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If we introduce any disease or deadly effect to a large group of living things, will such a group be able to develop a resistance?
Like for instance, introducing cancer or radiation,
to a large group of insects/animals that can reproduce very quickly,
would it result in the surviving population of these living things to be more resistant to whatever adverse condition that was subjected upon it?

Or how about conditions that should lead to cancer? I guess having that "pathology" tag wouldn't make sense in this case, I'll remove that.

From your edit, it seems that you are not interested in transmissible disease anymore (and so my answer would be off) but in cancer specifically. It feels like you may not really know what a cancer is (esp. when we consider what you wrote before the edit). You should definitely read a bit about cancers. Is the question "Is there selection to reduce sensitivity to cancer?", the answer is yes but almost by definition of what a cancer is, so I am unsure what you are really asking.

Thanks @Remi.b, Reading some general info about cancer, https://www.medicalnewstoday.com/info/cancer-oncology, I'm not sure how that could by definition imply "selection to reduce sensitivity to cancer". I really have zero background in any biology-related field, but this question had been an ongoing curiosity for some time.

@Remi.b As for what I'm really asking, I just wanted to know if it were possible to over natural selection, gradually evolve some group of living things to be more resistant to any harsh condition, such as extreme heat/cold, intense radiation, any disease, etc. This curiosity might have been inspired by new stories related to "tardigrades" (https://gizmodo.com/genes-hold-the-key-to-the-water-bears-indestructibility-1786814698), that are highly resistant to extreme conditions.

I'm not sure what you mean by to over natural selection?

@Remi.b By "natural selection", I meant, for instance, introduce an extreme condition to a group of ants (i.e.: low temperature that kills most but not all), then after several generations, the surviving ants should be more able to tolerate low temperatures. So if other things were applied the same way (introducing a disease that causes most but not all things to die), we should get similar results? I assume this is what you meant in your response by "selection against".

Yes, your description of the consequences of natural selection is correct. It is more the use of the verb over that I did not understand in the context of your sentence. Did you mean 'to put an end to selection' or something?

Selection against a trait is the same as selection for the opposite trait. For example, for mice living on white sand, there is selection for being white and against being black for increased camouflage (and the opposite is true on darker substrate; Nachman et al. 2002).

@Remi.b, I'm not able to edit the comment, but it should be rephrased as: "I just wanted to know if it were possible to, by the means of natural selection, gradually evolve some group of living things....", sorry for any confusion.

Oh I get what you meant now! No worries. Btw, I made a tiny edit at my answer you might want to have a look at.

Resistance is usually present in a population already and the selective pressure makes it apparent. So organisms don't develop resistance. They have resistance that is selected for. Even in bacteria that can survive ever more antibiotics at higher doses, they do not survive until a mutant arises that when exposed to the environment, survives.

Is there selection against cancer?
What is selection?
Let's start by explaining what selection is. Selection is a differential in fitness among different genotypes. In other words, if you consider a phenotypic trait for which there is some variance in the population. If, in the population, there is a correlation between this trait and fitness and there is a correlation between this trait and genetics, then there is selection.
The three ingredients for selection are

Variance for the phenotypic trait
Correlation between the phenotypic trait and fitness
Correlation between the phenotypic trait and genetics

These three bullet points are known as Lewontin's recipe. The last bullet point could be rephrased into "the phenotypic trait is heritable" and all bullet points put together could be rephrased into "fitness is heritable". Have a look at the post Why is a heritability coefficient not an index of how “genetic” something is? to understand the concept of heritability.
Is there selection on cancer?
Cancer is fundamentally a genetic disease. If this is unclear to you, you might want to read a bit more about cancer.
There is variance in the population in cancer (not everybody has a cancer but some people do) so we satisfied our first bullet point. Cancer is a genetic trait. So we satisfied our second bullet point. Cancer is a disease and therefore affect fitness (cancers kill) so we satisfied our third bullet point. In short, yes there is selection on cancer.
How does increasing the amount of carcinogens in our environment will affect selection on cancer?
From wiki

A carcinogen is any substance, radionuclide, or radiation that promotes carcinogenesis, the formation of cancer.

If you increase the amount of carcinogens in our environment, you are going to increase the prevalence of the disease, which will increase the variance for the disease (unless the prevalence would become very very very high) and therefore increase selection against cancer.
Does selection work?

I just wanted to know if it were possible [, by the means of] natural selection [to] gradually evolve some group of living things to be more resistant to any harsh condition, such as extreme heat/cold, intense radiation, any disease, etc.

Yes, it is possible. Natural selection does work.
Note that if you are interested in a short intro course to evolutionary biology, then you may enjoy having a look at Evo101 by UC Berkeley.

Thanks for edit to more closely follow updates in the the comments. I'll have a look into that Evo101 link sometime.

I don't think this answer answers the post given the discussion and new edits. I will leave it here nevertheless just in case I still misunderstand the OP's question.

[..] introducing cancer or radiation [..]

A cancer is not a transmissible disease (except very few cancer last the facial tumor in Tasmianian devils). A radiation is not even a pathology, it is a physical phenomenon which include light. Did you rather mean something like a virulent flu for example?

If we introduce any disease or deadly effect to a large group of living things, will such a group be able to develop a resistance?

The population may or may not survive. It depends upon many parameters such as how virulent is the parasite, how large is the population, whether individuals in the population have already encountered the parasite before, whether there is already genetic variants resistant in the population or whether de novo mutations will be needed, etc... There is no way to answer to this question in the general sense.
Note by the way, that an individual may be resistant or tolerant to a certain disease.
Most of the time, the population survive well. The population will likely decrease in size a little bit though.


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Are the fossil sites in Hadar geographically separated?
The Hadar fossil record is made up of, from oldest to youngest, the Basal Member, Sidi Hakoma Member, Denen Dora Member, and Kada Hadar Member.
Are these regions geographically distinct, or, are they layers on top of another on the same geographical region?

Here is a map of the region where they found the Lucy skeleton.

The researchers speak of the Hadar formation at Dikika, so they are giving it an expanse of 10-15 kilometers at least.
it's quite flat as well.
Why do you want to know?

source: Stack Exchange

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sort: votes


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Why does ostrich and other birds like pigeon swallow stones?
I have read in my book that birds swallow stone to help in their digestion process. What is the need of swallowing stones? And how does it aid them?

I have suggested an edit for your post for a possibility which I also think but not sure

Mention not :-)

there should be a textbook biology forum and an advanced one on here. it's confusing prefer to interact on a forum with a 1h incomplete response time, instead of geting a complete instant answer from google with illustrations and nice pages.

Birds do not have teeth so stones help in the process of grinding food.
Before even going to the stomach the food it starts to be processed in the "Crop". However is in the "Gizzard"  that the stones play a big role helping this muscular sack to mince and grind the food (the link sends you to an image of an open gizzard with pebbles inside).
Food and stones are present at the same time into this organ, therefore during peristaltic and contraction movements the friction between stones and food allow more efficient grinding.

Here you can a detailed description of the chicken digestive system that can be largely applied to birds in general.

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How does the body fight new infections?
I have read that the body contains T-cells and B-cells specific to all antigens in small amounts and that these are activated when the antigen presents in the body. If this is true then why are we not able to fight all types of infection?
If this is not true, how does our body learn to fight new infection or new foreign substances?

Disclaimer: This is mostly like canonical or "textbook" immunology. As with many biological systems, there are caveats to everything and it can't all be covered here. If you have questions outside the scope of this answer, please make another question!
The immune system consists of two subsystems: adaptive and innate immunity. Adaptive immunity as you know consists of T cells and B cells, and fronts much of the resistance to established infections. In fact, without adaptive immunity, you end up with a disease called SCID (severe-combined immunodeficiency), and HIV depletes CD4+ T cells resulting in AIDS. Important no doubt, but adaptive immunity has a process to it which makes it useless against brand new threats to which immunological memory doesn't yet exist. This is where the innate immune system comes in.
So we can either use the mucosal layer in the GI tract or the skin as an example, either way. Of course, the primary defense against foreign threats are such physical barriers as mucus, skin, the ciliary system of the lungs, and so forth. But lets say you get a cut or abrasion and now the skin barrier is compromised and a slew of bacteria enter the tissue. Your tissues contain resident cells such as macrophages (macs) and dendritic cells (DC) which have pattern recognition receptors that either recognize PAMPs or DAMPs. So what's a good PAMP? Lipopolysaccharide (LPS or endotoxin) comes to mind, and is recognized by toll-like receptors on DCs and macs, specifically TLR-4. These cells begin to produce mediators of inflammation such as IL-8 and IL-1ß which attract cells from the blood. The primary innate immune cell in your blood is a neutrophil, a type of phagocyte, which kill bacteria in a variety of ways. You also have a system of plasma (blood) proteins produced in the liver called complement which attempt to coat and directly kill the bacteria, or direct innate cells to targets of interest.
So say the bacteria is in the tissue, the tissue is inflamed, and a dendritic cell engulfs and digests a bacterium. The dendritic cell is what's referred to as an antigen presenting cell or APC, and APCs act to bridge innate and adaptive immune systems. Through an exogenous pathway sort of like this, they break down the bacterial proteins and "present" them on these MHC-II complexes (HLA in human). Macrophages, B cells and T cells may also be APCs. So when the dendritic cell is digesting the bacterial proteins and preparing to present them on MHC complexes, they move out of the tissues into the lymph system by expressing lymph node trafficking receptors such as CCR7 which responds to chemokines secreted by activated endothelium in the lymphatic vessels. The endothelium is activated by the inflammatory signals we talked about earlier. The DC goes to the lymph node where naive T cells and B cells aggregate, circulate in the blood, and re-aggregate.
Naive T cells tend to go back to the lymph node because they too express trafficking receptors such as CCR7 and CD62L that say "follow signals back to the lymph node." So this is where the magic happens. I'm not going to cover adaptive immunity but in short, typically APCs present antigens derived from foreign threats to naive T and B cells in the lymph node, thus activating them. These cells differentiate into a variety of lineages including effector and memory cells. As a note, you first adaptive response against a new threat takes about 2 weeks from start to finish to get antigens to an expanded pool of antigen-specific clones. Memory cells improve the second response by largely forgoing the wall of text above, proceeding directly to clonal expansion and elimination.

