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Does the use of "var", "x", and/or "ssp" in a scientific name provide specific information?
What exactly does it mean when a plant has a scientific name that specifies a vairety, for example  Nothofagus solandri var. cliffortioides, or when the name includes an "x", as in Populus maximowiczii Henry x trichocarpa, Populus xcanadensis, or "Crataegus x macrocarpa"?
All of these species are in the USDA Plants database (of plants that occur in the US). There are > 6000 occurences of the string " var. " ~500 occurances of " ssp. " and only a handful occurences of " x " in the database,

Does the x indicate that a plant is a hybrid, and are the varied uses indicate a different meaning?
Does the use of " var " mean that the plant is a variety?

Does it mean that each of these species has been cultivated and/or bred by a human?

Does "ssp"  mean that the plant is distinct yet compatible with others in the species?
is there a way to identify a that a plant is cultivated based on its scientific name?

Does the use of "var", "x", and/or "ssp" in a scientific name provide specific information?
Yes, those terms denote the rank of the taxon in question.
Does the use of " var " mean that the plant is a variety?
Yes, the use of "variety" or "var." in a taxon name indicates it has the rank of variety. There is also "subspecies", "subsp.", or "ssp." to indicate the rank of subspecies.1
Does [the use of "var."] mean that each of these [taxa] have been cultivated and/or bred by a human?
No. Subspecies and varieties are wild taxa found in nature (mostly, some common crops are called species, such as Zea mays subsp. mays).
Does "ssp" mean that the plant is distinct yet compatible with others in the species?
Probably. This is complicated because it gets into species concepts, but some kind of distinctiveness is required, and the biological species concept (where a species is basically defined as being able to interbreed) is popular.
Does the x indicate that a plant is a hybrid, and are the varied uses indicate a different meaning?
Yes. The multiplication sign × is used to indicate a taxon of hybrid origin. Its different placement can indicate whether the taxon is an intergeneric or interspecific cross. If the × glyph is not available, a lower case x is used (though, really, this should be rare these days). The × should occur before either the genus name or before the specific epithet (e.g., the species Populus maximowiczii is just a regular species name that happens to contain the letter "x").
Is there a way to identify a that a plant is cultivated based on its scientific name?
Yes. Names that include quotes (specifically single quotes), non-italicized text, or the addition sign + could all be indications that the plant is a named cultivar (or group, grex, or graft-chimaera).

Since the question references the USDA plants database, I'll limit the answer to plants. Similar rules are applied to animals and microorganisms.
Each entity being referenced is a taxon (plural taxa), that is, a group of populations of organisms that are seen by taxonomists as forming a unit. Taxa are hierarchically ranked, with the highest being kingdom2, such as Plantae (the green plants), the "basic" rank being species, such as Populus maximowiczii, and—most relevant here—ranks below species, such as subspecies and variety.
The rules for how (wild) plant taxa are named are defined by the International Code of Nomenclature for algae, fungi, and plants (the Code). There are similar codes for animals, prokaryotes, viruses, and, interestingly, cultivated plants.
While the Code recognizes that there are an indefinite number of ranks, it gives names for many of them from kingdom down to forma (grouping them as principle or secondary ranks). It also specifies that more ranks can be created by adding a "super" or "sub" prefix to the rank name to indicate a higher or lower level rank, respectively.
Species is the lowest principle rank, subspecies is below species, and variety is below subspecies (and, for completeness, there is forma below variety).
Strictly, since subspecies and variety are different ranks, a taxon could be classified as a variety that itself is a part of a subspecies. In practice this is rare, usually a taxon is assigned to one or the other.3
Besides denoting a different rank, what is the actual difference between a subspecies and variety? It turns out that the biological definition of these terms is basically up to the taxonomist doing the work. Just like there's no set definition of species, there is no set definition for intraspecific taxa. Some taxonomists might basically rank all intraspecific taxa as subspecies or as varieties, depending on their philosophy. Those that use both terms need some recognition that variety is a narrower term than subspecies, but what that looks like operationally is up to the person/group doing the work.4
(However, one should follow the resource they are using. If it's listed as variety in USDA, use variety. It's incorrect to just decide you don't like it and change it to subspecies [for example]; that would require a research publication.)
Species, either members of the same genus or of different genera can sometimes interbreed and form a natural population. One could refer to these by simply listing the hybrid parents in a hybrid formula, such as Agrostis stolonifera L. × Polypogon monspeliensis (L.) Desf.5 One could also formally name the resulting hybrid. In this case the hybrid nature would be noted by placing the × before either the genus or species name. The above intergeneric cross between Agrostis and Polypogon has been given the name ×Agropogon lutosus C.E.Hubb. The name Populus ×canadensis refers to the interspecific cross between P. nigra and P. deltoides.6
The basic unit of cultivated plants is the cultivar, which is an assemblage of plants selected (by humans) for a specific character, and that remains stable through appropriate propagation. The naming of cultivars is governed by its own code. This code only recognizes the terms subspecies, variety, or form, as they apply in the (wild) plant Code. (Note that other groups, such as the Association of Official Seed Certifying Agencies, do consider cultivar and variety to be synonyms.)
An example cultivar name is Clematis alpina 'Ruby'. Note the use of the correct botanical name, the cultivar epithet in plain text, and the use of single quotes. See other examples here.

1The Code recommends the abbreviation "subsp." for subspecies, but "ssp." is very commonly used.
2Kingdom is the highest rank recognized by the Code; there are generally recognized ranks that are higher, such as superkingdom and domain.
3For example, take the taxon Saxifraga aizoon var. aizoon subvar. brevifolia f. multicaulis subf. surculosa Engl. & Irmsch. This has been fully classified to a particular variety, subvariety, forma, and subforma. To refer to this taxon, one would almost always just write Saxifraga aizoon subf. surculosa, and that is in fact it's name as defined by the Code. One would only spell the whole thing out if they needed to give the full classification. Since no other plant can have the same name, there can be no other subforma within Saxifraga aizoon with the epithet surculosa, even if it were to belong to another variety, forma, etc.
4I could include forma in this paragraph, too, but this seems to have greatly fallen out of fashion as a useful rank.
5I've also included the author abbreviations here. They have their own set of rules. Just know they're not technically part of the name, but often included to help avoid ambiguity.
6This could be written as Populus ×canadensis or Populus × canadensis. The × glyph is not actually part of the name, and can be placed for best readability.


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How do fungi react to being grown in a tissue culture?
I know how plant cells and animal cells react to being cultured and grown this way, but what about mushrooms? Would they respond like plants, and result in embryos growing off the mass? Or does the mass just grow indefinitely as in animals? Has anyone done this? How do they react when grown this way?

Generally, fungi are cultured on agar with a food source such as malt extract. One way to do this is to clone a mushroom from the fruitbody of a mushroom or from colonized substrate (e.g. rotting wood). Another approach is to germinate spores.
The fungus will grow as vegetative mycelia until it runs out of food. At that time, some species will grow tiny fruitbodies or sporulate before entering a more dormant phase, dying out. Unless refrigerated, standard agar plates dehydrate. Also, fungi may take on different textures: wispy, bumpy, root-like (rhizomorphic), leathery, powdery, and may darken or change color as they age.
Some cultures start to adapt their metabolism to the media after a large number of transfers (based on observation and discussed in Stamets' "The Mushroom Cultivator".) at this point, cultures may also start to grow more slowly.
The mycelia can be transferred from one plate to another or to another media (substrate) such as a log, 'fortified sawdust' (sawdust with ~30% w/w wheat bran), or pasteurized compost. With the appropriate nutrition and environmental stimuli (CO2 levels, temperature, moisture, light, etc), the mycelia will fruit, creating mushrooms - generally after fully colonizing the substrate.
Here is a figure of 35 agar plates with 16 different fungal cultures that I isolated from the wild (soil, wood, mushrooms, as described in Allison et. al, 2009; LeBauer, 2010), and have transferred from a mature culture (about a 2 months old) to a new plate, which are about two weeks old in this picture. Parent cultures are in the first and third row, with children below (they are genetic clones; instead of counting generations, I count number of transfers.

You can also find cultures of fungi (Yeast) in unfiltered beer.
I have used many techniques to isolate and culture fungi (Isikhuemhen and LeBauer, 2004; LeBauer, 2010) but I would recommend the books "The Mushroom Cultivator" and "Growing Gourmet and Medicinal Mushrooms" by Paul Stamets for more information on sterile culture techniques used in mushroom cultivation.

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Where can I find comprehensive data on animal distribution?
I'm looking for vertical distribution or tidal height of several intertidal species, specifically from the Pacific Northwest.
I considered looking for published research for each species however, my search likely would not be comprehensive and perhaps be biased in site-specific differences.
Is there some kind of open database where I can find this information?
I've found that EOL draws some data from the Ocean Biogeographic Information System, but when I go to the site directly, I can't find the tidal height data. I've also looked through suggestions in response to this question but none are applicable.
Any help with these databases or suggestions on other relevant databases would answer my question.

This sounds both difficult and fascinating. I hope you can find these data!

