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How mosquitoes get their food and survive?
How do mosquitoes find and get their food? For how much time can they survive without food?

Only female mosquitos (of some, but not all species) need blood to reproduce, they find it by following cues that lead them to warm blooded animals. These include gradients of heat and CO₂. Pretty much all mosquitos feed on nectar and plants while they are adults...
As for how long they could survive without food, I don't know, but no longer than their normal lifespans of a few days to a couple of months as adult.

This answer would be greatly improved by linking to some study on the matter

@nico yeah, but during a cursory search I couldn't find any addressing the question at hand, how frequently must a mosquito feed (for any species), and I suspect it is because the question is kind of moot... most people don't care about how often a mosquito must eat its adult food... much less important to a mammal than: just when do they bite us?

blood seeking mosquitoes are attracted to CO2, lactic acid, and the bacteria that live in sweat (old sweat), physically active human emit all three.

Both Male and Female Mosquitoes feeds nectar and plant juice.
Only Female Mosquitoes feeds blood from Vertebrates. They find Lipid, protein from blood.
Lipid and Protein will help in nourishing egg nutrients. Their breeding proportionately increases with the amount of blood meal they intake.
I am not sure about their life expectancy without food.


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In what animal species is the sex ratio skewed in favour of the fertile female?
Ants have something like a single fertile female to several males. The same applies to bees, and larger animals - elephants too. Is the sex ratio universally skewed in favour of the female? What animal species exhibit this ?

You mean for animals, right? You get all sorts of crazy sex ratios (and crazy sexes!) going on in plants.

So just to be clear, you're looking for animals who have sex ratios of male:female <1:>1 in the population, right? Sex ratios within broods, as opposed to within populations can behave strangely.

@Oreotrephes: Yep. Thanks. Just updated the title

It is advantageous to have a skew towards more males. Males can be expendable as they are only required briefly for impregnation and can then focus on providing resources for the mother and young and protection. This breaks down when this is no longer the case, for example in humans we are closer to a 50/50 divide.
This article notes that in aphids, there are twice as many females as males, the same is true for daphnia. I don't think the reason behind this is known. In reptiles, the female to male ratio can depend on temperature of incubation thus this can lead to strong fluctuations.
An interesting principle is Fisher's principle:

Fisher’s principle explains why for most species, the sex ratio is
  approximately 1:1. Bill Hamilton expounded Fisher’s argument in his
  1967 paper on “Extraordinary sex ratios” as follows, given the
  assumption of equal parental expenditure on offspring of both sexes.
  Suppose male births are less common than female. A newborn male then
  has better mating prospects than a newborn female, and therefore can
  expect to have more offspring. Therefore parents genetically disposed
  to produce males tend to have more than average numbers of
  grandchildren born to them. Therefore the genes for male-producing
  tendencies spread, and male births become more common. As the 1:1 sex
  ratio is approached, the advantage associated with producing males
  dies away. The same reasoning holds if females are substituted for
  males throughout. Therefore 1:1 is the equilibrium ratio.
  Source

At least in some species, aphids have nested parthenogenic vivipary, that is, a female may be pregnant with a female child who is pregnant. Of course, this can result in rapid population growth, and if selected for would explain a higher female ratio.

In rock hyraxes, similar to elephants, the sex ratio of male to females are between 2:3 and 1:3. Since subadult males are pushed from the population by the territorial male just before they become sexually active. When looking at adult hyraxes, however, the females can outnumber the males by quite some margin.
Recent studies had shown an adult sex ratio of ♂1:♀17 & that the male to female ratio, in populations situated in residential areas, does not show such a big difference.
https://www.ncbi.nlm.nih.gov/pubmed/24899114

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How does a new species survive without suffering inbreeding?
Just what the title states. The thought came from reading When has an organism evolved enough to be called a new species?
I'm probably wrong but I understand new species happen sporadically rather than in whole-sale lot during breeding season. Is the new species capable of breeding with members of its parent species? How does a new species survive inbreeding initially?

I guess you should define "species" first. It`s kinda tricky term and at least in my opinion "child species" overlap with "parent species", "sister species" and so on.

Well, speciation is a process, not a single event thing.
Usually what happens initially is geographic isolation of some members of a species, so in that sense the inbreeding is something that is influencing and you can also think of it as causing the speciation process. The presence of special harmless or semi-harmless disadvantagious mutations - which increases in frequency from this isolation - influences how the species is going to evolve, but eventually shapes this species to better cope adapt to some environment, or evolves the new species out of existence.

This is indeed a very good question, that I have spent a long time thinking about myself.  My take on this is that there is indeed a very close relationship between inbreeding and speciation, but that inbreeding actually PRECEDES speciation ! The key to this rather counter-intuitive point of view is that inbreeding actually has several advantages, including that of resulting in cleaner genomes in those offspring that survive inbreeding depression.
In populations that have high degrees of inbreeding, because of, for example, small sizes of populations, or high tendencies to self fertilisation, the recessive mutations that cause inbreeding depression will be progressively eliminated, and there will consequently be very little inbreeding depression.
In such a context, there will thus be no barrier to exploiting other advantages of inbreeding such as reducing the cost of sex, or keeping together advantageous gene combinations. Small groups of individuals would thus be better off breeding among one another than with the ancestral stock, leading to speciation.
If you are interested, or just intrigued, by this kind of concept, I invite you to read the rather long essay I wrote on the subject (The existence of species rests on a metastable equilibrium between inbreeding and outbreeding. An essay on the close relationship between speciation, inbreeding and recessive mutations, Etienne Joly, http://www.biologydirect.com/content/6/1/62 ).
And please do not hesitate to get in touch with me directly  by email ( atnjoly(at)mac.com ) if you have comments or any further questions after reading this essay.

Is it possible to divide your post into paragraphs to make it easier to read?

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Is there a link between autoimmune diseases and X-chromosome inactivation?
I was reading about the necessity of niche formations to adequate development of blood progenitors and this idea reminded me of the patchy inactivation of the X chromosome which followed that maybe, if some of these pathways passed through X coded proteins, this might make women have different niches, that could account for the seemingly greater occurrence of auto-immune diseases in women.
Is there any sense to this idea? Was this ever researched?

Yes, here is an article on it: "The role of X-chromosome inactivation in female predisposition to autoimmunity"
Below see the method and results summarised.

Using a DNA methylation assay, we have examined the X-chromosome
  inactivation patterns in peripheral blood from normal females (n =
  30), female patients with a variety of autoimmune diseases (n = 167).
  No differences between patients and controls were observed. However,
  locally skewed X-chromsome inactivation may exist in the thymus, and
  therefore the underlying hypothesis remains to be disproved.

Not very assuring finding, but the size of sample and the heterogeneity of diseases maybe influenced the results. I have to read it again with more attention, but thanks.


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Is there any evidence that humans have faced extinction before?
Have we as a species faced extinction in the past? Resulting in a 'population bottleneck'?  If so, what genetic evidence is there of this occurring?

There is ample genetic evidence for a population bottleneck following the out-of-Africa migration. This would account for the reduced genetic diversity found in non-African populations.
There is further evidence for an earlier major bottleneck that reduced the human population to around 10,000 individuals.
These kinds of studies are typically done now via Coalescent theory using whole-genome sequences.

I just found this nice blog post summarizing the Nature paper I linked to.

Excellent information! I am also intrigued as to what caused these bottlenecks.  I used to follow the notion that an eruption of the supervolcano Toba, Indonesia caused an almost extinction bottleneck - but it seems that this is not the case anymore.


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Has synthetic biology created new plants or animals as of 2013?
I've seen a Ted.com talk where the speaker suggests that modern science can create new micro organisms, like bacteria with a pre- defined new set of traits. But has anyone create a new species of plants or animals using synthetic DNA yet? If so, what are their names?

None yet as far as I know.

Can you define "new"? Is a genetically modified species "new"?

nope, only bacteria as of this time.

Answering your question
Well, considering there is a plethora of facilities that deal with the cloning of plants and animals, as well as altering specific DNA in order to create a better plant or animal. Tests have been done with rats to try and create stronger and smarter rats, and tests have been done on countless other animals to try to develop immunity to dementia and Alzheimers. In the agricultural industries of the world, new types of corn, tomatoes, rice, and other types of crops are engineered on a daily basis, and new versions of these plants are made very commonly. The problem, however, is that a vast quantity of these plants are rejected from being planted. Some plants that are engineered either taste too bad, or they are less efficient than the plant at which they were modifying. As far as inventing a new species, you have to be more specific as to what you are asking. If science creates a new animal from another animal, it is likely of the same family and genus, like breeding a dog from another dog. Creating another type of mammal or reptile or bacteria that isn't part of a specific genus would be a breakthrough, as I am sure that all types of cloning and scientific pairing have been done to the same general Genus and Species... I am assuming, however, that it will be possible to engineer lifeforms at the molecular level by the next 50 to 100 years, as science and technology is getting more and more advanced. So, by the next few centuries, it would only seem logical to assume that new species would be created. However, the practice of creating new species, or even operating a laboratory/facility that deals with the concept, is illegal in a large number of countries, and has several guidelines in others.
I am only 13, so if any of this information is to be used anywhere else, I would advise not to cite me as a credible source. All this information is from my knowledge, and my knowledge is from school studies and personal readings. This is all my information, though. If any wording sounds similar to another source, keep in mind that one human brain functions similarly to another on several accounts and coincidences are often found.  I can assure you that if the documented information above is verified by plagiarism experts as my own wording, as I have taken the liberty to scan my own work. I hope I answered your question, and I am sorry for the long disclaimer ranting of this paragraph.

If you have referred to a source, it's okay to paraphrase as long as you cite where it came from.

hey its great to see someone 13 starting to contribute here!

