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Mutations, Death and the theory of Evolution
Evolution always made sense to me and I still find it to be true. However, I quite recently found a comment online that gave me some doubts and made me curious on the subject. Although a student of biology, I don't really know genetics all that much (I'm more of an ecology type), so I'm asking here - I hope there's somebody who can help. Without further ado, how would you respond to this comment (fyi the original post was on the subject of a woman denying evolution, then talking about her new short-eared dog breed):
"The woman was probably demonstrating that changes that we see in dogs (variation within one kind) is NOT Evolution because it cannot create new genetic info (so it cannot explain the origin of organs). It causes CHANGE with what is already there, and these changes are only NEGATIVE or NEUTRAL (but often negative, that's why our dogs are degenerate from wolves). I used to make a living out of Selective Breeding so I know that you can only change a fish's color and size but you can never add feathers or wings or limbs to it since the codes for those doesn't exist in a fish, nor can we create one just by random mutation. That's like trying to create Windows10 OS by relying on random bit-rot/data corruption -- death of program is ensured. The word "engineering" in Genetic Engineering isn't there for no reason. Coding genetic programs requires more intellect than coding binaries. Literally, we're all digital programs (but very intelligently coded). Welcome to modern science.
Having said that, you do realize that the reason why you grow old is because of mutations, right? I will be neutral here (neither Evolutionist nor Creationist) but let's be realistic. If mutations can improve us, why do we grow old and die from it even though our body undergoes "selection" too? And you do know that our genome as a population is also getting older, right? Let's math this out: Let's say you're Adam with no mutations yet. Your offspring will inherit an average of 50 mutations from you (you generated this mutations as you grow old). Let's say that we die when reaching 10,000 mutations (Natural Selection). Your offspring started his life on earth a little bit older than you. And he shall add your 50 mutation, plus his own 50 mutation to his offspring. The 3rd generation will now start his life with 100 mutations. Some may mutate faster, but since ALL organism mutates and pass it down, it's easy to see where all of us will end up. Think of your last PC. :)"

Welcome to Biology.SE. I read only the first paragraph which can be summarized into "Consider the following claim:". I am too lazy to read what follows. You should try to drastically shorten your post if you want the attention of people who can answer. Also, I am sure you can make a title that at least specify a little bit the subfield within the field of evolutionary biology.

Also if you have a quotation, please indicate the link and use the quote format (start the line with >)

I've changed your title to demonstrate that the length of your question does not preclude a short indicative title. You should do this yourself next time — it's an important part of the analytical process.

This question rambles a lot, has lots of misconceptions, and I don't see what exactly it is that is being asked. VTC.

@MarchHo What does VTC stand for? non-native english speaker here : )

@Remi.b Vote to close, I would guess.

It's very sad to see an "ecology" fellow that knows so little biology to ask such a question.

"The woman was probably demonstrating that changes that we see in dogs (variation within one kind) is NOT Evolution because it cannot create new genetic info (so it cannot explain the origin of organs)." ...  Simple answer, the woman is an idiot.

@Eli Korvigo Not everyone had the luck to be born in a country where evolution isn't taught for only one day in primary school and high school, where teaching evolution isn't almost a taboo and where you're not ridiculed by the general public if you accept evolution as true, while religious education is mandatory in both primary and highschool. I live with people who think that rain and thunder are the sign of God (whatever your stance on his existence might be, you understand how ridiculous that argument is).

Introduction
Welcome to Biology.SE. Please see my comment for issues relating the form of your question. Below my answers are very short as it would take too long to give complete answer. I just redirect you toward a source of information.
Questions

Having said that, you do realize that the reason why you grow old is because of mutations, right?

No, that's wrong!

I will be neutral here (neither Evolutionist nor Creationist) but let's be realistic. If mutations can improve us, why do we grow old and die from it even though our body undergoes "selection" too?

Nope, our body does not undergo "selection". (At least not in any way you may have meant it!)

And you do know that our genome as a population is also getting older, right?

No, that's wrong!

Let's math this out: Let's say you're Adam with no mutations yet.

