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Is evolution true as Darwin said?
I was telling the theory of evolution to my friends. But they asked me for the proof. They said, we are not seeing any such transition species at present. Neither we have such evidence for evolution. What should I do? I saw many proofs like archaeoptaryx, but now it has been proved that it is fully functional bird and others are also not supporting the theory of evolution given by Darwin!

You may want to look at the excellent series of links reported here: http://skeptics.stackexchange.com/questions/2057/demonstrable-and-repeatable-examples-of-evolution

There is no proving something outside mathematics, there is however the scientific process in which we determine the way reality likely is, in many cases to near certainty. You will not necessarily become convinced by one post here. You will have to learn trust in the scientific community, or learn about enough evidence for evolution yourself to convince you its a sound theory. Two points: there is no alternative to evolution that explains the data, or makes predictions as well as the theory of evolution, and the failing of one point of evidence is not necessarily evidence the theory is wrong.

It may be true that you're seeking scientific evidence but your friends are looking for the black and white answer. If they are, you can preface repeating some of the excellent responses below with a bit of what a scientific theory is. When someone asks me for proof of something I usually can't give them that, I can only give them evidence.

@ktamlyn Ok, seems logical. Mind the word 'seems'. See, even the atomic model that you studied in high school was based on certain observations. But they were all rejected when a more sound model comes up. For instance, Bohr's atomic model was rejected by Schrodinger, which itself was rejected because of just one fault in it, and the world got Quantization model. And even there were some faults in it and therefore, 2nd quantization model comes up and so on. And that is the whole story. The scientific world is always changing! You can't say illogically that Darwin is right.

You have to have prove if something is right. And just having some evidences doesn't make something true! As I mentioned earlier, even there were evidences that supported Bohr's model, but its no more acceptable.

As far as faith is concerned, I have in everything logical and scientific. But now on things given by scientists which have no solid basis! If I believe it today, can you take the responsibility that in this changing scientific world, this theory will remain unchanged? You will say yes only if you are not in depth with the science. I am also a science student. But its not bad to accept its limitations, which makes it changing.

@Smith, I am unsure I understand your response completely. You state "You have to have prove if something is right". No we don't, we "demonstrate that something is very very likely true". Black and white terms like "throwing out" an old model, when there is only "one fault in it" is a false characterization of what happens in science. What happens is augmentation, and modification. This false perspective on science is what leads to a sense we should throw out the entire theory of evolution because one detail is not understood. Minds that think this way cannot practice science.

I should add that augmentation and modification is generally common, not the rule. The examples you provided in my opinion are modification and augmentation.

I saw an excellent public science talk a few weeks ago. The speaker presented 5 questions which, if you answer yes to, you can only come to the conclusion that evolution exists. Firstly though we should define evolution: Evolution is the change in the inherited characteristics of biological populations over successive generations.
It was one of the best arguments I've seen put forward so I'll try to recreate it here. Put this to them and see what they say - and just in case they say no to any, I've put answers in for you ;) There is no hard evidence for the first four points because they are so damn obvious that if people say no, even after a logic based argument, then all they will ever say is no, they shouldn't need a scientific paper.
1) Do individuals reproduce?
The answer to this is undeniably yes, you were the result of reproduction. Reproduction exists.
2) Is there variation among individuals?
Yes, again this is undeniable. Do we all look and act the same? No. Are some people taller than others? Yes. Some more physically fit than others? Yes. Is everyone's hair or eye color the same? No. See, undeniable. Variation exists.
3) Do some individuals die before they get to reproduce?
Obviously yes. Children unfortunately die (of natural causes) which means they do no get to reproduce. Just go look in a cemetery or open the obituaries page of you newspaper and you'll likely find some one who died before they could have reproduced. Some people also never reproduce, because of life choices or fertility problems. Variance in reproductive success exists.
4) Do offspring resemble parents?
The answer to this is also yes, when two humans reproduce they (normally) produce something that resembles a human. And when that human reaches maturity they will likely look a more like their parents than a random stranger. Personally I was looking at old family photos recently and I honestly though I had found a picture of me marrying my mother, that's how similar my dad and I look. Heritability of variance exists.
5) Does heritable variation lead to differences in reproductive success?
If you've answered yes to all of the above then you really should be answering yes to this one too. As a hypothetical illustrative scenario, imagine two male deer. One has big antlers and one has small antlers. The size of antlers is largely genetically determined. The male with big antlers is seen as more attractive by a female. She chooses to mate with him. She gives birth to his offspring (n=2, 1 male 1 female) who inherit his genes for large antlers. This repeats with several females in the population (n=10). The smaller male has fewer mating events (n=2) and therefore sires fewer males in the next generation. The next generation contains more males with large antlers (n=10) than small antlers (n=2). This is evolution, the change in the inherited characteristics of biological populations over successive generations.
Another example is humans. We know some men have low sperm counts leading to low probability of successful mating. Further, we know that male infertility can be genetically caused for example by Y-linked genetic defects. Therefore we can expect that males with low sperm counts, caused by Y-linked defects, will have fewer offspring than a healthy male (given equal opportunity to mate) and because all males inherit their fathers Y chromosome they too will have low sperm counts. They will be represented at a lower level in the population's next generation. Again, this is evolution.
Speciation:
It then doesn't take much to jump from this to speciation. It involves the introduction of isolating mechanisms. These can be things like geography (allopatric speciation), or sympatric mechanisms like morphology, behavior, or any trait which prevents one group of individuals mating with another.
I'll illustrate first, and take the more difficult type - sympatric speciation. Again imagine our deer population. This time there is variance in sperm morphology, and female reproductive tracts. Males can produce two different types of sperm, one (male type S) is a slow moving but more resistant to the hostile female reproductive tract (because it is resistant to all types of antibody the females can produce), the other is faster (male type F) but less resistant (because it is resistant to only some of antibody the females can produce). Female reproductive tracts vary in the number of different antibodies they produce, one produces "all" that can be produced (female type R) and the other only a subset of the full array (female type W).
What will happen is that type S males will be more successful when mating with type R females because their sperm survive (whereas type F males have no sperm fertilizing the egg). However, type F males will be more successful in sperm competition than type S when mating to type W females. Repeated over many generations, these incompatibilities will cause distinct mating groups which do not overlap, i.e. species.
In reality it is much simpler to demonstrate this with allopatric speciation. Here two groups of one species become isolated by a geographical feature, like a river. Over time these populations evolve differently (because genetic mutation is random and selection might differ on opposite sides of the river). When they get the opportunity to mate after X generations, they can't because they have evolved genetic incompatibilities (offspring fail to survive, eggs can't bee fertilized).
One of the absolute classic examples is an experiment using fruit flies by Diane Dodd.   In her experiment she reared a population in two groups, one on starch based food, and one on maltose based food. After many generations (35 I think) the two groups showed mating preference, which is a reproductive isolating barrier, within their groups (mating pairs were more often formed from within treatments). Here is the paper.

Picture from http://evolution.berkeley.edu/

but still it doesn't prove evolution. When I say evolution, I mean formation of completely different species. In biology, two species are considered different if they can't produce a young one without mating. You are just proving that variations are inherited. I agree. But you didn't explain how this variation can lead to two different species. And this is exactly why I asked this question because I am facing a lot of similar questions.

@Smith That's speciation, not evoltuion. I'll add something in shortly, but you should be able to see how this extends to speciation.

Ok. But we have read that this evolution lead to speciation. And that what I want to know, how?

@Smith does this explain it for you?

@Smith. Speciation isn't so cut and dry as being able to mate. Reproductive isolation can exist in many forms. What about two animals that are able to reproduce and have viable offspring, but their reproductive organs have incompatible morphology so fertilization never naturally occurs? This would be a physical barrier to reproduction. Diane Dodd's fly experiment is similar, except that the animals have behavioural barriers.
You accept that variation can happen. What makes you not accept that variation can lead to speciation? What kind of forces would prevent it?

Going from variation to speciation is not that easy as you told. Why? Because different species have different morphology and anatomy. Variations only result in slight change of them. You can't expect a complete different species with variation. For an instance, human from monkey. But if humans evolved from monkeys, why we no more see any of the intermediate species? Even in the example of bee above, you will still get two closely related species. If you have any doubt, you can check with a DNA engineer, who can shower more light on it on the basis of more scientific DNA study.

@Smith Speciation isn't black and white, it is a gradual process.  To say we don't see intermediates between humans and apes is kind of wrong, some apes are closer to humans than others, humans 10000 years ago were more ape like than current humans and in 10000 years humans will be even less ape like, we are still diverging. Evolution and speciation do not stop, speciation is when we diverge enough to be considered separate species, but we will continue to evolve away from apes

@GriffinEvo I think you need to check the fossil records again in more depth which are contradictory to what you said! The human fossils found that are thousands to millions of years old, resemble the same shape. Caution: Dont depend on textbooks you are given. I faced a lot of criticism because of that. Search on internet the records. You would love to see this.

@smith As some one with a degree and a masters in evolution and two years in to a phd on evolution, I think I'm in a good enough position to judge what material to trust for myself but thanks for the great advice. Clearly you don't want to have your question answered by anything other than the answer you want. If you want an argument about the evidence of evolution go to a forum, this place is for questions and answers.

I also happen to work in one of the best departments in the world for the study of human evolution, I'd rather go to them for lessons on human evolution, not some guy on a website and a YouTube video. Science is peer reviewed, YouTube isn't, evidence that goes against the norm is welcomed by the scientific community, but the guy in the video is presenting weak subjective evidence against strong objective evidence.