The answer is no.
At this moment (2016) the are only two synthetic organisms that are being constructed or have been constructed.
The first is a synthetic Mycoplasma genitalium.https://en.wikipedia.org/wiki/Mycoplasma_laboratorium Made by venter
The second is synthetic yeast, S. cerevisiae http://syntheticyeast.org/
There has been talk of building a synthetic human genome... but that is only talk.


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Enlargement of joints in osteoarthrosis
If osteoarthritis (osteoarthrosis) is a degenerative condition, where the cartilage in joints wears down, what causes the joints to become inflamed? I'm reading through a book called Understanding Disease: Arthritis by Steven Tiger, and it mentions that Heberden's nodes are caused by osteoarthrosis. if things inside the joint are wearing down, why does it get bigger?

Osteoarthritis results from the gradual degradation of articular cartilage. When the cartilage is damaged extensively, e.g., all the way through the cartilage and into the bone, an inflammatory response ensues in the bone. This often happens when bone is rubbing against bone.
One of bone's responses to injury and inflammation is the production of new bone. In this case, the bone, called osteophytes or bone spurs, is produced pathologically (i.e., not like the bone laid down normally during growth). Heberden's nodes are the names given to these osteophytes at the distal interphalangeal joints, but the process is basically the same at other joints in the digits, ankle, etc.


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Competition with other individuals of the same species vs. adaptation pressure from predators
It is often said "You don't need to outrun the cheetah, just the other gazelles", thus emphasizing that greater part of the adaptation pressure comes from competing with other individuals of the same species and not directly from predators/parasites (which are seen as more indirect forces similar to the living conditions imposed by the environment (climate, geophysical factors, etc.))
My question is:
Isn't there a difference between competing with other individuals of the same species for food, habitats (i.e. resources) and competing with them in avoiding being eaten?

The correct answer is, "it depends."  The traits that will be under the strongest selective pressure will be those related to survival in the face of the most common causes of death for that species. If food is abundant but so are predators, then clearly predator evasion will be of supreme importance. If food is scarce, then perhaps metabolism-related traits will be under strong selective pressure. But it's important to remember that just because one selective pressure is stronger doesn't mean that the rest disappear. Thus, the individual's survival is dependent upon really a composite fitness that depends on a countless array of selective pressures, some of which may be larger components than others. The competition between individuals of the same species is really a complex interplay of fitness effects, then.

As for the maxim about outrunning a cheetah, what it's illustrating is that the gazelles are not competing with the cheetah for survival. They're competing with each other. If you want, you could expand it to say "...just the other gazelles and the rest of the herbivores in the environment". If a herd of gazelles and a herd of some slower animal are nearby and a cheetah attacks, one of the individuals from the slower species will probably get caught and all the gazelles will get away. The point is that the gazelles and the cheetahs fill very different niches in the environment, so they don't really compete for the same resources (as a matter of fact, one is the primary resource of the other).
When it comes to determining survival, one talks about fitness only within the context of the population (or, if you want, between species directly competing for the same niche). The less fit members of the population do not survive. Thus, the less fit ones that fail to evade the predator are simply doing a worse job evading the predator than the other members of the population. But it's not only the relative fitness that is important. Imagine that a new predator migrates into the environment, for which none of the prey has any evasive adaptation. Even though there may be a relative fitness between them regarding evading this predator, if even the best individual is not good enough to evade it, they would all have an absolute fitness that is too low to ensure survival. Then the saying breaks down, since none of the gazelles can out-run each other with respect to evading this new predator.
Of course, this idiom falls apart when you start talking about asocial species, since there aren't any other individuals around to out-run.

Thank you for your answer. I was rather wondering about why should the selective pressure caused by the imperative "avoid being eaten" should be viewed in the light of competing between individuals of the same species and not simply as competition between victim/predator

I was answering the specific question that you gave at the end. Nevertheless, I added a bunch of text about the saying.


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Any difference between inverted microscope objective vs normal microscope objective?
I'm planning to build an inverted microscope and I am not sure if I can use a plane achromatic objective of a normal microscope for the inverted microscope as well. Are there any specific needs for the objective of an inverted microscope?

Apart from the way it works and certain structural differences (reference), the decision of which kind of lens you need to use is left to your own personal choice based on your needs. You can find a list of the different lenses being offered by Olympus in this link.


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Is chlorophyll living or non living?
Is chlorophyll living or non living, and after boiling the water out of a chlorophyll extract would it still live, as in would it still maintain its properties after re-adding liquid to the dried chlorophyll?
Thank you for any help.

Do you want to know about chlorophyl or about plants? Chlorophyl is just a chemical contained for instance in plant cells.

If you meant "chloroplasts" rather than "chlorophyl", there might be an interesting debate, cf. Richard Smith's answer here about cyanobacteria as being almost "free-living chloroplasts" http://biology.stackexchange.com/questions/2848/photosynthetic-pigments-vs-chloroplasts/2850#2850

Chlorophyll is organic, not living, which is a fancy way of saying that it contains carbon. As for your question about boiling, it depends on whether or not the heat from boiling will disrupt the chemical bonds and destroy the molecule. According to Wikipedia, chlorophyll a will melt at around 117°C (I'll assume that chlorophyll b is similar), which is higher than the boiling point of water, so if the temperature is strictly maintained, the chemical should stay intact.


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Do the four cells produced by meiosis each divide into four cells again?
In the beginning of meiosis, there is one cell. During meiosis, 1 cell divides into 4 cells. Does each of these 4 cells divide each into 4 more cells?

No, meiosis is not a cycle like mitosis. In mitosis, haploid or diploid cells divide to create two genetically identical cells, and this process can go on and on. On the other hand, meiosis results in 4 genetically unique daughter cells which are also haploid. If a haploid cell was to try to undergo meiosis, there would not be enough genetic material and you would end up with half-chromatids.

...and, of course, haploid cells do mitosis too.

quite right @AlanBoyd - I should have drank my coffee this morning.

@AlanBoyd - I always taught that mitosis does not occur in haploid cells...

@siddhu99 ... perhaps I should qualify my comment: haploid eukaryotic cells do mitosis.

I'm only aware of this in some yeasts. Do mammalian haploid cells undergo mitosis?

Mammalian haploid cells do not undergo mitosis. In mammals at least, only meiosis during spermatogenesis result in 4 daughter cells (ironic). The meiosis in oogenesis results in a single egg and 2 polar bodies. Strangely MII in oogenesis isn't completed until fertilization.

In species where an individual can be haploid (for example in haplodiploidy) then cells produced by meiosis do multiply by mitosis in order for the individual to grow.
From a brief scan the Wikipedia article on ploidy nicely summarises the various possibilities.


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How do we memorize something?
When we see something, how and where in the brain do we remember it and are able to recognize it later?
What happens in the brain that makes this possible?

I'm afraid that we don't really understand this very deeply yet so there may not be an answer, but I may just be ignorant on the topic. I look forward to hearing what people know about this.

I tried googling but didn't found the answer. There must be someone that knows this.

A few terms that may help your googling: engrams, synaptic plasticity, hippocampus :)

The current working theory (note this is still an open question, but there are many leads being followed):
Sensory systems receive a combination of signals from an event, which are initially bound to the hippocampus (this is called episodic memory).  Then, typically during sleep, the memories are consolidated.
A simplified view is that consolidation basically consists of communication between the neocortex and the hippocampus, and the memories are thought to be "saved" in the neocortex.  Thus, amnesia patients with hippocampal damage still have all their long-term memories, they just can't create new memories (because their old memories were already consolidated to neocortex).
Your neocortex has many subregions with many functions.  One is the temporal lobe, where semantic memory seems to be stored.  So your episodic memory may record several interactions apples and, over time, your semantic memory will be updated (as memory consolidation occurs) to "consolidate" your concept of "apple".
The temporal lobe is highly connected with the occipital lobe (where visual information is processed) and the two likely work together to identify objects using the consolidated information.
On the molecular level, how the memories are actually stored.  The most well known concept is connectionism: different connection strengths between neurons carry different information.  But there's also genetic expression going on, and there was recently some research on prion-like proteins contributing to memory as well as astrocytes.
Realize, of course, that a lot of this is cutting edge research... and therefore could be wrong or contain numerous oversights and simplifications.

Great, detailed answer for an exciting field.


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Mass change in deamidation from Glutamine to Glutamate
To detect the deamidation from Glutamine to Glutamate in a protein, normal practise seems to be a mass spec, where it is claimed there is a change of 1 dalton.
EG It is claimed that:

Deamidation of an Asn to Asp/IsoAsp results in an increase in mass of a single dalton.

But when I look at their table, they are using Glutamic Acid as being 1 Dalton heavier than Glutamate, but at pH 7 the Glutamic Acid will be deprotonated to Glutamate. Do they  put the sample in pH 4 to protonate the Glutamate first? But then you are risking catalysing the hydrolysis of Glutamine anyway, rendering your results useless!
There should be a charge difference though, as you are going from neutral to a negative charge, so that would show up in a change in mass/charge on the mass spec, rather than a mass change.
Any help would be appreciated.

This might be better on chemistry SE.

Its more relevant to Biology as its to do with Proteins I think.

I am not an expert in this area but this is what I understand. Usually ESI based protein mass spec imparts a positive charge on the proteins by protonation. Formic acid is usually added to help in protonation. In deamidation -NH2 is replaced by -OH thereby increasing the mass by 1 dalton (14+2 -> 16+1). I think that glutamine may be also acquire multiple charge (by NH2 protonation). You can see this article, which talks about dealing with deamidation artifacts resulting from sample preparation techniques.

Ah, so the samples are put in acidic conditions to protonate the glutamate which can result in false positives, interesting.

Biochemistry is still chemistry :)

Are you performing native or non-native MS?

@harpalss I'm currently reading papers/data from other sources and was trying to work out how they were doing it. The details seem to be glossed over rather a lot!

