged prevents from predation from hawks) is enough.

I think a list of 10 or more such examples would be great.

Definition of local adaptation

Note that I define here local adaptation as differentially adapted subpopulation of a single species (with existing gene flow between subpopulations especially for sexually reproducing species).

Justification for the question

I found surprisingly complicated to find such list online. I think it could be a valuable post for many.

Examples

Examples of local adaptation (that you are free to add in your answer with a description) include beach mice camouflage, altitude adaptation in tibetans and peppered-moth camouflage.

Adaptation is a change in a trait as a response to selection. As you ask for local adaptation I assume you want examples where sub-populations have either come under different selection and adapted differently, or cases where sub-populations have come under similar selection but not all have had the necessary genetic variation to evolve, i.e. selection has caused differentiation between sub-populations. Local adaptation can lead to varying degrees of divergence, so some for some examples it may be worth exploring speciation events. Here's some examples:

Galapagos Tortoises

There are two general shapes to the shell of tortoises on the Galapagos Islands. On islands with little low-lying vegetation the tortoises seem to have evolved long necks & limbs and different shell shapes which allow them to reach up more easily.

  "The shell distortion and elongation of the limbs and neck in saddlebacks is probably an evolutionary compromise between the need for a small body size in dry conditions and a high vertical reach for dominance displays."

Silent Crickets

Marlene Zuk has some very famous work on crickets that evolved to be silent on a Hawaiian island where parasitic flies were using the call as a targeting method. It's a great example of rapid adaptation occurring under observation in the wild. During the 1990's the population of crickets was in decline as a result of parasitism. At some point a mutation arose where the crickets no longer produced song, and this allele spread rapidly and cricket numbers bounced back strongly.

Other possible examples. Some of these are not "classical examples" but serve as interesting examples nonetheless.

Peppered moth colouration in response to the industrial revolution
Sickle cell anaemia and Malaria
Artificial selection in crops, livestock, and domesticated animals
Darwin's Finches
Antibiotic resistance in diseases; resitance to pesticides and herbicides; resistance to diseases unique to/more prevelant in sub-populations
Seasonal and continuous breeding by species present in both temperate and tropical climates
The Stephens Island Wren adapted to life without predators, and then failed to adapt to life with predators
Barn owl colouration across Europe
Predator-prey co-evolutionary dynamics as demonstrated by Guppies in Trinidad and Tobago
Drosophila melanogaster and adaptation to starch and maltose based foods
Adaptation to different salinity across gradients in marine organisms


Thermoregulation Question I had the following question on an exam of mine and I got it wrong, so I was wondering if someone could help explain the reasoning to me. Below I list my explanation.

  An overheated and sick dog in a hot environment will have an impaired thermoregulatory response when its

  (A) evaporative heat loss increases

  (B) metabolic heat production decreases

  (C) body temperature increases to match the environmental temperature

  (D) blood vessels near its skin increase vasoconstriction

So here's how I approached this: A and B are clearly incorrect, as they aid the thermoregulatory response of the animal by allowing it to lose excess heat.

Thus, it comes down to C and D. I chose D because I thought that since vasoconstriction traps more of the heat inside the body, it would be counterproductive to what the dog actually needs (vasodilation). I'm assuming that the correct answer choice is C, but could someone please explain it to me?

Thanks in advance to all who reply :)

You're right, A and B both are normal thermoregulatory responses, so those can't be the right answer.

I'm guessing the rationale for C is that, if the dog's body temperature is increasing to match that of the hot environment, it must mean the dog has an impaired thermoregulatory response. It's kind of tautological.

But D also seems correct to me. If a dog is in a hot environment, and its blood vessels near the skin are constricting (say, because it's sick), that's counterproductive to the normal thermoregulatory response. If the dog isn't dilating its blood vessels near the skin, that's an impairment to the normal thermoregulatory response.

Perhaps the question is written wrong? Maybe D was supposed to say "vasodilation" instead of "vasoconstriction"? If this is a question written by a teacher I'd say you have a case for arguing it.


Plant Identification Help Can someone help me identify this plant? Flowers bloom in summer, then red seeds form afterwards.  Leaf length is about 10 inches max.  I live in Southern California and it is grown in a container under my patio.

Thanks for your help.

This seems to be Scadoxus Puniceus, also known as the Paintbrush Lily (not to be confused with other species with the same common name). The dutch originally cultivated scadoxus puniceus, and your specimen could be one of several hybrids of the original.

Dave's Garden has plenty of pictures of the species. He didn't have any fruit at the same stage of ripeness as yours, but the likeness is still rather compelling.