There was no such thing as a first human and no perfect human free of any deleterious mutations. Adam and Eve are characters from the christian mythology (kind like the equivalent of the first unnamed man Epimetheus and Prometheus created and Pandora (first woman) that Zeus created to punish men).

Your offspring will inherit an average of 50 mutations from you (you generated this mutations as you grow old).

Good job, this is a relatively realistic number (although a bit too high) of new mutations a human baby inherits. Note that these new mutations occur in the ovaries and in the testis either during mitosis or during the meiosis (mutation rate is much higher during meiosis).

Let's say that we die when reaching 10,000 mutations (Natural Selection). Your offspring started his life on earth a little bit older than you. And he shall add your 50 mutation, plus his own 50 mutation to his offspring. The 3rd generation will now start his life with 100 mutations. Some may mutate faster, but since ALL organism mutates and pass it down, it's easy to see where all of us will end up. Think of your last PC. :)"

Most mutations are neutral. Those that are deleterious are (most often) washed out by selection and therefore do not accumulate in the way you describe.
Source of information
I cannot provide complete answers as it would unfortunately be too much for a single post. Instead I redirect you to an online source of information.
There are great (free) online courses. Consider for example having a look at Understanding Evolution (by UC Berkeley). It is a very introductory source of information on evolutionary biology. It is quite short and you will quickly learn a lot!

In addition, the "change" argument of OP could be addressed by Glassford et al. 2015 http://www.ncbi.nlm.nih.gov/pubmed/26343453 and the "engineering" for circuits by the existence and results of a full research field (dedicated to evolvable hardware)

I like that you gave the OP a heads up with the "Good job". However, the approx. 50 mutations in a newborn are not really introduced in the aging process of the parents, but rather emerge due to error prone DNA replication. The actual number of mutations might be higher in case of older parents (increasing replication error with age), but that is not what the OP is suggesting.

Yes, you are right. I added a small comment. I did not want to go too technical. I had to use the terms mitosis and meiosis that the OP likely don't know though. Feel free to edit if you can avoid that the OP misunderstand the answer while remaining short. Thanks

Interesting, but growing old and mutation has nothing to do I guess. it's a common sense. but the starting arguments are quite convincing. What do evolutionists says to the argument that 'genetic engineering' can only turn switch on or off the current DNA and cannot make something new? This 'genetic engineering' is a form of what natural selection can do the creatures I guess.

Thank you a lot for answering! The part of the post in quotation marks was not actually mine, I just saw that comment on a site and wanted someone with better knowledge than I have to explain what might be wrong with it. I decided to copy-paste it because I thought I might leave out something important otherwise.
Also, please forgive my lack of knowledge, when my teachers got to the subject of evolution they (I guess?) were required to keep it very neutral while teaching, supporting neither side. I hope to learn more in uni now :)

You don't have to apologize for your lack of knowledge :) I understand how religious extremism (probably christian extremism given your reference to Adam and Eve) can try to restrict access to knowledge when the reality does not match their preconception. I hope you won't take any downvote and close vote as an offense. It was quite impossible to answer such question but you did well to ask and you are very welcome to come to this site to keep learning. If you come back for evolutionary biology, then I would recommend first having a look at Understanding Evolution (or other online resource).


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Why aren't all animals cold blooded?
At least, why don't all animals produce no more heat than the tiny amount that's a byproduct of walking or a bonobo climbing up a vine when the outside temperature is above 0°C? They won't freeze anyway.
After all, the amount of food controls the population size at whatever size makes each individual have just enough food, so shouldn't those with a lower energy demand be more likely to get enough food to rear more children? Shouldn't mutations that make a warm blooded animal able to thrive with a lower core temperature and produce less heat be selected for because there's more likely to get enough food to rear more children?
Also, shouldn't cheetahs evolve to produce extremely little heat in the day during rest even on not very hot days so they will be less hot and can chase their prey for longer? Have they already evolved that way?
If a species did evolve to produce less heat, would that also evolve to walk slower because it takes a lower speed to minimize the energy burnt per distance because they're producing less heat? I know there there will be a nonzero speed that minimizes the absolute minimum possible energy burnt per distance possible to evolve for that speed and a lower speed will actually increase the energy burnt per distance because the animal is walking for a longer time but the rate of energy burnt per time varies less rapidly with speed at such low speeds because of the energy burnt to fight against gravity.