Abul Abbas, Andrew H. Lichtman, Shiv Pillai (2014). Cellular and Molecular Immunology (8th ed.). Elsevier. ISBN: 9780323315906.

All understood but I familiar with this system. What I ask is when APCs carry antigens into the lymph node as you said, and they are NOT recognised by T-cells and B-cells, what happens? Assume there is a new strain of bacteria for which there is no particular T-cell or B-cell receptor, then how does the immune system respond?

@Person I can't recall there being a case like that. Typically your lymphocyte repertoire is sufficient to recognize something due to the amount of combinations of possible receptors and epitopes. Otherwise, see SCID or AIDS. To my best knowledge I can imagine the pathogen would either kill the host or your body would attempt an in-situ inflammatory attack. Tissue-resident cells such as resident memory T cells can respond to unrelated threats by recruiting tissue defenses in an IFN-y-dependent manner, for example (1).

These mechanisms heavily damage tissue, however, and present a double-edged sword.

Remember that APCs present hundreds of MHCp-II complexes loaded with different peptide antigens. You have thousands of TCR or BCR combinations, and if I can find the paper, you need as little as 100 MHC molecules to efficiently prime T cells in the lymph node*. The chance that you have an immune repertoire, are not immunocompromised and still don't have the necessary cells is slim.

I see, then why is that there are certain bacterial infections we die from? Considering the body has the T-cells and B-cells particular to the antigen, should the body not able to fight off all infections?

There are a couple good examples. For example, the causative agent of tuberculosis manipulates a number of pathways in innate cells that stunt the ability of adaptive cells to respond (ref). As another example, S. aureus strains can cause agglutination of fibrin with bacteria trapped inside, provoking a continually stronger and more damaging immune response as cells are unable to clear the complexes (see something like type-III hypersensitivity reactions).

In some cases the infection kills you, in others, the now-dysfunctional immune response kills you as a result of the infection.

Yes,it's true.In an overview, our body fights against all these foreign bodies and microbes in order to eliminate them and the threats caused by them.If u analyze deep, what you call antigen is just a protein on the surface of any microbe.Your body cells eg.RBCs, also have antigens on their surface.But your body's immune system doesn't attack them normally.Its because of the recognition of self antigens of our body by the immune system so as to prevent them from being attacked.If your body is attacked by a bacteria that has a new antigen on it that our system has never encountered, the so called antigen presenting cells for eg.,T helper cells, Dendritic cells ,etc. recognize each and every antigen on the microbe surface and present them to developing T and B cells.So the antibodies(the anti-proteins for the antigens) are produced to act against the antigens on the foreign cell surface and render them inactive.These antigen proteins have specific sites called epitopes an which the sites of antibodies ,called paratopes bind.In the set of  disorders called autoimmune disorders the body's immune system attacks some self antigens because of some pathology.For some conditions such as AIDS by HIV the body's immune system is suppressed by initial attack on the T helper cells so that the recognition of antigens is suppressed and the immune system fails.And some microbes have the ability to modify the antigens on their surface.This is the reason for resistance of microbes to drugs.
Reference:Pathologic Basis of disease..-    Robbins and Cotran
----Combining a second answer into one---
It's simple...it has already recognized what are all self and thus any new microbe attacks your body it doesn't need to recognize it earlier...since it is something new the defense system starts working. Naturally when it is not known as self, it's some new invader which is read by the patrolling WBCs and by the effects produced by it( such as inflammation) which draws the attention of other WBCs to the site through some chemical attractants called inflammatory mediators...these attacking happens only when the foreign substance crosses the first line of defense our body has(the so called innate immunity plays an important role in it).WHEN THAT MICROBE IS ALREADY KNOW BY RECOGNIZING THE ANTIGENS PRIOR TO EXPOSURE (i.e. during a second or successive attack) the reactions start immediately i.e. the antibodies already programmed are released immediately along with inflammatory mediators ( which accouts for allergic response).If it is new microbe a recognition process takes place and after that anibodies are produced.HAVING T AND B CELLS FOR ALL POSSIBLE ANTIGENS IS NOT POSSIBLE BECAUSE THE CORRESPONDING T AND B CELLS ARE PRODUCED ONLY AFTER FIRST EXPOSURE and stored as memory cells... during second attack the memory cells are cloned and response is produced.Antigens are just proteins and can be infinitely many(just a single alteration in a protein structure produces a new antigen)...IT DOESN'T NEED TO KNOW WHAT IT DOESN'T KNOW which is not possible if not exposed once... Because of the need  for this first exposure attenuated antigens are given in vaccines so that during the first attack of the corresponding microbe T and B cells readily attack them.

Please add references for your claims and edit spelling and punctuation, at the moment the answer is not intelligible

I understand but what I'm asking is how does the body fight a foreign substance that it has NOT encountered before (with an antigen it does not recognise and simply knows that it is non-self). Does it have T and B cells for all possible antigens?

In my next answer

So you've said ''HAVING T AND B CELLS FOR ALL POSSIBLE ANTIGENS IS NOT POSSIBLE BECAUSE THE CORRESPONDING T AND B CELLS ARE PRODUCED ONLY AFTER FIRST EXPOSURE'', but how does the body produce NEW T and B cells to attack the bacteria?

They are produced in Bone marrow along with other blood cells...The process of maturation of Lymphocytes (B and T cells) take place in Bone marrow and Thymus respectively.Hence the name B and T. It is in this process the T cells learn to differentiate self and non self antigens.90% of the T cells fail in this and are naturally killed by apoptosis(Programmed cell death).After they are produced they release corresponding antibodies against the antigens of the invading microbe.The matured Lymphocytes play the roles of recognition and fighting.


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Why don’t humans have eyes at the back of their heads?
How does evolution rule out the possibility of humans or others fragile herbivores from having 2 pairs of eyes, one at the front and the other at the back of their heads? Why didn’t that ever happen?

I’m sorry but I’m not a biology student; currently pursuing mechanical engineering. So, I don’t have any knowledgeable viewpoint over the same. The idea was that you people could hopefully provide some intellectual insight.

“Given limited resources” - what does that mean ?

@user115962 A limited resource is any element an agent utilizes, in which the quantity, or frequency of use, of the element can not be fully assumed throughout a completely defined process. The most general form of any limited resource is free energy.

On top of the question marked as duplicate, you might want to have a look at Why don't mammals have more than 4 limbs?.

First, humans aren't fragile herbivores, they're omnivores, and quite successful hunters even pre-technology :-)  Now that that's out of the way, the basic vertebrate body plan - four limbs, two eyes, &c - was fixed hundreds of millions of year.  Herbivores, such as horses, have the eyes located at the sides of their head, and have nearly a 360 degree visual field.  Predators tend to have front-facing eyes, the better to focus on potential prey.

Vertebrates have ears which sense 360 degrees for a range of many meters, and they have social eyes, where they group many eyes and ears into one social group, it's easier to listen and live in groups, than grow eyes in the back of the head.
2 eyes exists in nearly all bilateral animals, arthropods, flatworms, sea-slugs, crabs, crickets, squids, flies. Arthropods have compound eyes and it would be easier for them to have 4 eyes, and only spiders and horseshoe crabs have more than 2.
It would be easier for a vertebrates to develop 4 nostrils and ears than 4 eyes because they are simpler than the orbs of the eye.
Same reason as 5 fingers has been the optimal numbers for all vertebrates since early lizards. in short, it's very easy to lose extra organs and to modify old ones, but it's very difficult to evolve new organs, and to relocate ones around the nerves and veins... centrally connected organs travel around the body and the circulation moves in front of them, i.e. if you did get 4 eyes and two of them moved to the back and sides, the nerves for your face expressions that are next to your ear would have to go in front, around, and through the moving eye pathways.

To simplify, we stopped evolving our symmetrical archetypes when we were related to starfish, ammonites and ediacaran fauna, and the fastest most versatile animals all had 2 sided symmetries, with entirely symmetrical nervous systems, and forwards moving at that point in time, using binocular compound vision, which did have 180, and that binocular compound vision afterwards became our 2 eyes. We share the kingdom Animalia with starfish, our common ancestor experimented with shape during the Ediacaran era.
To understand the difficulty of adding new eyes later, you should learn why nearly all vertebrates have 5 fingers, except some frogs which have 4. it
google: why do animals all have two eyes?

The mysterious downvoter is back I guess.

I should post more to compensate then.

2 eyes and 5 fingers has been the optimal numbers for all vertebrates this is fantastically wrong (might want to have a look at Why don't mammals have more than 4 limbs?). we stopped evolving our symmetrical radiation is wrong. when we were starfish sounds like you mean that the common starfish is our ancestor which is wrong. You seem to equate symmetry with binocular vision which is also wrong. Your only two links are google search!

We share the kingdom Animalia with starfish, our common ancestors experimented with symmetries during the Ediacaran era resulting in worms, corals, urchins, bivalves. Terrestrial vertebrates have 5 fingers.... you send me to a page called "mammals have 4 limbs" I send you to 4 pages called "why nearly all vertebrates have 5 fingers" .... bi-focal vision is a common theme in planar symmetry or in radial? PLANAR symmetry.

"Optimal number" is wrong.  It's much more of an accidental number: the long-ago last common ancestor just happened to have 4 limbs, 5 digits per limb, 2 eyes (and ears &c), and those are buried so deep in the genes that any changes make the organism non-viable.  See e.g. Hox genes.