I do alot of ESI mass spec, so i might be able to help. Alot of my work is on native MS. Are you looking at the whole protein in the mass spec or a peptide fragment?


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What insect is in this photo?
Found in Russia, in the kitchen. It is about 1–2 cm length.

This is an immature "True Bug", order Hemiptera. You can tell this from the general shape of the wings, and from the big "beak", a feature of the Hemiptera.
Within Hemiptera, it's possible that with those enlarged front legs, it could be an Assassin Bug, family Reduviidae.

This isn't a nymph, but a short-winged adult; enlarging the second photo shows that the front wings are not fused to the mesothorax (which would be the case in a nymph).

It may also be a squash bug, they look pretty similar. They even have enlarged front legs too.


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How many honeybees are there, and how has the number changed across time?
How would you begin to estimate the world population of the European Honeybee (Apis mellifera)? Would recent colony collapse disorder show up as a blip? How about the spread of A. mellifera from Europe to Asia and the New World?
Ideally, I'd love to see a chart with estimates of the kept and feral populations of A. mellifera across time. I realize that this is a tall order; but given that we have available to us:

the complete genome,
current data from agricultural organizations, and
historical and archaeological records,

it seeems that with a combination of genetic and historical methods this shouldn't be impossible. Or is it? There seem to be plenty of articles arguing about A. mellifera's African or European origin, but none that I see that mention actual population sizes.

1 billion hives
(at 10,000-50,000 bees/hive this is 10-50 trillion bees)
Managed: 100 million hives
Based on country-level data from FAO, supplemented  for a few countries with Apiservices, in 2011 there were about 80 million managed hives. Because FAO lacks any data for some countries, and other countries under-report (for instance US figures don't include hives kept for pollination service and hives kept by small-scale operators) a reasonable round estimate of managed hives in the world is 100 million. (This implies a 128% correction to the FAO numbers). (Aizen and Harder 2009 give context on FAO figures).
Wild/Feral: 900 million hives
Wild/feral hives of Apis mellifera are difficult to count via direct observation. Jaffe et al 2010 use a genetic sampling method, and also report a reasonably strong correlation between the total number of hives (managed and wild) per square kilometer and the mean annual temperature of the area.
I used the best fit line from their data to estimate the "hive-carrying-capacity" by country using (the admittedly very general) land area and mean annual temperature. Then I subtracted the number of managed hives from the carrying capacity to estimate wild hives.
Although this formula probably overestimates large, cold countries and underestimates Africa (the formula gives 211 million feral hives in Africa when literature suggests closer to 300 million), in general, it seems to give not unreasonable estimates in comparison to the literature. Globally, this formula gives an estimate of 984 million wild hives. Given that land area included desert and other unsuitable habitat, it seemed reasonable to round down, and I took 900 million as my estimate.
Historical Populations

1961-2011
FAO statistics date to 1961. I plotted their numbers, with the 128% correction for each year. I assumed that during this time the number of wild bees has remained virtually unchanged, at 900 million, because it was defined by mean temperature and land area, which have not changed.*
1650-1961
This period represents the globalization of Apis mellifera. Before 1600, there were no European honey bees beyond their native range (Western Eurasia and Africa). However, once established in new areas (the usually cited first beehive in the USA in 1622), Apis mellifera rapidly spread in both managed and feral populations, in North America (17th c), South America (18th c), Australia (19th c) and East Asia (20th c) (Crane 1999)
.
I used carrying capacity of native range countries (just about 35% of the carrying capacity of the globe, or 350 million hives) as a before-1650 estimate,  and then assumed a geometric increase of about 2% per decade in available land area (ALA), as Apis mellifera bees and beekeeping made their way around the globe.
To estimate the number of managed bees during this period, I assumed a human:hive ratio of 35:1**, and modelled hives based on historical estimates of human population, multiplied by the ALA for the decade. The 1650 estimate was 5 million managed hives.

*Although diseases, pests, and pesticides have been reported to affect feral populations, I didn't find any solid information on this. For instance, feral populations of Apis mellifera mellifera and A. m ligustica have been widely reported to be in decline in the USA, but at the same time, feral populations of Africanized honeybees (Apis mellifera hybrids) have been rapidly spreading. Even with 90% losses in the USA, Canada, Japan, and Europe (areas affected by varroa) my estimates would only be decreased about 10%. However, it's also possible that land-use change has greatly affected feral bee populations (Moritz et al 2007).
**This wasn't a totally wild guess. I first calculated the human:hive ratio for 1961-2011. This ratio was increasing - there were 71 people / hive in 2011, and 47 in 1961. Initially, I assumed the rate of change in the ratio to be constant, but this led to unrealistically large estimates for historically managed hives. However, the rate was clearly increasing (just, perhaps in a nonlinear way I didn't want to estimate), so I decided instead to compromise on a number less than 47 and greater than 4. I decided on 35, as it produced what seemed like a realistic estimate of 5 million hives in 1650, compared to around 20 million today for Eurasia and North Africa (excluding sub-saharan Africa where wild-harvest remains important and likely was even more so in the past).

 Aizen MA, Harder LD. 2009. The Global Stock of Domesticated Honey Bees Is Growing Slower Than Agricultural Demand for Pollination. Current Biology 19: 4–4.
 Crane E. 1999. The World History of Beekeeping and Honey Hunting. Taylor & Francis. (Chapter 12).
 Jaffé RR, Dietemann VV, Allsopp MHM, Costa CC, Crewe RMR, Dall'olio RR, Rúa PPDL, El-Niweiri MAAM, Fries II, Kezic NN, et al.. 2010. Estimating the density of honeybee colonies across their natural range to fill the gap in pollinator decline censuses. Conservation Biology 24: 583–593.
Moritz R, Kraus FB, Kryger P, Crewe RM. 2007. The size of wild honeybee populations (Apis mellifera) and its implications for the conservation of honeybees. Journal of Insect Conservation


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How diverse are dogs in their traits other than appearance?
I've asked this question about dogs not so long ago, and the short answer was - dogs are the most diverse looking species of mammals because they got a small number of genes that have a big impact on appearance.
I would like to ask a follow up question- differences in appearance are easy to notice, and I would like to learn about other traits that might be genetically based.
Are there other major differences between dog breeds, like longevity, cognitive performance, friendliness, etc? Or are all dogs more or less the same in traits other than appearance?
Are there plots of traits like these among different dog breeds that identify outliers?

Since diversity isn't absolute, or doesn't have a maximum, it might be good to compare it to a wild species, like wolves, or something similar with a broader range and larger population.

Dogs are highly diverse in their patterns of copy number variation (variation in the number of copies of different genes). This has been shown to be probably related to the diversity in morphology. It would thus presumably also affect other traits such as those that you list, and it seems to at least have been shown for disease susceptibility. Interestingly, wolves have less copy number variation on average than dogs (citation).


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Is it really detrimental to humans as a species to reproduce with one's own first cousin?
Tired of hearing of these urban legends and popular opinions, I ask this question here to see if there really is scientific merit to this belief. My questions is, is it really "harmful" for a person to reproduce with his/her own first cousin? Everyone, at least in America, seems to think that this is incest which I completely dismiss because incest is purely a religious concept. The next argument I get is that we want more genetic diversity and having offspring with a first cousin is detrimental to our survival as a species. If you have any genetic weaknesses then your cousin is likely to be carrying them as well and then the chances of your offspring carrying them increase and so on.
I don't really believe any of this. It is rather well known (or may be not so well known) that only a very small percentage of a human individual is different from another human individual's genome. Differences due to skin color, race, ethnicity, and such are literally skin deep. So one reproducing with her cousin or someone half way across the globe is only negligibly different.
Forgetting about religion, has this been scientifically systematically tested and/or proven? Has any research been done on this? Is it true one way or the other? I don't mean to spark any debates here. Opinions are of course welcome. But if anyone can point me to any reputable sources or published results/references, that would be ideal.

Inbreeding depression, "the reduced survival and fertility of offspring of related individuals" (quoting the linked article), is a well-known and well-understood biological effect. It does, indeed, affect humans.
The problem is that recessive mutations become more likely to affect the survival of the offspring of relatives. Imagine that you have a mutation affecting, say, some gene that's critical to your metabolism, which is entirely possible. But, since you have two copies of the gene and only one of them is faulty, you are not affected by this. Nevertheless, you, by chance, pass the non-functional one on to a couple of your kids, who are also not affected due to only having one copy as well. They, in turn, pass it on to one or more of their kids. Now, two of them, cousins, have a kid. The kid gets both copies and can no longer properly metabolize something due to having two faulty copies of the gene. This can prove to be fatal or at least severely debilitating.
Now, lest you think this is improbable, there are on average 70-something mutations per generation. Some of those will be neutral in effect, others will be detrimental. Once an offspring gets two copies of those detrimental alleles, then there could be serious health effects. The likelihood of an offspring getting two copies decreases as the relatedness of its parents decreases. So, sibling or parent/child pairings would be the most likely to produce offspring with the problems. Pairing between 3rd generation (First-cousins) or any pairings between them and their siblings, parents, aunts/uncles or grand-parents would be the next most likely.
So yes, first-cousins marrying and having kids is a bad idea for very basic scientific reasons.

I missed the "as a species" part of your question. Inbreeding will only likely have an effect within small, closed populations, though it will continue to have a lasting effect even as those populations grow and open up. Two textbook examples are French Canadians and Ashkenazi Jews. Even now, there is continued elevated risk of certain rare genetic diseases in these populations. As for the species as a whole, it is likely to be really detrimental only if the effective population size of the species becomes really low: a general rule of thumb used by conservation biologists is that the effective population size should be at least 50 to avoid the effects of inbreeding (and 500 to avoid the effects of genetic drift) (50/500 rule).
Sorry about the confusion.