I like your question a lot! I think what you're trying to achieve is the best way of solving your problem. Unfortunately, although I do have a few links for you that might get you a little bit further, a perfect solution is, I fear, not available. Tides are extremely complicated and depend on many factors. Some of these are large scale effects such as the relative positions of earth, sun and moon, but others are more local, such as ocean currents or the shape of the coast. Especially the latter can make a surprisingly large difference on a relative small spatial scale. Luckily, it is possible to come a long way and have very decent approximations.
The best option, as far as I'm aware, is to use XTide, a software program that can calculate tides at thousands of locations worldwide, making use of actual measurements as well as mathematical models. This will give you by far the largest amount of information, and the most detailed information. better still, it's open source software and completely free. The drawback is that it is complicated to use. Also, if you are a windows user, it is even more tricky as this is an X-windows program, developed for UNIX and UNIX-like operating systems (it should run fine on linux and macos). It is definitely possible to run it on windows, but I wouldn't recommend it for the faint of heart.
My second option would normally be to use rtide, an add-on package for the statistical program R, though in your specific case it's probably not good enough. The rtide package is fairly easy to use if you're familiar with R, and runs equally easily on all operating systems supported by R. The drawback is that it doesn't give as much detail as XTide, and it is based on data from a mere 637 stations, all of which are in the USA, so it's only of limited use for the Pacific Northwest. In addition, it takes more work to calculate certain variables such as the tidal range than to do the same calculations in XTide
A third option would be to use a website like https://www.tide-forecast.com/ where you can click your way to the relevant data. The number of stations they cover is even smaller than those offered by rtide, but they do cover the entire world. If you do not want to go the XTide way, then combining rtide with https://www.tide-forecast.com/ would probably be the best way to go: the former gives you a large number of stations in the Pacific US, while the latter will add some stations in the rest of the Pacific Northwest.
I hope this helps!

Hi Yuri, I appreciate your thorough answer however I'm looking for the vertical distribution (aka tidal height) of species. Effectively their vertical range along the shore. I'm not so concerned with the height of tides in a region but rather where animals live with respect to chart datum.

Oh, sorry. From your question I had understood that you had found the animal data in EOL and only needed the tidal height data that were missing there.

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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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Why do only two sexes exist for animals?
Why, from the natural selection point of view, do only two sexes exist for animals?

What avantage would you see in more than 2 sexes?

Mushrooms have a lot of sexes. So where is the advantage for them?

Fungi have a completely different type of reproductive cycle when compared to vertebrates. For instance they often switch between haploid and diploid during their life cycle. To be honest I am not sure of what you consider "a lot of sexes" in mushrooms. Could you elaborate (my microbiology courses are very far away in time...)

The meaning of my comment is: If i can say that more then two sexes does not bring any advantage then i can ask: where is the advantage of having only two sex?

Having sexual reproduction has several advantage over asexual reproduction. Having 2 different genders (rather than 3 or 4) is the easiest way to have sexual reproduction. Which bring us to my original question: 2 genders (sexual reproduction) is better than 1 (asexual reproduction). What would be the advantage of 3 rather than 2?

His question is actually a big one in biology. Why is there sex at all? It seems obvious but it goes a lot deeper than you would think.

Chance. Evolving another gender is hard, especially if you are a large multi-cellular animal, losing a gender is easy. Single celled animals do sometimes have more than one sex however.

@nico The benefit is that if there are $n >1$ sexes, than it is possible to mate with $1 - \frac{1}{n}$ of the remaining population for any given individual -- this approaches 100% as $n$ goes to infinity. For $n = 2$ this is a measly 50%.

Is there evidence for this statement? "More than two would confer no further genetic benefit for either repair or diversity, and would likely introduce complexity and inefficiency." – kmm Sep 30 '15 at 2:37 Evidence? No. Just logical reasoning. – Anthony X Sep 30 '15 at 2:46
2 I don't think you can say whether or not additional sexes would be beneficial or not, without some theoretical or empirical basis. Just because a trait hasn't evolved, doesn't mean that it wouldn't be beneficial if it did (e.g., wheels). – kmm Sep 30 '15 at 12:15

@TinaGallant - Please do no re-port other users comments as "answers". They are here anyway and are not answering anything.

I've upvoted as I think this is a good question, but I would ask you to add some content to show that you've done some research into the purpose of sex and the systems used by other organisms beforehand.

I'm voting to close this question. It shows neither research on the subject or presents any arguments or explanation for their being a problem. It appears many people think there is a problem, but this is extremely broad. If they wish the question to remain open they should modify the question so that it is appropriate.

Good row of comments... E.g. "not sure of what you consider "a lot of sexes" in mushrooms" (not too many references there to). "Identy" seems to be the key. Horse and donkey may not  be identical enough for meiosis and their crossing over. Not the whole story: there is the male and female of the mule. Refering to mushrooms: if the mule had some, optional, non-sexual reproduction, and assuming not all gametes of horse and donky would suffice, would that correspond to "many sexes of funghi"?

To get a non-circular answer to why humans and other mammals have only two sexes, it's helpful to take a look at our evolutionary history.  While mammals possess several adaptations to a terrestrial life cycle, including internal fertilization and gestation, which require substantial anatomic specialization between males and females, these are all secondary features that evolved long after our aquatic ancestors had acquired two distinct sexes.
Indeed, if we look at animals like fish, which reproduce via external fertilization, it's not at all obvious why they might not have more than two sexes.  After all, for many aquatic animals, mating involves little more than the female and the male releasing their respective gametes into the water, where they meet and fuse to a form new zygote, which can then divide and grow into a new adult.  Seen that way, there seems to be no reason why there could not be more than two "mating types", as in many fungi, such that gametes of any two distinct types could fuse into zygote.
The answer lies in the fact that the male and female gametes aren't actually that similar: the female gametes, or eggs, are typically large cells that contain all the nutrients necessary for the new zygote to develop into a viable individual, whereas the male gametes, or sperm, are tiny and produced in huge numbers.  This asymmetry is known as anisogamy, and modeling its origin has been an important topic in the theoretical study of evolution.
Without going into details on the evolution of anisogamy, once it exists, it clearly forces the mating types to also split into two groups: there's no advantage in two microgametes (sperm) fusing, since the resulting zygote would lack the nutrients it needs to be viable, whereas the fusion of two macrogametes (eggs) would simply be inefficient — eggs, being large, are comparatively rare and expensive, and wasting two of them to produce only one offspring would be suboptimal even if the resulting zygote was viable.  Nor is there really room in such a scheme for gametes of intermediate size: they'd be too small to fuse into a viable zygote with sperm, but too large to be produced in sufficient amounts to be effective in fertilizing eggs.
Of course, there's nothing that would stop a single adult from producing both micro- and macrogametes, but such an adult would not really be a third sex — it would just be male and female at the same time, a mating strategy known as (simultaneous) hermaphroditism, which indeed occurs relatively often in nature.
So, if pretty much all animals are anisogamous, why do fungi remain isogamous (and often have multiple mating types), then?  Well, one explanation is that the main drivers for the evolution of anisogamy — sperm competition and transportation risk — don't really apply to fungi, which mate when two sessile haploid mycelia grow and come into contact with each other.  Since the gametes are not motile, there's no advantage for either/any sex to produce more of them (at the cost of smaller size) in order to increase the chance of successful mating.  Thus, isogamous mating works fine for the lifestyle of fungi, and having multiple mating types is then a useful adaptation to make successful mating between neighboring mycelia more likely.

@emanuele you seem to be asking why there are only 2 sexes for animals, in contrast to fungi which can have many sexes or maybe bacteria which have mobile sex - the ability to donate genetic information can be acquired or lost.
Some animals - worms and fish for instance are hemaphrodites - they can accept sperm or donate them to produce offspring. Fungi are even simpler - the mating is by haploid fusion on the cellular level, since they have single celled life cycles.  The mating type allows mating with any cell that is not of the same mating type.  Its just a matter of how much genome space you want to dedicate to mating and there can be 2 mating types of 10,000 mating types - the only rule is that you can't mate with your own mating type.  Its a simple mechanism to restrict mating with yourself - probably to encourage genetic diversity.
Physiologically, for single celled animals and simple egg layers like fish and worms, you can see why sexual roles might not need to be specialized; its a matter of which gamete you will deposit.  If the egg is no more than an especially fat cell, becoming male is not necessarily a big change.  But when eggs are more complicated structures or live birth becomes an adaptation, the expense of being the gamete donor (male) or recipient (female) becomes a significant commitment and changing roles is not so easy to do in an evolutionary system.
Ultimately, Unlike worms or snakes, committed females are specialized such that turning into a male, with the requisite development of a womb, changes in bone structure, etc is such an elaborate phenomenon that we don't observe it.

Sex reversal, however, is observed for example in fish (notably salmon)

"For animals and humans" -- do you mean mammals? (Snakes and worms are also animals.)

I think the OP is likely asking why mammals only have 2 sexes. This is quite different to asking why we don't spontaneously change sex (as you quite rightly point out, the physiological changes required are too much). But what you don't touch upon is why there are no examples of 3 sexes, for instance, in mammals (that I know of) - I think this would then be a very complete answer.

"Its a simple mechanism to restrict mating with yourself - probably to encourage genetic diversity." - Are there any animals known to exist as hermaphrodites only? Because: self-mating makes sense as an exception to a rule, the rule refering to a whole lot of very diverse ancestors being integrated in that only one, the one and only.

Richard Dawkins describes an elegant solution to the puzzle in his memorable Selfish Gene: in the beginning, all gametes were similar, and many sexes could coexist (like in fungus). But when some lineages began to specialize in different strategies (ESSs, Evolutionarily Stable Strategies), with some increasing and other decreasing the size of the gametes, then there was room for two sexes. Probably a third sex would only compete with one of the others, without space for niche drift, and thus one of them would usually become extinct, driving it back to two sexes again.