@smith http://www.nhm.ac.uk/nature-online/evolution/what-is-the-evidence/morphology/hominid-skulls/

@GriffinEvo I know these, I am not a non-evolutionist. But there are evidences of human fossils millions of years old. Thats what I have to say.

@smith that says nothing, yes there are human fossils, but what is that supposedly telling us which goes against what Darwin or the theory if evolution says?

@GriffinEvo and thats why I am sure that Darwin was wrong. Have you read his book The origin of Species? Highly unscientific, although logical. He is assuming a hell lot of things on his own. ID is better option.

@smith so quote me what he said, why your evidence goes against what Darwin or (more importantly) the theory of evolution say, and how does it better suit ID?

The best proof of evolution is not in the fossil record, but perhaps in the living things you see around us right now.
For instance the rise of antibiotic resistant bacteria is the direct result of selection. The environment for the bacteria changed - we introduced antibiotics.  The vast majority of the bacteria die, but eventually the survivors are resistant- just in the space of a few years.
Adaptation and even speciation is occurring around us and can be observed directly.
A case that all of has seen, and was one of the most important to Darwin's argument in the Origin of Species is how we breed domestic animals.  By selecting animals with characteristics they find desirable, all sorts of animals are created by the use of selection - breeding the animals you want and then not breeding animals with characteristics that are not desirable.  Cats, dogs, horses, sheep - using selection any animal you want can be modified nearly to the point you can't recognize it.  This is a multibillion dollar industry when you think of all the livestock and pet breeders in the world.
The most famous scientific experiment along this lines is Dmitry Belyaev's domesticated fox experiment where over 40 years the foxes who were the friendliest to humans and bred them together.  As a control experiment the most hostile foxes were also bred together.  The result is an animal which is as friendly as a golden retriever, even though no fox had ever before been taken as a pet.
There are dozens of other stories.  Selection for breeding plants is another such success story.  Though it takes more work and time, Selection is as reliable as electronics as a technology.
Making someone believe something that they don't want to is much harder though.

ok. May be you are right. But still, this may be valid for asexual reproduction. What about sexual reproduction case. Is there an example in that too?

added another case above

Despite evolution is generally macroscopically appreciable after a long time, there are some examples observable right now.

A classic example is the evolution of the peppered moth (Biston betularia) in the last two hundred years. Originally the predominant color was white, which camouflaged them against light-coloured trees such as Betula plants, while dark-colored moths were rare. During the Industrial Revolution in England the pollution blackened many trees, causing most of the light-coloured moths to die off from predators. The black-coloured ones (called carbonaria) flourished because of their ability to hide on the darkened trees.
The best example about whole species evolving is the ring species. Here is a good definition from wikipedia:

In biology, a ring species is a connected series of neighbouring populations, each of which can interbreed with closely sited related populations, but for which there exist at least two "end" populations in the series, which are too distantly related to interbreed, though there is a potential gene flow between each "linked" species. Such non-breeding, though genetically connected, "end" populations may co-exist in the same region thus closing a "ring".
Ring species provide important evidence of evolution in that they illustrate what happens over time as populations genetically diverge, and are special because they represent in living populations what normally happens over time between long deceased ancestor populations and living populations, in which the intermediates have become extinct. Richard Dawkins observes that ring species "are only showing us in the spatial dimension something that must always happen in the time dimension."

You can continue the reading at the related wikipedia article.

peppered moth just adapted to this change and their body colour changed. But are both different species?

No, they are not. It's an example of current evolution. You can look at the "ring species" example for the speciation (read the wikipedia article!).

I added a larger quotation from wikipedia, now is self-explanatory.

The ring species is an excellent example of evolution of species.  The two endpoint populations are essentially different species, and you can find the gradations between them in the ring around the globe.  Remove the intermediate populations and all you have are two (related) species.

@mgkrebbs - Great comment about ring species.  Here's a nice explanation: http://www.pbs.org/wgbh/evolution/library/05/2/l_052_05.html

But lets become somewhat practical. If you read from that wiki page only, it says only four species are found to follow this concept of ring species. So, again, if this is the right concept, atleast majority of species are supposed to follow it. And thus, this idea still is just a concept and not a law, which is universally applicable. Any comments?

Ring species is a special case in which the intermediates haven't become extinct. The general trend is the contrary. The theory of evolution will be forever a theory: you can't pretend to see the evolution of every single specie in the planet. However, like Stephen Jay Gould said, it is "confirmed to such a degree that it would be perverse to withhold provisional assent." Sure the ring species concept alone can't prove evolution.

so, in the end it comes to faith only! We have to just accept. Then what is the problem in Intelligent Design? Even you have to put faith there! But that is more scientific than saying that everything we see around evolved by chance. I have never seen any discovery taking place by chance. A scientist may be working on something and not getting results. But he may get that by chance. But to believe that anything just came up by change is illogical and unscientific! In ID, atleast they tell its a design by a designer which is more logical than saying chemicals combine on their own and life came!

You have several misconceptions about the theory of evolution, however you wouldn't have written certain things. I can't explain you all because I'm italian and not a good english speaker and because you will need a long answer. Moreover, your question was about present transition species. I suggest you to read a popular-scientific book about evolution. You can ask a new question for suggestions about it!

Of course you dont see a transition species at present! A transitions species is what existed between two other species. When it "becomes" the new species, the transition species no longer exists. Transition species only exist in the past. Its also important to remember that species are a spectrum. When we divide things up into discreet species it makes it seem all neat and tidy but really it is not because of the large amount of variation that exists within a species. When the variation becomes so great that certain members of the species may not be able to interbreed, we break it into two species.
I also do not see why you need to visually see evolution to believe it exists. The strongest evidence can be found in DNA or protein sequences. Look at any conserved protein and see the similarities. I will give you a link that shows the difference between the mouse and human version of a protein called p53. p53 is studied a lot because it is thought to have a role in cancer. Im not even sure if p53 is considered a "highly conserved" gene, but look at how similar it is!
ps53 protein alignment*
How many generations difference do you think there is between a mouse and human? [remeber humans did not evolve from mice, they just had a common ancestor, so what I mean is how many generations have elapsed since the last common ancestor]? It is estimated that mice / humans disverged some 70 million years ago. Lets say a generation (age difference between parent and child) is ~30 years in humans (it is much much much much less in mice but lets forget about that) that means there were some ~2 million generations, and thats being conservative. This website claims there are 74 de novo[new] mutations in humans each generation. Technically this is not all mutations but again we are being conservative. So that is about a 150 million mutation difference between humans and the ancestor that became both humans and mice
My question to you is this: Look again at the similarities between human and mouse p53. You see how there are some differences? Dont you think it is entirely possible that the differences can be accounted for after having 150,000,000 chance mutations?**
Now imagine this happening to every gene, not just p53. That is evolution
*Not sure how long this link will be valid but you can see the sequences at these links and do the alignment yourself here
http://www.ncbi.nlm.nih.gov/protein/200203?report=fasta
http://www.ncbi.nlm.nih.gov/protein/23491729?report=fasta
**Actually double that to account for mouse evolving from the common ancestor but like I said, wanted to be conservative

There are six different types of evolution and they all happen on different levels.

Cosmic evolution- the origin of time, space and matter. Big Bang
Chemical evolution- the origin of higher elements from hydrogen.
Stellar and planetary evolution- Origin of stars and planets.
Organic evolution- Origin of life from inanimate matter.
Macro-evolution- Origin of major kinds.
Micro-evolution- Variations within kinds. Only this one has been observed. For instance poodles and great danes are descendant from the same thing. A wolf.

Are you asking about macro evolution or micro evolution? Or one of the other 4?
Speciation does not show macro evolution in any way, shape, or form. And the ring species you refer to moths changing colors, that is micro evolution. A moth changing into another moth would even be micro evolution.
Man thought up species and defined them. If it looks like a duck and quacks like a duck, it didn't evolve into a different animal because it changed the color of it's feathers.

You're using some rather strange terminology, your first 4 points are generally not called evolution, the Big Bang and abiogenesis are not part of the theory of evolution. And the division into macro- and microevolution is misleading, it is exactly the same process.

It is not the same process and they are all forms of evolution. Define macro and define micro and let's see if they are the same. Micro are finite changes that can happen independently of macro evolution. Are you saying you can't have micro, without macro? Or are you saying you can't have macro, without micro? If you can have micro without macro then they are different.


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What makes a metal safe to use for an artificial joint?
What determines if a metal is suitable for transplantation such as in the hip? What I am most interested in however is why might some metals be toxic to animals once in the body?

There are a number of reasons why a given metal may be toxic to an animal:

Radioactive metals are the easy ones.
Some metals can affect the normal biosynthetic pathways within the body.  Lead is a good example of this, as it can take the place of calcium; I believe beryllium does the same for magnesium.
Some metals themselves are very reactive.  Hexavalent chromium ($Cr(VI)$) is highly reactive, and will cause damage through severe oxidative reactions, whereas $Cr(III)$ is largely okay.
A lot of metals are okay, even required, at some level, but become toxic at too high a concentration.  Iron, for example.
People can simply have allergies to metals.  Nickel in silver jewelry is a good example, although in my experience it can be overcome.

The basic gist is that some metals are required for life, some aren't but aren't too terrible, and some are completely toxic to it.  Different organisms can vary a bit in which metals are useful or not.  A good implant will of course not be toxic at all, and will be strong and long-lasting.  Titanium is often used, given its strength and general nonreactiveness, but so is cobalt, despite being toxic to some degree.