This is a good explanation of the mechanics, but maybe you could add a bit about the rates here. Inbreeding certainly can have an effect, but is it a big one? Somehow, cousin-cousin marriages are permitted in many cultures and even encouraged in some; likewise, at points in history, effective population size in many human populations has been very small, without any lasting negative effects. It takes a seriously concentrated effort of sustained intermarriage within families over hundreds of years (European Royals and pituitary hormone deficiency or haemophilia) to actually produce an effect.

Just because cousin-cousin marriages are permitted or encouraged does not mean that they're wise. On the other hand, there are many examples of elevated genetic disease rates originating from  small, closed populations: French Canadians, for example, or the textbook example of Tay-Sachs disease in Ashkenazi Jews. And it only takes one or two generations to see an effect, unless you're looking for a population-wide elevated frequency. Of course it's possibly harmful for the 1st gen offspring...

I can't edit my comment anymore: but it only potentially takes one generation (not "one or two") to see an effect, and I mean one generation after the cousin-cousin mating. I read the question as "Is it detrimental for cousins to marry" and the answer is "Yes, for the offspring it is likely to be detrimental". I missed the "as a species" part.

OK, I edited the answer to contain some extra information.

Good points, good examples, and good answer: +1.

Technically.. it just reduces diversity in the population and moves the it towards homozygosity. It may increase the likelihood of a disease but it may also select for a good trait. So the societies which promote consanguineous marriages are perhaps thinking that they are selecting for a trait that they think is good. But what happens most times is that we don't really have an idea of all the traits and their combinations and inbreeding leads to amplification of deleterious mutations.

@BrandonInvergo Wow good answer. Exactly what I was looking for. Thanks! +1 and accepted.

An allele causing individuals to mate preferentially with their counsins might evolve if the inbreeding depression is not too high. The reason is that the inbred offspring is more related to the parents than a half as the parents are themselves already related more than two randomly picked individuals in the population


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Is it possible to make humans extinct artificially?
Verging on the realm of science fiction, my question is that is there any theoretically possible way, biologically/chemically, with which the entire human race can be killed without affecting the rest of the biosphere at all? I am only curious about theoretically possible no matter how unlikely. If we encounter a sufficiently advanced alien civilization bent on our destruction, would it be possible for them to make sure all humans die without harming any other living organism on our planet?
Is there anything biological/chemical which makes us unique or different than other lifeforms on Earth? Something which can be used against us? Or are we just so similar with a bunch of other species that we cannot be wiped out without other lifeforms getting harmed or our destruction cannot be ensured? Is it possible to artificially make humans extinct?
Thanks you.

Does it have to be an external mechanism? (i.e. not human-caused)

This question appears to be off-topic because it is not about biology as defined in the FAQ. It would be much better suited to scifi.stackexchange.com

@BrandonInvergo Actually I would be okay with either one. I prefer an external mechanism but just for the sake of intellectual curiosity, internal mechanisms will also be interesting.

@MattDMo I though about this very carefully and decided to put the question here instead of at scifi.stackexchange.com because I am looking for scientifically theoretically possible methods. This is specifically related to human biology and I don't think scifi.stackexchange.com is the proper place to ask bio questions. This is a "question about biological concept". Is there anything biologically different about us which makes us different enough from other species on this planet?

I think it's a fine question. It's a bit abstract and probably impossible to answer conclusively, but it's grounded in actual biology (immunology, etc.). I think such hypothetical questions are fine as long as nothing gets too speculative so as to no longer be based on modern scientific knowledge.

In 50 years time, if you had a 20 billion dollars and a space program, you could probably make a fleet of 1 ton sattelites which can track the entire planet using 1cm resolutions and that uses a 20 kilowatt laser to destroy all vehicles except tanks and then to destroy humans, including all agriculture vehicles, and visible crops, so humans would be decimated by hunger. It would need to take out human space launching first, and then it could at least prevent humans from using cars or walking without 3 inches of steel over them. The sattelite would aim for all non-plant/animal structures.

Infectious diseases is probably the only way I can think of. Viruses for example may have tropisms based on receptors to which they attach. These receptors may be and often are unique to a species, and thus an infection could target humans very specifically. Differences between humans and animals present the weaknesses and resistances we would have to such an infection. As an international species, spread of the disease can be quite rapid. However, our increased intelligence means we could given time, understand the threat and combat it.
If an infectious disease killed rapidly enough that development of a cure or administration of one was not easily possible, the disease itself would be wiped out by quarantine measures (theoretically). For an infection it is not wise to kill the host too quickly as this prevents survival of the infection which is dependent on its host.
Thus we want an infection that is non-pathological at first then rapidly pathological but affected the whole world as a whole. This infection would need to spread to every individual so would have to be incredibly infectious and for no individuals to have any resistance to it and also ideally to kill everyone at roughly the same time or at least quickly enough to prevent us having time to come up with a cure. The only way I can think of that would fulfil all of those conditions is if the infection on it's own was non-pathological but then a novel secondary universal factor made this infection pathological. This factor would have to be in low levels prior to infection but then rapidly escalate to worldwide distribution.
Disclaimer: Obviously this is theoretical and probably not at all possible.

Apart from not being extremely infectious, HIV/AIDS had some appropriate characteristics: long incubation period and initial deaths being attributed to diseases taking advantage of a weakened immune system (initially predominantly affecting people that could be marginalized--at least in the U.S.--might also have made the disease more effective). If initial symptoms appeared among the poor (no health care, somewhat marginalized), a disease might be undiscovered and later mostly ignored until it is too late (but a trigger factor would seem more effective).

Thanks, +1 and accepted. A virus specifically engineered is the only way I could think of as well but wasn't sure. I was thinking of something which would lay dormant for a long time to make sure everyone is infected and then all of a sudden become active and just wipe out everyone very fast. Not sure if this is even theoretically possible or not.

Trick question. By driving humans to extinction, you almost certainly will be driving all human-specific parasites and pathogens to extinction as well.

Such would probably also tend to reduce populations of some animals such as cockroaches and raccoons which exploit human-created niches better than other animals.

Wow, good answer. I didn't think of this at all. I wish I could accept both answers. +1 anyway. Thanks.

This answer is building on the answer by @BrandonInvergo and focusing on the "..possible way...the entire human race can be killed without affecting the rest of the biosphere..." part of your question.
No, it is impossible to remove humans without affecting the biosphere (barring some extremely made-up scifi scenario) because many species are adapted to us. It doesn't stop with the parasites and pathogens in Brandon's answer. Most obviously, the majority of all domesticated animals and plants will go extinct, and these number ~750 species (Duarte et al 2007). A large number of other species (e.g. plants, insects, birds) are also adapted to man-made environments and many are likely to go extinct if humans disappear, and these effects will cascade into their respective ecosystems. Just look at what is happening to species adapted to traditional low-intensive pasturelands in e.g. Europe.

Really? All of those species would go extinct as well? Wouldn't they all just adapt back, meaning adapt to live without man-made environments? That's how they were living before.

@FixedPoint For domesticated species most will go extinct since they have been so heavily modified and cannot compete successfully in the wild. For other species dependent on man-made environments the outcome depends on how rapidly their living environment changes, but many are likely to go extinct. Some are likely to find refuge in their native habitats, e.g. natural grasslands. However, the original habitats are sometimes lost or the species is extinct from their original range, and some have evolved adaptations to their current antropogenic environments.


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why water is a proof of a life?
I read that NASA looks for water on Mars or other planets as a sign of a life.
I wonder why scientists look for water as proof of a life? isn't there any animal that drinks another liquid like alcohol or something?

duplicate: "An identical copy; a facsimile." please see the definition of the duplicate on http://www.thefreedictionary.com/duplicate it is not a duplicate...

A "duplicate" means the same or a very similar question has already been asked and has one or more sufficient answers. If there is something that has not been addressed to your satisfaction, feel free to edit your question to explain what further information you're looking for.

sorry, I shouldn't have fed the troll...

Water is not a proof of life. It is just indicating that life might be possible there.


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Ecomorphs as evolutionary definitions
There have been demonstrations of ecomorphs in different taxa, where each morphology type is associated to a single environment. I know that it happens because special morphological characters increase the fitness and therefore will be positive selected.
My question is; if we find similar places (talking about natural pressures and climatic conditions) on earth and given enough time, can we expect to see more or less the same ecomorphs living in different places? Also, assuming that, could evolution be a regarded a non-stochastic process?

The phenomenon you describe, where the same result comes about in more than one time/location via evolution, is called "convergent evolution." It is when the same character, or trait, evolve independently of one another. One example is the wing, it has evolved (at least) several times independently, in bats, birds, and insects. Parallels can also be drawn with other traits like dispersion methods of seeds, or the evolution of fins in fish, dolphins, and whales. Here is a classic paper by Ernest Williams from 1972 which describes one of the earliest examples given of ecomorphs, the anolis lizard, also talked about on this site.
This is from a good article on the new scientist website that would be worth reading:

"Evolutionary convergence occurs at every level, from proteins to
  societies. An unusual antibody once thought to be unique to camels has
  a close equivalent in sharks, for instance, while naked mole rats form
  social colonies like those of ants and bees.
"What this means is that if we could wind the clock back and let life
  evolve all over again, life might take very different paths but still
  produce organisms that, in some ways, resemble the organisms alive
  today.
"There would almost certainly be streamlined swimmers in the oceans and
  winged creatures in the skies. In fact, some argue that the evolution
  of intelligence is also virtually inevitable, though intelligent
  organisms could be very different from us."

The answer to your question is yes, with enough time and the same selection effects we would not be surprised if there was a similar pair of independently evolved characters. However, selection acts on random mutations which is not a directed process, therefore for the same characters to evolve you would need mutations to occur that had similar effects. This is why given enough time we can see the same responses. Despite the non-random effect of selection, we could consider evolution to be a stochastic process, it only arrives at the same converged point by chance. This is because selection (the main driver of evolution) acts on randomly generated genetic variation thus the direction of the evolutionary trajectory is random.