This answer focuses on the gametes being different or not. However, think of  donkeys and the horses. 4 sexes of one bastard? It's 2 x 2. Is that, roughly speaking,  the idea of Dawkins...? Can you cite? More comment: Key to me is "identity". Funnily, considering ordinal and cardinal numbers brings up that you end up in two, don't think twice: it's all "right to copy" as long you pay allegiance to the two, there are only two: the original and its copy. Just the two of us. The more you diverge from perfect identy, and what's the use of diploidity if you don't... ("donkeying by numbers")

The purpose of sexual reproduction is to combine the genetic material from the contributing parents to produce a new individual. That combination has the potential to replace genes which may be defective and generally increase diversity in the offspring, improving resistance to certain pathogens. Bottom line: sexual reproduction confers an evolutionary advantage.
Where it occurs, why only two sexes? Simply because two is sufficient to get the job done.
Consider the perspective of one "parent", and the goal to combine genetic material from some other source of the same species in order to produce an offspring having some blend of genetic material. If that "other source" was one randomly selected individual, how does an additional randomly selected source qualitatively change the result? By the principals of statistics, it doesn't. One other source containing some random variation is no more or less random than a combination of two or more such sources. Therefore, to meet the requirements of a random genetic shuffle, two sexes suffice.
If a third sex was required, then three individuals would have to play their respective roles for successful procreation, where only two are required for the two-sex system we understand. If you compare asexual reproduction with two-sex reproduction, you might wonder why asexual reproduction exists at all given the genetic benefits of sex. The answer is in simplicity. No need to find a partner. To go from two sexes to three, there would have to be a benefit to overwhelm or at least balance the added complexity of bringing three partners together instead of just two. As previously discussed, there isn't any. Even if a three-sex system just happened to occur, it would be out-competed by its simpler two-sex rivals.

Is there evidence for this statement? "More than two would confer no further genetic benefit for either repair or diversity, and would likely introduce complexity and inefficiency."

Evidence? No. Just logical reasoning.

I don't think you can say whether or not additional sexes would be beneficial or not, without some theoretical or empirical basis. Just because a trait hasn't evolved, doesn't mean that it wouldn't be beneficial if it did (e.g., wheels).

@kmm As I said in my answer, a third sex adds complexity. We all know how complex partner-seeking and relationships can be when only two sexes are involved. For a trinary sex system to survive, it would have to confer a benefit which would overwhelm the added challenges of fitting in the third "contributor". Since the primary purpose of two sexes is to shuffle genes, and a third contributor isn't going to introduce any more randomness than two is capable of, there's no room left for any benefit from a third component, so it would never survive.

@kmm Also, it's reasonable that in 3.5 billion years of evolution, terrestrial life ought to have had the chance to give a three-sex system a try. If it could succeed, we ought then to be able to find extant examples.

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What causes fingerprints to form and why is the pattern formed unique?
I've found research that suggests that the reason we develop fingerprints is because they aid us with feeling surfaces (Scheibert, et al. 2008) and not to increase friction  and help with the gripping of smooth objects (Warman and Ennos 2009).
One thing I am still curious about is at what stage of growth the pattern is formed and why a unique pattern is created in the fingerprint of each person (including identical twins). I assume it has something to do with the mechanism by which the patterns form, but I couldn't find any detailed research into this. Any insight would be very welcome.

We can expect this uniqueness in foot[toe] prints as well. I suppose, all derivatives of germ layers should have their identity and heritability. Many forensic literature have explored these areas for personal identification.

I would say genetic diversity is the primary reason which results in other reasons that you are looking for. At the lowest level, random crossing over at prophase I, random separation of homologous chromosomes at anaphase I, random separation of sister chromatids at anaphase II, and random fertilization: one sperm fertilizes one egg randomly.
The skin is developed from ectoderm so need to look at the formation of embryonic disc and specifically to the genesis of germ layers: ectoderm.
However, I would stick to the primary reasons, since it is extremely difficult to visualize the given formation - actually we do not have resources for it at the moment.

Very good question the last part. I have an intuition that skin develops randomly because of the above reasons. You would also need a lot of memory to make identical skins for twins! It has not been useful to have identical fingerprints between two people so evolution has not resulted into it.
Feeling surfaces and gripping are movements - not much space taken things, in contrast to the memory needed in storing the exact surfaces of skin from one generation to another. - Learning is a way to save resources here and it is a lot more efficient and than storing static information to species from one generation to another.

Answer
Fingerprint pattern formation has two components to it: developmental and genetic.
Firstly, this article's abstract describes how fingerprints are physically formed in the womb.

[...] fingerprint patterns are created as the result of a buckling instability in the basal cell layer of the fetal epidermis. Analysis of the well-known von Karman equations informs us that the buckling direction is perpendicular to the direction of greatest stress in the basal layer. We propose that this stress is induced by resistance of furrows and creases to the differential growth of the basal layer and regression of the volar pads during the time of ridge formation.

Also, this OMIM entry describes a study which suggests the function of genes directly related to fingerprint formation.

An assumption is that the basic pattern is all ulnar loops and that a variety of genes cause deviations from the basic pattern. These include (1) a semidominant gene for whorls on the thumbs (one homozygote has whorls on both thumbs, the other homozygote has ulnar loops on both thumbs, and the heterozygote has two ulnar loops or one ulnar loop and one whorl); (2) a semidominant gene for whorls on the ring fingers that acts like the gene for whorls on the thumbs; (3) a dominant gene for arches on the thumbs and often on other fingers; (4) one or more dominant genes for arches on the fingers; (5) a dominant gene for whorls on all fingers except for an ulnar loop on the middle finger; (6) a dominant gene for radial loops on the index fingers, frequently associated with an arch on the middle fingers; and (7) a recessive gene for radial loops on the ring and little fingers. They suggested that these genes may act independently or epistatically.

The first source explains why everyone has different fingerprints, but the second explains why family members and identical twins have increasingly similar patterns.

References

Kücken, M, and A. C Newell. “A Model for Fingerprint Formation.” Europhysics Letters (EPL) 68, no. 1 (October 2004): 141–146.
Slatis, H M, M B Katznelson, and B Bonné-Tamir. “The Inheritance of Fingerprint Patterns.” American Journal of Human Genetics 28, no. 3 (May 1976): 280–289.


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Molecularly, why can you straighten or perm hair?
I'm aware that hair can be curly because of the disulfide bond interactions in between cysteine amino acids in alpha-keratin filaments. However, I'm curious as to the biochemistry involved in straightening hair with a straightening iron, as well as with "perming" hair.
What happens at the molecular level? I suspect that a straightening iron simply disrupts the present disulfide bonds, but I'm only speculating.

Pretty much yes. However, temporary things like wetting your hair or using an iron merely disrupt the hydrogen bonding network. http://www.ccmr.cornell.edu/education/ask/index.html?quid=708

Related: https://biology.stackexchange.com/questions/42760/how-do-disulphide-bonds-in-hair-cause-curling

For straightening hair with a flat iron:
This source provided by bobthejoe states that temporarily straightening hair involves the breaking of hydrogen bonds between keratin molecules within hair.

One of the reasons hair is curly is because of hydrogen bonds between the proteins (keratin) that make up your hair [...]. Another way to alter hydrogen bonds is with heat; electric straighteners work because of this principle. The platters on electric straighteners are flat so that when your hair cools it takes the shape of "flat" as the hydrogen bonds reform. The same thing occurs with curling irons, but since the heating element is circular, the hair stays curled as it cools. The effect of heat, however, is temporary, over time the hydrogen bonds eventually return to their original form and the hairs goes back to the way they were. This rearrangement happens because moisture in the air hydrates the proteins.

This source provides a similar explanation.

Running a flat iron through blown-dry hair breaks the hair’s hydrogen bonds. It flattens hair until water or water vapor (from humidity, drizzle or the shower) penetrates the hair fiber and allows the hydrogen bonds to revert to their natural positions.

Thus, the straightening of hair with an flat iron does not involve the breakage of disulfide bonds as I had originally hypothesized.
For perming hair:
This article suggests that perming involves the chemical treatment of hair with reducing agents to break the present disulfide bonds between cysteine amino acids, followed by the reformation of the disulfide bonds in the desired curled shape.

In a standard “cold” perm, hair is put into curlers and the reducing agent ammonium thioglycolate is added. The disulfide bonds break and keratin molecules are now free to move around and adjust to the shape of the curl. Then a “neutralizer,” such as hydrogen peroxide, is added to reverse the effect of the reducing agent. New disulfide bonds form so the keratin molecules are locked into the shape of the curls.

This Wikipedia article also suggests that the chemical straightening of hair is obtained with the same process.

When disulfide bonds break it leads to hydrogen bonds, which then changes the shape of the alpha keratin protein. Therefore, that is why the hair changes from straight to curly or vice versa. It's the ability of the hydrogen hydrogen weak force that allow the protein to fold differently.

Welcome to Bio and thanks for your answer. +1 could you add a reference?

Both actions- whether by heat or drying naturally by moisture evaporation break and restructure the ionic hydrogen bonds.
This is why a wet roller set has staying power despite no heat and when using heat esp., if the hair is damaged or if temp. Gets too hot, it will denature the hair and will not be able to be set to the desired shape. (Damaged hair can not longer hold moisture-- hair is made of a protien, keratin)

Hi welcome to Bio.SE! Short answers are not typically well received on this SE site. We also ask that all answers provide citations or other kind of reputable support. Please add more context and support to your answer to avoid having it deleted. Thanks.