Ref: Metal Sensitivity in Patients with Orthopaedic Implants.  Hallab, et al. J Bone Joint Surg Am, 2001 Mar 01;83(3):428-428

If the question is why a transplant implant like an artificial hip may be made from a metal, then toxicity issues of the metals are not the main question.
I think it would be better to focus on metal sensitivity.
Metal sensitivity is not a specific immune response as with transplanted organs, but a non specific response to a foreign substance in contact with the body. While  Surgical stainless steel and similar hardened alloys which contain iron, nickel, chromium and molybdenum are popular for metal components of implants, even plastic coated pieces can cause scarring and irritation.
This reaction is highly variable from one individual to the next and can have no effect or cause further surgery or rejection of the implant.  the cause is poorly understood and so diagnosis is still in an exploratory state.
Since oxidation and rust seem to cause more irritation, it seems that corrosion resistance is an important part of implant metal choices.   Hardness, durability and Cost is also an issue since I'm sure gold and platinum would also be great choices from a cost perspective.

I think the question is specifically interested in what makes some metals better or worse than others.

i agree, though I feel that within the the set of metals that might realistically be chosen for implants might be a more focused answer.

I think  @Amory answer is a good one but I would like to add a new point for the last part of your question.
Our normal body cells can recruit the immune system when there is infection but the transplants can not. Some findings suggest that bacteria can form a biofilm over that part and  so can become difficult to treat with antibiotics.
Source : I read this in a book called Good Germs, Bad Germs by Jessica Snyder Sachs

yes this is i think more to the point. why is surgical steel better for transplants than say, iron or copper?  immune rejection is a big part of the problem, but i don't know the answer myself

@shigeta I don't know why surgical steel is  better but I can only say that whatever artificial material we use, biofilms are going to be a problem .

Biofilms can form on materials within body cavities exposed to fluids. But can it form on implant materials within tissues surrounded by tissue fluids? Are there any references?

then why do they bother to use some alloys of metal at all?  its not for the looks... lmgtfy  http://emedicine.medscape.com/article/1230696-overview

@shigeta I really don't know why.

ok i'll ad a bit on that below.

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What is an 'ex vivo' experiment?
Simple terminology question:

Is there a hard boundary between in vitro and ex vivo?
Is there a hard boundary between in vivo and ex vivo?

Suppose a sensory neuron is electrically recorded in the following settings:

Surgically accessing through the animal's skin, and patch-clamped,
Tissue surrounding the neuron is almost separated, but still dangling from the larger part of the animal, and patch-clamped,
Same as above, but the slight dangling connection is cut,
The sensory neuron is isolated and put in an artificially oxygenated medium

The sensory neuron is assumed to have purely feedforward signal, and is perfectly healthy in all conditions. Which conditions, if any, are in vivo, in vitro, or ex vivo? (Feel free to propose better hypothetical experiments. I know this example is not the best.)
Am I the only one confused about these terminologies?

It's simpler and broader than that. All depends on the source material for the experiment, if you're talking about experiments: in vivo: animal models
ex vivo: cultured cells
in vitro: purified molecules

The terminologies are there to be helpful shorthands, i.e. they are not mutually exclusive terms and are not strictly defined jargon. Case 1 is in vivo, the rest are not. Concerning Case 2, removing the environment of a neuron cannot guarantee its native state as it exists in the organism, so it is not an in vivo experiment (at least not to most electrophysiologists). In vitro is just a shorthand for where it's taking place. You can simulate an observation on a computer in silico, or make observations on a plate in vitro. If you can't be clear with a shorthand, don't use it!

Ex vivo simply means "outside the normal, living organism", whereas in vitro means "within glass", usually in a cultured system.  They are not exactly same as there is no need for the work to be done in a culture system, although both are not in vivo.  Harvested tissue could be examined ex vivo without being in a test tube, or surgical systems could be tested ex vivo on artificial organ models.  In vivo requires the natural, living organism, although it depends on just how much you are perturbing the natural.
To answer your scenarios,

in vivo
ex vivo, as it is not within the normal organism, although I could understand someone taking issue with that; definitely not in vivo, which is usually for normal conditions only, even including temperature.
ex vivo
If you mean the artificially oxygenated environment of a tissue culture system, then in vitro; if you mean the artificially oxygenated environment of a lab bench with an open $O_2$ valve, then ex vivo would suffice.

Comment to top answer (from Amory): in vivo is not for normal conditions only, half of the times it's not in the "normal" "natural" conditions, that's how you can learn something, you always have to compare a mutated version or diseased version to a healthy control, all is in vivo anyway (when it's in vivo), regardless of the conditions. So in the example 1, are you trying to say that if it is the mouse model for Alzheimer disease, for example, then it's not in vivo anymore?!
Also, "vivo" doesn't mean "living organism", it just means "living".

@kjf That was intended to convey the typical case of a living organism.  Cell culture is living and is an organism, but it is not a "normal organism."  It was intended to be colloquial, as noted where I say "although it depends on just how much you are perturbing the natural."

(Not only) Wikipedia states that in vitro and in vivo have a very hard boundary between them. I something is studied in the context of an organism, without being extracted, it is in vivo, as soon as it is extracted it is in vitro.
Strictly speaking, I would count only the first of your neuron examples as in vivo, because it is still expected to be working like it does inside the organism. As soon as you start having it dangling out, the original "environment" is destroyed.
The relation between ex vivo and in vitro is less defined.
I would count example 2 as ex vivo, but not in vitro, as the Wikipedia article for ex vivo  describes. Same goes for example 3.
Example 4 is of course in vitro. Debatable is, if in vitro excludes ex vivo. It is still taken out of an organism, not grown artificially, so I would still consider it ex vivo.

if you check articles in different fields, chemists and biochemists will usually say cultured cells is in vivo ("the molecules we always study in the tube are now inside a living cell!"), clinical doctors will say it's in vitro ("we take some cells from the patient and put them in a tube"), cell biologists working with clinical samples, animal models, cell cultures, purified molecules, the whole set, will say it's ex vivo ("the molecules that we study are in a living cell, but that living cell that we also study is out of the organism, ex vivo!").

Can you add some reliable references please?

The term in vivo refers to a medical test, experiment or procedure that is done on (or in) a living organism, such as a laboratory animal or human.
The term in vitro, in contrast to in vivo, refers to a medical study or experiment which is done in the laboratory within the confines of a test tube or laboratory dish.
In contrast to in vitro studies, in vivo studies are needed to see how the body as a whole will respond to a particular substance. In some cases in vitro studies of a drug will be promising, but subsequent in vivo studies fail to show any efficacy (or, on the other hand, find a drug to be unsafe) when used within the multiple metabolic processes that are continually taking place in the body.

Please provide a citation or link to supporting evidence. Thanks!

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Change of phase from juvenile to adult in plants
I tried googling this but couldn't get much information on this. Most of the articles were about induction of flowering.
I am more interested in knowing what factors influence the conversion of juvenile phase to adult phase in plants and not the induction of flowering.
Can a plant survive if it is artificially kept in a juvenile phase ?

there are no distinct developmental stages in most plants.. a plant which will grow up to become a big tree may still bear flowers when it is smaller.
there is no juvenile phase in many animals too.. just that they are sexually immature.. only arthropods and some amphibians have a distinct larval stage which is very different from an adult.. they undergo metamorphosis whereas other organisms just grow and develop. you can stop the growth and also inhibit the sexual development but that would be just called as growth retardation

@WYSIWYG There ares some plants like Acacia koa which produce distinct types of leaves in juvenile and adult phase.

After a cursory reading on Acacia koa i gather that even the smaller plant bears the phyllodes along with the compound leaves. So i guess there is still no distinct compound leaf only stage. Just that perhaps the development of the compound leaf ceases after a stage. I am no expert in this topic so cant comment more. But if we go back the the original question - if an organism can be retained in a developmental stage: i guess it is possible to retain an animal in its larval stage by inhibiting metamorphosis.

I know a genetics professor that found the reason for the juvenile leaf into a adult, a gene (151) in the RNA. He is presently working on what factor that promotes this to happen.


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Need of Creatinine Phosphate
In muscle cells most of the ATP's phosphate is with creatinine phosphate.
So why is the displacement of the phosphate group done ? Is it because creatinine phosphate would give it's phosphate more easily ? Is it done so that the negative feedback by ATP on mitochondria is not there and more and more ATP can be generated ?

Creatine phosphate is used as a buffer in high energy using cells, such as muscles. In a cell you have a pool of ATP, which is needed for things like muscle contraction, and then you have your pool of creatine phosphate, which can not directly be used as energy for muscle contraction. The cell only stores so much energy as ATP. And during high energy activities it can be depleted quite fast. The problem is that it takes a lot of time to make ATP through oxidative phosphorylation. And while glycolysis is faster, you dont get nearly as much ATP. Creatine phosphate solves this problem by acting as a reserve of ATP, so when ATP is depleted, the creatine phosphate can transfer a phosphate to ADP, and thus restoring ATP without needing to wait for glycolysis or the electron transport chain to complete.


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Why are Lymphatic trunks part of the Cardiovascular system?
According to Wikipedia the Terminologia Anatomica (international anatomy standard) the lymphatic trunks are part of the cardiovascular system instead of the lymphoid system.
Why did they make that choice?