"..often used to represent the evolution of some random value, or
  system, over time. This is the probabilistic counterpart to a
  deterministic process (or deterministic system). Instead of describing
  a process which can only evolve in one way (as in the case, for
  example, of solutions of an ordinary differential equation), in a
  stochastic or random process there is some indeterminacy: even if the
  initial condition (or starting point) is known, there are several
  (often infinitely many) directions in which the process may evolve." -
  wikipedia entry on Stochastic Processes

Following the quote above it may seem that evolution is a directed process, i.e. selection is aiming for a specific target. It is not, selection can only weed out the least fit genotypes and increase the frequency of the better ones, selection has no goal or pre-existing aim. Thus, when discussing stochasticity in evolutionary terms it is perhaps better to use evolutionary trajectories, to describe the randomly created paths they move along, instead of "directions."

As an example of convergent evolution we could use the peppered moth and a little imagination because this is purely a hypothetical illustration I am making up on the spot.
The peppered moth is famous for once being a white moth that turned dark during the industrial revolution, when towns and cities grew and pollution killed the light coloured lichens that helped the light morph hide. This meant, rather suddenly by evolutionary time-scales, the white morph of the moth was not very well camouflaged against the dark bark of the trees. This created a positive selection for darker morphs, as such, alleles which made for dark moths would have spread rapidly in the population.
Using a little imagination we can think about two different parts of the world where this same event occurred independently - e.g. Glasgow and Plymouth in Britain which are quite far apart but both grew expansively during the industrial revolution. In both of these locations we would have seen a simultaneous rapid loss of lichens and increase in the dark moth ecomorph. This would have been convergent evolution because it is likely that they were independent of each other, i.e. the dark moth probably did not evolve in Glasgow and then fly itself down to Plymouth.

Evolution by natural selection is not a stochastic process. Only the generation of genetic variation is stochastic. The question is how much evolution is governed by natural selection versus genetic drift, which is stochastic, and it has been shown that natural selection is dominant. Since convergent evolution is a selection-mediated process, it also would not be stochastic.

@BrandonInvergo In my opinion evolution is stochastic because "there are several (often infinitely many) directions in which the process may evolve" because evolution can occur through drift or selection. Convergent evolution is when one identical or similar direction of evolution is achieved. It relies on random mutations, a stochastic process, which selection, a deterministic process, then acts upon, or the more unlikely possibility of genetic drift to the same result.

You are conflating the result (evolution) with the process (natural selection or genetic drift). Even the quote you gave indicates evolution as the result. Also, watch your wording: evolution is not directional. (I'm not sure why I can't add your name with an @; it's not working. Sorry)

@BrandonInvergo I'm not sure I say evolution is directional, maybe I missed that, but I definitely agree, it is not a directed process. Where do you mean (I'd like to change it to make it clear)? Perhaps you mean "directions in which the process may evolve" - this is where evolution proceeds along a trajectory, it's motion along the trajectory is random (therefore not directed) but it is still a direction (away from the origin) nonetheless.

No, I meant "...or similar direction of evolution is achieved." I understood what you meant but the use of the word "direction" might be confusing or misleading to some.

Although I do take issue with the wording of the quote as well (not your fault, obviously): it is some state that may evolve in several directions, not the process itself. In biology we look at allele frequencies; the fate of alleles via natural selection is predictable and thus heads in one "direction". Under genetic drift only, their fate is unpredictable. Under a combination of the two, their fate is of course unpredictable. But again, this is the result, not the process!

@BrandonInvergo ah yes, perhaps misleading, too late to edit the comment, future note: "similar direction of evolution is achieved" in my above comment better stated as "similar evolutionary trajectory and result is achieved". I'll also give the answer a tweak later to make it clearer that evolution is not directed.

Thanks @BrandonInvergo and GriffinEvo for your answers!, both where too much good and im gonna read the paper that Griffin suggested me. Returning to the discusion and looking only the results of evolution, ¿the achieve of ecomorphs in all the places under similar conditions makes the result predictable (high fitness), so we can say is directional (deterministic), even if the "process" is stochastic or deterministic?. ¿Could ecomorphs been the final result of the evolutive process?, ¿Can we expect homoplasy in all linages in enought time?

@CristianRomán No, the journey to two ecomorphs is not deterministic, it is merely the result of similar mutational effects occurring in scenarios with similar selection. Using the moths example, the selection is created when the camouflage is less effective and thus leaving them more prone to predation. Group A might develop mutations which make them darker which selection would then favour, whereas Group B might instead evolve mutations to fly quicker or see better, making them better at avoiding predators. In convergence they arrive at the same result by chance mutations, not determinism.

If you have two similar environments and you allow the organisms to evolve indefinitely, then you would, indeed, expect to see convergent evolution, in which different species evolve to have very similar adaptations. However, because the species in the two environments have different genetic backgrounds, they would most likely arrive at these these traits through distinct genetic adaptations (see: analogous traits). Thus, they might look similar but not exactly the same (think: bird wings vs. bat wings vs. insect wings).
Note that this should still be the case even if you take a population of some species, split it in two and put one half in the one environment and the other half in the other environment. Over time, there will begin to be novel traits popping up only in one of the linneages, resulting in the accumulation of genetic differences despite their initial shared history. It's probably that, in the evolution of some new trait, these two populations will have attained it through distinct genetic routes: either through mutations on distinct genes (or their regulatory mechanisms), or through distinct mutations within the same genes (not to mention other mechanisms such as gene duplication).
As for your other question, it's important to remember that evolution by natural selection is a deterministic (non-stochastic) process! All else being equal, the most fit individuals will survive. However, the "raw material" that determines the fitness of individuals, such as mutations and recombination, are stochastic. There is also a stochastic evulotionary process, namely genetic drift, however the actual process of evolution by natural selection is entirely deterministic. So, that's why you would see convergent evolution: species will develop similar adaptations because they deterministically give advantages under certain environmental conditions, but the adaptations will not be exactly the same owing to the stochastic manner in which mutations arose to give rise to those adaptations.


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Is there are practical lower limit to gene length in E. coli?
Question is rather self-explanatory.
Putting aside other post-transcriptional factors like rate of degradation of transcript, what is the smallest gene ever reported to have successfully been transcribed in E. coli or other similar prokaryotic systems? Why couldn't this gene be any smaller?
Note that in the context of this question, I am disregarding factors like promoters, operators and terminators. Also note that this gene does not necessarily need to code for a protein.

One example of short transcripts in bacteria would be transcriptional riboswitches when they are in the "off" state.

In terms of naturally-occurring "genes" I think that the record is probably held by the attenuator peptides.
In bacteria, the regulatory mechanism known as transcription attenuation involves the ribosomal biosynthesis of very short peptides. In the trp operon, where the phenomenon was first described by Yanofsky's group, the peptide, MKAIFVLKGWWRTS, consists of just 14 amino acids. Other examples, described subsequently, are of comparable size.
Now that I have written this answer, I have reread your question and I see that you are really interested in transcripts. In the case of the attenuators, the peptides are encoded by the 5' end of a much larger transcript, so they probably don't count for you.

Non-coding transcripts can be as small as 10-15 nucleotides. Once the RNA polymerase initiates, the DNA is melted and the transcription bubble forms. This region is about 10 nucleotides long.
But if you are asking the limit of mRNA length, then the answer is different. First of all, to get a protein, the ribosomes have to translate the transcript. To do that, they need some space to land on, and initiate the translation process. We know that ribosomes protect about ~30 nucleotides from  ribosome footprinting experiments
Moreover, bacteria wouldn't need to utilize the genomic space and the ribosome machinery to produce small peptides (even if the peptides were useful), since the small peptides are already around as the degradation product of other proteins. Hence, once you add 3 times the shortest produced polyaminoacid length to the minimum length required for the ribosome landing, you get somewhat physical (or let's say physiological) limit of the transcript length.


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What is this insect I found in Russia?
I found this in Russia. It is approximately 2cm long.

What area of Russia? it is a large country so that could be a good clue to rule some options out.

@GriffinEvo, Volga Region. However I think it is an international insect.

This is a wasp, (see that nice slim "wasp waist" it's got?), which means taxonomically that it is in the order Hymenoptera (which it shares with bees and ants).
Within Hymenoptera, wasps are diverse and often difficult to ID, but it's possible that this is a Braconid or Ichneumon (family Braconidae or Ichneumonidae). If you take a good closeup of its wing veins, chances are an expert (not me) could ID it.

I'd agree it's definitely a kind of parasitic wasp - I'd be inclined towards the Anomaloninae subfamily - perhaps get in touch with the Russian Entomological Society
http://www.zin.ru/societies/res/index_en.html also http://www.opsu.edu/Academics/SciMathNurs/NaturalScience/PlantsInsectsOfGoodwell/ichneumonidae/default.html and
http://en.wikipedia.org/wiki/Anomaloninae

The ichneumon wasps I've seen all have long ovipositors not seen here, so I doubt it's one of those.

Since it got bumped and no one seemed to be too clear on an identification. Based on the presence of two recurrent veins in the forewing, following identification guidelines here, I'd identify the above wasp to be a member of Ichneumonidae. The identification of the subfamily, however, is difficult without access to the wasp itself for close observation. Ctenopelmatinae is a good candidate in my opinion, however, due to the close morphological features, and the geographic distribution of many genera tends to be holarctic.