For a slightly more reliable source (if a little older), the South African Medical Journal also identifies Scadoxus Puniceus in a study of accidental poisonings by herbal medicine. The flower might be a touch wider than yours, but you almost certainly still have a Scadoxus, and within-species variations can easily account for such a small difference.

Copyright Disclaimer: All included photos would typically fall under fair use due to their limited scope compared to the original work and due to their non-commercial use as a benefit to the public. If any of the copyright holders disagree, feel free to contact me so we can resolve the problem.


Is there a way to measure the amount of bytes that are possible to encode in a DNA molecule? When I saw a DNA molecule for the first time, it kinda reminded me of a hard drive. It consists of slots and there are some possible combinations for each slot; in the hard drive these possible combinations would be 0's and 1's. In DNA, these slots would be G's, A's, T's, C's.

So, is there a way to measure the amount of bytes that are encoded in a DNA molecule?

I've made this question before in another forum, but the answerer provided me only with Shannon's theorem, which is $K=L-\frac{(1-q^L)^n}{q^L}$ and told me a little about genetic redundancy. I could only search for the ammount of slots which are present in the DNA, but this genetic redundancy thing got me stuck.

Unfortunately the answer is highly dependent on what you mean. In the simplest terms, comparing it directly to how we measure data storage in digital media, the number of different states of a DNA string of length $n$ can have is simply $4^n$. A byte holds $2^8$ different states so the number of bytes in a DNA string of length $n$ is $\frac{n}{4}$. Of course, actually accessing this information would be more difficult than simply having it in a strand of DNA.

DNA in real organisms is not random, however, so sequences are not randomly distributed meaning that you could compress that information down into less bits than that, Shannon information style.

However, you can decently argue that this doesn't really tell us how much information is in real DNA because real DNA has structure that matters. It has exons and introns and promoter regions and so on. Meanwhile, the sequences in protein coding regions are a lot more important than sequences in non-coding regions for the most part. Large parts of the genome are functionally irrelevant but because of this they tend to be more random and thus have higher Shannon information.


About acetyl-coA in the Krebs Cycle of respiration In respiration, Krebs cycle starts with acetyl coenzyme A which is made from pyruvate.

However, it is said that the cycle keeps repeat it self with oxaloacetate turning back to citrate and cycle starts again, so why is acetyl coenzyme A constantly supplied to the cycle?

According to that logic, shouldn't there be no need for acetyl-coA after the first round?

Pyruvate transfers an acetyl group to coenzyme A.

The acetyl group from acetyl co-A is the molecule that provides the 2 carbon atoms that get added to oxaloacetate to form citrate, and as you said, citrate starts the cycle over again.

Without coenzyme A, pyruvate cannot transfer the acetyl group to oxaloacetate to form citrate so without coenzyme A/acetyl co-A, the process would stop.

This is a slightly busy version of the diagram, but it does let you see how molecules in the cycle are formed and where carrier molecules interact with the molecules in the cycle.

- By Narayanese, WikiUserPedia, YassineMrabet, TotoBaggins [GFDL (http://www.gnu.org/copyleft/fdl.html) or CC BY-SA 3.0 (http://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons


Does sex-chromosomes exist in all the cells in a human body? Each cell of a human body contains 46 chromosomes. So every cell must contain a pair of sex-chromosome. Is it true? Then a cell of a male and a cell of a female are always different and never be the same?

Like the other answer already said: yes, all cells in the human body contain all 2x 23 chromosomes (with the exception of cells that loose all nuclear DNA during maturation, like red blood cells, or cell produces by meiosis, which contain only a single set of 1x 23 chromosomes).

However, the more interesting part of your question remains to be answered:

  Then a cell of a male and a cell of a female are always different and never be the same?

Technically it is true, that cells from a male and female can never be the same, however that difference is vanishingly small.

Genetically the difference is that female cells have two X chromosomes and male cells have one X and one Y. However:

in all female cells one of the two X chromosomes is permanently silenced (turned off), so essentially they also have only one (active) X chromosome.
the male exclusive Y chromosome is tiny. Size wise it is ~1% of the human genome, but it only has ~200 genes (of which only a portion is protein coding), which is even below 1% of all human genes (there are ~25.000 protein coding genes, around twice that much in total). Many of these genes are also only used/active in male exclusive organs.

These two points taken together mean that the majority of male and female cells do actually have the same active genes - and are therefore "the same" (there are of course many many other factors in biology, including individual differences, that require putting this into quotes).


Bio-fuel efficiency as aviation gasoline Can biofuels replace petroleum for aviation fuel?