The definition of "vascular" is as follows:-

of, relating to, affecting, or consisting of a vessel or vessels, esp.
  those that carry blood:

By this defninition, the cardio-vascular system doesn't need to include only the blood vessels and the heart. It includes all conducting and distributing vessel elements including those which carry the lymph-Lymphatic vessels. The cardiovascular system stands for the "circulatory system"+ the heart tissues and since lymph is an essential part  of the circulation (of nutrients, hormones, wastes etc), the cardiovascular system must include the lymphatic system.
Lymphoid system is a completely different entity which includes spleen, the lymphoid tissue (MALT), the lymph nodes and the lymph vessels. Hence the lymphatic vessels belong to both, the cardiovascular system and the lymphatic system, but the MALT and Spleen (arguable and disputed) are only a part of the lymphatic system and not of the cardiovascular system.
MALT= Mucosal Associated Lymphoid TIssue


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Fear in elephants
It has been noted that elephants trained for war, as was done occasionally in earlier times, have still shown a tendency to panic in battle much more often when compared to a war horse trained for the same purpose.  However, is this due to an innate quality of elephant behavior, or a result of poorer training methods due to humans simply having less experience training elephants than horses?  Are elephants naturally more fearful creatures than horses or other beasts of war?

Do you have any reference on the fact that elephants are having a higher tendency to panic than horses in the same situation?
Elephants were much more involved in the fight, than horses, since a horse rider would never run into the middle of the battlefield, but elephants were used in the first rows!

I doubt if a comparison between these two animals in war situation is in order. These two animals serve different roles.
Here is a reference to an article in Wikipedia on War Elephants. Elephants have been used in war for thousands of years pretty effectively till the enemies discover their weakness and use it to their advantage. Making the elephant panic is one of the ways to counter them. Here is a list of methods from the above article:

Elephants had a tendency to panic themselves: after sustaining painful wounds or when their driver was killed they would run amok
One famous historical method for disrupting elephant units was the war pig......
At the Megara siege during the Diadochi wars, for example, the Megarians reportedly poured oil on a herd of pigs, set them alight, and drove them towards the enemy's massed war elephants. The elephants bolted in terror from the flaming squealing pigs.

It is for sure that many horses also panic in war situations. However a panicked elephant can cause more havoc than a horse. It appears that to prevent a panicked elephant from running amuck back into the ranks

The driver, called a mahout, was responsible for controlling the animal. In many armies, the mahout also carried a chisel-blade and a hammer to cut through the spinal cord and kill the animal if the elephant went berserk.

In recent times elephants in temple festivals in india do occasionaly panic and run amuck when the high explosive fire works are set of. However most of the elephants seem to tolerate it.

authors: Андрей Беньковский


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Male behaviour during breeding season
The mountain blue bird build nests to attract females and exhibit aggression towards other males during breeding season. Which of the following is likely to give the birds maximal evolutionary fitness?
a) stronger aggressive behaviour only during egg laying
b) stronger aggressive behaviour during nest building rather than during hatching of eggs
c) stronger aggression when egg is first laid than during nest building
d) greater aggression during hatching eggs than during nest building

Can you provide some of your thoughts on what the answer should be (and why?)? I personally think it is too less information to decide upon, but taking a thought-out guess, I think it can be (b).

@SatwikPasani Yes the answer is b. What did you think ? I am really confused with the question.

For the trait to be beneficial it needs to happen before mating. If the male scares off other males but the bird has already mated with another bird it wont be beneficial. So the answer is B, because its the only answer that happens before mating

a) stronger aggressive behaviour only during egg laying
c) stronger aggression when egg is first laid than during nest building
d) greater aggression during hatching eggs than during nest building

These all occur after the stage which determines fitness. Egg laying (a and c) and Egg hatching (d) occur after the male has won the right to mate.

b) stronger aggressive behaviour during nest building rather than
during hatching of eggs

Assuming the behavior increases mating success and fitness, the answer is B because this is the only strategy that attracts more females and gets rid of rival males before it is too late (i.e. before the female mates). This is also assuming that the female can/will only mate once.
In chronological order the answers run "B,C/A,D" (C & A are really one and the same in my eyes). Mating occurs between B and C.


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If I built a concrete pool, would it ever contain fish?
Imagine that I built a concrete-walled pool the size of a football field and filled it with fresh water - obtained from another lake but free of bacteria, plantlife, eggs, etc.
Would it ever, over time, become a life-filled "lake" - with fish, amphibians, algae, plants and other water-dwellers?
If yes, how?
What would the chain of events look like?  I'm assume plant-life would get there first but how would it develop an established eco-system?
Please re-tag as appropriate as I am new to this SE site.

The short answer would be yes, given enough (long++) time. The situation would be similar to e.g. newly formed volcanic islands or when bare rock is exposed after a glacier disappears. However, the specifics are really hard to answer and would depend on the geographical location and stochastic colonization events, and you won't get a definite answer on a Q&A. Look into the vast ecological litterature on colonization and succession. A likely chain of organisms would be someth. like: Bacteria & phytoplankton-> zooplankton-> invertebrates & plants-> vertebrates (e.g. birds and amfibians first).

Also look at Hydrosere succession, which describes long term succession in fresh water bodies.

@fileunderwater Assuming that you don't also build a bunker around the pool, and that you live near or in the path of migrating species (especially birds, and you probably do), it actually doesn't take long at all.  Higher level animals are going to land/bathe/drink it, as they do they are going to bring a whole host of life with them, including the possibility of fish through eggs.

@AtlLED The "long++" part was referring to fish. I agree that birds and flying insects will visit quickly (they will spot a fotball-field sized pool). I read the questions mostly as asking whether a natural lake ecosystem will develop over time.

If the pool was stagnant, I can imagine that algal spores would be among the first to reach the lake. The algae could 'suffocate' the lake and make it very cold and even poisonous if certain species of algae bloom. I hope one/some of the answers discusses this.

@goodgravy your scenario requires a healthy dose of nutrients

@Abe A very good point about nutrient rich water, especially considering we are starting from a blank slate. There many are trace elements in concrete, notably calcium. This is usually one of the limiting factor in algal growth. The other problem is nitrogen. This is where my theory has a weak link, yet I don't think we should dismiss that algae could thrive on whatever other micro organic matter found itself in the lake. Obviously if we were to discuss this further we would need more specifics on types of concrete, geographic location, animal contamination, pollutants etc.

@goodgravy algae don't thrive on organic matter, they thrive on mineral nutrients, N and P in particular. Ca is important but rarely limiting.

@Abe If you are intentionally trying to grow algae, you get a pot of water and leave it in the sun. Algae will grow. This is sped up by the nutrients, but there will be enough for slow growth from microscopic spores, fish eggs, seeds bacteria etc. This question is a scaled up version of growing algae in a pot.

if the pool were just sitting out in open air, on earth and all that good stuff, it certainly would, given enough time.
This thought experiment is in the same vein that inspired Darwin when he reflected on his experiences on his visit to the Galapagos islands.
Think about it - the many islands which are formed by upheaval were lifeless when they first emerged from the ocean.  Over time, the winds or storms eventually populated them all - just about every island has animal life on it.  Not all animal types are found there that are best for the climate; its a matter of accident that some birds or lizards are found on the galapagos islands.  These accidental landings don't happen very often and sometimes a single animal will generate many species which will fill the role that other animals would normally fill on the mainland continents at the same latitude.
This is what happened on the islands- in different islands, Darwin found finches of sizes and shapes would be eating insects from bark or ant hills that might be done by an animal
Eventually, if you wait long enough a frog, then maybe a couple of fish will find their way into the pool from a nearby waterway (yeah that could take a long time I know).  If it takes too long then a new species will show up.  If you build walls around the pool it might not happen.  These accidents of animals showing up by accident can take millions of years.
This experience of Darwins' has inspired an entire field of biology - Island biogeography.  Each island is an experiment and ecological niches can be observed by taking a series of islands and seeing how different animals take up the various ecological roles on each.  A famous experiment EO Wilson and colleagues did was to fumigate some mangrove islands and watching them repopulate.

I recently dug a pond in a forest, and the first things to happen was not actually plant life. First I found small aquatic animals that lived in the mud, then I found salamander axolotyls and water striders, and crawdads. Salamanders (especially newts), water striders, and crawdads all migrate between ponds to breed and when old ones dry up, as well as various other aquatic animals. The aquatic mud dwellers might have been washed there by rain, or they might have migrated there like the others. In the case of a lake, all of these will happen, although slower because of a lack of sediment with concrete walls. The fish would depend on whether or not there is a waterway connecting the lake to an area where fish already live. These events would happen in the first year except for fish, and pretty soon algae will be growing right after the animals moved, or during, and plants will start to grow as well, their seeds or whatever they use to spread will make their way to the lake. I have found though that lakes, especially man made ones, often contain very little large plant life. As for the time it takes, one year will start it off with basic predator prey relationships, and will slowly grow from there over the course of years.

I believe that's why the question used concrete, to avoid the fact that a pond/lake in the dirt is actually still quite open and in contact with life.

I did mention the fact that it would occur slower with concrete, but eventually enough debris would fall in the water that there would be sediment.