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Could sex alone drive complexity?
Imagine that complexity is measured by a positive number $f_n$.
If one has no prior knowledge about the positive number $f_n$ then from Bayesian theory one can assign $\log f_n$ an "improper" uniform prior over the range $-\infty$ to $\infty$.
A random mutation might increase or decrease the complexity of the offspring $f_{n+1}$. If we assume the offspring's complexity is likely to be close to the parent then we could simply model the random change in complexity by:
$$log f_{n+1} = log f_n + \Delta\ \ \ \ \  \hbox{with probability 0.5}$$
and
$$log f_{n+1} = log f_n - \Delta\ \ \ \ \  \hbox{with probability 0.5}$$
where $\Delta$ is some small number.
Such a random evolution will lead to the log of the complexity performing a random walk.
But now add sex.
Assume the complexity of a sexual organism is the average of the complexities of its parents.
$$f_{child} = \frac{f_{male} + f_{female}}{2}.$$
If one evolves the simple model now one finds that the complexity of the population grows exponentially.
Is this idea interesting or not? :)

What is complexity? I think you need to very explicitly define what this concept is, with regards to your model.

True - I could have modeled simplicity instead but that seemed a bit perverse!

Replace the word "complexity" with any other word..."height", "weight", "resting metabolic rate", etc. and the model would still be solvable in a mathematical sense and it would read the same way. So, it's hard for me to accept the model as relevant to the evolution of complexity.
I think you need to make the model have a more robust definition of complexity (as mentioned in the comments) but you also need to consider the costs and benefits of complexity in your model, which will greatly affect the dynamics and actually carry biological relevance.

Is it interesting?  Perhaps, but "complexity" is a vague notion.  If you want to simplify and just say "variation" then sure, sex increases variation.  But so does that random mutation you brought in.  Really, all you need for increased variability is some difference between generations and genetic Drift will take care of the rest.  Mutation is enough, which is clear from asexual organisms.  Sexual reproduction tends to increase diversity, but that has nothing to do with "complexity."  The environment, in particular interaction with other organisms, drives complexity more than anything.

A concrete theoretical version of my model could be a population of random computer programs or Turing machines. I would define the complexity of a computer program as its run time not the size of its code.
Mutating programs will have varying run times whose logs just perform a random walk.
But if you allow pairs of those programs to occasionally combine in such a way that they generate a child program with a run time that is the average of their own then the run times of the population will grow.


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What is the mechanism of labeling a DNA molecule with deuterated water?
I have seen a paper in which deuterated water was used to follow dividing cells. The assumption was that deuterated water will be incorporated into newly synthesized DNA molecules. Is there any direct incorporation of water in the replication process? Is there any proton exchange?
The paper describing the method can be found here:
http://www.pnas.org/content/105/16/6115.full.pdf

Please add a reference for the method. I imagine that deuterium could be incorporated at several points in the pathway for de novo synthesis of dNTPs, either into the bases or the deooxyribose.

proton exchange always happens (i dont have anexact reference right now but i have read about it in spectroscopy texts) .. and hydrogen incorporation is also there as @AlanBoyd said..

@WYSIWYG Exchanging protons wouldn't be useful to follow cell division as they exchange all the time. The deuterium would be incorporated into both new and old DNA, and would also be gone if you remove the D2O again.

Thank you all for the comments and answers. Just added the reference. The de novo synthesis pathway of dNTPs sounds like a reasonable place to start looking. Thanks, Alan.

I would assume that the labeling occurs in the reduction of NTPs to form dNTPS.
This process (catalyzed by ribonucleotide reductase) involves protonating the hydroxyl group on the 2' carbon, allowing it to leave as water, and then adding a hydride to the newly formed carbocation. The two hydrogen atoms (the proton and the hydride) come from two thiols on the enzyme, which in the process are oxidized to form a disulfide bond.
The crux is that, in the presence of heavy water, the two thiols would rapidly exchange their hydrogen for deuterium. That means that the hydride that gets added to the carbocation would be a deuterium, and the resulting dNTP would be deuterium labeled.
This is the only step that I can imagine the labeling working for, as a carbon-hydrogen bond is formed (which doesn't exchange rapidly with the solvent) using the hydrogen from a sulfer-hydrogen bond (which does exchange rapidly with the solvent).


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Is Nerve Growth Factor (NGF) commercially available?
I'm curious if NGF, or Neurotrophins in general is available commercially. Can I order it online? If not, what are the medical/biological reasons. Does it breakdown quickly after synthesis/capture? Is it a regulated protein?

No.  Any use in humans is strictly experimental and should only be done by physicians.  Using it like a nutritional supplement wouldn't do anything for the body anyway.

Nobel prize Rita Levi-Montalcini begs to differ: http://www.independent.co.uk/news/science/is-this-the-secret-of-eternal-life-1674005.html

It's awful hard to study something with an N=1.  Given that she put it in her eyes in the form of drops, it probably just degraded away.

(also, she is a physician)

I'm voting to close this question as off-topic because it’s not about biology but commerce, and is intrinsically temporarily transient.

recombinant human NGF is available for purchase.  You might not be able to buy it without some sort of a research lab affiliation.
http://products.creative-biolabs.com/symbolsearch_NGF_1.htm

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Cloning two fluorescent proteins with different promoters in the same plasmid?
I want to clone two fluorescent proteins both driven by different promoters in a plasmid to be used to transform B. subtilis at the amyE locus. For this I want to use plasmid pSG1729 (Lewis and Marston, 1999), because this plasmid can be used for homologous recombination at this specific locus.
Now the problem is, because of a few reasons (i.e., the locations of the restriction sites, keeping the spc resistance gene and deleting the current GFP gene), if I want to clone two genes into this plasmid, they will be very close to each other (~10bp). Will this be a problem either technically or biologically after transformation? I don't think that possible read-through will be bad, as I want one of the fluorescent proteins (pHluorin) to be continuously expressed. Maybe an option would be to clone the two genes in opposite directions?
This is the current genotype of the plasmid:
Ori amyE5' currentGFP Spc amyE3' bla

you can use bidirectional promoteror you may extend the spacer to ~100bp just use the 10bp spacer in tandem or better, with some reshuffling..

The spacer is a good idea, can you maybe elaborate on the reshuffling?

just use similar sequence but not exactly the same sequence.. you can move some bases here and there.. though, not really essential to do so, it will reduce repeats..

If you want to express them in an operon, make sure you have an RBS at the 5' end of each coding sequence. If you place one 10bp downstream without it having an RBS, it will be transcribed, but not translated... If you want more help, paste the DNA code of each as a comment.


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Why not produce protein based on condensation reaction?
I'm fairly new learning about protein. As I know protein can be synthesis by condensation reaction. And the current method to produce protein is purify them from an organism. So why not produce protein based on condensation reaction instead of purifying it from an organism?

can you give a link to the "condensation reaction"? I'm not sure what exactly you're referring to...

@MattDMo http://www.google.co.uk/search?q=protein+synthesis+condensation+reaction&bav=on.2,or.r_qf.&bvm=bv.49784469,d.aGc&biw=1366&bih=640&pdl=300&um=1&ie=UTF-8&hl=en&tbm=isch&source=og&sa=N&tab=wi&ei=XYjwUZmLIYSWiQeTpYHQBw

@ĐứcUltraSoft, because it is difficult to synthesize long proteins that way.. small peptides can be synthesized like that..

@WYSIWYG Thank you so much, now i understand.

The chemical synthesis of peptides has actually been used for a long time, see the Wikipedia entry or this schematic for some examples.

It is important to first remember that to do anything useful, the sequence of the amino acids in the protein must be exact. For example, sickle-cell anaemia is caused because one amino acid in a haemoglobin protein is incorrect. Because of this, peptide synthesis involves rather complex chemistry in order to ensure that amino acids are added in the correct order and number, and is only effect up to a chain of a few dozen amino acids.
Now it is possible to produce peptides of various lengths in a cell-free extract, which basically involves taking the cytosol out of cells (with all the ribosomes, tRNA's, and other factors therein) and adding the mRNA template to be translated and an ATP source. This way, a peptide can be prepared by using the cell's own machinery for protein synthesis without actually needing a viable cell.
Remember also that even if it were possible to chemically synthesize a correct peptide sequence, the protein would still need to fold into a correct 3-dimensional structure to work properly, which in some cases is impossible for any artificial method currently available.


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Why are there no organisms with metal body parts, like weapons, bones, and armour? (Or are there?)
Reading this question, Why are there no wheeled animals?, I wondered why no organisms seem to make use of the tensile and other strengths of metal, as we do in metal tools and constructions. I am obviously not talking about the microscopic uses of metal, as in human blood etc.
Why are there no plants with metal thorns? No trees with "reinforced" wood? No metal-plated sloths? No beetles with metal-tipped drills? Or are there?
I can think of some potential factors why there are none (or few), but I do not know whether they are true:

Is metal too scarce near the surface?
Are there certain chemical properties that make metal hard to extract and accumulate in larger quantities?
Is metal too heavy to carry around, even in a thin layer or mesh or tip?
Can metal of high (tensile etc.) strength only be forged under temperatures too high to sustain inside (or touching) organic tissue, and is crystallised metal too weak?
Are functionally comparable organic materials like horn, bone, wood, etc. in fact better at their tasks than metal, and do we humans only use metal because we are not good enough at using e.g. horn to make armour or chitin to make drills?

As a predator, I would like to eat a lot of vertebrates and save up the metal from their blood to reinforce my fangs...

A bonus question: are there any organisms that use the high electric conductivity of metal? Animals depend upon electric signals for their nervous system, but I do not think nerves contain much metal. The same applies to the few animals that use electricity as a weapon.

one possible answer is that metals have to be molten and forged.. they dont crystallize by deposition..

@WYSIWYG: Never? So things like pyrite either do not exhibit the desirable properties of metals, or they crystallise under high temperatures or pressure?

There are magnetotacti bacteria. One problem would be oxidation. Also spider silk has greater tensile strength per unit mass than steel. Metals like magnesium and iron are (each) more than five times less common in the human body than sulfur much less carbon or even calcium, hinting at general biological availability.

Homing pigeons?