I've read in the news that Alaska Airlines was flying with 10~20% biofuel and 80~90% petroleum. Is biofuel efficiency comparable to the efficiency of petroleum? I am curious whether or not the maximum speed of the airplane is same when it uses bio-fuel 100%.

The term biofuel refers both to the source of the fuel, as well as (currently, at least) the compounds contained in it. If the production quality is strictly controlled, eventually there should be no detectable difference between a fuel mixture derived directly from biological sources, and one derived from petroleum products (which, technically speaking, are of biological origin themselves, just a few million years removed). However, due to technological limitations, biofuels and petroleum-based fuels do have different chemical components today.

The reason we hear of differences in mileage or "energy density" in biofuels used to power automobiles as compared to gasoline/petrol is because they are not the same mixture of chemicals. This page goes into detail (the whole site is actually quite clear with its explanations), but the basic difference is that petroleum products are essentially 100% hydrocarbons (only containing hydrogen and carbon atoms) while nearly all biofuels contain oxygen as well, which has numerous effects on the fuel's physical and chemical characteristics, altering everything from polarity to reactivity to stability over time to the types of byproducts (and pollutants) produced during combustion.

There is much more to the story, but the basic answer to your question is yes, biofuels could replace petroleum-based products for aviation and many other types of fuels, and not impact the maximum speed of the aircraft. It may require engine modification, and the energy density may not be exactly the same (possibly reducing range), but for the long-term health of our planet we MUST reduce and eventually eliminate our use of petroleum.

By the way, the Aviation or Chemistry StackExchange sites would likely be able to provide you with much more in-depth answers, as ultimately this question is better suited to either or both of those sites than Biology, which would be more concerned with the production of biofuels by living organisms.


Is it possible to use two forward primer and one reverse primer? I have eGFP and the gene fragment i assembled by pcr.The next step is that i have to join my fragment fragment into 3'p end of the eGFP.I have three primers FP1 is forward primer for eGFP, FP2 has overlapping between eGFP and my fragment. RP1 is just revcom of my fragment 3 prime sequence. How can I assemble this by pcr. is it possible to mix all the three primers together with GFP and my fragment.

Well, technically yes but no. Why yes is because on paper this looks simple enough but think about the technicalities. Your FP1 and FP2 will have different TMs, meaning the temp required to make the complete fragment with FP1 and RP1 will be different than to the MP of FP2. Effectively when the temp for FP2 reaches it might cause FP1 and RP1 to detach.Or the opposite might happen, where FP1 and RP1 are attached whereas FP2 might not.
Another problem I could think of is that as the PCR is cycling, the difference will lead to random length amplifications if at all you get any. The maximum amp product you might see will be of Frag-2.
If you want to fuse such fragments, I suggest going for OE-PCR (Overlap extention PCR).
This is a highly effective method to join two pieces of DNA using PCR. the concept is similar to what you have proposed.
Look at the wiki page- https://en.wikipedia.org/wiki/Overlap_extension_polymerase_chain_reaction

This image also explains the process...


Insect species identification I think it's a moth and need further identification like scientific name, order and family.

The picture was taken on May 30/2016 in my university laboratory window in South Korea. At that time there were so many moths on this building. The temperature was also high and it was also daytime around lunch time. What I want to ask related to flying time is do moths fly at daytime? as far as I know moths are nocturnal. Please clarify this too if this insect species is moth.

It is a moth and all moths and butterflies belong to the order of Lepidoptera. Based on the shape of the forewing and the orange color of the hindwings I think this moth belongs to the genus Catocala https://en.m.wikipedia.org/wiki/Catocala, see also here for some pictures.

EDIT:
theforestecologist did a excellent suggestion that this might be Catocala streckeri based on the wing pattern. This species does occur in Korea, see this website for a distribution map. So it may indeed be Catocala streckeri. However, Asia is very rich in Catacola species, and I know that this family often has species looking very alike, so I can't say with 100% certainty.

Most, but not all, moths are nocturnal. Some Catocala species are known to fly on sunny afternoons (Waring&Townsend 2006).


Why do we perceive colour? (i.e., distinct values?) This is a question I often asked myself, but never really found a satisfactory answer to. It may be that I always went about it from a wrong starting point because the question is induced by physics. But I think an evolutionary perspective may be the most satisfactory one to explain this.

Humans and other animals had much to gain from differentiating not only dark and light but also colors to identify edible things, or threats etc. For this purpose we developed multiple types of cone cells. But what reason is there to not perceive light as we perceive sound, in a spectrum? We could easily distinguish said things by just knowing how high or low the light frequency is (or for that matter, what the spectral 'fingerprint' of specific objects is). Why differentiate between an - albeit big - array of colors?