The answer is yes, absolutelyvne enough time. You can do this experiment yourself. Get a clean glass jar, hell even sterilize if if you like (your oven overnight at 250 F will do it).   Fill it about 3/4 with clean (or even sterilized) water, and leave it outside in a mixed sunny shady spot for a few weeks, in moderate weather. It's small volume will get cooked by constant direct sun, which will impede the results.
After a few weeks (might be faster), look closely into the water (through the sides of the jar) with a magnifying glass, or better still, sample the water and look under a microscope. You won't see, but they are there, multiple bacterial species.
You will see single celled algae, small pond creatures (hydra, rotary-topped species (multiple)), paramecia, and multi-celled algal forms in strings. These are all fallen in from airborne dust and windblown particles.  You likely won't get fish, but if you are lucky, you might get a few brine shrimp.  And yes, particles of blown or bird-carried dirt etc can easily carry shrimp, amphibian, or plausibly, viable fish eggs.
But what do they feed on?  There's no food in the water you put in !!  CO2, nitrogen, Oxygen, etc are readily available from the air. A few cells of bacteria or algal forms seed the clean water, and begin fixing CO2, nitrogen etc, and now you have a food source. Wind-carried (or bird-carried) small organisms can now survive in a web of bacteria-plant-animal interactions.
By the way, you can also run a control jar, where you sterilize the jar, fill it with boiling hot water, and quickly cover it tightly with foil. Place it beside your open jar, and it will grow...nothing.
As a side note, "toxic" algae are often not toxic to small organisms and other algae. Their toxins (neurotoxins usually) affect mostly only higher organisms, such as fish and humans. Algal blooms kill fish and birds, they seldom sterilize the pond.


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Basic text/notes on DNA structure (for non-biologists)
I am a mathematics grad student researching knot theory, and I've recently discovered that there is a connection between knot theory and DNA structure (if I understand correctly, when DNA strands repackage, they do it in a way similar to what is known as Skein relations in knot theory, therefore tools from knot theory can be applied to DNA research).
The problem is that I have almost no background in biology, therefore it is difficult for me to understand how exactly DNA repackages and what happens on the molecular level.
Could anyone suggest some basic (and preferably not too long) text which gives an introduction to the structure of DNA? I have some basic background in organic chemistry, and I am not really looking to understand the topic thoroughly, just to visualize what's going on so I could see the analogy to the mathematical theory.
Thanks in advance!

I found this thesis online. For an introduction to the DNA look at paragraph 1.3

We could help you more if you explained how DNA is similar to Skein relations or, conversely, explain what Skein relations are so we can understand how they're similar to DNA.
As always, the best and most accessible resource will be a university text book. I would recommend Alberts, as I recall, it explains this topic quite well.
If you're after something a bit more visual, I found some nice ones (click on an image to be taken to its source):

this is a special topic, I'm assuming you have looked over the basic Watson and Crick stuff.
Maybe closer to your interests DNA does tangle and needs constant maintenance of the amount of winding to keep it properly ordered.
I would look at topoisomerases and DNA origami to start with.
Topoisomerases are a class of enzymes that help DNA pack up and wind up into the compact forms of the chromosome when its wound into solenoids in chromatin and unwind into the looser forms when it is loose.
DNA origami is a field of study which uses DNA as a self assembling template for making three dimensional structures.
Maybe this helps?  let me know if we can narrow the specifics of your interests.


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Are there echolocating insects?
Echolocation is the ability to obtain spatial information of the surroundings from echos generated by the animal. There are bats and other vertebrates that naturally use it.
I was wondering if this is limited to vertebrates, or if there are examples among the invertebrate, especially insects.

Some moth actually do use clicks for their own echolocation: "Noctuid moths (Noctuidae) are the only group of invertebrates for whom echolocation was
demonstrated":

Lapshin & Vorontsov 1998
Lapshin et al 1994.

Cool. Thanks for the references. It's good to know some people believe in it, but those articles have no citation and are published in somewhat minor journals. So I must say I don't fully trust them. Do you know of any other group replicating their results?

Well, I would of course keep some degree of skepsis. And I'm not aware of something published by other research groups: it's true, that they provide principally only self citations. But this, coupled with the fact, that nearly all of the papers of this lab were originally published in Russian, is just another example of the continuation of the Soviet school. I can confirm, that the author still considers his findings valid and has a very elaborated description of the story and his experiments (in Russian): http://www.lapshin.iitp.ru/project1/index.htm

As others have indicated, I also haven't seen direct evidence of echolocation in insects. However, there is much evidence that the auditory system of e.g. moths can hear ultrasound generated by bats (Waters, 2003). According to Waters (2003) moths mainly use this to avoid predation. The review also contain many useful references and examples of moth ultrasound detection, and specifics on the physiological adaptations. Since moths apparantly can detect ultrasounds (and generate them), this also opens the possibility that some species could use it for echolocation. But from what I have seen, no direct evidence.
In general, many insects use high-frequency sounds, but we often do not know exactly for what purpose. If you are interested, this webpage on sounds in butterflies (in Swedish) have a couple of examples that you can listen to (recorded by a professor emeritus as my old department). Look at the subpages for each species for embedded .wav where the ultasounds are played in slowmotion. Again, the exact use of these sounds are mostly unknown, but they are believed to be used to attrach mates or scare predators, but might potentially (if we are speculating) be used for echolocation in some species.

My understanding (as a PhD holder in toothed whale echolocation) is that insects do not use echolocation themselves as a means of hunting or sensing their environment more generally, but some do produce clicks which serve to jam/confuse a bat's echolocation. This is an anti-predation strategy. Their production of clicks being a means of defence is supported by this recent publication (O'Reilly et al., 2019, Scientific Reports), which shows that even deaf moths exhibit this behaviour. Additionally, this recent PhD thesis (T. Hugel, 2020) thoroughly explores this predator-prey interaction between bats and moths.

Welcome to Biology.SE. This looks like the start of good answer. Two suggestions for improvement: 1) Can you add more support for saying that insects don't use echolocation — as written it sounds like some moths are clicking to "jam" bats, but that doesn't seem to disprove echolocation in moths let alone all insects; 2) Please include the complete reference information since links can (and do) break. One easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information.

As far as I can tell, the answer is no.  It's hard to prove a negative so the best I can do is that none of the articles in the literature I've been able to comb through have any mention of invertebrates at all.  What I can give you is that some moths use clicks to jam bat echolocation and some fish are sensitive to echolocation, "raising the possibility that fish may exhibit negative phonotactic behaviour in the way that moths do."


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Identification of this Salamander
This salamander was found in a small forest pond somewhat near the Oregon coast. In the area are many rough skinned newts and a small number of another type of salamander that I still can't find the species of. I'm guessing it is either the salamander species or a rough skinned newt.

I found what it is, it's a torrent salamander.

It is a torrent salamander. Most likely this is the southern torrent salamander (Rhyacotriton variegatus)

I'm not convinced this is a Torrent salamander (Rhyacotriton variegatus)... I'll look into this a bit...


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what is knob heterochromatin?
I am reading a paper which discusses Maize Genome Structure. Descriptions of the  structure is given in the papers introduction.
I know about heterochromatin "heterochromatin stains intensely, indicating tighter packing. Heterochromatin is usually localized to the periphery of the nucleus"
but, could someone explain what is knob heterochromatin?
thanks for help.

Here's a good summary of knobs, which says that they are "typically telomeric," "tandemly repeated DNA sequences [that] appear as distinct, heteropycnotic regions located at certain sites on specific chromosomes and look much like beads on a string" and are involved in:

increased recombination
neocentromere activity
preferential segregation
chromosome breakage and chromatin loss
sex differences in recombination

The introduction to this paper gives some of the same information.

I found it in this article :

Heterochromatic knob
  A chromosomal region that can
  be identified microscopically as
  being darkly stained compared
  with surrounding chromatin.
  DNA sequence analysis has
  shown that knobs often contain
  highly repeated DNA
  sequences. They were
  described initially in the
  1930’s by McClintock during
  her studies of maize
  chromosome structure

If you copy a paragraph verbatim from another source, please indicate this clearly by naming and linking the source and using a blockquote. Else one might get confused about which parts of the answer you wrote yourself, and which are taken from other sources.


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What is the equivalent of shutter-speed in Human eye?
I just learned that in video cameras, every frame of the video has its own shutter speed.

And I know how frame-rate in human eye works out, well, not completely, hence the question.
http://en.wikipedia.org/wiki/Frame_rate

The human eye and its brain interface, the human visual system, can process 10 to 12 separate images per second, perceiving them individually.

How much (or what is the equivalent of) shutter-speed in those individual images?

Related Q?: Is it a limitation of the eyes or the brain that we cant see a moving bullet

See also http://en.wikipedia.org/wiki/Flicker_fusion_threshold

Many people can tell the difference between 60 FPS and 144 FPS monitors. Cameras and LCD's are changing from 30 to 60 to 120 FPS. Conversely, even professional gamers can't really tell the difference between 120 and 240 FPS monitors. That's not exactly equivalent to the eye shutter speed though, it can be because of eye tracking of lower FPS movement.

The light receptor of the eye is a protein called Rhodopsin.  To me the equivalent of shutter speed for the eye is the (de)sensitization of rhodopsin by phosphorylation.  The brighter the light, the more sites on rhodopsin are phosphorylated, diminishing the intensity of the signal coming from the photo receptor via the transducin G protein that conveys the visual signal onward.
This process takes a few seconds, but then it's possible to see when stepping into sunlight or in a darkened room.
This is more like a volume knob than a shutter speed since the same signal comes out at the same rate of each light sensor, but it has a similar effect — it modulates the intensity of the image.
Actually I feel dumb but there is a simple answer to this question.  You can get lost in the above physiology. The simpler answer is about 20 fps.  Whenever strobing stops and persistence of vision takes over to create a continuous image is an interesting way to answer this question.  That's how television and movies (and videos) work. 30 fps looks pretty smooth.  It's not a perfect answer because 60 or 100 fps are functionally useful for situations like video games where fast reaction time is important.