Oh, and caddisfly larvae, in symbiosis with French artists

On chemistry SE, I've asked a similiar question (or rather a question inspired by this train of thought): http://chemistry.stackexchange.com/questions/4009/is-it-possible-to-crystallize-a-solid-ingot-of-metal-from-an-acidic-aquaous-so

@mart: Ah, cool!

Link to a previous Q on magnetic bacteria

Almost all metals corrode, and non-living parts of the body (as horn), cannot be renewed. That's all I think.

@TomášZato: Hmm corrosion is an interesting factor indeed. But there are plenty of metals that don't corrode very much, like gold, silver, aluminium, stainless steel...
Horn can be renewed, as in our finger nails and hair. Couldn't metal body parts be renewed in a similar way? Even teeth can be renewed in a way, as sharks do.

Gold and silver are rare, aluminium reacts with water upon acidic conditions and stainless steel oxides to produce highly toxic waste.

@TomášZato: You may be onto something; care to post that as an answer?

Steel really isn't something that is going to happen naturally... :p

@theforestecologist: Why not?

Beaver teeth are heavily impregnated with iron, which makes them stronger and tougher. http://www.dentalproductsreport.com/dental/article/new-study-finds-beaver-teeth-could-provide-insight-human-tooth-decay

Some molluscs incorporate iron into their radual https://www.researchgate.net/publication/44120196_Radula_synthesis_by_three_species_of_iron_mineralizing_molluscs_Production_rate_and_elemental_demand

@John: Ah, very interesting; hence their reddish colour! But the article mentions resistance to corrosion, not tensile strength.

In molluscs and beavers it also results in increased hardness, which makes them more wear resistance. Incorporating iron in small quantities will not do much for tensile strength. Bone already has a quite high strength, comparable to magnesium alloys. Metallic iron is not very chemically resistant and would quickly breakdown. If it did evolve I image a defensive enzyme from plants to encourage corrosion would be easy to evolve.

@WYSIWYG At risk of getting really off-topic now: metals don't have to be forged into a shape, they can be cast or machined instead. (Sorry, I couldn't stop myself and yes, I realise I have a problem.)

Related: How to form biological metallic tissue?

Your bones are largely made of metal, calcium is a metal as is potassium sodium and a dozen other elements in the body.

@John: All right, but I was looking for ways in which we use the tensile strength of metal, as when metal is present in the form of a grid/roster; I believe that is not the case in bones? See my full Question above.

The hemoglobin in your blood contains four iron atoms per protein, whereas the hemocyanin in a number of invertebrates contains two copper atoms.

Ad "reinforced wood": cellulose fibers have comparable tensile strength to steel "cabels" of equal diameter. Cellulose fibers in wood are just really really thin (1 fiber = 36 molecules) and arranged in a way that allow cell growth.

@BagiM: Hmm but could those be used in the specially useful ways that metal can, in tools and weaponry?

There are some cases of bio-metallic materials, as hinted at by the comments. But these are relatively small amount of metal.
It's not that there is a lack of metal available. Iron in particular is the fourth most common element in the earth's crust. Most soil that has a reddish color has iron in it.  There are several reasons you don't see iron exoskeletons on animals all the time.
Firstly, metallic iron (in chemistry terms, fully reduced, oxidation state 0) has a high energetic cost to create.
Iron is the second most common metal after aluminum on the earth's crust but it's almost entirely present in oxidized states - that's to say: as rust.  Most biological iron functions in the +2/+3 oxidation state, which is more similar to rust than metal.  Cytochromes and haemoglobin are examples of how iron is more valuable as a chemically active biological agent than a structural agent, using oxidized iron ions as they do. Aluminium, the most common metal on Earth, has relatively little biological activity - one might assume because its redox costs are even higher than iron.
As to why reduced biometal doesn't show up very often, inability of biological systems to deposit reduced (metallic) metals is not one of them.  There are cases of admittedly small pieces of reduced metal being produced by biological systems. The Magnetosomes in magnetotactic bacteria are mentioned, but there are also cases of reduced gold being accumulated by microorganisms.
Bone and shell are examples of biomineralization where the proteins depositing the calcium carbonate or other minerals in the material are structured by the proteins to be stronger than they would be as a simple crystal.  most of the examples here have very little or no metal, but rather minerals like the Chrysomallon squamiferum cited by @navyguymarko and @loki'sbane here.  The Iron Sulfide looks metallic but it is a mineral, akin to a bone.
While iron skeletons might seem to be an advantage, they are electrochemically unstable - oxygen and water will tend to oxidize (rust) them quickly and the organism would have to spend a lot of energy keeping it in working form.  Electrical conductivity sounds useful, but the nervous system favors exquisite levels of control over bulk current flow, even in cases like electric eels, whose current is produced by gradients from acetylcholine.
What's more, biological materials actually perform as well as or better than metal when they need to.  Spider silk has a greater tensile strength than steel (along the direction of the thread). Mollusk shells are models for tank armor - they are remarkably resistant to puncture and breakage.  Bone is durable for most purposes and flexible in addition.
The time it would take for metallized structures to evolve biologically are likely too long. By the time the metalized version of an organ or skeleton got started, the bones, shells and fibers we know probably have a big lead and selective advantage.

mineral deposition is different from free metal deposition and thats what i was implying.. deposited metals hhave to form metallic bond else they'll remain colloidal

While minerals tend to include oxides of elements and metals are different a chemical state, I'd just say that the creation of reduced metal structures could be created by similar sorts of genes.  they can structure the lattice into layers and introduce defects of specific amounts.  i would say that they represent a degree of control that genes could exert on the structure of deposited minerals if necessary.  I see no reason that reduced metals could be built with less control over their structure.  If so, then there are probably other reasons you don't find organic metal structures often.

Thanks for your answer! So you are mainly saying the energetic cost of building and maintaining metal constructs is too high for organisms to be a good investment compared to other materials.

yes - I should have just said this :)   I think its the cost relative to other minerals and organic compounds is high for what you get from using metal.  Metal based tissue could have a hard time healing after damage too.

Beavers and molluscs both incorporate iron into their teeth/radula for increased strength and resistance. there is a high metabolic cost however https://www.researchgate.net/publication/44120196_Radula_synthesis_by_three_species_of_iron_mineralizing_molluscs_Production_rate_and_elemental_demand

@John: Very interesting article. One of the other answers also mentions molluscs. But a comment says they use oxides or other compounds, not metal rosters, so I don't think metal's tensile strength is used?

teeth and shells are nanocomposites they exploit a mixture of materials with various properties, and many iron oxides are plenty strong, hematite comes to mind. in these cases they want hardness and chemical resistance, which metallic iron would not give you.

Gold is the ONLY actual example of a material that is metallic in and of itself being formed by biology, and it doesn't seem to be used. All the other examples in biology that I know of are oxidized rust essentially. Even the "copper" bloodworm teeth which are called "metallic" are just atacamite and organic polymers and maybe other minerals.

A few minor points to add to shigeta's excellent answer:
Biological enzymes don't work well on metals.  Some often incorporate metals (see chelation) but elemental atoms aren't easy to process.  For one, a large molecule would be identical everywhere, so cleavage, for example, would be indiscriminate and just leave a bunch of tiny tiny atoms.
More to the point, once an organism incorporates metal there certainly isn't a lot it can do about that.  A lot of shell-based organisms swap out their shells because of the inflexibility of those designs, and metal would be no different.  It's difficult to grow when you're encased in a self-made iron maiden.

Thanks for your additions! I'm not sure I understand all the chemical terminology, but you seem to be saying that there are chemical reasons why metals are hard to work with for organisms, don't you? // As to metal shells, they could be segmented, or the metal could only cover certain vital areas in patches, or the metal could be used in joints, or other body parts...

good point Amory.  I think the metal could be replaced/resurfaced as calcium carbonate is, but it would degrade much more readily because molecular oxygen is everywhere too.

A self-made iron maiden would have organ-puncturing sharp spikes on the inside. A plate mail would be a better approximation, but not even these are form-fitting in the chest area. Another useful comparison would be to look at how the brain can't grow after birth because it's encased in a solid layer of bone from all sides.

There are good reasons why tissues/structures with a very high metal content might cause problems (I defer to the other answers here).
However, I am aware of one other example: some molluscs incorporate high concentrations of iron into the points of the radula (basically a ribbon of teeth, used for grazing). This is especially important for grazing molluscs, as they essentially make a living by scraping a thin layer of microalgae directly off the rock surface.

That is very interesting, a nice counter-example! So these molluscs use iron to make their radula stronger. Now I wonder why not many other animals or plans to this too...those molluscs don't happen to live in an en environment rich in metals?

Good question. These molluscs (primarily chitons) occur all over the world, so it's not a question of some local abundance of iron, but I guess it's possible that their rock-scraping habits give them quite a high dietary intake of iron (particularly on non-sedimentary rocks). However, I think it's probably more to do with their need for especially durable teeth, which outweighs any physiological/chemical costs associated with iron impregnation. It's just one of many solutions in the animal kingdom for dealing with tooth wear.

Right! It is interesting to note how humans have fairly recently switched away from metal teeth. I think dentists now use ceramic materials.

@Cerberus according the linked article, their teeth are not metallic, but of iron oxide (rust, a ceramic meterial).

@Anixx: Hmm you're right, they use oxides, not pure crystals. Perhaps it is still relevant, if metallic oxides are still harder than most materials?

some beautiful pictures and the slug looks awesome.  the iron in references are Iron Sulfide, which is a mineral form of Iron(II) its not really metal in the sense that the iron in our bodies is iron, nor is the calcium in our bones metallic (Calcium can form a metal, but its a mineral in our bones. )

Well there is the common Bloodworm (Glycera dibranchiata)which people use for fishing bait. The animals are unique in that they contain a lot of copper without being poisoned. Their jaws are unusually strong since they too contain the metal in the form of a copper-based chloride biomineral, known as atacamite.
http://www.sciencemag.org/content/298/5592/389.long
And unlike the clamworm (Nereis limbata), whose jaws contain the metal zinc, the copper in the mineral in the jaws of Glycera is actually present in its crystalline form.
http://www.pnas.org/cgi/pmidlookup?view=long&pmid=12886017
It is theorized that this copper is used as a catalyst for its poisonous bite.
(I got this from Wikipedia)

Evolution is incredible.