Or, to go one step further, why did we need an extra type of cone in the middle, the yellow-green wavelength? Is there an evolutionary reason? I'd settle for using the three more or less distinct cone sensitivities as explanation that the brain just has enough information to arbitrarily differentiate these into very discrete cognitive signals.

But evolutionarily, there has to be a purpose, so that one of the questions is the right one. The colors must bring something to the table. Or not?

Thanks in advance. I am also grateful for anyone nitpicking my arguments, because it always helps.

"But what reason is there to not perceive light as we perceive sound, in a spectrum?"

We do perceive light in a spectrum. Not just in a spectrum, but in a combination of spectral components (because we rarely in nature observe true single-wavelength light). If you are thinking about names of colors, those are just words we made up to describe colors to other people, and the range and spacing of those colors differs across language groups. We do the same for sound in the context of music: B-flat versus an E, for example.

  Or, to go one step further, why did we need an extra type of cone in the middle, the yellow-green wavelength?

Colors are perceived in vision by the ratio of activity of different cones, and intensity and spectrum can be confused. If you have no "green" cones, there are big stretches of wavelengths that only activate one of the other two cones. In that situation, there is no way to discriminate between intensity and color.

If, on the other hand, you are wondering about transduction, it's because sound and light have different physical properties. The cochlea effectively "maps" sounds onto a physical arrangements of hair cells. You could do something similar with a prism, but you would lose spatial acuity (effectively, you would need a whole spectrum analyzer for the receptive field of each photoreceptor: your retina would have to be absolutely massive). Instead, color vision works by differential chemical sensitivity to different light wavelengths.

Your question doesn't seem to be much about evolution, besides the title, so I left off that part.


use of antibiotics in selection of good plasmids I have not understood the role of antibiotic medium in filtering the bacteria containing the recombinant plasmids with the ones having normal plasmids. Since all the plasmids of a certain bacterial species have a antibiotic resistance gene regardless if its recombinant or not , shouldnt there be no effect of the antibiotic on the colony?

Short answer: selection protocols are designed to work
When choosing a selectable marker for a plasmid, one chooses a gene that is known to be absent in the host organism of interest. For example, standard lab strains of E. coli are free from extragenomic plasmids and are susceptible to the antibiotic ampicillin. As such, plasmids that confer resistance to ampicillin are commonly used to maintain plasmids in E. coli lab strains.
Other things worth noting:
1. Antibiotic resistance genes are not universal.
That is, a bacterial strain that has a gene imparting resistance to one antibiotic may still be susceptible to many other antibiotics.
2. Not all plasmids carry antibiotic resistance genes.
Many naturally occurring plasmids are selected for in the wild because they carry genes that enable the bacteria to perform new metabolic functions, or impart virulence genes that enable bacteria infect a host organism: (https://en.wikipedia.org/wiki/Plasmid#Properties_and_characteristics).
This is also true of recombinant plasmids. Many commonly used yeast plasmids are selected for by enabling the host strain to produce a necessary nutrient that is absent in the growth medium.


Does anyone know what this purple plant is? (picture taken in Turkey) Is anyone familiar with this plant species, picture taken in the Dalaman region of Turkey. It has large purple leaves.

This shrub is called Tradescantia pallida. You can read more about this shrub on this website https://florafaunaweb.nparks.gov.sg/Special-Pages/plant-detail.aspx?id=2521

I hope this helps you


Detecting cancer in the hyperplasia phase using image processing and SEM I was wondering if it possible or have someone tried before to use SEM or some other spectroscopy to detect an cancer evolvement in its hyperplasia phase:

It sounds like a good way to do it? I guess that's how biopsy works, but maybe there is a way to do test people in the risk groups using this method.

Not exactly spectroscopy, but microscopy is common for detecting pre-cancerous tissue as part of the standard Pap Test given to women at regular intervals throughout their life:

https://en.wikipedia.org/wiki/Pap_test

This is typically done by a team of cytologists (with pathologists confirming results, particularly in abnormal cases), but is beginning to have automated screening (with human oversight).

One of the problems with any form of screening is that the potentially problematic tissue needs to be observed, which is typically quite an invasive procedure. A potential melanoma is usually cut out prior to analysis, and I expect that any procedure involving a scanning electron microscope will also require tissue removal prior to analysis.

A more interesting development in the area of cancer screening is in looking for cell-free genomic DNA in blood; blood tests are much better tolerated for screening purposes in comparison to other tissue removal. With high-throughput short-read sequencing, it's possible for some cancers to see DNA changes before their effects are detectable through histological methods.