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What is the correct model for enzyme-substrate complementarity?
This Wikibook shows both proposed models of enzyme-substrate complementarity, the Lock and Key model and the Induced Fit model. I've always been taught that the Induced Fit model is  the proper one. However, my biochemistry professor mentioned that often times, enzymes behave as lock and key. I also noticed that the Wikibook doesn't mention which model is in fact true.
The Lock and Key Model

The Induced Fit Model

Is there currently one accepted model? Which is it, and why?

IIRC there's no "accepted" one--depending upon the enzyme, it can be either.

This is true of all protein binding as well as the special case of enzyme-substrate interaction:
Various proteins are more dynamic than others: some have only one or two overall conformations and are relatively implastic otherwise. An example would be a receptor tyrosine kinase like Kit (or CD117, or Mast Stem Cell Growth Factor Receptor, whatever you want to call it), which has a very stable structure and binds its substrates in a lock and key manner.
Others, for example p53 (not an enzyme), have much more structural placiticity - even to the point of being mostly disordered when not bound. They tend to be induced fit binders (of other proteins, not catalytic substrates) and often exploit that to bind a broader range of possible targets than lock and key proteins.
The point is, it is a continuum between lock and key <-----> induced fit rather than discrete classes you can sort proteins into.

Thanks for the answer, like mention of continuum. I'll wait to see if there are more answers before I accept though.

Both models are true depending on how you frame the mechanisms of catalysis. As mentioned by @Blues, proteins are highly dynamic. In that manner, a protein will adopt both the unbound active state shown in the induced fit model and the complementary shape shown in the lock and key model.
(apologies since this is the only figure that I could find to explain this concept). Using the above description the induced fit model (E) will change its structure to the ES model. In the lock and key model, the E state will be equivalent to the ES state. According to the below figure, this would imply that the ES state always exists but as it is a few kcals higher in free energy, the state is rarely seen. Thermodynamically, this means that the "lock" always exists but it is an unstable configuration. When the substrate is added to the system, it will stablize the lock and thermodynamically favor an ES state.

Long story short, the induced fit model is a good explanation of how enzymes morph into an active state but depending on how you frame the mechanism, you are always seeing a lock-key model (at least according to my enzymology professor). Unfortunately, the majority of biochemistry textbook continue to teach using the induced fit model since it is a much easier concept to understand given the majority of undergrads; and 1st year graduates' understanding of statistical thermodynamics.
The induced fit model is more appropriately used to understand the mechanisms of substrate specificity. As hinted by your professor, enzymes will perform their function in the lock-key mechanism. This is true for many serine proteases which all do the exact same reaction. However, substrate specificity can be incorporated by unstabilizing the E*S complex which largely has to do with the E state.


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Is there any reason for the variation in mitochondrial DNA size?
As my textbook An Introduction to Genetic Analysis points out, yeast mitochondrial DNA has approximately 78 kb of genetic data, while the human mitochondrial DNA contains 17 kb. Is there any evolution reason for this drastic change in size? Also, are there any particularities about mitochondrial function that have been compromised with this reduction in size?

References

Griffiths, Anthony J. F. An Introduction to Genetic Analysis. New York: W.H. Freeman, 2000.

I know yeast is supposed to have very little non-coding DNA, but could it be possible that mitochondria in yeast have more intron regions?

There is a diagram showing the decrease in intron regions for humans. Nonetheless, could the sole evolutionary reason for the decrease be that it's simply more efficient in replication, or the efficiency of use of nucleic acids?

I think that to look at the evolutionary aspect of this question fairly, one needs to consider many other organisms in addition to human and brewer's yeast. An alignment of the genomes, or perhaps a simple list of the encoded genes will address the question of compromising of function with changes in genome size.

One of the contributing factors the size of the yeast mitochondrial genome are 'selfish' mobile genetic elements termed homing endonucleases genes (HEGs).  These genes are typically found in introns that encode site-specific DNA endonucleases.  These endnoclueases cleave the HEG- alleles during yeast mating leading to DNA recombination using the HEG+ allele as template.  I suspect over time as organisms became more complex and HEGs become unable to mobilize they would become fixed in the organisms genome.  Upon being fixed there is no selection pressure to maintain the open reading frame of the HEG or the intron its encoded within (ref).  This causes the eventual loss of the HEG and intron since they provide no real benefit to the organisms genome.
I don't know how much of the yeast mitochondrial genome is taken up by these introns.  I believe that there are 4 of them in yeast some of the introns also require reverse transcriptase for splicing and mobility.  Other fungal species can have many more introns and sometimes weird things like introns embedded within introns.

Shorter DNA would allows easier synthesis, but more introns could  allow for more different transcription factors to influence gene expression.
Human mitochondria probably does not need to be as adaptable as mitochondria in yeast, since the a human cell's environment tends to be more stable. This could provide a viable reason as to why human mitochondria does not need as many introns, but this is only how I imagine things. I have no proof or experience to validate any of this - its just a possiblility.

Multicellular have mt-DNA that contain 14 - 20 kb  but planta have mt-DNA that contain 200 -2500 kb.
Yeast mt-DNA ís in between.
It seems that the role of the mitochondria determines its size rather than its evolution.lífið

Hi and welcome to biology.sx. It would be great if you could add some references so that interested readers can follow this up.


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X chromosome "weight"?
According to Wikipedia, the X chromosome has approximately 153 million base pairs, while the Y chromosome has only 60 million base pairs. Thus, the difference is roughly 93 million base pairs.
My question is: Could this "extra" 93 million base pairs in virtually every single female cell of the human body slightly contribute to the "extra" relative weight of the female as a whole, in comparison to a male (of course) with a similar amount of cells? Or would this weight be so small that we can consider it negligible?

Theoretically...
93 million bp/cell x 650 daltons/bp x 10^13 cells/body x 1.66 * 10^-27 kg/dalton = 0.001 kg
So I would say it's not too much of a difference :P
however this ignores the rest of the chromosomal material: histones

Not too much of a difference, but it's something! Thanks.

Girls take note, this is not a valid excuse. Seriously though, this difference is exploited in some (albeit minimally effective)  techniques to sort sperm for gender selection.

Yep. Believe it or not, X sperm swim slower than Y sperm.

So, what is the difference in weight between X and Y sperm?

Very small. Using the same method as above yields an answer of around 0.1 picograms.

@ bobtheowl2, @ jp89: Could you provide some reference for the sorting procedure?

Is that difference due to the weight or rather the metabolism of the sperm due to having a different sized genome?

Hmmm, is it really true that Y sperm swim faster? If that were the case, you would expect that there be more men than women.

And indeed we do see such an imbalance. There are more male conception to female conception. Estimated 160 male conceptions to 100 female. There are 107 male birth to 100 female birth. But you can see males are losing individuals due to spontaneous abortions. This comes from males have only one X chromosome. A bad copy of a ChrX gene and you die if you are male.


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Electricity generated by the body and its applications?
I recently came across this article from Nature. In it, it states that the snails have "tiny biofuel cells that extract electrical power from the glucose and oxygen in the snail’s blood", and that the power obtained is dependent on "how quickly sugar and oxygen can be taken from the creatures' blood". They go on to say that the power obtained decreases over time, and that these implants could power future pacemakers in humans.
Would this application in humans require that a patient eats more and "breathes more" than average? Why does the power output decrease over time, and couldn't that potentially lead to the malfunctioning of a pacemaker?

References

Van Noorden, Richard. “Cyborg Snails Power Up.” Nature (March 12, 2012). http://www.nature.com/doifinder/10.1038/nature.2012.10210.

You'd think if such devices were used in humans, they wouldn't require a change of lifestyle.
They don't say the power always decreases over time:

Katz’s snails, for example, produced up to 7.45 microwatts, but after
  45 minutes, that power had decreased by 80%. To draw continuous power,
  Katz’s team had to ramp down the power they extracted to 0.16
  microwatts.

This is really a chemistry question. The glucose has to be brought to the fuel cell some way. In this case, the glucose is oxydized directly in the hemolymph. As oxygen PP in the hemolymph is always greater than glucose concentration(1), your limiting rate (which is related to the power you can get from the device) is that of glucose intake at the fuel cell. Therefore, the more you oxidize glucose per unit time, the greater intake you need to keep the output from dropping.
The glucose intake at the fuel cell is a function of biological parameters such as quantity eaten, metabolic efficiency, metabolic speed, blood flow, but also diffusion. The kinetics of glucose intake at the fuel cell are such that you can't ask for too much power for too long.
I suggest you read the article to get a more detailed answer. Nature news is good, but there's nothing like reading the real paper.
1 http://pubs.acs.org/doi/full/10.1021/ja211714w

Would this application in humans require that a patient eats more and "breathes more" than average?

From the cellular standview, each glucose and O2 molecule that you substract to the cell for use in a second futile cycle, should be replaced. However, I doubt that the amount of glucose/O2 required per hour will be so important to require additional food intake.
By the way, each cell in the body normally generates electricity from glucose and O2: just think at the electron transport chain during the mitochondrial cellular respiration.