Great example! So the copper serves a double purpose: it makes the jaw stronger, and it works as a catalyst. Smart worm.

Looks like some parasitoid wasps have zinc coated barbs on their ovipositors which may function to help them bore through wood and lay their eggs.
Here's the blog entry about it on IFL Science, and the original article:

parasitoid ovipositor specimens had a weight percentage of zinc of 7.19±3.8% (N=42) in the tip regions, which was significantly higher (P<0.05) than that in pollinator and parasitoid remote regions (<1%; N=10).

Kundanati and Gundiah (2014) Biomechanics of substrate boring by fig wasps. J Exp Bio 217: 1946-1954

https://en.m.wikipedia.org/wiki/Scaly-foot_gastropod
Gastropod that incorporates greigite, pyrite, and graphite on it's shell and foot.
Due to the large quantities of these compounds in dissolved form surround the hydrothermal vents.
Speculation for purpose: the shell is extremely resilient, the metal does improve this greatly. Though whether evolution deemed this adaptation necessary because of an abundance of strong predators, or as a means of detoxification of the injested compounds, is unclear.
The three populations of these snails have varied compositions, one which even being magnetic, due to the different compounds produced by the vents.
Appologies, here is non wiki http://www.esa.org/esablog/research/iron-plated-snail/

Very interesting example! It does seem to be a compound, but it's probably still the iron atoms that make the compound strong?

Digging a little deeper into the references there is more speculation than answers.

Out of the three independent populations, the Solitaire Fields population, does not utilize the granular greigite in scerlites at all. Original hypotheses theorized that the granular pyrite(Dodo field) and granular greigite(Kairei fields) was utilized by the Gastropod to improve defense. Further analysis concluded it is not the compound alone, interfacial geometries, layering, and the incorporation of other materials do aid in penetration resistance, energy dissipation, mitigation of fracture and Crack arrests, and other beneficial traits. Predators include, cones nails and seafaring crabs

I belive it is the structure of the greigite molecules that aid more in the scerlites and shell strength. Shell using layering and scerlites arranged in a shingling manner resembling scale mail. Furthermore, Greigite is only a 4-4.5 on Mohs hardness scale, by itself is not all that hard, comparative materials(Flourite, Nickel, Iron, Steel). Arogonite(polymorph of calcium carbonate) makes up the majority of the tertiary layer of the shell(core), hardness 3.5-4. Secondary layer composition periostracum, fleshy material. Primary layer composition pyrite, greigite, or none(solitaire).

Hmm so...the effectiveness of the shell may not be the result of the typical tensile (or other) strength of metal after all? P.S. I'll believe that crabs might crack shells, but I don't imagine a cone snail could penetrate or crack any half-decent shell anyway, don't you agree? Or does it have special, boring radulae that can do so?

The metal does help greatly for the 2 groups that take advantage of it. My comment on how the 2 minerals are not that hard was addressing that a hardness of 4-4.5 is just under average. Steel has the same hardness. Apatite has a hardness of 5, whivh is harder than steel, and hydroxylapatite is the main component of tooth enamel and bone. For the snails though the greigite and pyrite are harder materials than the shell materials alone. So combination of the metals and Arogonite, and the way they are structured, aid in the tensile strength, heat dissipation, and reflective abilities of the shell

But in other animals the bone and tooth are a harder material than either of these 2 iron compounds.

OK that's clear. I wonder whether hardness or tensile strength would be more interesting for shells: against drilling predators, you want hardness, but against crackers (like crabs), you want tensile strength, don't you?

Though not in metallic (0) stage; an Iron ore called "Bog-Iron" is formed via microbial process.

Fig-1: Bog iron

  (Wikimedia)

It is formed inside bogs and swamps, classically in Sphagnum-moss-bogs. It is also found in peat.

Fig-2: a bog

  (Wikipedia) , (Wikimedia)

Fig-3:  Sphagnum sp, common bog moss of temperate and cold regions.

  (Wikimedia)

When Fe(2) or ferrous ion, the more soluble form, obtained in the groundwater of bog region from some mineral-source such as spring, the anaerobic iron oxidizing bacteria, such as Gallionella and Leptothrix etc, oxidized it into Fe(3) or ferric form; which very easily get precipitated as insoluble compounds.

Fig 4: Spring acts as iron source.

  (Wikipedia) , (Wikimedia) , (USGS) , (USGS url).

Fig. 5: Leptothrix sp. , found in ferruginous environment.

  (Wikimedia)

The iron components found in bog-iron, is commonly iron(III) oxyhydroxides (FeO)OH of varying compositions; geologically Goethite and Limonite.

Fig. 6: Samples of "bog ore" from Nassawango Creek show vugs lined with goethite around massive "ochre".

   (USGS) , (URL)

Sources:
>

Wikipedia.
Iron Production in the Viking Age, at http://www.hurstwic.org
http://www.hurstwic.org/history/articles/manufacturing/text/bog_iron.htm
Google books: Topics in Ecological and environmental microbiology/   Edited by Schmid and Schaechter/ AP; Chapter-37 ---> metal precipitation
Google Books: Environmental Microbiology: Fundamentals and Applications: Microbial Ecology/ Jean-Claude Bertrand/ Springer.
  Chapter 14 (Biogeochemical cycles)
Google Books: Bryophyte Biology / Edited by Shaw and Goffinet / Cambridge;
  Chapter 9: Mineral nutrition, substratum ecology and pollution/ J. W. Bates
Metal depositing bacteria and the distribution of Manganese and Iron in Swamp- waters/ Ghiorse and Chapnick/ jstor.org
Bog iron formation in the Nassawango Creek watershed, Maryland, USA/USGS (photos)

im no biologist, but while not commonly cosidered, calcium IS a metal, so technically skeletons count.
additionally, while not technically a metal, limpet teeth are quite impressive.
http://www.bbc.co.uk/news/science-environment-31500883

Quite interesting, thanks for the link! As to calcium, while bones are strong, do they actually contain calcium in the form of a metal grid/lattice? I think not?

bones are mineral composition of a Calcium Phosphate called hydroxyapatite

Have you ever looked up the scaly foot gastropod? It uses iron as a form of body armor. Literally scale armor on It's foot.

Oops sorry I just realized someone posted this information already. My apologies.

Now just imagine if the snail had weaponised love darts lol. Metal tipped spears to fight back with instead of reproduction. Yes I know about the conch and it's venomous attack. More proof that nature is just as alien as anything we can imagine.

Your answer provided this great picture, and you explain more clearly how it actually uses pieces of (partly) metal as scale armour on its foot; the other answer was mostly about its shell. A bit more of an explanatory text would improve your answer, though! Incidentally, I wonder why it has a greenish hue, while iron is usually reddish?

yeah i like it too!

@Navyguymarko What is the scientific name (identity) of this snail? and which other answer already mentions it? (i could not found that, sorry). Could you please provide the source of this image, and some other links, so the information could be verified?

Barden et al (2017) have discovered an extinct species of ant (hell ant) that was alive 95 million years ago that had naturally occurring metal mandibles. Mandibles on ants are essentially the same as fangs on spiders or teeth on humans.


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What is the difference between the Ureter and Urethra? also between the Renal papilla and Renal pelvis?
Differentiate between the following:

Ureter and Urethra
Renal papilla and Renal pelvis

It is not given in my book.
Please help.

This sounds a bit like a homework question...

Yup, it is. But it is not given in my book. So I needed help.

@siddhu99 See our homework policy for reasons your question may have been downvoted.

overall though, homework is okay though.

The ureters run from the kidneys to the bladder whilst the urethra runs from the bladder to exit the body:

The renal papillae are the site where urine drains into one of the minor calyxes of the kidney.   Multiple minor calyxes join together into a major calyx, and multiple major calyxes join together to form the renal pelvis which then drains into the ureter.


text:
How to compare SNP from genotyping results for multiple people with a known phenotype?
I'm looking at different genotyping profiles available at opensnp.org and am trying to compare profiles for people with different phenotypes.
For example, given 10 profiles of people who can roll their tongue and those who cannot, I am trying to identify what is different between these people and what's similar.
A typical record is in this format:
Rsid, chromosome, Position on chromosome, actual 2 letter mutation

How can such records be compared to identify similarities for a given phenotype? Does RSID uniquely identify a mutation, or is it a combination of rsid and position?
In other words, if one user has rsid 123 at position 555 and another one has rsid 123 at position 666, and the mutation is the same, is this a similarity, or does position matter?

Each rsid identifies a unique SNP in the genome. Thus there should not be any entry in the files that have the same rsid but different chromosomes and/or positions. If you do find this, it is likely that you have data from different versions of the assembled genomes.
To find genetic variants associated, i.e. correlated, with your trait, you need to focus on the genotype at each of the SNPs. For example, SNP rs3094315 is an A/G polymorphism, i.e. an individual can either have the genotype AA, AG, or GG. To find if it is associated with tongue rolling, you would count the number of AA, AG, and GG individuals (alternatively you could sum the number of A and G alleles) in the group that can roll their tongue and compare those numbers to the group that cannot. You would then repeat this for each SNP that you want to test. For most SNPs, there will be no difference in proportion.
That being said, this is not a modest undertaking as this a cornerstone of human and statistical genetics. There are many issues that could strongly bias your results (e.g. population stratification, genotyping error, linkage disequilibrium, multiple testing). To learn more, you can read about the Cochrane-Armitage Trend Test and the PLINK software. If you are really serious I recommend Applied Statistical Genetics with R by Andrea S. Foulkes.