Life on Earth is thriving, it's not just surviving on the edge. This leads to organisms with a high power to weight ratio. Energy efficiency does play a role, the less energy you waste the higher you can make the power to weight ratio for a fixed weight. But there is no need to keep the maximum power at some very low value.

Having a warm temperature allows body chemistry to happen more easily, move muscles faster, etc. That would be the advantage. When it's cold, reptiles can't do much, but mammals can. When it's too hot, reptiles suffer from heat and need shelter just like mammals.

Cold/warm blooded are misleading categories
The terms cold blooded and warm blooded is very misleading as it gives one the sensation that animals may warm up their internal temperature for the only reason of warming it up.
The terms homeo-, poikilo-, exo- and endo- terms are much more useful in thinking about control of body temperature. Have a look at this post and this post to understand these terms. Make sure to really read these posts to correctly understand these terms and how they interact.
Reformulating your question
What people, in general mean by cold vs warm blooded animals is whether they actively control their body temperature or not. That is cold blooded would mean exotherm while warm blooded would mean endotherm. As such the question becomes "why would any animal care about being endotherm if the body temperature won't go under freezing point anyway?"
Answer
Any metabolic pathway is affected by temperature. A change of temperature of only a few degrees can drastically affect the rate of chemical reactions. Homeotherm individuals (often homeotherm thanks to endothermy) are able to keep a quasi constant level of activity despite external change in temperature. It allow them to forage during hot and cold whether for example. This is a very important advantage but it often comes at the important energy cost. It is a trade-off between the benefit of homeothermy vs the energy cost of endothermy that will define the best interest of an organism.

Absolutely. Also, although it's fairly obvious once you think about it, I would complete the explanation by highlighting that it's easier to achieve and maintain a relatively stable body temperature that is higher than your surroundings than one that is lower than your surroundings...

Maybe for a lot of species, it's because being a poikilotherm would necessarily come with a costly trait because they reproduce sexually. Maybe if they reproduced sexually, they would have evolved to be poikilotherms because that would come with a much smaller costly trait.

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What is this wasp killing insect?
I spotted these two in my garden.  What is this insect?  He had firm control over the wasp and was just hanging on by one leg.  He appeared to hold on until the wasp stopped moving and then flew away with it.
I live in Ohio (USA). The wasp was a bit less than 2cm long while the other insect was about 2.5cm long.

Nice pic +1! What country do you live in? What privince/state/bundesland/etc.. do you live in? What size do they have approximatively?

I'm the United States, Ohio.  The wasp was regular size, maybe 3/4 inch long and the other insect was slightly larger, maybe 1 inch long

Given the large eyes, the almost non-existent antennae, the humped back, elongated abdomen and the wings, I'd say it is a robber fly.

It is one of many insects known to prey on wasps.
Note the description on the linked page:

This spindly piece of nastiness is a Robber Fly in the genus Diogmites. It seems that it's members of this particular genus that are adorned with the name Hanging Thief. You may remember that this was to denote their habit of dangling from a leg or two while the other limbs held onto prey, stabbed it to death with venom and then sucked out the insides. [Emphasis mine.]

Fun fact: They perform 'extra-oral digestion', meaning they extrude digestive enzymes onto/into their prey before ingesting them.
Not so fun fact: Those enzymes burn. I had one of these land on my arm once and try to digest me. I do not recommend it.

Interesting convergence with spiders: dangling system and extra-oral digestion.

@n_b I saw your username at the end of the post and did a double-take, thinking that it was some kind of an emoticon to express the pain.

Wow, don’t know who gave a bounty, but thanks! Hope all is well.

@anongoodnurse Charles gave you this bounty!

Maybe worth adding (info about the venom):  "Robber ﬂies are capable of incapacitating large and dangerous prey quite rapidly, depending on thesite of venom injection, and they can deliver painful bites to humans . Recent studies have described over 300 venom proteins and have organized novel venoms into ﬁfteen ‘Asilidin’ protein families, using the taxa Eutolmus ruﬁbarbis,Machimus arthriticus,Dolopus genitalis, and Dasypogondiadema." ..