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Why does muscle tissue have relatively constant AMP + ADP + AMP?
I was going over slides of energy expenditure in muscle cells. It mentions that in muscle tissue, the cell's energy charge ([ATP] / [AMP]) is the principle factor controlling glycolytic activity, and also that glycolysis’ primary role here is to provide ATP for contraction.
However, the slides also mentions that "Keep in mind that [ATP] + [ADP] + [AMP] remains relatively constant in the cell over short time frames" with no further explanation. I was under the impression that ATP was actively consumed in muscle tissue during intense activity (which is why lactic acid builds up in muscles: oxidative phosphorylation can't keep up with your rate of energy expenditure).
Thus, my question is Are my slides wrong? During muscle activity, is there a general lack or constancy of ATP?

Adenosine triphosphate (ATP) is often thought of as the energy currency of cells. It is not "used up" per se, but energy is released from the conversion of ATP to ADP (adenosine diphosphate), and yet more can be obtained by removing another phosphate to make AMP (adenosine monophosphate).
Here's a chemical schematic of ATP, you can see the three phosphates to the left.

Your slides state that the amount of (ATP + ADP + AMP) remains constant in the muscle, which makes sense because ATP is not used up, but converted to ADP. So as cells use energy, they do not actually reduce the total concentration of (ATP + ADP + AMP). Energy is required to add the phosphates back onto an ADP or AMP molecule - the process is called oxidative phosphorylation in cellular respiration (although this is not the only way).
I hope I didn't misunderstand your question.

Ohhhhhhhhh, I think I may have just misunderstood the professor's wording in the slides. This makes total sense of course (and must be what the prof is referring to) but didn't occur to me. I was understanding that the concentration of EACH nucleotide remained constant (which is not so), and not the SUM of all three. Thanks for the epiphany :).

The pluses stand for addition, not "and".

In fact there is even a certain balance ATP/ADP/AMP + GTP/GDP/GMP + IMP/XMP as these are all interconvertible purine nucleotides.


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How did the nucleobases in the Murchison meteorite form?
The Murchison meteorite is an important piece of evidence for abiogenesis, because it contained nucleobases from extraterrestrial origin, as this Wikipedia article explains.

These results demonstrate that many organic compounds which are components of life on Earth, were already present in the early solar system and may have played a key role in life's origin.

My question is: How did these nucleobases arise? Is it possible for these nucleobases to have been synthesized naturally from simpler molecules in a specific environment, like in the Miller-Urey experiment for amino acids?

I think it's fine here.  Biochemistry is on topic to a degree on both sites, but I think this is closer to Bio's scope (I'm a mod on Chem).

The Wikipedia article about the meteorite mentions nucleobases, you're asking about nucleosides. Which one of the two are you asking about?

Just to clarify, what are you actually asking? I mean, what would be the alternative to them having been synthesised naturally? The only alternatives seem way out of scope for a biology site – namely, either spontaneous formation (e.g. supernatural creator) or aliens.

@KonradRudolph I think the alternative would be that we have no idea how they formed spontaneously.

@MadScientist Sure. But whether we have an idea or not how they formed, they still formed naturally, or not at all. Or am I overseeing something here?

I've edited the question to read nucleobases. A professor had told me nucleosides. Guess he was wrong.

See my response below. The problem with Urey-Miller is that they assumed a strongly reducing environment which probably was not the case on the early Earth thereby giving them very high yields of lovely organic stickies.

@LanceLafontaine I agree with Konrad - it is meaningless to ask if they formed naturally. The only alternative is supernatural (i.e. not real). Do you perhaps mean 'is it possible for [them] to have been synthesized abiotically' i.e. without requiring a life-form as the environment of synthesis?

Also @KonradRudolph oversee != overlook :)

@Richard Duh. I’m still slightly hung over.

@Poshpaws From what I’ve heard, that criticism of the Urey-Miller experiment has been refuted by recent findings (see the section on the Wikipedia article ff). Also, didn’t early life probably form deep under the sea in environments similar to black smokers, rather than in the atmosphere?

@KonradRudolph The argument about reducing vs non reducing atmosphere goes on, but it probably was not as reducing as Urey Miller assumed. Not to take away from their very important contribution however. Regarding black smokers, yes they are favourite candidates for early life, but their chemical environments are not much like Urey Miller either!

It is interesting to note that, in the Wikipedia article, it states that

The amino acids were racemic (that is, the chirality of their enantiomers are equally left- and right-handed), indicating that they are not present due to terrestrial contamination".

This implies that, if a 'life form' did create these proteins, they are fundamentally quite different to life on earth. (Particularly in light of the 70 unique amino acids they described!).
We cannot ever 'know' how they were made, unless a pretty revolutionary discovery is made that undisputably confirms evidence for extra-terrestrial life (although this is the best evidence yet!), so we are left to speculation.
The nucleobases either formed 'randomly' in one of the countless celestial events (although the chances of this seem pretty remote given the complexity of the molecules and the homogeneity in the sample), or they were made by extra-terrestrial 'life' (much more exciting, and indeed probably more likely, as we will see). (Or the 3rd option: intelligent design, however this is dramatically less probable than either of the other two).
The Miller-Urey experiment to which you refer has been subsequently enhanced, and evidence for the "catalytic potential of cosmic dust" is now reasonably robust (Hill, 2004). They demonstrate that simple nebular iron silicate catalysts can yield methane and water from CO₂ and H₂, and ammonia from N₂ and H₂. Allowing these to react yields nitrogen-containing organics such as methyl amine.
It is not a huge jump to suppose that with enough time, mass and energy, these reactants could combine and form a molecule (chain of amino-acid-like molecules - a protein) capable of faithfully replicating itself, and thus initiate life. There is no reason to suppose that Earth is unique in this respect; there are billions of suns in our galaxy alone, and billions of years of time for these reactions to take place.

I am not sure that I would say that we are left to speculation. The fact that these chemicals are racemic would suggest that they were formed abiotically. This being the case, we can probably get to understand the chemistry which should be pretty basic.

But certainly the importance of dust should not be underestimated!

I think it's fair to say that we don't really know how these more complex organic molecules formed abiotically, but we can say that carbonaceous chondrites - a class of carbon and organic molecule bearing meteorites to which Murchison belongs (specifically CM2) - have experienced at least three distinct chemical histories:

In the interstellar medium (ISM) in cool (10 - 30 K), dense clouds where cold gas phase chemistry can lead to the formation of species such as HCN, C₂O₂ and CO.Polycyclic aromatic hydrocarbons (PAHs) have also be identified here.
In the early solar nebula. These simple organics can stick to dust grains forming "tarballs". The ultraviolet radiation field from the young star can then create some interesting chemistry through things like radical reactions and during the evaporation of ices. Things like diethyl ether have been detected in the pre/proto stellar nebulae of young stars.
In the parent body of the meteorite, such as in a meteoroid. Here most chemistry would occur through hydrothermal alteration over long timescales as the body orbited the parent star. As these bodies will invariably describe elliptical  orbits, it will undergo many freeze-thaw cycles all in the presence of an intense radiation field.

Carbonaceous chondrites in particular undergo aqueous alteration due to the presence of water in liquid form.
Figure 2 of this article gives an basic overview of some of the chemistry involved. It actually refers to the chemistry in cold molecular clouds, but is almost equally applicable to that in things like meteroids/asteroids/comets.
Ehrenfreund, P, and Charnley, S.B., 2000, Annual Reviews of Astronomy and Astrophysics, 38, 427

I've not read of complex molecules form in clouds before - are these molecules faithfully replicated in such a way as to call them living?


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What causes knuckle "popping" and the feeling of relief that comes from it?
Many people like cracking their knuckles. I have always been curious about it.
What happens when we crack knuckles?
What creates the POP sound?
Why do we get a relief-like feeling after doing it?

A paper was just published that explains this in PLOS One, found here. It looks like it is caused by the formation of a gas cavity in synovial fluid of the joints. They do mention that contrary to what is stated in the previous answer the sound does not come from the collapse of the bubble, but rather its formation. And in response to the comments, as mentioned in the paper, this does not seem to cause any harm to the meniscus or surrounding tissue. See http://biology.stackexchange.com/a/31582/107

@cagliari2005 - it has overlap but the relief factor is added to it. That justifies it as a new question I think. As more and more questions are asked, more and more questions are closed for being duplicates. As such, subtly different questions should not be closed, but just answered and perhaps linking the other question, or edited first and answered.

@AliceD makes sense and I agree

Nobody really knows where it comes from. The currently most popular theory is that pulling the joint apart leads the gases in the joint's cartilage to accumulate and form a bubble which then pops when you let it spring back. The only thing that has been researched is whether it has an effect on the joint, but people who do it regularly don't seem to have any problems with their joints more than anyone else (I'll find the reference once I have time). Apart from that it's hard to get funding for this kind of research because it has little practical use.
Relief like feeling? That must be subjective to you, I used to do it every now and then but I don't remember getting any relief from it. In that case, it's probably the same relief as other people get from picking their nose, their ears, biting their nails, etc. It's called compensation reaction.

anecdotal I know, but I also enjoy popping my knuckles. May be all in my mind, but I can 'feel' when I haven't for a while, and having done so there is a feeling of 'relief'. People have always told me that it increases your chances of arthritis - if you have a reference that says otherwise I'd much appreciate seeing it also. Thanks

Not on-topic enough to warrant an own answer but if you want to add the reference to the research about the harm, here’s an explanation and the link to the Ig Nobel prize research on Skeptics.