Quadruped 5 digit number = "The number chosen by natural selection of fitness" was "optimal" because there were 7, then 6, then 5 digits on Both limbs of archetype quadrupeds. Neither 7 nor 6 digits could have been optimal, because they were both lost by selection against ray fin derived Hox Genes for 6/7/4 digits. Eyes: Planar symmetry arthropods can all develop multiple eyes, and they dont. Even all Flatworms and seaslugs have two eyes, which is certainly the chosen number of eyes for planar symmetries, for the same reason that we have 2 ears, it's genetically efficient.

I downvoted too.  This is the very worst kind of answer for StackExchange; it's superficially plausible and written with great confidence and authority, so a naive reader will probably think that the author is deeply knowledgeable; yet the answer is simply bluster, mistaken stereotypes, and sweeping claims based on ignorance. If you don't actually understand the field, you shouldn't answer questions. The fact that you think you understand this is simply Dunning-Kruger in action.

@comprehensible Even the expression natural selection of fitness is non-sense.

You don't know the difference between a limb and a digit, Remi.B. Also, learn to speak english. natural selectrion of fitness for purpose. https://www.google.fr/search?q=%22natural+selection+of+fitness%22&oq=%22natural+selection+of+fitness%22&aqs=chrome..69i57j0l5.6993j0j7&sourceid=chrome&ie=UTF-8 <--- check that, selection according to fitness of a phenotype and morphology... iaYork you yourself are like tim-nice-but-dim. WHY? hyper beginner question = beginner answer, at least i bothered. It just shows that you don't have basic knowledge of evolution, you reply without facts/content, vaguely

Remi.b, you must feel like an idiot telling me "that doesnt even exist' and then reading it www.genetics.org Ph.D texts ... and confusing 5 digits (polydactylism) with 4 legs? you are truly the one talking nonsense.

@comprehensible: Then by your argument, 5 digits aren't optimal either, since many vertebrate lineages are evolving away from that.  E.g. snakes with no digits (or limbs), dogs with four (plus a largely vestigal dewclaw), cows and such with two, horses with one...

That's a fair comment, snakes are not quadrupeds, there are 4 species of dogs (40 species of cats) and 350 species of primates including humans, 5000 lizard, 200 species of squirrels, 5000 frogs, all 5 digits, a dog and a horse can never evolve back into a forest environment. losing all grabbing ability is not an optimal design unless it gets wings/trunk/aquatic. all land vertebrates that survived after the dinosaurs had 5 digits except snakes? all non grasping species didn't survive, and ungulates would all vanish when there is another apocalyptic winter.

@comprehensible: If you think that having single-digit hooves means the critter loses all grabbing ability, I can deduce that you've never spent much time around horses.  And hooves seem to work pretty well if your niche in life is as a grazing herbivore :-)

ok, so the dominant big species of african ecosysters have soft pads and hooves. That knocks over my theory. perhaps hooves are not digits, so when 1 finger vanishes the limb ceases to have a hand a very fast becomes a clawed pad and a hoof. no rodents, marsupials, lizards and salamanders have 4 finger hands, and pandas, koalas, opossums and some frogs have opposable thumbs. It's a theory I read on a Polydactyly biology page, I only copied it.


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Are proteins a different shape in space?
Is the shape of a protein affected by gravity? In space, will the shape of a protein be different to what it is on Earth?
If the structure and shape is in fact affected, then would it be enough of a change to cause a change in protein function?
I've found studies from NASA saying that when protein crystals are grown in space, they are larger and form more perfect crystals than on Earth but I want to know about the effect of gravity on proteins that have already been formed.
Thanks!

Can you provide a link to the NASA article please ?

https://www.nasa.gov/mission_pages/station/research/experiments/1320.html

Please note: Life depends on enzymes and other proteins. People have lived in space for long periods of time. If protein structure (3-D) were affected by being in space, do you think life would be possible there?

Yes of course I've considered that before asking the question but I thought there could be minute changes that wouldn't cause serious illness. Also, space flight definitely takes a toll on health and the weightlessness does mean muscle mass is lost. I thought perhaps as opposed to this simply being because of the lack of use of muscles, it may be because of changes in the shape of proteins that govern their structure and the production of muscles. So, I just wanted to know if gravity would have an effect on protein structure.

You can also do a rough estimate about the energy involved - the amount of energy a protein would gain from moving a distance of its radius (protein mass)(acceleration of gravity)(protein radius) is about a billionth of the typical scale of thermal energy in the cell (kT = 4 piconewton nm).

However, once you get around the range of hundreds of microns in length scale, there can be some gravitational effects in the cell: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3789854/ - this is why protein crystals (at a large length scale) can be distorted by gravity, even though proteins aren't.

Proteins are not made to be one way up or the other as they flow around and surround cells, so sea-level to space gravity gradient will not be the major cause of change to proteins at different altitudes.
Pressure is more of a factor on proteins, and it has been studies very much, both for protein shape and protein interaction with elements and other molecules.
http://www.annualreviews.org/doi/abs/10.1146/annurev.pc.44.100193.000513?journalCode=physchem
People have awesome health when they are born and raised at altitudes of 4000 meters, there are even people living at 4800 meters OK. the pressure gradient there is halfway in between sea level and space. 100m depth also stresses nitrogen toxicity and other severe effects more than proteins, but deep sea fish do have specially adapted proteins because depths at 10000 meters require different proteins than the surface.

Note: the sea-level to space gravity gradient is much lower than sea-level to even geostationary orbit gradient.


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Identifying a weird Texas tree
I recently saw this tree in Texas, with many bees on it. I think it attracts   bees. However it didn't have any specific smell, so I don't know why there were so many bees (they were bee for sure). I tried to identify the leaves but couldn't. Dear experts: could you please identify this tree?

Could you be a little more specific regarding where within Texas? It's a big state.. hah. Thanks.

Yes. Thank you. It was in Mt Pleasant, TX 75455

an in-focus picture of the fruit/nut will help as will a picture of the whole tree. just from this it could be hickory or one of the  walnuts.

almost certainly not a hickory, walnut or other member of the juglandaceae family. No compound leaves for starters...

That looks like a live oak covered with oak galls

Welcome to Biology.SE! Your answer seems reasonable, but you are more likely to get a positive response if you explain why your identification is correct and specify the genus and species since "live oak" can refer to many species. Specifically, please edit your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

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Identification of an insect found in Edmonton, Alberta, Canada.
It's 8.5mm long found in front yard. Unusual wing shape. Sorry about the images: the insect is so small my camera was struggling.

That is a caddyfish (Thrichoptera).

Thank you but I'm looking for more specific answer,the species name or at least family

I know that. That's exactly why I wrote a comment, not an answer.


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What causes puberty to begin?
I understand that puberty begins when hormones are released from the pituitary gland as instructed by the hypothalamus, but why does the hypothalamus instruct this to occur?
How is this process timed by the body?

Too broad, sorry.

partial answer: https://biology.stackexchange.com/a/3609/460

Possible duplicate of How are long time periods measured in biological systems?


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Reference request: neocortex creating 11 dimensional structures
I've come across several pop science articles like this one that vaguely describe a method of analyzing brain tissue involving algebraic topology and 11 dimensional structures. They all seem to cite each other. One of the researchers involved was Kathryn Hess. I've searched the web, a community college library, and the UCLA library and haven't been able to find the original paper. Does anyone know where I could learn more about their methods?

Welcome to Biology.SE! You say They all seem to cite each other. It would help if you could directly tell us what papers you found and eventually why it feels like they all just cite each other.

New Frontiers is surrounded by controversy mostly becasue they have no restrictions about what they publish regardless of methodology or ethics. They also fired a bunch of their editors for trying to impose some scientific integrity. The fact the "journal" is owned by the first authors to publish in it is another bad sign. You can safely assume anything published by Frontiers is garbage.

That's a shame I thought the mathematical model that the researchers developed was really cool. I didn't pay much attention to their methods though.

I finally found the work. It was in the sources of the sources of the article that I gave as an example.

you should edit your question not answer it, especially just to add and not answer.


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Hardy Weinberg Explanation
I am able to calculate frequencies for allele and genotype, but I don't understand how to tell if the population is at equilibrium. Or how to determine how many generations of random mating would be needed to reach HW equilibrium. I thought the proportions didn't change from generation to generation?
number of individuals: TT-200, Tc-200, cc-600
observed frequencies : TT-0.2, Tc-0.2, cc-0.6
HW frequencies       : TT-0.05, Tc-0.35, cc-0.60
p=.33, q=.77

The answer is logical if you understand the reasoning behind Hardy-Weinberg. I recommend that you to have a look at the post Solving Hardy Weinberg problems and try to answer the question yourself. Once you've done that, you can hover over the yellow zone below for the answer to compare against what you've understood.
The answer:

 If the assumptions of Hardy-Weinberg are respected (see Assumptions of Hardy-Weinberg rule), incl. random mating, then a population is back to Hardy-Weinberg equilibrium at the beginning of any single generation. H-W equilibrium is directly caused by the random sampling of gametes. This random sampling is happening at every single generation and therefore a single generation is enough to get back to H-W equilibrium.


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Stink bug identification
This is a stink bug that I found in Indiranagar, Bangalore. It was dead at that time and had become stiff, so the following are the best pictures I could get. It is 2cms in length. I tried searching on the net on various websites but I didn't find a match for the colouration on the dorsal side. Also, I would like to know what those protrusions on the top half of the shield ( excuse me if 'shield' is the wrong terminology) are. They seemed to be quite a troublesome feature as none of the reference pictures I saw on the net seemed to have bugs with these 'protrusions' .

First that comes to mind are Euschistus sp., which are known for these kinds of protruding shoulders, but I'm not sure if they're in India or not.. also considering Halyomorpha sp..

I agree, but none of the species (which I found on the net) of Euschistus sp. Have such pronounced protrusions. Maybe I'm missing something?

No, I don't believe you are.. to me, it is confusing because the shoulders on the OP are saw toothed, which would indicate a common brown stink bug, as apposed to marmorated brown stink bug, but the antenna would indicate marmorated. The same can be said about the black/white checker pattern. Hmm..