.. "Some of these venoms are species-speciﬁc, consistent with observations of variable venom toxicity between species demonstrated by previous authors. Toxicity assays of crudevenom or isolated components have shown paralytic and other neurotoxic eﬀects in insect and mammalian subjects. "  Source/publication:  https://www.researchgate.net/publication/347161201_Pick_Your_Poison_Molecular_Evolution_of_Venom_Proteins_in_Asilidae_Insecta_Diptera

@iLuvLogix - They asked for an ID, not a lot of information on it. I tend to answer the question. The rest is superfluous.

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How do poikilotherms thrive in a wide range of core temperatures?
What is it about the metabolism of a poikilotherm that enables them to adapt to the surrounding temperature?

I guess the answer lie mainly in (1) they stop all activity outside their comfort zone, (2) they spend time to control their internal temperature through behaviour (sun bathing or sun avoidance typically) and (3) their biological pathway are relatively not too sensitive to temperature change. I am not sure (3) is really a thing!

Do they thrive in a much wider range of temperaures than usual but regulate their temparture to within that large range by controlling where they go?

I do not understand your question. Could you specify what you mean by "what is it about ..."? Metabolic reactions are chemical reactions and therefore not extremely sensible to temperature changes, unless you are looking at reaction rates. You do not need special adaptations to being poikilotherm as this is life's (and dead matter's) status quo. This means that the metabolism of poikilotherm animals reacts (more or less, see Remi.b's comment) passively to temperature whereas homoiotherm animals have an actively reacting metabolism that creates it's own constant temperature.

I'm not an expert in this topic but I have read a reasonable amount on animal thermal regulation, especially in insects, so maybe I can give some insight into your question.
First of all, an important thing I learned is that one must differentiate poikilotherms from homeotherms and endotherms from ectotherms.
According to Randall et al (1997):

Endotherms are animals which generate their own body heat through metabolism, while ectotherms have a hard time generating enough body heat to maintain their physiological functions, as they have low metabolic rates.
Homeotherms are animals which are able to maintan their body temperature at a more or less constant rate, while in poikilotherms body temperature fluctuates more or less with the environmental temperature.

This a somewhat troubling classification. Insects, for example, are considered ectotherms/poikilotherms, but they may show a condition called heterothermy: they are (most of the time) ectotherms, but they may be able to generate heat through some metabolic activity, and in this situation, they are showing endothermy. This happens quite often in winged insects, which may raise their body temperatures by flapping their thoracic muscles which move their wings. They may also ventilate themselves using their wings, lowering their body temperature, which (I'm not sure about this) may be considered an endothermic behaviour, as they are lowering their temperature in spite of the ambient temperature. Bees and wasps are even able to control their nest temperatures when the whole colony uses their wings to heat or cool their nest. So classifying animals in one of these categories is not so straightforward, but I'm just pointing this out because this is important. I don't think this invalidates your question, so I will talk about poikilotherms/ectotherms for now on.
One important thing to know about these animals is (Randall et al 1997):

Often, ectotherms have low rates of metabolic heat production and high
  thermal conductances-that is, they are poorly insulated. As a result,
  heat derived from metabolic processes is quickly lost to cooler
  surroundings. Accordingly, heat exchange with the environment is much
  more important than metabolic heat production in determining an
  ectotherm's body temperature. On the other hand, the high thermal
  conductance allows ectotherms to absorb heat readily from their
  surroundings.

As for how they control their temperatures...well, there are lots of mechanisms. I'll state some of them.