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Why are some menstrual cycles irregular?
A friend of mine asked me this today, and I didn't know. I remember studying the menstrual cycle a few years ago, but I can't remember the details (other than it was very hormone-related), and so I don't have a good base in the matter anyhow.
What makes some women have irregular periods? Why?

You get things like nutritional factors and cortisol (stress) intermingling with sex hormones. Also, sex hormone secretion is primarily steered by the hypothalamus (through pituitary) which may be influenced by the general state of your mind. Would be interesting to see if a woman actually has a regular cycle if she manages to maintain the exact same mood and diet.

@Armatus true, that'd be pretty interesting, given that I read somewhere that 30% of women are irregular. You have to wonder if its always the same 30%.

Actually, I'm pretty sure the rest of the brain plays a role there; be it through the hypothalamus or not. I've read about studies with students sleeping in the same room whose menstrual cycles apparently adapted to each other slowly until they all roughly menstruated at the same time.

That's actually should be another question altogether, I'd be curious to know exactly what's going on there (if it's known).

@Armatus: what you are describing is called the McClintock effect and the extent to which it actually exists are still under debate. A similar effect is a quite well known phenomenon in mice, and it is due to pheromones in urine.

There's two phases of a menstrual cycle, before ovulation known as the follicular phase and after ovulation known as the luteal phase. The second phase is not very variable, it's the same length almost always as it is governed by how long the corpus luteum (remnants of the follicles after the ovum bursts out) survives. The first part is variable and is what causes periods to be irregular. In this phase the eggs mature. The body picks several eggs to mature but only one will "win". However, how fast it wins changes. It all depends on how fast it grows and much it manages to suppress growth of the other eggs and that in turn depends on the quality of the egg. But then this also branches out, as it is controlled by levels of hormones this is heavily affected by stress and diet among other things.
It's unfortunate that the first phase is variable otherwise knowing which day you were going to ovulate would be easy.


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How can I accurately predict proper transgenic protein function/structure from different species?
I am currently building a synthetic system in E.coli, and am often faced with the need to use genes from other distant prokaryotes. I know that myself and most of my colleagues resort to an educated trial and error approach. Besides the obvious (elimination of introns from eukaryotes, codon optimization, genetic relatedness), is there any predictable or semi-rational way of knowing if a transgene for a different organism will function properly in any given organism?

There seems to be something missing at the end of the second sentence.

other things such as the nature of the protein should also be considered (Glycosylation and other PTMs which make the protein functional). Also it is important to make the GC content of the transgene comparable to that of the host. I have heard that certain organisms such as plants silence transgenes with drastically different nucleotide composition (it is something like an innate immune response).

By looking at the sequence only?  This is an unsolved problem.
Its not clear to me exactly what you are looking for, but here are some thoughts...
On a relatively narrow question as to whether any gene you plug into a bacterium, yeast, mouse, goat or other transgenic organism - the rna may not translate into protein in detectable levels or at high enough levels to get the desired result.  changing the sequence of the DNA of the gene for better transcription/translation is a common necessary experimental.
On the broader systems biology level, other cofactors, substrates that are necessary for the function of the gene may have to be engineered in the host organism. That is also an open question.
All this is assuming the gene in question codes for an enzyme to make a new or different amount of the metabolic product from the host organism, a commmon synthetic biology target.  If you are adding signaling pathway components, tinkering with a more specific mechanism in the cell, getting the function you desire could be a lot of work.  E.g. if you were inserting a new ribosomal component or a gene related to mitosis, that would be hard to imagine a priori how it would function in the new cell or if it would just kill it.
Also, Olga Troyanskaya at Princeton CS is working on the related problem of finding the function of a gene by looking at its sequence and cross referencing to other known data. Electronic functional inference is difficult, esp when we have no complete gene functional description of any living organism to start with.


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Can two hammerhead ribozymes simultaneously cleave each other?
I am working on a project in which an XOR gate is being built by having two hammerhead ribozymes simultaneously cleave each other when both are expressed, but have these ribozymes cleave a target transcript when expressed alone. Has it ever been shown in the literature that a hammerhead ribozyme was able to cleave the flanking arms of another ribozyme?

In principle it can. Ribozymes can be designed to target small RNAs too. But unless the ribozymes have highest affinity for each other, they will continue to cleave the target, when both are expressed together. It will cause leakiness of the gate.

@WYSIWYG, I plan on having longer flanking arms and 100% complementarity between the ribozymes, and less so for their target.

[ For the sake of answering a question that is long unanswered ]

Can two hammerhead ribozymes simultaneously cleave each other?

Yes, in principle they can.

two hammerhead ribozymes simultaneously cleave each other when both
  are expressed, but have these ribozymes cleave a target transcript
  when expressed alone.

This may be realized only when ribosomes have higher affinity for each other than for the target. As you said in the comment, inserting few mismatches in the ribozyme-target interaction may work. You may need to notice that since the two ribozymes are complementary to each other but cleave the same target, the target sequences will form a set of two mutually complementary regions. If separated well enough, there may not be much of a problem. From your design strategy I guess that UTRs are the best place to keep the ribozyme target sequence. If you keep both the target sequences in the 3'UTR (lets say), then they may form a hairpin structure, which may interfere in the targeting. So you can insert mismatches that also destabilize the possible hairpin.

Has it ever been shown in the literature that a hammerhead ribozyme
  was able to cleave the flanking arms of another ribozyme?

Not yet. Self cleaving examples are there but not mutually cleaving ones.


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Why isn't there a standard unit of promoter strength?
Sometimes in synthetic biology, we need to know rates of transcription of one promoter in relation to others (particularly inducible vs constitutive) in order to perform tasks like balancing transcription products and ensuring an excess of one product over another. As far as I know, there is no standard method of characterizing promoter strengths in relation to one another. However, a logical unit for transcription rate made (by organism or in vitro) could look something like:
Promoter Strength = number of transcript made / (concentration of RNA polymerase) (length of transcript) (unit of time).
Why hasn't this been done yet? What other factors could contribute to rate of expression in a particular organism? Is there another system for comparing promoter strengths?
Note: a similar system could be used for strength of repression.

What if there are multiple regulatory elements acting on a given locus?

I think the quantity you suggest is suitable only if the relations between the different factors is linear. Is there any proof of that?

@Amory, this is exactly why a characterized number would be useful to define promoter strength. You would be able to quantify a particular promoter's strength with or without activators/repressors, as well as in relation to other promoters with their respective regulatory elements.

The destruction ratio of the mRNA also varies, for example. Also, different mRNAs may have different affinity to the ribosomes (for instance, differences in Shine-Dalgarno sequence in prokaryots). Finally, unless you're using retrotranscriptase RT-qPCR, you shoudn't have a fiable method to quantify gene expression.

I think this paper defines a standard unit: https://jbioleng.biomedcentral.com/articles/10.1186/1754-1611-3-4

Transcription rates are very context dependent. This shouldn't surprise you, since the same genes aren't expressed in your lungs and your eyes. They're also very environment dependent, this shouldn't surprise you either, since it's pretty obvious every organism is going to respond to temperature, their current nutritional state and so on.
So, in order to define promoter strength, you'd first need to define the exact conditions under which you're measuring it, including the exact strain you're measuring it in. Because if you get any of those even slightly different you're going to get a different answer. Doing this might get you a consistent number but you're abstracting away the most important parts of differences in transcription anyway: how it varies between cells and contexts.
Moreover, even if got past these hurdles you'd not have a particularly useful answer anyway since the rate of transcription is only a small part of the whole process. Why not consider mRNA durability, or rates of translation, or protein durability? What matters very much depends on what you're considering.

I do realize that transcription is very context-dependent, but disagree about its importance. Even if strictly used in characterized in vitro systems, a number associated with a promoter is very useful, and can be extrapolated to its general abilities for transcription in vivo.

No, it can't. Consider DUO1 in Arabidopsis: it's a gene that expresses strongly in the germline but is entirely unexpressed in somatic tissue (and, in fact, is detrimental if it is). How will expression in vitro be extrapolated then? If your in vitro model is similar to the germline you'll get results irrelevant to any other cell; if your results are relevant to the somatic tissue you'll fail to understand key processes in the germline. The major issue in gene expression is its variation.

Not all genes need to be expressed in their "proper" context. Think of the Tet and lambda pR promoters being expressed in E coli (or really synthetic biology as a whole). If the purpose is exploiting or engineering and not discovering novel protein functions at a particular developmental stage, these promoters strengths are extremely relevent.

the measurement - counting # of mRNA from a specific cell state over a period of time would be difficult to do.  a single cell measurement where you are simultaneously monitoring the promotion state of the gene.  Sounds like quite a bit of work!

@LanceLafontaine: Extremely relevant for a particular purpose carried out in a particular way. That doesn't call for a standard measure; instead if you want to compare the effectiveness of two promoters you can simply compare them by Western Blotting or qPCR and see what you find. If you are desperate for a number, this will quantify the difference.

It's true that the expression of a promoter is context-dependent, i.e. depends on the overall status of the cell, but some work has been made to boil down such context-dependency into some measurable parameter. For example, for constitutive promoters such a parameter seems to be the growth rate. You could characterize promoters by that:
Gerosa, L. et al. Dissecting specific and global transcriptional regulation of bacterial gene expression. Mol. Syst. Biol. 9, 658 (2013)

I realize this is an old question, but in Synthetic Biology, we nowadays use the Relative Promoter Units (RPU)1. This is a standardized measurement of promoter strength to circumvent inter-wet-lab variability.
Reference:
1: Kelly, J. R., Rubin, A. J., Davis, J. H., Ajo-Franklin, C. M., Cumbers, J., Czar, M. J., ... & Endy, D. (2009). Measuring the activity of BioBrick promoters using an in vivo reference standard. Journal of biological engineering, 3(1), 4.