If we are comparing with a camera, I would say this is more like the ISO rather than the shutter speed.

good point.  the right answer might be the speed with which the optical nerve assembles the information from the eye.  that is harder to explain or define though.  nerves each act independently and do not synchronize the way a machine does.

There is nothing comparable to a shutter of the camera in the eye. The eyelid is like a lens hood. When the eyelid is open the image is continuously projected on to the retina unlike in a movie camera. However if the question is on frames per second (number of static images) required to produce a sense of seamless motion this article might be of some help. In video camera instead of a shutter speed it is the number of times the image on the sensor is sampled(recorded) per second electronically. The eye is more similar to a video camera. The retina has rods and cones which has variable 'refresher' rates which makes it more complicated to calculate exact figures.

Not all of your rods/cones fire at any given moment.  Exception is when a bright flash of light is viewed.  Recovery time from the resulting flash blindness is pretty slow -- seconds.  But there's some photobleaching there, so maybe that's not fair.


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How is RNA of retrovirus converted into cDNA?
The retrovirus (oncovirus) contains RNA. It also has a molecule called reverse transcriptase. This molecule transcribes RNA into cDNA. This cDNA is the DNA copy of viral RNA genome
RNA has Uracil instead of thymine and DNA has thymine instead of uracil. So, how can RNA be converted into DNA? Where does Uracil go and where does thymine come from?

RNA has Uracil instead of thymine and DNA has thymine instead of uracil. So, how can RNA be converted into DNA?

I think you may want to ask a more basic question.  DNA and RNA are extremely similar, with only an oxygen being the difference.  This has vast consequences for organisms, and life as we know it uses DNA and RNA for very separate purposes.  DNA stores the genome providing the instructions for life, and RNA in a nutshell is how that message gets converted into protein for a useful action.  RNA is generally less stable than DNA, so this arrangement works out well.
DNA is regularly and constantly transcribed to RNA, so Thymine is regularly used in favor of Uracil.  There is a fantastic answer here on Biology.SE already dealing with why so I suggest reading that.  The how is pretty straightforward, there are different molecules used!  DNA polymerases incorporate Thymine whereas RNA polymerases incorporate Uracil.  The reverse transcriptase that is encoded by the retrovirus does just this: it transcribes RNA to DNA, using Thymine instead of Uracil.  Both Uracil and Thymine are present in the cell and are thus available for use.

Does reverse transcriptase CONVERT rna to cDNA or is cDNA transcribed from RNA just as RNA is transcribed to DNA in cells ?

Transcribed, of course; sorry for the lack of clarity, fixed.

I think it might be of use to show you the difference between uracil and thymine

They are very similar structures. The part that is involved in base pairing is actually the Nitrogen and the  oxygen furthest from the sugar. See below:

So having an extra methyl group on the other side of the molecule does not interrupt basepairing. And remember, with DNA/RNA synthesis you have a template, and the new strand is based on the template. So, when the RT enzyme Medhat mentions encounters an adenine in the template RNA, it will pair it with a thymidine. And when it encounters a uracil, it is able to pair it with an adenine. The enzyme is structured specifically to only allow in thymine and not uracil, which is how it makes the distinction.


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The antibiotic 'kanamycin' in the growing of culture E. coli
I'm a first year student and I'm not sure if I understand correctly the role played by the antibiotic 'kanamycin' in the growing of culture E. coli (Rosetta).
Can anybody explain me why we use 'kanamycin' antibiotic and kanamycin resistance gene during that process?

Absolutely, Positive Selection
You are looking for the bacteria which have the gene (probably a plasmid) you (or someone else for you) put into the bacteria.  That gene lets them live in the presence of kanamycin, and any bacteria that don't have it, or that try to get rid of it, will die.  Thus you can select for the bacteria you want by killing everything else off (hopefully your sample is not contaminated with other bacteria also resistant to kanamycin).
I totally thought there would be a good wiki article on positive selection but there isn't.  The reason it's positive selection is that you are selecting for bacteria that have something; instead of negative selection where you would be killing them for having something.
You can find plenty more if you search "positive selection" or more generally "artificial selection."

According to this data sheet, the genotype of the strain RosettaTM(DE3)pLysS is F- ompT hsdS (r- m-) gal dcm (DE3) pLysSRARE (CamR).
This strain carries certain tRNA genes on the same plasmid as the LysS gene, and these tRNAs boost expression from genes containing rare (in E. coli) codons. The plasmid encodes chloramphenicol resistance (CamR).
If you have a protocol that suggests growing your strain under kanamycin selection then presumably you have an additional plasmid present which carries your gene of interest. Then, as the accepted answer says, you are selecting positively for the correct strain.
I don't know how stable the pLysSRARE plasmid is, but I would have expected that you should also maintain selection for chloramphenicol resistance.


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Does our DNA change during our lives?
As far as I know, DNA is the construction protocol of all organisms on Earth.
Does it change when influenced by time and environment (physical laws)?
As parents with schizophrenia are more likely to have children with schizophrenia and an individual with no genetic predisposition for schizophrenia can suffer from such a condition because of drug abuse or environmental influence, does this prove that human DNA is changing during our lifespan?

This question is more appropriate for a biology Stack Exchange. But the answer is that "yes, each cell's DNA changes over time." I think what you might mean though, is "does all my DNA change in precisely the same way?" and the answer to that is "no."

Changes in your DNA occur pretty much every minute of your life. You have trillions of cells, each of which contains about a meter of DNA. Tiny changes happen all the time.

I think this perspective in Science about genome mosaicism is appropriate here PMID:23888031. Basically, not only our genomes change, but it changes differently for each cell.

This related post will probably interest you

To quickly answer your question, yes DNA changes over the life time of many organisms including humans.  You have a whole host of mechanisms in your body that try to prevent your DNA from changing, but they are not perfect.
A good example of this is DNA degradation due to aging.  When discussing aging in biology, we use the technical term senescence.  Of interest here is the shortening of telomeres due to mistakes made in your cells as they continue to divide (copying the DNA to each new daughter cell).
In a grown adult, there's not some master well of DNA somewhere such that if you change it there it will immediately change the DNA throughout your body.  Most of the cells in your body have DNA in them (red blood cells are just one example of cells that don't have DNA in the traditional sense). Most of these cells can and will divide over time (mitosis) to produce new cells with copies of that DNA.  However, there are also plenty of cells that don't divide often or at all in healthy adults.  If one is concerned about schizophrenia, it would be important to note that many neurons in the CNS are in this group of static cells.
Considering environmental effects, there are plenty of things that can change your DNA. Radiation, gamma and x-rays in particular, do a great job of disrupting, degrading, and occasionally mutating DNA.  The class of chemicals and physical agents that can change DNA are called mutagens.  This shares a root with the verb mutate, which is when something is acting on genetic material to cause it change.
You will note that I said genetic material, and not DNA.  Without getting too far into the debate of what is "alive," DNA is most certainly not the only "construction protocol" for earthly organisms.  RNA is one common alternative, but there are weirder ones that are hard to describe like prions.

I have read that in parents DNA there is a code that guarantee their children to will more likely be proned to be better musicians or have better logic or just be better in something specific than other children.
If this is true does it mean that during my life part of my  way of thinking , my gifts will affect my DNA over time?
So for example if my 10xgrand mother was musician and my 9xgrand mother was musician and so on untill i was born
Does it mean that im proned to be musician and its coded in my DNA because of DNA changes in our geneological tree

@Flux your last comment makes no sense. Yes, you inherit characteristics (including, possibly, musical ability) from your ancestors. That does not mean that events during your life time will affect your DNA. Your DNA will change during your life because of damage and mutations but not because you become a better musician.

@terdon: see my comments to vonMises's answer. Epigenetic changes to the genome happen because of environmental changes, mutation is not the only way to change genetic information.

@nico of course, but do you really think that learning to play an instrument will result in inheritable epigenetic changes? And whether or not epigenetic changes are actually changes in DNA is debatable. Anyway, my main point was that I simply could not understand the OP's comment: "I have read that in parents DNA there is a code that guarantee their children to will more likely be proned to be better musicians or have better logic or just be better in something specific than other children." Can you?

@nico Darn.  After reading his comment, I was thinking about coming back to include info on epigenetics, but you beat me to the punch.  There are of course some really good questions not being asked here which are the subject of current research.

@terdon: I doubt there is a specific change for "piano playing ability", but I would not be that surprised whether there were changes to, say, genes involved in neurotransmission in cognitive areas of the brain. As for whether epigenetics changes are or not changes to DNA... well definitely methylation of DNA is a change to the DNA, that is really not debatable. I guess that strictly speaking histone modification are modifications of chromatin and not DNA, but that's nitpicking...

@nico I just said it was 'debatable', I did not specify my position in the debate :).

A DNA change will only be passed on if it occurs in a germ line cell (the cells that become eggs or sperm). If you have a mutation in, say, a liver cell, that will not be passed on.
But I dont think thats what you are talking about. From reading your question and comment closely I think the answer is "no". A person who becomes schizophrenic because of drug use does not become any more prone to having schizophrenic kids than a person who doesnt do drugs. Drugs can upset the chemical balance in your brain and that can mimic certain genetic diseases, but what happens in your brain because of drug use can absolutely under no conditions be passed on to your child.
In your piano comment things are slightly more complicated. Being good at playing piano is a result of a complex interaction of many factors, some of which may be genetic. A long line of pianists generation after generation may be a result of genes that, say, sharpen a persons auditory perception so they can hear and interpret notes better. However, I am sure that the parents encouraged piano playing and practice for their children, which is just as important.
But most importantly, playing the piano a lot will not in any way cause changes to your DNA that will make your children better at playing the piano. Your genes dont care how well you play the piano. Mutation is random, and that is the only way DNA can change.