As Remi.b stated, behaviour is an important mechanism of temperature regulation in poikilotherms/ectotherms. This happens with basking/avoiding sunlight (as previously said), but also happens in the example of wing flapping I mentioned. Another interesting behaviour mechanism for temperature control is microhabitat selection: desert ants, for example, may face soil temperatures as high as 70° C when searching for food. They lower the harmful effects of such a high temperature by standing high on their legs and/or climbing onto small grasses or rocks which they find through their way. This may seem useless to us, but it plays a big difference between life or death for them (Marsh 1985).
Some animals have antifreeze substances in their blood which prevents them from freezing to death (see Randall et al 1997). This is common in arthropods.
Colour may play an important part in temperature regulation, as lighter body colours make the animal absorb heat less quickly than darker colours.
Some bumblebees may heat up by producing heat at the cost of ATP (a clearly endothermic characteristic) (May 1979).
Body size plays a huge part in body temperature regulation, not only in endotherms, but in ectotherms too. Lighton et al (1994) demonstrate that bigger workers from a species of ant called Veromessor pergandei can withstand dessication from higher temperatures for longer than smaller workers (and they show only a few milimeters difference in their sizes).

Well, as you may see, I don't think there is a straightforward answer. The way I look at it is that, as almost anything in biology, different organisms may show different strategies of coping with thermoregulation. I suggest you take a look at the following book if you want to know more or if I haven't quite answered your question (and the articles I have cited are the ones below):
Book: Randall et al. 1994. Eckert Animal Physiology: Mechanisms and Adaptations. W. H. Freeman  and Company.
Journal articles:
May, M. 1979. Insect thermoregulation. Annual Review of Entomology.
Lighton et al. 1994. Is bigger better? Water balance in the polymorphic desert harvester ant Messor pergandei.
(The name of the ant above changed, that's why I called it Veromessor pergandei)
Marsh, A. C. Microclimatic factors influencing foraging patterns and sucess of the thermophilic desert ant, Ocymyrmex barbiger. Insectex sociaux.

I want to know how they thrive in a wide temperature range and don't want an explanation of how they avoid extreme temperatures outside that large range to be instead.

I have some ideas on your comment, but first I must understand something: you're stating poikilotherms are able to withstand a wider environmental temperature range than homeotherms, is that so? Why do you think that? I see no reason for that being true (if you've read it somewhere please tell me where, because I'd like to know if I'm wrong).
Also, the mechanisms I talked about are not necessarily ways of dealing with extreme temperatures only, they are, most of the time, ways of coping with a temperature range.

I once saw a page that mentioned the word poikilotherm and described what it was that I can't find anymore then I searched for the Wikipedia article https://en.wikipedia.org/wiki/Poikilotherm.

What the article says is "A poikilotherm is an organism whose internal temperature varies considerably". That does not mean that poikilotherms can withstand wider environmental temperature ranges than homeotherms. If a poikilotherm is in an environment in which the temperature ranges from, say, 10° C to 30° C, its body temperature will vary acordingly (10° C-30°). If a homeotherm is in the same environment, its body temperature will be always, say, 28° C, independently of environmental temperature. But both of them can thrive in that environment.

I fixed the title of the question to be what I meant it to be all along.


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Does protein structure depend on phylogeny?
Proteins have two basic secondary structure forms - beta strand and alpha helix. Do these depend on the organism or do the two forms exist for every protein?
For tertiary and quaternary structure: do such motifs depend on the position or does each organism have a specific form of protein structure?

Welcome to Biology SE. However I am afraid your question is too general and at a very basic level. You can learn about proteins by carefully reading information available on the internet, for example sections such as this in Berg et al. or the entry in Wikipedia. If, after studying the examples there you are still confused, come back with a well-formed question.

The OP asks what is the relation between levels of protein folding and phylogeny. It's a good question, I think it could be rephrased with the aid of a native speaker.

I agree with @David - this question is exceedingly basic and should be understandable by reading textbooks, websites, etc - it is not a very well-formed question.

@Rodrigo Although I tend to agree with David on this, and I think you re being generous in assuming it's about folding and phylogeny, it is possible the question is good.

@Muna Ar : What do you mean by 'depend on the position'?

@gilleain I mean in the those structural motifs may vary when we change the position we are in the protein for example , the beginng of the chain or at the end ...

@MunaAr I see  - the position along the chain. I think that the answer is : no, there is no strong dependence of secondary structure on chain position.

@gilleain so if a protein folds into a tertiary structure having a zinc finger motif  for exemple , that would be all along the chain right  ?Sorry I'm newbie in the domain

@MunaAr I assume so - but I haven't actually checked. That could actually be a good question just by itself : "Are there any motifs whose frequency depends on position along the chain?" or something like that.