I looked through the appropriate volume of Fauna of British India but couldn't find a good match (not surprising; the volume in question dates from 1902 and illustrates 201 of the 542 species known at the time); at the time Euschistus had not yet been found in India, and the species of Halyomorpha illustrated is not a good match.

I've been searching for quite some time in different subfamilies of Pentatomidae and have to admit defeat. Until now I'm unable to retrieve any information about the marvelous bug you have found.
The pictures you took are really great, by the way!
Maybe you can ask Dr. Salini for help? :)
She studied 94 species of Pentatomidae according to the following website: http://www.nbair.res.in/salini.php


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Mathematical representation of "gene signatures"
According to Wikipedia's definition, "a gene signature is a group of genes in a cell whose combined expression pattern is uniquely characteristic of a biological phenotype or medical condition."
While the above definition is very useful to understand the concept, I am looking for a "more practical" definition or, rather, a mathematical representation (e.g., a vector) of gene signatures. Hence my question.

Possible duplicate of Is there a formal definition of signature of natural selection?

I think the WGCNA package in R is an interesting and relevant take, the related paper is here.

Let's say you have a list of genes that you derived from a RNA-Seq and made a differential expression analysis. You can rank genes by p-values or fold-change values, or convert to membership values between 0 and 1. This ranked list and any its subsets are gene signatures.

@MaximKuleshov thanks for your reply. Could you, please, provide a full answer listing the three methods you just highlighted (attaching a short discussion of applications would be great)

@mrb If you could comment on whether or not you think your post is a duplicate of the one I marked as possible duplicate. If it is not a duplicate, could you please highlight why? That would help to know what you're after.

Hi @Remi.b, the other post provides a definition of the concept, which is very useful, but my question is about a common mathematical representation (eg, the comment above by @MaximKuleshov).

@mrb You edited your post from genetic signature to gene signature after the question had been answered. You should rather roll this edit back, accept or comment on the given answer and open a new post for your new question. Also, it will bring more attention to your new question to open a new post than to change a previous one.

No, i haven’t. I am sorry about the confusion but i edited the post immediately after the first comment a few days ago. Dunno way you could not  see the edited version until now.

There are mathematical definitions of "gene signature". Please have a look at the supplemental material of Subramanian et al. PNAS 2005, one of the first papers on "gene signatures", and a method and tool which is still commonly used in basic research.
Note that Subramanian et al. have multiple definitions and that copying them here would exceed the scope of this page.

There is no mathematical definition of genetic signature. Please first have a look at Is there a formal definition of signature of natural selection?. As explain the term genetic signature is used in a very broad sense.
There are a number of processes for which one might be looking for a signature of this process. Such signature can take the form of various statistics. For example, a historically important statistics is Tajima's D defined as
$$D = \frac{\Pi - S/a}{SE}$$
, where $\Pi$ is the average number of pairwise differences between two randomly sampled haplotypes, $S$ is the number of segregating sites, $a=\sum_i^{k-1}1/i$, where $k$ is the number of sampled haplotypes. $SE$ is the standard error for the numerator which takes a complicated formulation (have a look at Tajima 1989 for more information).

Why would anyone use pi as a variable?!

@canadianer What do you mean? $\pi$ is very commonly used to represent the expected heterozygosity. Note that to avoid confusion, I used $\pi$ to $\Pi$ in my answer.


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Are the 5 digits of all land vertebrates an accidental number?
All land verterbrates except some frogs have 5 fingers on hands and feet.
The first vertebrate lizards came out of the water and had 7 fingers ( -370mn yrs), and then 6 fingers, and after 30 million years, all their descendents had 5 fingers on both limbs.
someone told me "5 is much more of an accidental number", so if all land vertebrates had 7, then 6 fingers, why did that get selected to 5?

Related (if not duplicate): Why don't mammals have more than 4 limbs? and Why do some bad traits evolve, and good ones don't?

There are more exceptions than frogs. It depends a bit upon what you call a finger, but typically snakes don't have fingers, ungulates don't have fingers, cats have 4 toes at each hind paw, ....

Note also that the first vertebrate coming out of the water was not a lizard (not a squamata).

By the question why did that get selected to 5 there is a potential false assumption that make it clear that your question is a duplicate of Why do some bad traits evolve, and good ones don't?. I'm voting to close as duplicate. Please have a look at this post and if you think it did not answer your answer, please clearly explain why.

The general question is a duplicate. Articles here, here, and here emphasize the contingent nature of the five-finger tetrapod.


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Do eye's muscle share the same nerve?
When I try to rotate my eye, both of my eyes will rotate the same amount and in the same direction (obviously).
I'm wondering if it is possible to control each eye separately. I've never seen anyone that can do this (except some pics on the internet which I'm not sure if they are digital edits simply for fun).
Is it possible? If not, why? Is it because they are both controlled by the same nerve? Or is it simply because we are not used to it and it's super difficult (but possible)?

"I'm wondering if it is possible to control each eye separately" - have you ever tried focusing on the tip of your nose? Maybe not quite the same thing as e.g. controlling your arms separately, but you certainly can move your eyes in different directions.

Each eye is controlled separately. Three cranial nerves emerge at the brain for each eye to control the so called extraocular muscles. That we usually move both eyes in one direction is due to that our brain is trained that way. Nonetheless, we sometimes move each eye individually, for example when looking at an object that is very close to our face (convergence). I wonder that you have not noticed it on yourself, since it is a pretty common eye movement. Further, you can train your brain to perform other, rather unusual movements, as you can see in this video.

Ops thanks for the tip! I forgot about convergence, since I was busy thinking about moving them both outside.

So it's like when you play Mario and you instinctively start pressing B when you press over. You don't think about it, you just do it!

There are basically four different types of eye movements:

smooth pursuit (think about following a moving target with both your eyes, note how smooth the movement is)
saccades (think about moving your eyes without fixation on a specific target, note how jerky the movement is)
vergence (the other answer mentioned "convergence", this is an example of a vergence movement)
vestibulo-ocular movements (these are mainly reflex movements which depend on the "position-sensing" apparatus of the inner ear)

The motor control of the eyeballs (globes) is mediated in a fairly complex way via the third, fourth and sixth cranial nerves. The coordinated movement of the eyeballs is mediated neurologically in a really complex way involving multiple brain and brainstem centres (nuclei).
To explore this in detail, you really need a good textbook in neuroscience. For what it's worth, I've found a web reference that covers the gist: https://www.ncbi.nlm.nih.gov/books/NBK10991/


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Blast databases
I am helping a colleague setup a local blast server. My background is computer science so I apologize if I use incorrect terminology.
Using the NCBI blastn webpage, one of the databases listed is "NCBI Genomes (chromosome)." I'm unable to find this database listed on the database download page (ftp://ftp.ncbi.nlm.nih.gov/blast/db/).
What is the name of this database as listed on the ftp site?

Have you tried contacting NCBI help?

In addition to NCBI, you can also use genomes from UCSC and Ensembl.

With the blast binaries you get a perl script update_blastdb.pl which you can use to download preformatted databases from the ncbi (it's pretty much a script that fetches the data from the location you found, anyway).
With update_blastdb.pl --showall will list all available blast databases and probably refseq_genomic is what you need, unless your query is human data only.
However, that's based on the assumption that your query data is nucleotide data - you might need to choose different databases and tools for proteins
Unlike Maxim Kuleshov claims, the NC and NT accession prefixes don't differentiate between organisms, but genome assembly status, as stated in the linked documentation and the refseq release notes, section 3.8

human_genomic.*tar.gz is Human RefSeq (NC_######) chromosome records with gap adjusted concatenated NT_ contigs and other_genomic.*tar.gz for non-human organisms (more about RefSeq accession numbers such as NC_ and NT_).
You can find more information in the readme file.


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How do plant cell vacuoles form?
Does the plant cell vacuole form by the invagination of the cell membrane?

Does the plant cell vacuole form by the invagination of the cell membrane?

Yes, in part, but the complete answer is way more complicated than that.
Endosomes (the vesicles formed by "invagination" of the cell membrane, as you said) are responsible for (part) of the biomembrane of the cell vacuole. However, some biomembrane comes from the Golgi-ER system, and almost all proteins come from ER (having passed by the Golgi apparatus).
Have a look at this image (Marty, 1999):

Its legend says:

Seven basic pathways are used for the biogenesis, maintenance, and supplying of vacuoles. Pathway 1: entry and transport in the early secretory pathway (from ER to late Golgi compartments). Pathway 2: sorting of vacuolar proteins in the trans-Golgi network (TGN) to a pre/provacuolar compartment (PVC) via an early biosynthetic vacuolar pathway. Pathway 3: transport from PVC to vacuole via the late biosynthetic vacuolar pathway. Pathway 4: transport from early secretory steps (ER to Golgi complex; pathway 1) to the vacuole via an alternative route with possible material accretion from Golgi (indicated by the asterisk). Pathway 5: endocytotic pathway from the cell surface to the vacuole via endosomes. Pathway 6: cytoplasm to vacuole through autophagy by degradative or biosynthetic pathways. Pathway 7: transport of ions and solutes across the tonoplast. AV, autophagic vacuole; E, early endosome; ER, endoplasmic reticulum; PVC, pre/provacuolar compartment; TGN, trans-Golgi network.

According to the same paper (Marty, 1999):

Experimental evidence suggests that material within the vacuolar system in plants derives confluently from both an intracellular biosynthetic pathway and a coordinated endocytotic pathway. (emphases mine)

Source: Marty, F. (1999). Plant Vacuoles. THE PLANT CELL ONLINE, 11(4), pp.587-600.


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Insect Identification (even the family name would do)
I found this insect in Bhopal,Madhya Pradesh,India could you please help me identify it??
I think it is some kind of beetle. Approximately 2-3 cm in size.

Welcome to Biology. SE! Thanks for taking the tour before posting. From the wing case, it looks like a true bug (Hemiptera). Any chance you can add something to show the scale?