A person who becomes schizophrenic because of drug use does not become any more prone to having schizophrenic kids than a person who doesnt do drugs. This is not that obvious. First, if drugs are taken during pregnancy/nursing they may as well influence the child. Second it is now well known that many drug can produce epigenetic modifications that, in certain situations, can be transmitted transgenerationally.

Mutation is random, and that is the only way DNA can change.. This is not true. Mutation is not necessarily random, mutagens may be more or less selective. Also, again, mutation is not the only way DNA can change, there are plenty of epigenetic changes that can play a big role in shaping behaviours. Just as an example, you may want to have a look at this paper: http://www.ncbi.nlm.nih.gov/pubmed/22941276

in response to your first comment, you completely ignored the second half of the sentence. I dont care that drugs can affect a fetus, they are not specifically going to change the fetuses DNA so that it has a schizophrenic gene

I understand the need to nit pick, and you are correct, but unless there is an epigentics paper that comes even close to doing what the OP is asking, I think saying "yea but sometimes..." will only mislead him.

sorry, but how can you say that it is impossible for a drug to affect a foetus so that it becomes schizophrenic? I can see many biologically plausible mechanism for that. Your answer is misleading because you are saying that the effect of the drug "can absolutely under no conditions be passed on to your child". Which is not necessarily true.

The key word is "specifically". What you are talking about is a non-specific effect of drug use. The fetus would be schizophrenic by chance. The asker is not looking to find out if a non-specific effect of drug use can be passed on. He is looking to find out if the DNA is specifically changed to a schizophrenic phenotype because of a specific trait acquired by the parent. The answer is an unequivocal "no". The fetus would be schizophrenic because of DNA damage, or brain damage done by the drug. It would not be "inherited" from the parent in any sense of the word

I see the question as much more general. "Does DNA change during our lives?". The answer is yes. Schizofrenia is meant to be just as an example...

It's become quite clear that your active genome changes all the time, due to various effects.  There is also gathering evidence that epigenetic changes can occur in somatic cells and be inherited by the offspring.  But these seem to be stress-related.
So, for schizophrenia: If the family had a gene that triggered schizophrenia, which was normally inactive, then stress/drugs could cause an epigenetic change which would make the "schizophrenia gene" active.  And this epigenetic change could conceivably (see what I did there?) be passed along to offspring.

+1, however it is to note that stress (depending on the definition of stress that you want to use, some are rather large) is not the only stimulus that can generate epigenetic changes. For instance maternal behaviour is well known for having epigenetic effects (e.g. http://www.ncbi.nlm.nih.gov/pubmed/15220929). Surely, you may say that at the end it is stress-related, as you modulate GR, but it is not directly caused by stress (again, you should define stress more clearly so we know we're talking about the same thing).

http://biology.stackexchange.com/questions/53406/any-dna-changes-inconsistent-with-its-genetic-ancestry

Are there any stimuli of any kind that have been observed to change a certain gene to change in a specific manner (specific chain). Can lived daily experience change an individual's spermatozoa genetic makeup (say over the course of days)


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Does Darwin's Theory of Evolution refute Terence McKenna theory "Stoned Ape" theory of human evolution?
I haven't read it but I'm asking for a quick answer.
As far as I know, Terence McKenna's theory of evolution in humans main concept is that a hominid has tried in their diet psilocybin mushrooms, and the experience they integrated changed their mind in a way that led to "us."

to call it a theory is seriously stretching the term. it barely qualifies as a hypothesis.

@user1136 I know of no paleontologist working on hominids who takes it seriously, it sets out to explain something that does not need explaining and does so with bad outdated psychology and just so stories. Worse it ascribes behaviors as unique to humans that we no are not, and that non existent uniqueness is what it pretends to explain.  It is not based on any paleontological evidence, and even the author of the study it cites for the effects the mushroom criticize it for grossly misreading the effects of said mushrooms.

How can one theory refute another theory? And you haven’t read it? And nobody has removed this in seven years! Let’s do it!

Briefly the "Stoned Ape theory" posits that psychoactive Psilocybin mushrooms in the diet of pre-Homo sapiens primates catalyzed the change Homo sapiens.  It suggests that the mushrooms conveyed selective benefits to consumers of the mushrooms, dissolving the 'egos' of our ancestors and allowing them to form communities.  It may also be sexual stimulant, goes the theory and so may have conveyed an advantage there.
I think this theory is not terribly popular now, but it is difficult to refute or to prove.  The only real proof would be to take a hominid or any other species and give them the fungus and see if they become intelligent.   Just because this has not happened does not disprove the theory.  the only other way to prove this really would be to have a time scope and look back and see what happened.  Its a similar question as to how life emerged on Earth.  We have some interesting evidence but conclusive proof is going to be hard to get.
I found a large collection of supporting evidence.  Even the definition of human intelligence and whether it is so unique is subject to debate.  Certainly there are other primates who appear to be as or more social than we.  I think other theories seem as or more likely.
Darwin's theory of evolution doesn't refute many theories of how something happens in evolutionary history.  The Panspermia hypothesis is taken quite seriously at this point - could it be that life originated elsewhere then was introduced here by meteorites.  The origin of Species doesn't have a lot to say about that.  I think the same is true for the emergence of human intelligence, which at this point we believe is unique on Earth.  Hard to make an irrefutable theory based upon a single example.

its fairly easy to refute, since the author of paper it cites on the effects of mushrooms has criticized it for completely misinterpreting the effects, and the timeline it predicts as well as the changes it posits do match the paleontological record. its refuted for the same reason a theory that humans coevolved with wolves 8 millions years ago is refuted, it doesn't match the fossil record in the slightest, regardless of the reasoning.

Refute?  No.
Shigeta summarized the work pretty well, and though I have my own opinions on McKenna's theory the fact is that Darwin and McKenna are not opposed.  The "Stoned Ape theory" is a specific idea for how human intelligence might have appeared from earlier hominids.  Darwin (and Wallace) proposed a broad theory that has borne out for the process of evolution by natural selection.  Evolution applies to populations large and small, whether human, primate, or bacterial.
Evolution, however, is not particularly predictive and would say nothing about what might happen should some primates eat some entheogens.  McKenna's idea could fit into reality, although as Shigeta said it is difficult to prove, but there is technically no Darwinian reason why it couldn't have happened.  Darwin did write about human evolution in The Descent of Man.

a belated thanks for the props... - 8 years later...lol

The stoned ape "theory" ("we owe our very existence as a species to psychedelics") isn't theory, despite it's pretense. There is no support for it in evidence, or in theory. Nor can there be because in its own terms it defies both. It's founder seems to have thought himself a genius, and solicited a cult-like following determined to spread his message, as their own. He had no college-level science education - see facts and citations below (*).
Bear in mind the "theorist's" target audience when he wrote Food of the Gods. Not scientists nor anyone scientifically literate. In his own words: "[The target audience is] the 18-25 year old group that is drug-friendly but has no rationale except that it's a good time" (Gracie, Zarkov & McKenna interview).
As for his understanding of evolution, the scope of his grasp, here's what he thought science says - if you believe what he says. No harm to have smelling salts in easy reach if you're minimally educated in biology, i.e. high school level:
"Conventional evolutionary theory tells us that small adaptive changes eventually become genetically scripted into the species" (OMNI interview)
Obviously that's 180 degrees backward from true or accurate, a recitation of what Lamarck thought - over 200 years ago, and before anyone ever heard of Darwin, or natural selection.
There's nothing theoretical in the "stoned apes" storyline, despite its claim. It's not a theory, its malarkey of the same type as Creationism - but from the opposite fringe: new age psychedelia, not old time religion.
(rolls eyeballs)
*TM was at quite a disadvantage for science ed. For any major in college, even liberal arts - there's normally a 'general studies' science requirement. Its a minimal basic in higher ed, across the board. But TM's college program (Tussman Experimental) is one that specifically, uniquely excluded science. And short-lived as it was, the college was roundly criticized in its day on that very point. Its founder made excuses, e.g. this quote (from Tussman's book EXPERIMENT AT BERKELEY):
"It is recognized that the program does nothing in the way of integrating science with the social sciences and humanities. We leave this two-culture problem for wiser men to solve. In this respect, however, our students are either better OR WORSE OFF than others" (caps added for emphasis).
Obviously lame? Colleagues in education didn't buy it. For example, this remark from Sidney Rosen (Univ of Illinois): "By his admission that he cannot find a way of integrating scientific ideas into a basic two-year program, Mr. Tussman is guilty of contradicting the educational goals he defends ... It is difficult for me to see how the curriculum can flourish without science as an integral part." - Journal of Research in Science Teaching 7: 271 (1970)
Prescient? The college didn't flourish, it floundered. It was already crashing when Rosen wrote that. In fact, the 'experiment' seems to have perhaps been a case of politics in education, masquerading as 'educational reform.' TM himself offers an interesting remark along just such lines:
"... it was an experimental program... this thing called the Tussman Experimental College. I arrived at Berkeley the year after the Free Speech Movement ... in an effort to keep the place from blowing sky high they had told this left-wing professor that he could have an experimental section of the university" (www.tripzine.com/listing.php?id=terence1)
This is the kind of info those who think they're all into McKenna, all about his rap and 'ideas' - have no clue.  Zero, none.  Knowing anything whatsoever, that's able to be factually established, double-checked and verified as true and accurate, valid - ain't its ticket.