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Years of discussion about this:
"Polymerases Per Second.
A standard unit to measure the inputs and outputs of a BioBrick Device.
PoPS have yet to be directly measured in vivo."
http://openwetware.org/wiki/PoPS
*understanding this would be a great feat and it would get us one step closer to measuring complex systems.


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Two subunits connected by only one disulfide bridge: quaternary structure?
I've always simply assumed quaternary structure to be characterized by non-covalent interactions such as hydrogen bonding, van der Waals interactions and whatnot. However, if two distinct polypeptides were only connected by one covalent disulfide bridge, would this be considered as quaternary structure, assuming that non-covalent interactions between the subunits are either negligible or even repulsive?
In other words, can a disulfide bridge, on its own, convey quaternary structure?
On a side note, are there any notable examples of this type of interaction?

I don't know of any examples of this but I would say no doubt, that's quarternary structure. Quarternary isn't so much defined by the kind of interaction but much more the fact that it's between different polypeptides; all lower-level structures are within one polypeptide. (Wikipedia agrees.)

I've always just gone with the name hetereodimer but there isn't any technical reason why it isn't a quaternary structure. As for an example, I work with antibody fragments or FAbs and cys-diabodies which are exactly that, two distinct polypeptides that are connected by a disulfide bond linkage.
These do have a significant amount of non-covalent interactions. For something with less, maybe ricin?

authors: Vladimir F Героям слава


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The genetic and physiological origins of laughter?
This Wikipedia article  defines laughter in many terms, such as...

"a visual expression of happiness, or an inward feeling of joy"

and

"a part of human behavior regulated by the brain, helping humans clarify their intentions in social interaction and providing an emotional context to conversations".

Note: the emphasis was added by myself.
The article also states that laughter is "probably genetic", and that

"Scientists have noted the similarity in forms of laughter induced by tickling among various primates, which suggests that laughter derives from a common origin among primate species."

According to this report which the Wikipedia referenced, the expression of laughter in general is present among other great apes. Phylogenetic trees were reconstructed to represent the evolution of this trait among primates (which concludes that the ability to laugh must have a genetic basis, at least to some degree).
Note: I also found this WikiAnswers post, but it clearly can't be that reliable.
A search on the OMIM database yielded this result, where children with Angelman syndrome were characterized with "excessive laughter", this result, in which Charles Bonnet syndrome was characterized with "inappropriate laughter", as well as many other genetic mutations which resulted in some sort of uncontrollable laughter.
I understand that laughter is a complex psychological expression of emotion likely associated with more abstract thought, and that there simply can't be "a laughter gene", but my question is:
Is there any known genetic or physiological origin of laughter? What is biologically different in great apes which allows for laughter, in comparison with a panoply of other animals? I'm looking for more of a molecular answer rather than an ecological or psychological one.

this question (or any follow ups you might have) would also find a good home at CogSci.SE.

I recommend this article: The Evolution and Functions of Laughter and Humor: A Synthetic Approach by M Gervais and DS Wilson, 2005, University of Chicago Press.
For your question about the origin, firstly they explain that all laughter is induced by stimuli which are unexpected or unpredictable, experienced in a non-serious (unthreatening, safe) context. Given examples include peek-a-boo, which can make a child laugh but also cry if the child is not perceiving the situation as safe. Also that we can't tickle ourselves and tickling is induced by stimulating vulnerable body areas. Similarily, apparently in apes laughter is mainly induced by "tickling in conjunction with mock aggression and chasing".
They explain the function of (Duchenne, that is stimulus-driven "honest" as opposed to voluntary) laughter to be propagation of "positive affect" in a group, as it utilises the chameleon effect (it is contagious) which apparently has been shown to exist for its "cooperative value". Other studies seem to have shown that a) we are thirty times more likely to laugh in a social context than by ourselves and b) the contagiousness of laughter response increases with group size, making it an efficient tool for coordinating a group and getting everyone into the same emotional state.
As for other animals, the article doesn't address that. It does seem like a different question to me so I would consider separating that into a second one.

Informative and relevant response, but I'm also looking for some sort of a more "molecular" explanation as well. Any more insight?

Molecular in what sense? The neural pathways, anatomy?

Hmm. Signalling pathways, anatomy as well, but I'm mostly interested in the molecular genetics of it. Your answer is certainly a fine one, but doesn't quite cover that area.

Could you give a different (unrelated if you wish) example that could explain what you mean by molecular genetics in relation to a pattern of behaviour?

Rather than the behavioural act of laughing itself, I'm more concerned with the biological ability to laugh that humans and some great apes have, according to the report. As laughter also has some sort of genetic component, there must be some genes being expressed within specifically primates that allows us to laugh. I'm thus interested in the expression of these genes, and how they interact to create the phenotype of being able to laugh.

@LanceLafontaine The road from genes, to proteins, to neurons, to neural systems, to behavior is a very long one. It has not been parsed out yet so what you're asking for can not yet be delivered. Keep in mind that laughter (like all behavior) is an extremely complicated emergent property of many underlying systems. It's never as simple as "having some genes for X". Basically, the question your asking is too vast.

@Preece, notice that I mention exactly that in the question. I'm not looking for the impossible, but rather what's already known, if anything. And if nothing is known, an answer explaining why would be sufficient.


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Is there an evolutionary advantage to crying when sad?
It seems as though the act of crying when sad does nothing to relieve that sadness. Is there an advantage to crying from an evolutionary perspective, or is it the end result of a different process? Also, why is there the same physiological reaction of crying when in sadness or in pain?

Purely anecdotally it stirs empathy in peers so could lead to protection from other members of the group when an individual is vulnerable.

Just a note, not every behaviour (or generally phenotype) has to be advantageous. This question just assumes that there has to be one, and while I agree with Rory about the probably effect of this one, it’s not a valid assumption in general.

@KonradRudolph thanks for the specification, I'll edit the question.

@RoryM Yes but why does it stir empathy in peers rather than, say, blinking quickly?

I've seen various odd theories, but most commonly, it's just assumed to be a social signal. There's no inherent survival advantage to turning up the corners of your lips when you feel happy, either, but there is probably an advantage to letting other members of your group know how you're feeling. There may even be specific advantages to having this happen automatically and in ways that are slightly difficult to fake (tears or duchenne smiles).

As for why we use tears rather than some other kind of signal: the "choice" could have been a fluke of evolution (people coordinated around the first good signal that happened to develop). There's also some work suggesting that our physiological and behavioral responses to pain and sadness are mediated by proinflammatory hormones, so maybe it's not a coincidence that being sad superficially resembles having hay fever...

@octern some great comments, would be a good answer.

First, here is a link to an article that discussion the answer to your question:
Why Cry? Evolutionary Biologists Show Crying Can Strengthen Relationships
The original article to which it refers can be found here:
Emotional Tears as Biological Signals
To speculate a bit on Jez's question, crying in adults could be a result of our possible Neoteny. Crying in infant animals is extremely common as a way to elicit attention and sympathy from the mother. If we are neotenous apes, crying could be a left-over behavior that was seized by evolution, instead of being discarded.

It seems to me that your neoteny hypotesis just shifts the question. How did crying evolve in human infants? Animal pups only have the "vocalization" part of it, by the do not shed tears... (also, as Wikipedia reports, human newborns often cry without weeping, probably because of insufficient development of their nervous control)

@nico You're right, it's not a very satisfying hypothesis. I don't have the answers to your questions, but they are good questions.


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Are cells really the basic unit of all life?
Please see comments as to the appropriateness of this question on biology SE.
All known life on Earth is made up of cells. It is thus safe to say that all known life is characterized by the presence of cells. But is having cells as a basic unit a requirement for life?
I'm thus asking if life is currently existent and/or possible without biomembranes, and to what degree cells actually matter in our present understanding of life.
An all-encompassing, comprehensive and cited answer would be very much appreciated.

You're basically asking for the definition of "life".

I'm asking whether or not cells are part of the definition of life as we know it, or all potential life. Is that a bad thing? Clearly related to biology.

And in some respects, the question is similar to this one:http://biology.stackexchange.com/questions/90/life-without-dna

I think it's a fair question - perhaps very closely related to "life without membranes".

Well at the moment, there isn't a question related to what is the definition of life. Meanwhile, I think that most evolution of life specialist will say that no, cells are not the basic unit.

Maybe I should ask another question about the definition of life ahah! Although I feel that it'd be more of a debate than anything...

@bobthejoe: and what they would say it is then?

The impression I get is that the inquirer hasn't put much thought into his question. If you were a kid, I wouldn't mind of such a question, but you're not. It's exactly because there's no clear cut definition of life that your question is in fact not a question.

@CHM, just because a question does not have a clear-cut answer, it doesn't mean it isn't a valid question. Exploring such questions and explaining why or how is what scientific thinking is about.

I've flagged this as off-topic. I could go on and explain the reasons, but I think it should be pretty clear.

@LanceLafontaine: I do not think lack of a clear-cut answer is a problem per se. The impossibility of giving a proper scientific answer is, though (for questions on this website, that is). Calling on the possibility of undiscovered extraterrestrial life which is not cell based is like claiming you have an invisible, incorporeal, floating dragon who spits heatless fire in your garage...