I am sorry I can't add anything to add to show the scale as I was just passing by when I saw it,but I suppose it was 2-3 cms besause if the size of the leaf which seen in the photo.

I suppose it belongs to superfamily Pentatomoidea.

That's a hemipteran not a coleoptera

You've found a specimen of Coridius janus or cucurbit stink bug or red pumpkin bug (don't mix up with the red pumpkin beetle). They betong to the suborder Heteroptera (True bugs).

(picturefrom Wikipedia)
Also see:
projectnoah.org: red pumpkin bug
nbair.res.in: Coridius janus
indiabiodiversity.org: Coridius janus

It would be nice if you could embed at least one image of the proposed ID in your response, instead of just providing links to those images.

We really discourage linking to pictures or any other valuable info off of SO because if the link dies (which it often does), your answer becomes useless to future viewers. So, to follow up Charles's comment, please make sure your answer here on SO is as complete as possible without requiring users to visit external links


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What are some examples of non-homologous sequences having similar functions?
I am trying to find some proteins that are non-homologous but functionally similar. However, I cannot seem to find concrete examples. Can someone please point out any resources or provide examples?

Would something as broad as a gene involved in the development of wings in insects and one involved in the development of wings in birds be a satisfying answer?

Yea, sure, that would work.

By, homologous gene, do you mean gene with independent origin and similar function or independent origin and similar sequence?

I mean examples of sequences that are not similar(i.e. you cannot find them by BLASTing) but their functions are similar.

Serine Protease Catalytic Triad
This is classic example of convergent evolution in catalytic mechanisms. Shown below are chymotrypsin (4CHA, green) and subtilisin (1ST2, blue) aligned on their catalytic triads (Ser/His/Asp, darker colours). There is no obvious sequence or structural similarity.

You can check out the MEROPS database for a list of protease clans ("represents one or more families that show evidence of their evolutionary relationship") and this paper for a discussion on convergent evolution of the catalytic triad:

Although the biophysics of rate acceleration are intricate and sensitive to even minor structural perturbations, evolution has converged on a catalytic triad (or diad) with a reactive Ser, Cys, or Thr nucleophile more than 25 separate times to facilitate central biochemical reactions such as hydrolysis, transacylation, and phosphorylation.

Hoxd12 and Hoxd13 are involved in the development of wings in birds (Vargas and Fallon 2004).
pdm and aptorus are involved in the development of wings in insects (Williams et al. 1993, Averof and Cohen 1997)

Thanks. But, which of them are non-homologous?

Hoxd12 and Hoxd13 are of independent origin than pdm or aptorus but all are involved in the development of wings.


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How do transitional forms survive without the full adaptation?
This may be an odd question, but this is one thing I've always wondered. How does a dragonfly ancestor with early structures that will one day become wings gain any benefit from these useless limbs that don't work?
It seems in an intermediary context like this, that the adaptation would almost fall under a category more along the lines of something vestigial--something defunct.
I understand the creature adapts with no understanding or control of the process, and it takes extremely long periods of time to see any significant changes from one anatomy to another, but it would seem that statistically that would work against the animal, not for it. It's not like the dragonfly goes from the land and water to having fancy new fully operational wings.
The longer a species is stuck with an unhelpful adaptation, the longer they would be exposed and at a disadvantage. There is one way in which I could see this happening, and that is a prolonged series of random mutation in favor a winged route for the insect with no real input from their environment.
We all know that mutation and variation drift (all of which are relatively random) are part of the evolutionary process, but it is often described in more concrete terms, and the creatures in between an ancestor and a descendant have been discovered and described, but often not very well to the public.
The mutant albino bear ancestor being better suited for arctic stealth and eventually becoming the polar bear and diverging from the brown bear is an example given in the new Cosmos that actually could happen overnight. The bear is born with the full adaptation.
Even if the bear weren't instantly white, fur slowly becoming lighter leading to better hiding capability, or having a thicker coat to help it keep warm makes more sense than the precursor to an entire limb like wings or a tail though.
I suppose that it's possible to say the that random mutation is the primary method of evolution, and the apparent improbability of plants and animals surviving with incomplete, underdeveloped adaptations can be answered by realizing that the plants and animals alive today are the cousins of countless species that actually weren't helped by the wings, and some of that is random too.
And with that in mind, it's slightly more obvious, but I'm wondering if there's more to it or something I'm overlooking.
I've struggled to find any discussion about this topic in the literature, which I may have simply missed because it often goes over my head. I'm hoping my conclusion is helpful.

It is always a little disturbing that some high rep users can close questions as duplicate without the opinion of other users! It surprises me when the question closes while I just wanted to cast a vote. Anyway, @RealisticWuxia, please have a look at the ost marked as duplicate and if it did not answer your question, please try to explain why the other post did not answer your question.


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Why was the intramuscular route selected for palivizumab administration to infants, instead of the subcutaneous route?
The majority of monoclonal antibodies administered by an extravascular route to adults are administered subcutaneously.  Does anyone know or have hypotheses about the reasoning behind why palivizumab and motavizumab were designed for intramuscular administration?  A key point may be related to the fact that they are administered to infants as young as one week old, rather than adults.
FDA documents are at this link:  https://www.accessdata.fda.gov/drugsatfda_docs/bla/2003/103770Orig1s5033.pdf


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Under which circumstances does muscle hyperplasia happen in humans?
What circumstances allow humans to have muscle hyperplasia in the prenatal and immediately postnatal period that doesn't exist later?
Is it about specific hormones that follow through our veins?

IMHO, this question would be a better fit on Health.SE.

@Remi.b : Given that it's about developmental biology I don't see how it's better at Health.SE

You're talking about a medical condition at birth. It sure is related to human developmental biology but also human health. The fact that you phrase your question as "Under which circumstances" make the question sounds like a medical question to me. But that was just my opinion and I tend to be willing to migrate more things to Health.SE than most users I think. Other users might disagree with me.


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DNA Longevity in Keratin, Ivory and other Bioplastics
For how long is DNA viable for extraction and/or sequencing in bioplastics created by the human body? I checked out a few links online, and this article gives a record of about 7000 years for frozen mitochondrial DNA, and Ötzi's DNA remined viable for 5000 years. However, I suspect that the samples used to analyze both were not taken from anything that was like keratin or ivory, with their limited cellular matrix. What is the longest record of sequence-viable DNA being stored that way?


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How do parents give their offspring a chromosome?
Whenever an organism sexually reproduces, it gives its offspring one chromosome from each of its pairs of chromosomes. My questions are

Is this done randomly?
Is it uniformly random?
If so, what mechanism allows it to be random, considering that the laws of physics are deterministic?

(Note: I'm a little rusty on this subject, so if there are any errors in the question, feel free to correct them.)

Are the laws of physics deterministic? I think no one knows, currently.
In any event, yes, the segregation of homologous chromosomes during meiosis I is random: there is an equal probability for each chromosome of a homologous pair to segregate into a given gamete, and this is independent of other homologous pairs. This idea dates back to Mendel, who observed that the heritable “factors” (what we now know as genes) responsible for macroscopic phenotypes are inherited independently of one another (this is his Law of Independent Assortment). This isn’t actually true when considering linked genes, but is certainly true of chromosomes, as was described by Sutton in 1903:

...many points were discovered which strongly indicate that the position of the bivalent chromosomes in the equatorial plate of the reducing division is purely a matter of chance - that is, that any chromosome pair may lie with maternal or paternal chromatid indifferently toward either pole irrespective of the positions of other pairs...


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Are the changes required to produce genetically manipulated organisms (GMOS) considered to be mutations
By definition, are mutations required to be natural, or are synthetic lab-induced genetic changes considered mutations too? Furthermore, are genetically manipulated organisms (GMOs) considered forced mutants?

What is a mutation?
A mutation is any change to the DNA sequence. From wikipedia

In biology, a mutation is the permanent alteration of the nucleotide sequence of the genome of an organism, virus, or extrachromosomal DNA or other genetic elements.

Whether a given alteration to the DNA sequence occurred in nature or in a lab changes nothing to the fact that we call this alteration a mutation.
How common are mutations?
Just so that you realize how common mutations are: In humans, a couple having a baby typically transmit about 40 new mutations to this baby. This mutation rate is not quite the same between women and men (see Kong et al.(2012)).
What is a GMO?
I have never seen the term "forced mutants" before but it sounds like you might have a misrepresentation of what GMOs are and esp. in your misrepresentation, you might think that there is such natural category which are GMOs and other that are non GMOs but the boundaries between the two is more than vague.
Consider for example that the vast majority of our food has been manipulated by humans through artificial selection. Check out the ancestor of modern-day corn (from Genetic Society of America; original source: teosinte.wisc.edu; thanks @John)

This evolutionary change occurred via artificial selection mainly and without using modern genetic tools.

What's the source of that image?

It is some google image I found. I forgot the link. I put another one where I could verify the source a bit better. Why the question? Is it just for legal reasons or was there something wrong about the image?

Well I think attribution should be given for other's work, but I was more interested in reading about it. Thanks for the edit.

Orriginal source for the image is here, https://teosinte.wisc.edu/images.html, I use it in my classes. The small ancestral plant is called Teosinte.

I've downsized the image as I assume you didn't know how to do that. 1000px high was hardly necessary.

You quote the Wikipedia article for a definition of ‘mutation’ and then go on to imply — although not to state explicitly — that this means GMOs are produced by mutations. That, after all, was the question. However the extensive Wikipedia article on mutation does not feature a single mention of ‘GMO’ (or genetically manipulated organism). I suggest that this is because, as I have stated in my own answer, the manipulations used to produce GMOs are not generally referred to as mutations. Do you agree or not?

From NIH :

A gene mutation is a permanent alteration in the DNA sequence that makes up a gene, such that the sequence differs from what is found in most people. Mutations range in size; they can affect anywhere from a single DNA building block (base pair) to a large segment of a chromosome that includes multiple genes.