Hi, whilst I wasn't involved in the original editing of your answer please be aware that the Stack Exchange model allows anyone to submit edits for peer review.  Please refer to this page for further help.

Thank you for the page link.  After reading it along with your comment, I can only conclude the policy you cite - as explained - is critically unclear and suborns tampering with posts, such as has happened with mine.  Thanks to your page link, I see five criteria specified for edits.  And I find that what was done with my post - violated not one, or two of them - but all five:

The other answers have done excellent job explaining how the stoned ape theory contradicts the Darwin's own theory of human origins. What remained unmentioned is that Darwinism have been the basis of the modern evolutionary theories for more than a century, and in this modern light there are even more glaring contradictions between the McKenna's theory and the reality.
More specifically, there is little to support this theory from the point of view of molecular and population genetics. One could imagine two scenarious here:

Consumption of the psychoactive mushrooms was a single event that triggered a germline mutation in the most-recent common anscestor of the modern homo sapience (pretty much in the same way as cancerous mutations are known to be triggered by exposure to toxic substances). Note that this scenario, tracing our ancestry to a single mutant, already contradicts the McKenna's picture of a mushroom consuming prehistoric culture. Moreover, divergence of species requires more than a single mutation, and it is improbable that multiple beneficial mutations could have arisen this way.
The psychoactive mushrooms could have been a part of the diet of homo erectus throghout hundreds of thousands of years - sufficient time for accumulating enough mutations to evolve into a separate species. While these mutations could make humans more adapted to surviving while being stoned, they are no replacement for mushrooms. In other words, the effect of mushrooms would disappear once their use was discontinued, leaving a species with a doubtful benefit of adapted to survival while being stoned (any evidence that drunk or stoned people are less likely to harm themselves in dangerous situations is at best anecdotal).

Let us finally note that McKenna's time scale for homo sapience diverging from homo erectus (100,000 BCE) is at odds with the established paleontological scales. In fact, it even post-dates the humans common ancestor with Neanderthals and Denisova people (about half a million years ago), which is attested on genetic level for both neandertals and densova people.

@user1136 I think that the only way it may not contradict the modern synthesis is, if we assume that homo sapiens had already existed as a species capable of consciousness, and the mushrooms only served to wake this consciousness. This is even more so for language, since it requires specific physiological particularities, which many apes simply do not possess.

@user1136 I don't know that there are many, if any, serious neuroscientists who would claim consciousness is in any way unique to humans. There is no gap.


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Is it possible for two brown-eyed parents to have blue-eyed child?
Here's the (real) story: A young man has stunning blue eyes. On his mother's side are lots of instances of blue eyes, but on his father's side is no history of blue eyes. Both parents have brown eyes.
When he was born, with these bright blue eyes, it was considered a "miracle". As an adult, he still has these potent blue eyes.
How is this possible?
I obviously understand the popular science behind dominant and recessive genes. The mother could be Bb, but if the father was BB, it doesn't seem possible that he could have blue eyes... but I've read more on eye colour recently, and it appears to be a lot more complicated than I initially thought.
For example, this article goes into some detail explaining How Blue Eyed Parents Can Have Brown Eyed Children, but I've not seen anything that talks about it being the other way around: Could a BB parent have a bb child?
If so, how? And what is the rough probability of such a thing?

Possible, yes but probable, no. (I assume that the history of the parental family as you mention is important)
Let us first consider HERC2 (H=brown, h=blue) and OCA2 (O=brown, o=blue) as per the names mentioned in the reference you cite, to be completely unlinked, such that they are independently assorted. Since the father's lineage has no history of the recessive phenotype(blue), and the genes segregate independently (our assumption), we can conclude that the father is homozygous for the dominant allele in both the genes(HHOO). In this scenario, it is very unlikely to get blue eyed children, but is still possible in the following two ways:-

The father's lineage does have a recessive gene (which probably entered his family gene pool due to non-consanguineous mates carrying a heterozygous phenotype in either of the gene pair HERC2 or OCA2), and has evaded expression by pure chance or because the recessive gene carrier entered into the family very close to the father,i.e. probably just one or two generations above the father(so that not enough generations have passed to allow the homozygous recessive trait to develop). In each of these cases, one or both the gene loci in the father might be heterozygous(HhOO or HHOo or HhOo) and coupled with the mother's heterozygous genotype(a good guess considering the history of many recessive phenotypes), might produce a blue-eyed child due to homozygosity in any one of the gene.
There is a mutation in the germinal cells of the father which creates a non-functional mutant allele and thus can give a blue-eyed child with a heterozygous mother.
But in either case, considering independent assortment, the chances are very bleak.

But if we also take into account the linkage of the two genes, then the probability rises significantly. Now there is a good chance that the father's lineage might contain a heterozygous (or homozygous recessive) allele pair on a single chromosome, which due to their tight linkage, might pass on without any recombinations and therefore might evade phenotypic expression more efficiently(although, since a dominant allele in both the genes is required for the dominant phenotype, the extra evasion efficiency due to linkage is less). As given at the end of your reference, suppose there is one chromosome in the parental ancestry that carries both the recessive genes. If they are linked, the chances of brown eyed parents to have blue eyed children decreases (and the chance of being heterozygous also decreases) thus making it more likely that the father's lineage could have a recessive allele in spite of there being no significant expression in his family history. Therefore, more tightly they are linked, greater is the probability that the father is heterozygous. Linkage does not significantly lessen the possibility for the father to have a blue-eyed child since the mother does contain a recessive linked- phenotypic pair in all probability. (Actually, the probability is also based on which combinations are linked, but the possibility of there being a heterozygous allele remains positive with most combinations).This again gives some chance for brown eyed parents with the history you mention, to have a blue eyed child.
In any case, there is a chance but the probabilities depend a lot on the linkage, the linked combinations, and the actual genotypes of the parents but there is always a possibility.
ADDITION
Just to add a bit of information, the kind of recessive epistasis we described here, where the homozygous recessive (at the hypostatic,HERC2, loci) phenotype resembles the phenotype for the recessive condition at the modifier pair (OAC1), is only a part of the story. Actually, certain polygenic influences further complicate the situation by introducing a variety of phenotypes.

Nice answer, +1. Could you tone down the bold and italics please? It's really hard to read.

@terdon Sure. On reading the answer after all the boldifying and the italicizing, I could see what your concern was! I have already toned down quite a bit, however, feel free to reformat my answer according to your aesthetic understanding as I am not much of a formatter.

its worth mentioning that many babies are born with blue eyes, even those of african descent - it can take several months for pigment to start up.

@shigeta That's good to know, but in this (real life) case, he's now in his 30s with the same stunning blue eyes.

It's also worth mentioning that the example suggested is incorrect. Human eye color is multigenic (i.e. MORE than 2 genes, probably more like 7) with more than one possible allele per gene. Epistasis can certainly occur, and combinations can happen which give rise to very uncommon colors, such as yellow. A simple one or two gene model will suggest brown eyes can't have blue eyed kids, and that is incorrect. This also ignores the frequent occurrence of mosaicism at the tissue level, which can yield kids with two different eye colors, or irises with two colors within them, which neither parent might have shown.

Can you please add some references?


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Would I still exist if
I've been wondering for some time, but say that my mother's egg chose another sperm cell, and a baby was eventually produced. Would I still be born, but end up with different characteristics/features?

Sorry but this is not a real question. What makes you you? If you have different characteristics how can you be you? Also, the egg does not choose sperm, where did you get that idea?

I, as in being an entity that can perceive the world. Let's Ignore the extra features like hair, eye color, etc.

Well, yes, just about any sperm with any egg would produce a human being that could perceive the world. How would we decide if that's 'you' or not?

I was hoping someone would have an answer to that.

consciousness and awareness and in fact a brain develops long after fertilization.. i hope that clears your doubt

@terdon This is a legitimate philosophy question. Not biology, though.

For every sperm that fertilises an egg there are millions/billions/"a sh**load" that don't make it. Within that pool of unused sperm there is considerable genetic variation. If we assume that DNA is the only factor which makes "you you" then the chance of picking one of those  sperm and it having the exact same DNA is small. Of course environment also has a large effect so even two identical sperm and egg combinations would produce two people with different physical and mental attributes.
If this does not answer your question then this is not really a biological question though and should really be on the philosophy SE.


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Identify this spider
I found this spider on my balcony in Sunnyvale, CA. It sat in a irregular net. The body was approx. 6mm long. Which species does it belong to?

That's a Western Black Widow subadult female.  The banded legs, with dark 'knees' and lighter brown intervals, become all black as the spider matures, just as the bands on the body disappear as it becomes all black.
Below is a slightly older one, where the center stripe is beginning to turn red.
Your first clue is the irregular web, characteristic of the Theridiid cobweb spiders.  The second clue is the robust body and legs, with especially long first and last pairs.  The key field mark, if you had seen the underside, is the red or orange hourglass.  It is clearly not any kind of orbweaver, simply from the web; and none of the several sorts of Argiope look anything like this spider.
Be aware that this spider can give quite a potent bite (although they often don't, preferring to hide, and not biting unless endangered).  Like the other Black Widows, they are best not handled, just in case.
https://bugguide.net/node/view/1458045/bgimage