@nico and CHM, I can see your points. I'll go ahead and edit the question for it to read something less fantasy/science-fiction based ahah.

Lance, I don't think you're getting the point of my objections. This is not about you or your question: its about maintaining this stack's purpose and quality. You will not get an "all encompassing, comprehensive" answer from anyone - discussion is all that can be done about it. Before even drafting an answer, you'd have to define life. I suggest to close this question and move discussion to the chatroom. I also suggest you go talk with your professors, I'm sure they'll have things to say. Again, don't think this is not interesting, it's just inconsistent with this site's purpose.

As a point of community management and education: This question is not appropriate for THIS type of Q&A. It may be an interesting discussion and even educational, but we forgo these types of question to preserve the purpose of building a canonical knowledge base. Questions should be specific problems you might encounter in your day to day work. But the question above is really a "discussion starter" likely to solicit extended discussions, opinions, and debates. That type of activity is better left to the chat rooms and discussion forums, and not really what we do here.

According to Gerry Joyce: "Life is a self-sustained chemical system capable of undergoing Darwinian evolution."
From a meta-analysis of 123 definitions of life: "Life is metabolizing material informational system with ability of self-reproduction with changes (evolution), which requires energy and suitable environment."
According to Alexander Oparin: “Any system capable of replication and mutation is alive”.
At hand are some key elements in order to match these criteria. Maintaining a Darwinian cycle requires replication, mutation, and selection. Thus, we can break down the above into 5 criteria (personal communication with Gerry Joyce).

Life stores information
Life reproduces its information
Life alters that information
Life does something with that information (uses energy)
Life does all of this in a self-sustained manner

I would point out that the above criteria is quite different from what is currently on wikipedia described by metabolism and homeostasis. There are certainly additional criteria that certainly raise the threshold for what may be considered life. The common discussion revolves around viruses which do many of these things but not in a self-sustained way.
The question at hand then asks if cells are the minimum unit of life? What makes a cell a cell is that there is compartmentalization. The underlying reason behind this compartment is due to the necessity of tying the phenotype to the genotype. Paraphrasing using our definition of life, it links the information with the function that the information carries out. In the modern biological scheme, it keeps the proteins (phenotype) with the DNA (genotype).
The necessity of compartmentalization is negated when the phenotype is already linked with the genotype. The most frequent example is RNA where the material that carries the information is also the material that carries out its function. It tend, is reasonable to hypothesize that life can be made entirely with RNA without the need for compartmentalization (although compartmentalization certainly helps see Paegal and Joyce and Chen and Szostak).
Recent experiments by Gerry Joyce and others have been able to satisfy several of the requirements of life. The have self-replicating RNAs, that store information, that reproduce their information, that introduce alterations to their information, and do it in a self-sustained manner. What Gerry and his colleagues agree on is that their current self-replication Ribozyme system doesn't do anything particularly novel. However, by introducing a larger variety of functional elements to their ribozymes perhaps they will.

I disagree with your conclusions. Otherwise should we say that a virus or a prion is alive?

Also, please link to the sources of the papers that you mention and give relevant extracts of the authors conclusions about ribozymes being a life form (or otherwise clearly state that that is your personal interpretation of their results, which is absolutely fine, of course).

@nico, I think I have pointed out that viruses do not qualify under the above definition. Likewise as mentioned in http://biology.stackexchange.com/a/96/389, prions are dependent on host factors. Citations will come after I finish my experiments.

sorry I had missed the sentence about viruses

What about self-replicating computer software?

@CHM intriguing. I guess we have to start considering the battle against entropy.

Where are you getting those criteria from?

@Preece Gerry Joyce.

@bobthejoe His website is disappointing :(

@nico, CHM, Preece. You guys better be satisfied.

OK, I am not sure I necessarily agree with their views but your answer now deserves a +1.

@nico: As someone who studies mathematical modeling of ecology and evolution, I see no reason not to consider viruses to be alive. They pass the duck test for it: they replicate like life, they consume resources like life, they evolve like life. True, they depend on a host to do so, but so do all parasites. For that matter, all heterotrophs, including us humans, are just as dependent on other life forms — none of us can live on just water, air and sunlight.

@Ilmari Karonen: there is a subtle difference between a parasite and an obligate parasite

This discussion thread is begging to be closed. The chatroom isn't used, people. Why not move there and have a very interesting talk about this subject, where it belongs?

Life is a physical entity that creates copies of itself,sometimes in a slightly changed form.
That's it.
A cell is not the basic unit of a life but a large number of molecules that have bonded together to reap the benefits of specialization.
Like what is happening today, humans coming together to form a society which collectively starts to function like a single living organism again.
So no, a cell is a far cry from being the basic unit of life, it is a very advanced form of life.
All it takes for life to start is for a single self replicating molecule to form, that's it.
Evolution takes over from there.

Molecules aren't "alive". An intricate synergy of a mind-blowing quantity and variety of molecules can be. Would you consider H2O a self-replicating molecule, since it spontaneously undergoes dissociation to form H+ and OH-, at equilibrium?

Not all molecules are alive, but molecules that produce copies of themselves are. H2O is not alive,when it undergoes dissociation there are no extra copies of it being created.

Agree. This is extremely interesting, but I just feel like it belongs in a forum, not a Q&A, since there's no answer to be had, only discussion. Mind giving some sources where I can read more on self-replicating molecules?

"The Selfish Gene" and "The extended Phenotype" by Richard Dawkins.

Now that I've actually sat down and thought about it, this definition does fit; +1. H2O can't be life since it doesn't add any variation to itself.

Well, that's only partially true - while H2O does not create extra copies of itself after dissociation, there can be a difference in its quantum state before and after the dissociation, which constitutes a variation.


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Is it more likely that the very first living organisms had a linear genome?
Is it right to assume that the first living organisms on earth had a linear genome? I base this on the fact that linear macromolecules are clearly much more common in nature that circular ones. To be honest, I can't even think of any naturally-occurring circular macromolecules that aren't already a part of current living organisms.
Were the very first living organisms more likely to have linear genomes? If so, when during evolutionary time did circular chromosomes originate?

I would say this is a question that might not be resolved yet.
Going back to the earliest days of DNA - a billion years ago - its hard to imagine circular DNA being the first sort to show up.  Its speculated that in the transition from RNA world to DNA world, early on each gene had a separate piece of nucleic acid coding for it which would not have been circular.  It's been proposed for example that RNA viruses might have been a next step to cellular life.  Although I can see an old electron microscopy reference, not it does not seem as if any RNA viruses with circular RNA have ever been found.  How the first DNA chromosomes came about and what they looked like seems unclear to me.
In any case, though not typical, its not unusual to find linear chromosomes in prokaryotes.  I could not find reference to archaea with linear chromosomes, but in prokaryotes, the link above points to the observation that even close relatives can have linear or circular chromosomes.

A remarkable property of the 8.2-Mb chromosome of S. erythraea was that, contrary to the expectations and the earlier data (Reeves et al., 1998), it proved to be circular. The chromosomes of its close relatives, Streptomyces coelicolor and Streptomyces avermitilis, are both linear, as is the chromosome of Rhodococcus sp. strain RHA1. These chromosomes are the largest in actinobacteria (8.7, 9.0 and 7.8 Mb respectively) and comprise some of longest DNA molecules in the prokaryotic world. In contrast, the shorter chromosomes of other actinobacteria are all circular.

It seems that linear vs circular genomes are a 'lifestyle' choice or connected to selection critera we don't understand yet:

Hence, it was tempting to speculate that the linearity of streptomycetal chromosomes was somehow linked to and perhaps beneficial for the maintenance of these extremely long DNA molecules, even though it resulted in the instability of their termini. This idea has been contradicted by the discovery of equally long but circular chromosomes in the acidobacterium Solibacter usitatus (9.97 Mb), δ-proteobacterium Myxococcus xanthus (9.1 Mb), cyanobacterium Trichodesmium erythraeum (7.8 Mb), and, now, in the actinobacterium S. erythraea.

I really doubt the instability of the chromosomal terminii is a real consideration - there must be genes that help maintain those, just as there are in eukaryotes.  S coelicolor is a soil bacterium that is so common most people can find it in the dirt right outside their door - its not hard to live with a linear chromosome as a bacterium.

Nifty! Learn something new every day.

It is hard to give an answer to this question that is not just speculation.  We can be reasonably confident that the most recent common ancestor of bacteria and archaea had circular genomes.  However, we currently have no way to get any conclusive evidence earlier than that.  3 billion year old DNA doesn't fossilize.  So it's just speculation what DNA looked like back then.
On the other hand, my understanding is that most experts think that RNA genomes predated DNA genomes.  These RNA genomes would be linear.


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What are polytene bands, and why are they there?
Drosophila polytene chromosomes have been particularly useful in genetic research, as it made cytogenetic gene mapping possible with very little effort. This was primarily accomplished due to polytene bands, which are naturally-occuring (no stain) fixed bands seen along the chromosomes via microscopy.
We have been exploiting these bands for decades, but it seems as though their function isn't quite clear.
What is the cause of the visible polytene bands, and what function do they serve?

well, Wikipedia says that they are formed by numerous rounds of replication without cell division, and their function may be in gene dosage [but this is not really clear].  However, this is all without proper references, so you should probably wait until someone comes along with citations to verify.

This review has more information than you will ever want to know.