So both naturally occurring, and lab-induced modifications could be considered mutations.
I've never come across the term "forced mutants", but for perspective, a GMO can be created by purposefully exposing the organism to radiation in a controlled manner. In the wild, it is possible that organisms are thusly exposed as well, but in an uncontrolled manner.
For further reading, see this article.

This really is semantics.
There is no clear-cut definition of mutation, whatever you find in a dictionary or in an anonymous article in Wikipedia. However most molecular biologist have a certain picture in their minds when they see or hear the word ‘mutation’, and a certain picture in their minds when they see or hear the phrase ‘genetic manipulation of an organism’.
The two pictures in my mind are very different, but tend to be related to the extent and complexity of the changes rather than whether they occur in the environment or are produced in the laboratory.
Mutation
In plain English mutation just means change, but in molecular genetics one thinks of small-scale changes: base changes, additions or deletions of a base or a short stretch of bases. Those that occur in the environment are random in the general sense, and originally this was also true of those induce in the laboratory through agents such as mutagenic chemicals or ionizing radiation. With advances in recombinant DNA technology the changes could be directed: introduced at particular points in order to produce the desired mutation — site-directed mutagenesis. However the picture is one of small changes, even if they can have major consequences. Certainly the fact that the mutation is directed to produce the desired outcome (presumably what the poster means by ‘forced’ — although this term is not in common use.)
Genetic Manipulation
Genetic manipulated organisms (whether bacteria or mammals) often have a completely new gene inserted into them so that they can produce an entirely different protein — something non-functional like a fluorescent protein, or practical utility like insulin or a protein that provides a plant with resistance to pesticides. The organism is certainly changed, but ‘engineered’ would seem more descriptive of the extent of the change and the technology involved than ‘mutated’. (And although one of the other answers suggests there is no difference in principle between directed plant breeding and and such manipulations, this seems a little ingenuous to me. There is no way you could breed corn so that it expressed the green fluorescent protein from jellyfish.)
My apparently subjective remarks on genetic manipulated organisms and the non-use (or less frequent use) of the term ‘mutation’ is supported by the abstracts you find on googling for GMOs. I cite the first four below:

A genetically modified organism, or GMO, is an organism that has had its DNA altered or modified in some way through genetic engineering.
A genetically modified organism (GMO) is any organism whose genetic material has been altered using genetic engineering techniques (i.e., a genetically engineered organism).
Agricultural plants are one of the most frequently cited examples of genetically modified organisms (GMOs). Some benefits of genetic engineering in agriculture  ...
Genetically modified organisms (GMOs) are living organisms whose genetic material has been artificially manipulated in a laboratory through genetic engineering.


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What factors may lead to a difference in whole-cell potency compared to cell-free potency?
For studies of protein-ligand binding, the reported whole-cell potency may be higher or lower compared to measured cell-free potencies.
For decreased potency, this may represent an increase in non-specific binding of the ligand. Are there other factors that may contribute?
On increased potency, I've noticed this applied to the BACE1 protein in which the IC50 may go on the micromolar scale in a cell-free assay to nanomolar scale in a whole-cell assay. This seems counterintuitive to me. Are there possible reasons for this trend?

You are correct in saying that whole-cell potency and in vitro/cell-free potency often differ by quite a bit. There are actually a lot of factors that can contribute to this, but I'll try to give a couple illustrative examples, for increased and decreased potency (when moving from cell-free to a whole-cell assay).
When moving from cell-free to whole cell assays, decreased potency is the more common outcome. As you mention, a big reason is just that you get a lot more things the drug can bind to, so you tend to have less drug effectively engaging the target. However, there are other factors at play as well. Ultimately, the main reason that one sees decreased potency in the whole-cell format is that one is often asking for something fundamentally different than what was asked for in the cell-free assay.
For example, let's say you do some CRISPR of RNAi screen in cancer cells, and you find that if you shut down gene X, the cells die. You look it up, and gene X codes for an enzyme.
So you think, "Great! I'll design an inhibitor for the enzyme, and then kill the cancer cells with that!"
In order to screen for inhibitors and test their effect on this enzyme, you set up an in vitro with purified enzyme, substrate, and some way of measuring the generation of product. You screen, find compounds, and optimize your lead. You eventually end up with a compound that has an IC50 of 1 nM in this assay. Then you decide it is time to move into cells. You treat the cancer cells with the compound, and you notice that your IC50 for cell death is 100 nM - 100x what it was in the original assay. The reason is that you are asking much more of your compound.
In the first assay, the compound had to bind to the enzyme, which may have been the only protein in solution, and inhibit it. You were directly measuring enzyme activity. In the second assay, the compound had to diffuse through the cell membrane or find some other means of getting into the cytosol, where the target protein resides. Then, despite the complex milieu in the cell, it had to bind that specific protein and inhibit it. But inhibiting the protein isn't enough. It has to inhibit the protein enough to kill the cell. Maybe the cells die when the enzyme activity is 50%, in which case you would expect your IC50 values to be fairly close between assays. But maybe it doesn't. You may need 70 or 80% inhibition before the cells start to actually die. Plus, the cells may not go down without a fight. Maybe they up-regulate expression of drug-efflux pumps, which are ATP-powered proteins that literally pump small molecules out of the cell. This reduces the effective concentration of drug you are giving the cells. There are also many other adaptations that the cells may undergo to improve survival, which are beyond the scope of this answer. So what you are demanding from your compound in the whole-cell assay may actually be much more than in the cell-free system.
The other effect - seeing increased potency in whole-cell vs cell-free conditions is much less common. Without seeing the exact study you are referring to, it is difficult to comment. However, one thing to remember about BACE1 is that it is part of a huge complex that is embedded in the cell membrane. Reconstituting this complex in vitro is non-trivial, and it may be that the complex is not functioning the same as in the cell depending on how the reconstitution was performed. For example, maybe BACE1 binds better to the drug only when a binding partner is present that stabilizes a conformation suitable for inhibitor binding. It could also be that the inhibitor is actually targeting another protein in the complex that is not present in the cell-free system.
Anyway, I apologize if this was a bit long, but I hope this answered your question and shed a bit of light on the complexities of assay development and drug development.


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What is this insect species? It lives in damp places in a cocoon like structure and can protrude its head from both ends
Lives in damp places and can protrude head from both directions, 1 cm long approximately

Yeah its a case bearing moth.. Thanks for responding! I was looking for it since long..


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How is the Guide RNA created for Crispr?
It seems that to modify DNA a guide RNA and Cripr are introduced.
But I'm unable to understand how the Guide RNA is made or created.
Is it a simple method which can be done with simple lab equipment or is it complicated?
What is the equipment need to create it?


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Binary fission in amoeba
When a parent amoeba undergoes binary fission, two amoeba are obtained. Are those two amoebas, both daughter, or 1 parent and 1 daughter?

During binary fission in unicellular eukaryotes ,the nucleus of parent organism divide into two it is followed by the divison of cytoplasm so two daughter cells of almost equal in size are formed

Binary fission is found in unicellular organisms like amoeba.After attaining an optimum size,the adult individual undergoes a simple division to firm two daughter cells of equal size. During this fission in amoeba,first of all nuclear division takes place followed by cleavage of cytoplasm into equal parts.

I think concept of parents and offspring (daughters) is not very useful for unicellular organisms.

In binary fission, the fully grown parent cell splits into two halves, producing two new cells. After replicating its genetic material, the cell divides into two nearly equal sized daughter cells. The genetic material is also equally split. The daughter cells are genetically identical (unless a mutation occurs during replication).

Source: Binary Fission - Wikipedia
This corroborates with what I was taught in school as well.
A quick Google Image Search also shows that most diagrams on the subject involve one parent producing 2 daughter cells.

But it doesnt make sense. The parent is still alive, how can we call it daughter?

From here "Fission is a process by which an unicellular organism splits(/divides) to form two or more new organisms.When the parent organism splits to form many new organism it is called multiple fission. If the parent organism splits(/divides) to form two new organism it's called binary fission. When this happens the parent ceases to exist and two new organism is formed. Amoeba reproduces with the help of binary fission."


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How can carnitine enter the mitochondrial matrix without OCTN2?
Some people have defects on the gene SLC22A5, giving them problems with their OCTN2 transport protein (Organic cation transport).
OCTN2 transports carnitine into the mitochondial matrix where it can be used to create cellular energy.

Treatment indications for individuals with the defect on SLC22A5 includes oral or intravenous carnitine supplementation.
But one piece is missing...
If their OCTN2 is defective, then how does supplementing carnitine solve the problem? If they are deficient or lacking in OCTN2, how does carnitine even enter the mitochondrial matrix? (with no functional OCTN2 to transport it through?)
But the condition of these patients often improves with supplementation. So the carnitine is getting in there somehow.
Is there another route via which carnitine enters into the mitochondrial matrix?

Where is the picture from? As far as I can tell SLC22A5 (OCTN2) is annotated as a plasma membrane protein, and the disorder is related to defective uptake into the cell, not into mitochondria. The protein labeled OCTN2 in your picture rather looks like the carnitine-acylcarnitine translocase, SLC25A20.

The image is from here: http://www.kanazawa-u.ac.jp/research_bulletin/feature201309F003.html (Dr. Tamai actually responded to me that he thinks it's a mistake and that the person who created the image might have misunderstood the paper it was based on). I will update the answer according to his response.

Short answer -- looks like the image in my question might be flawed, and OCTN2 probably isn't even involved in inner mitochondrial transport. Lesson: don't believe everything you find on google image search!
Longer answer - So I went back to the page where I originally found the image and saw that Dr. Ikumi Tamai was featured as one of the researchers who originally described OCTN2 back in the late 90s.
So I contacted Dr. Tamai via email-- and he responded to me a few hours later!
In his response, Dr. Tamai stated that while OCTN2 is expressed in various places in the body -- it is mostly active in the kidney -- and works there to conserve blood carnitine by re-capturing it from urine and returning it to the blood.
He added that jvm mice (which have defects in OCTN2 that cause carnitine deficiency) respond favorably to carnitine supplementation because the defect mostly just lowers blood carnitine levels, and simply raising those levels improves the condition of the mice.
This seems to suggest that OCTN2 does NOT play any role in transporting carnitine within the mitochondria.
Dr. Tamai noted that the image, which seems to depict OCTN2 sitting on the inner mitochondrial membrane, might have been designed by someone who did not fully understand the science of OCTN2, and that different transporters are likely responsible for the transporting of carnitine into and out of cellular and mitochondrial membranes (not OCTN2!).
In short -- it seems like that little pink blob in the image above should NOT be OCTN2 (even though it is labeled as such) and should probably be another transporter altogether.