Here's a review paper on cfDNA screening, which is is generally negative about the whole thing:

http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1002205

And one that is generally positive:

http://cancerres.aacrjournals.org/content/76/14_Supplement/LB-136.short


Why we have just 2 teeth cycles, primary and secondary not more? After baby teeth go, secondary teeth grow, is there a scientific reason why they are just 2 sets not more?

Humans are diphyodont animals, which means we are having two sets of teeth cycles, on contrast, the polyphyodont animals which are having multiple tooth cycles. The first deciduous teeth(milk teeth,baby teeth or primary teeth) then followed by the permanent teeth. Milk teeth develop from the embryonic stage and continue to develop for 6-7 years and gradually erupts forming the permanent teeth. The permanent teeth is developed and it pushes the milk teeth from the bottom which result in the shredding of milk teeth.

Most of these polyphyodont animals uses their teeth for more severe purposes like grabbing and slashing. Due to these massive work load, their tooth are considered as their main advantage for survival. Also their tooth are subjected to heavy flaws while they grab or slash, so having multiple tooth cycles help them ensure healthy teeth all over their life time. On the other hand considering the diphyodonts, their tooth have been using for chewing and grinding and they will having low flaws compared to the others. So from the evolutionary standpoint increasing the number of tooth cycles are not so economic for them.
Reference


What types of light can't a plant photosynthesize in? I have a plant on my desk, and it got me to wondering: Can my plant use the light from my monitors to photosynthesize? If so, what light (apart from green light, to a degree) can't plants use to perform photosynthesis?

I know that plants have the photosynthetic pigments to absorb many different wavelengths of light (primarily red and blue) but would there be certain types of light it can't use?

(The specific plant by the way is Schlumbergera truncata)

Chlorophyll can use a quite broad range of light for photosynthesis, the only range where it is not working is approximately between 500 and 620nm. See this adsorption spectrum of chlorophyll (from the Wikipedia article on Chlorophyll):

The lack of chlorophyll to absorb light between 500 and 620nm (roughly) results in the green color of leafs, because this light is reflected.
Besides the wavelength also the energy of the light is important, so plants will grow better in sunlight than in the light of your monitor. This link about the maximum effectiveness of photosynthesis is also interesting.


What is the reason for having an extra recognition site for a restriction enzyme? Can the size of a supercoiled plasmid DNA be determined by using standard DNA size fragment electrophoresed in parallel? 2. An unknown DNA molecule was cleaved using several restriction enzymes individually and in various combinations. The DNA fragment sizes were determined by agarose gel electrophoresis and the restriction enzyme recognition sites were mapped. Subsequently, the DNA was sequenced and an extra recognition site was found for one of the enzymes. However, all the other mapping data was consistent, within experimental errors, with sequence data. What are the simplest explanations for this discrepancy? Assume the DNA sequence had no errors.

My answer:

the  extra enzyme recognition site was cut-off with the fragment due to partial digest that occurred because of insufficient enzyme was added or the rxn was stopped after a very short time.

Am i wrong? my logic here was such that they only found the extra recognition site after they sequenced the DNA thus it was not available during the rxn and thus it was either cut off unevenly in one of the fragments OR it could have had the complementary sequence to it that was methylated that hid it.

Detailed answers are appreciated!!

The scenario in your question can be explained if the "extra" recognition site mapped very close to another recognition site for the same enzyme.

For example, if there were 2 EcoRI sites separated by between 0-50 bp of plasmid DNA, then depending on the type of gel being used, the resulting tiny DNA fragment generated could be difficult to detect (either because small fragments run off the bottom of the gel, or because they don't resolve well unless the gel contains a higher percentage of agarose or acrylamide).

Similarly, depending on the size of the adjacent fragments in the various digests, and this assay's limitations on estimating fragment sizes, you might not detect that an "extra" fragment was generated, and "missing".


What is disease risk? I would like to find an accurate definition of disease risk for virus ecology.
I am searching in articles and in none of them this term is defined, they only mention it.
Schematic of the relationship between habitat heterogeneity and disease risk.
Disease is greatest in fully cultivated plants, intermediate in wild plants
that are tended by humans in anthropic habitats, and lowest in fully wild plants.
On the other hand, biodiversity is highest in the habitats of wild plants, and
lowest in those of cultivated plants.

Roossinck, M. J., & García-Arenal, F. (2015). Ecosystem simplification, biodiversity loss and plant virus emergence. Current opinion in virology, 10, 56-62.
I have defined it as the probability of a host to develop a disease. However, I have the feeling that this definition is somewhat lax.

To my knowledge disease risk is not a generally acepted epidemiological term. You may want to look at the incidence rate or prevalence and follow the suggestions from the "See also" section.