Nice way to get the answer! The protein in the image is carnitine-acylcarnitine translocase.

@canadianer thanks! And more thanks for filling in another piece of the 'puzzle' for me regarding carnitine-acylcarnitine translocase.

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


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Why can't pyruvate be used directly in the Krebs cycle?
Why can't pyruvate be used directly in the Krebs cycle? Why does it have to be converted to acetyl before it enters the cycle?
Excluding the reason that the shape of pyruvate is different than acetyl and therefore it would not fit the enzymes involved in the Krebs cycle, what is the advantage of converting pyruvate to acetyl?

"Excluding the reason that the shape of pyruvate ... would not fit the enzymes involved in the Krebs cycle" -- that's a pretty big exclusion. Obviously pyruvate cannot be used directly because it doesn't fit. It rather sounds like you're asking why the cycle isn't made up of completely different enzymes? But metabolism is evolved, and there is no special reason why it looks the way it does, except that this solution was found by evolution. I'm not sure the question is answerable. (But maybe I don't understand it correctly.)

Oxidative decarboxylation of pyruvate to acetyl-CoA by pyruvate dehydrogenase is coupled with reduction of NAD+, which can feed into the electron transport chain.
CoASH activates the acetate: hydrolysis of the thioester is thermodynamically favourable and drives the reaction catalyzed by citrate synthase.
Conversion of pyruvate to acetyl-CoA commits it to a subset of possible fates (including the tricarboxylic acid cycle) and is therefore a key regulatory step.

You can read more about this in most introductory biochemistry texts, like this one.
Also note that pyruvate actually can enter the TCA cycle via carboxylation by pyruvate carboxylase to oxaloacetate. This reaction requires energy in the form of ATP and is used to regenerate TCA cycle intermediates as they are siphoned off for anabolic pathways.


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Which matched normal(s) to use when computing CNAs from exome data with a Read-Depth approach
I want to use a Read-Depth algorithm to call copy number alterations (CNAs) from Whole Exome Sequencing data (WES) of a specific tumor.
I have a set of WES tumor samples, some of which also have the matched normal sample. My question is: would be more effective, to call CNAs for each tumor, the whole set of matched normals or, if available, only the corresponding matched normal sample?
I thought that using only the single matched normal could spot only somatic variations, while using the whole set of normals would also add germline variations into account. Is that right?
Which best strategy do you suggest?

For the detection of somatic copy nuber alterations it is best to compare each tumour sample with its matched normal. If you want to call CNVs for all your tumour samples and some don't have matched normals, then pooling together all the normal BAMs to create a reference may be the best way to standardise your calling.


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How come large herbivores have such thin legs?
Edit:
This question is very similar to this and related to this one (though the latter focuses on homology instead of scaling laws). However, the answer to this question is far more comprehensive, in particular it offers a plausible explanation why horse legs evolved as they did (vs human or even rhino legs).
Large grazing mammals such as horses, moose, and cows tend to have relatively thin legs despite being up to ~1000kg. For example, this rider's and her horse's legs appear to have about the same cross-sectional area both for below and above the "knee":

If this horse is 500 kg (a mid-range mass for horses), each leg would have to support 125 kg, compared to only 37.5 kg for a 75 kg adult. Why don't we see a corresponding difference in cross-section?

Possible duplicate of What is the anatomical term for a two jointed leg?

Possible duplicate of Comparative leg sizes

On that photo, the horse's shoulder is easily twice as broad as the woman's gluteal region whereas the horse's gluteal region is over 4 times as broad. That translates to 4 times and 16 times more cross-sectional area (mostly equal to strength). The calf is admittedly slimmer, but you should note that on the horse it's about 90-95% bone whereas on the human it's more like... 8-10% bone, the rest being muscle (... which a horse doesn't need due to its anatomy...).

Elephants? Just saying.

Elephant, rhinoceros, &c all have much thicker legs in proportion.  The answer, I think, lies in the fact that the animals you mention all evolved as cursorial animals (that is, they run to escape predators).  Less mass in the lower leg means it swings easier, so the animal can run faster.
There are two things you're apparently not noticing in that picture.  First, the the horse's lower leg is almost entirely bone (and some tendon), and it's bone that does the supporting.  The propulsive power comes from the large muscles of the hip, thighs, and shoulders.
Second, the lower part of the leg (with the white wrappings) is not anatomically equivalent to the human's lower leg, but to the bones of the hand and foot.  You can see this if you look closely at the rear leg in that picture.  The femur, equivalent to the human's thigh, ends at the knee just above the belly line.  Then the tibia extends about halfway down, ending at another joint which you might think is the knee, but which is called the 'hock' in horse-speak.  The white-wrapped part is a metatarsal, equivalent to human foot bones, then there pastern bones equivalent to human toe bones, ending in the hoof/toenail.
So consider that you can, if reasonably fit, walk around on tiptoe without crushing your foot and toe bones, then imagine the end result of your ancestors having done this for the last several tens of millions of years :-)
PS: With horses, there is some effect from human selection, too.  Racing & show breeds tend to have thin lower legs, draft horses & working breeds have proportionately thicker ones.  My first horse, a thorobred/arab mix, had legs about as thick as my wrists (granted, I'm a fairly muscular guy); my current mustang, about the same height & weight, has legs about twice as thick.

May I suggest you add (Or can I do this?) a picture of the horses leg structure? As you say a lot of people don't know the lower part of a horses' leg is more equivalent to the bones of a human hand or foot.

@JaneDoe1337: It would indeed be a help, but I have no idea how to do it (since SE insists on using its own arcane methods for such things).  Feel free to do so yourself.

@jamesqf there's a little button that appears when you are writing an answer and that lets you upload images or link to them from other places in the web. See the "Images" section at the bottom of this page. That doesn't seem too arcane, really.

@terdon: Maybe the little image appears in your browser.  It doesn't seem to in mine.  Also, I'm dysiconic: unless a button has actual words spelling out its function, I am highly unlikely to be able to "intuit" its function.

This is a mistake in comparative anatomy which is somewhat common. When looking at four-legged animals, people often mistakenly map the parts of the hind legs.
Here is an image that shows the different morphology of the same bones in horses and humans:

What people often think of as the thigh of a four legged creature is really our calf and shin bone! And what is often mistaken for the calf is actually our foot.
Horses evolved to run on what is actually our toenail. You can see a similar pattern when humans sprint, our fastest running pace — we pull our heels up, and land on and launch off of the balls of our feet and our toes. That foot-strike is actually how animals such as the cat and dog walk habitually.
There's an urban myth that "dog's knees bend backwards", but by looking at this graphic, you can see that what appears to be the dog's knee is actually its ankle. And both the dog's ankle and knee bend the same way ours do.

Habitually landing on our heels in a normal walking pace makes us plantigrades, alongside raccoons and kangaroos. Dogs and cats walking on their toes is called digitigrade, while swift grazers such as deer and horses we classify as unguligrade, which means walking on their toenails.
So, other answers are correct, and flesh out the full information. I just wanted to give a visual indication to correct this common error.

Can you source the first image, I want to see if I can use that.

That image of the skeletal dog standing upright is both amusing and alarming, and I will never be able to look at a dog again without imagining it wandering around like that while people aren't looking.

@WayneWerner https://www.youtube.com/watch?v=7f1ovurzU2s

@John sorry, I grabbed it off of Google image search. If you do a search for "human horse comparative anatomy" you can find many copies of it, but I don't recall which one I originally got it from.

How come large herbivores have such thin legs?
They don't. The following book does an extensive comparison of the bones of humans with other animals:
Adams BJ, Crabtree PJ. 2008. Human vs Horse. In: Comparative Skeletal Anatomy. Humana Press.
Here are some images of human bones (left) next to horse bones (right):
Radius/Ulna (fused in horses)

Humerus

Femur

From these images, the bones of horses are clearly larger than their homologous counterparts in humans. Another answer gives a good picture of where these bones lie. Even if you were to consider the horse hock as its knee/elbow and compare, you would find that:

the horse radius/ulna is ~1.9 times larger than the human humerus at the smallest diameter
the horse tibia is ~2.3 times larger then the human femur at the smallest diameter
the horse metacarpal is ~1.3 times larger than the sum of the human radius and ulna at the smallest diameter

This is a homological comparison, but we should compare the part of the leg that is visible for both animals and "forget" that the horses knee is really it's ankle; it's more relevant for scaling laws. In that case horses do have human-sized but bonier legs. Though the femur difference is still illustrative of the more robust skeleton in horses.

@KevinKostlan I've updated the answer to address this. I understand your point though, and I think even with the rough measurements I made the horse bones are still supporting more weight. I just wanted to provide some data to show that the horse bones are not that small.

@Kevin Kostlan: The important part of the like-part comparison is, I think, that the muscles remain much the same.  The hip and thigh have the largest muscles, the fingers/toes have little, even though the corresponding bones are greatly elongated in the horse.  So when you grasp something with your hand, the power is coming from muscles in the forearm - you can see the tendons moving in the wrist.

You're assuming that horses and cows are still subject to Darwinian evolution.  In fact breeding of domestic animals has mostly been controlled rather carefully by humans, to breed for characteristics which we feel are favourable, even if those characteristics are detrimental to the animal's survival in the wild.
This became most obvious in the Agricultural Revolution, with selective breeding work pioneered by Robert Bakewell and others, where animal size increased dramatically.  African cows today give you an idea of how big cows would have been before this breeding effort, but even they are the product of thousands of years of fairly selective breeding.
Horses are a similar case.  Genghis Khan's Mongol warriors used ponies of around 12hh, and these would have been relatively wild animals.
Fragility of limbs is just one way modern animals are rendered less fit in the wild, of course.  Many breeds of domesticated animals have problems giving birth without assistance, or have genetic defects which can cause the animal distress or reduce its lifespan.  These issues are usually tolerated or managed somehow, because humans prioritise the desirable features of the breed.

Your answer is evidently overstating the importance of artificial selection if you consider that wild animals, such as zebras and deer, also display this characteristic.

Wild equines are not really morphologically distinct from domesticated ones. This isn't a phenotype that's emerged in the last 6,000 years since horses were domesticated. Humans have absolutely nothing to do with why horses have thin legs.

@NuclearWang Look at different horse breeds, though. Draught horses (speed isn't important) have a lot thicker legs than racing horses (speed is of prime importance). The differences between various domesticated breeds and wild horses are many (and don't confuse wild horses with domesticated-horses-gone-wild). But there's no need to reiterate James' answer, which is a lot closer to the mark.

"You're assuming that horses and cows are still subject to Darwinian evolution." They still are. It's just that most of their evolutionary pressures are human driven, and humans are a part of nature. This is just another case of one species exerting evolutionary pressure on another.

Evidence suggests that horses may have been domesticated as early as 3500 BCE, strong evidence exists at 2000 BCE. Khan's horses would have been bred for at least 3000 years. They were hardly "relatively wild". https://en.wikipedia.org/wiki/Domestication_of_the_horse


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How not to kill a spider while moving out of my flat?
About two weeks ago, when it started getting cold, a house spider (tegenaria domestica I believe) has chosen my flat for spending the winter. I like those spiders so it's not a problem for me. Only problem is, two weeks from now, I'm moving out. I don't know anyone around here who would want to take the spider in.
Would the spider die if I move it back outside now ? In the morning it's around 10°C / 50°F
Since I got a liking to the little guy, is it reasonable to try to take it with me ? There's going to be 5 days between moving out and moving in the new flat, if I go down this road how should I take care of it during those few days ?
What should I do to have the least chances to accidentally kill it ?
Thank you very much

Not that it's absolutely important, but, do you happen to know the species of the spider? Or, it's common name? This may help with environmental conditions & feeding.

It looks like the standard tegenaria domestica, I'll try to catch a pic this evening but it runs fast.


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How medical studies induce cancer in lab animals?
To test the effectiveness of drugs, they are typically tested on animals. How cancer is induced in lab animals to test the effectiveness of cancer drugs?

That depends on the cancer. There are many mouse models which are susceptible to develop cancer or can be induced to do so. This might be a starter: https://www.ncbi.nlm.nih.gov/pubmed/20936938 Another way is to inject cancer cells from humans into immunodeficient mice, which then can be able to "settle" and grow.

What is the success rate of cancer transfer from human to mouse method? And why not extract cells from the mouse,   induce cancer in vitro and place them back in original organ? In this case there will not be any immune response?

I am not an expert, otherwise I would have written a full answer. You can induce some cancers directly in genetically susceptible mice, but not all of them. Also, doing that many operation on small mouse organs is quite likely to kill them before they develop any cancer (not speaking of the ethical implications of the amount of additional discomfort they would have to endure).


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Is there any difference between hydrogen acceptor and hydrogen carrier?
As what i have learnt, hydrogen carrier (NAD+ and FAD) gets H (H+ and e-) from glyceraldehyde 3 phosphate dehydrogenase or Pyruvate dehydrogenase, and then transport H to electron transport cycle.
Do NAD+ and FAD act as hydrogen acceptor, hydrogen carrier, electron acceptor, and electron carrier?
Does this mean hydrogen acceptor = hydrogen carrier = electron acceptor = electron carrier?

Actually, both NAD and FAD accept a hydride ion, H$^-$ (a proton with two electrons), not a hydrogen atom (a proton with one electron). For this reason, I would not refer to NAD or FAD as "hydrogen acceptors" or "hydrogen carriers" at all. It just gets confusing. (I guess you could call them "hydride acceptors" if you want, but it's not common terminology.)
"Electron acceptor" is the right name for NAD and FAD when discussing a redox reaction where they in fact accept electrons, in the form of an H$^-$ ion. Pyruvate dehydrogenase which you mentioned is one such example. This is not unique to biology, it's standard chemistry terminology: any molecule that accepts electrons in a redox reaction is (cleverly ;-) called an electron acceptor. For example, oxygen is an electron acceptor in combustion reactions. So "electron acceptor" is just a name for the role that the molecule plays in a redox reaction.
"Electron carrier" refers to the fact that NAD (and also NADP, and quinones, and some cytochromes ...) can carry electrons between reactions that occur at different places. For example, after NAD picks up an H$^-$ ion in the pyruvate dehydrogenase reaction to form NADH, it can carry the two electrons over to complex I where it donates them to ubiquinone. (And here, NADH acts as an electron donor, while the ubiquinone is the electron acceptor.) So the term "carrier" emphasizes the transporting role of the molecule. FAD is actually a bit different in this respect, because it is not soluble; it's a prosthetic group bound to certain enzymes like Complex II, and therefore it cannot really carry anything anywhere, or at least not very far. So to be precise, I personally would rather not call FAD a carrier. But maybe that's just me.


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Difference in multicellularity between prokaryotic and eukaryotic organisms
As most prokaryotic organisms are single-celled, and in eukaryotic organisms this is the reverse, is there some evolutionary advantage that led to these features evolving? Or is it purely the fact that features of eukaryotic cells allow functions (i.e. enabling multicellular organisms) not possible in prokaryotic cells?

What matters is how many times multicellularity evolve and not so much how many species are multicellular. Have a look at this answer section How many times did multicellularity evolve independently?

Your title question does not match with you content question. Are you interested in the evolution of size or of multicellularity?

Multicellularity - apologies, I thought the terms were almost synonymous


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Microsatellites and Minisatellites: Which of these form the basis of DNA fingerprinting?
I'm in a fix.
 Prepare yourself for a long read
We've just learned about minisatellites and microsatellites at class (okay, by "learned", I mean we were told their definitions and essentially nothing else... hardly surprising, since we aren't expected to know more than that at school).
Shortly afterwards, we touched on the topic of DNA profiling, and my textbook went on to state:

Minisatellites are hypervariable and are specific to each individual. This uniqueness is employed in DNA profiling.

Which would imply that the repetitive DNA fragments used in DNA profiling (VNTRs - Variable Number Tandem Repeats) are (only?) minisatellites.
Fine.

However, the Wikipedia pages on minisatellites and microsatellites (I linked both of them earlier on in this post) mention:

(Minisatellites and microsatellites)... together are classified as VNTR (variable number of tandem repeats) DNA. Confusingly, minisatellites are often referred to as VNTRs, and microsatellites are often referred to as short tandem repeats (STRs) or simple sequence repeats (SSRs).

If I interpreted this correctly, it's saying;
"Both minisatellites and microsatellites are classified as VNTRs. But when one normally talks about "VNTRs" he/she is referring to minisatellites. Microsatellites are, instead, commonly referred to as STRs/SSRs."
Okay, so far so good.
The Wikipedia page on microsatellites explicitly states that they (the microsatellites) are the ones you deal with in DNA profiling. However, the Wikipedia page on minisatellites carries no clear indication of their (minisatellites) use in DNA profiling.
Ugh.
And to compound my confusion, the Wikipedia page on DNA profiling states:

DNA profiling uses repetitive ("repeat") sequences that are highly variable,called variable number tandem repeats (VNTRs), in particular short tandem repeats (STRs), also known as microsatellites, and minisatellites.

Which suggests that both minisatellites and microsatellites are used in DNA profiling (as they're both VNTRs), but microsatellites are more relevant in this regard.

Summing up what I said:

My textbook  says that DNA profiling makes use of VNTRs.
My textbook (and teacher) says DNA profiling makes use of only minisatellites.
Wikipedia says that VNTRs refer to both minisatellites and microsatellites.
Wikipedia says that VNTRs are typically mentioned in reference to minisatellites. Whereas microsatellites (which are strictly "VNTRs") are better known as STRs/SSRs.
Wikipedia says (explicitly) that microsatellites are used in DNA profiling. It doesn't mention minisatellites in this regard.
Wikipedia says that both minisatellites and microsatellites are used in DNA profiling, but minisatellites are use more often.

 This inconsistency over the three Wikipedia articles I've linked is seriously annoying

My question(s),
1) I'm told that VNTRs are used in DNA profiling. Does this refer to both minisatellites and microsatellites...or just minisatellites?
2) If only one of them is used, why disregard the other? They're both (technically) VNTRs aren't they? So shouldn't either of them work just fine?

I have complained many times about too long questions in the past. It is good to see here a long question, which has good reasons to be long. Also, it is nice to see a long question with a pleasant format.+1

1) I'm told that VNTRs are used in DNA profiling. Does this refer to both minisatellites and microsatellites...or just minisatellites?
Actually, it refers mostly to STRs. I worked a bit in forensic genetics and we always published works using STRs markers (one example here, there are plenty in the literature).
In addition, I would not be surprised if current forensic identification used SNPs instead, e.g. as proposed in this paper
2) If only one of them is used, why disregard the other? They're both (technically) VNTRs aren't they? So shouldn't either of them work just fine?
I really don't know, but I am sure that it has to do with one of a) level of variation, i.e. if minisatellites have lower mutation rates and are less variable, then they also are less useful, b) ease of genotyping.
Browsing in the web I found this website from which I understand that the minisatellites were the first to be used to perform DNA profiling (using a method different from sequencing) and that "modern" DNA profiling is performed using STRs. However, I insist that modern DNA profiling should be better performed using SNPs.