Beta sheets and alpha helix are secondary structures that are simply very common to proteins. Their formation depends on the Amino acids that make up particular stretch in the primary sequence. For example alanines in a row will naturally tend to twist up into a alpha helix in water (medium matters). There are no hard and set rules to determine Tert. Structure or quart (aside from modeling but you have to validate in the end so its not entire end case)

So the tertiary and the quarternary  depend on the protein , it could have a tertiary or quart as it could not right ?

Tert depends on primary sequence and environnment. Quart depends on some level of symmetry in tert structure that allows for optimal contact between subunits


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Human Blood vessels,
Why is blood drawn from veins? Is it because veins have a large lumen? Or is it because the blood is flowing at a lower pressure and makes discharge easier? Is it safer to draw blood from veins?

If you draw blood from arteries,it will spout out because the arterial blood flows at some pressure. Moreover, it is too hard to stick a needle because arteries consist of thick blood walls.


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How do we know that our genetic similarities to other species is actually due to common ancestry?
I know all about how the fossil record shows more human-like species coming about over time, and how modern testing proves we have genetic similarities with other animals.
All that says is we have similar genetic blueprints to animals in the past and present. How do we know these similarities are caused by having a common ancestor?

I don't believe in evolution, it's like saying 'similar' => 'come from'. But every various things inherently have similarities and dissimilarities. don't they?

That's why people in science field keep looking for physical evidences and study them. It's a very very long process and will take years to know the answers..... it's like you're studying the vast universe and wondering if there are alien life forms out there..... so difficult and still unknown.

@ChanKim Your implication reveals a massive misunderstanding of evolution and, in evolutionary terms, is plain wrong. No wonder you do not "believe" in it.

You should have a look at this highly related post and at Demonstrable and repeatable examples of evolution

If you want a short and very introductory course to evolutionary biology you should have a look at Understanding Evolution by UC Berkeley.

I think a major misunderstanding that could be coming in to play here is the misconception that DNA is like a engineering document, e.g. "this strand of DNA says i will have an arm with 5 fingers of certain proportions, this strand of DNA says I will have a facial structure like this.", and not realising that it appears our DNA is full of junk "data" that doesn't appear to be active or serve any purpose, and that even this "junk" un-used DNA is common between believed-to-be ancestors. It would be like throwing a dice in two sets of a thousand and getting results that are 80% the same order.

We don't know, and we never will. Science doesn't work that way. But evolution is the simplest hypothesis that is both falsifiable and consistent with lots of experimental data. Therefore it is the currently accepted scientific theory.
I would agree that genetic similarities between current species does not in itself suggest that they evolved from a common ancestor. But knowing the genome sequence of various species let's you do much more than simply measure pairwise similarity between species. The structure of genetic variation (losses, duplications, inversions, mutations ... ) also fits with evolutionary models. And crucially, genome sequences confirm predictions made by the evolutionary theory --- evolution is not just a post-hoc explanation of data, it has actually been tested many times over, and has never been falsified.
A good example is the sequencing of the human and chimpanzee genomes. We knew long before any genome was sequenced that humans have 23 chromosomes (23 pairs), while chimpanzees have 24. If the theory of evolution is correct and we do have a common ancestor, then that ancestor should have 24 chromosomes, like the chimps do, and it must be that in humans, one chromosome is a fusion of two ancestral chromosomes$^*$. This is a strong, testable prediction: if we don't find this arrangement of chromosomes, then evolution is proven wrong! In the 1980's, the sought fusion chromosome was found using high-resolution cytogenetic banding: it's chromosome 2. Modern genome sequencing later localized the precise fusion point on the human chromosome.
Also, the fossil record provides a timeline, not just a bunch of more or less similar organisms. In general, we don't find old fossils of modern-day animals (including ourselves), but we do find old fossils of species that no longer exist today. And when piecing together the findings, it looks like there is a sequence of gradual changes over time. That's a pretty good clue. What hypothesis might fit this data?
If you are suspicious about the theory of evolution --- which is fine, you should think critically about everything in science! --- then you must look for an alternative hypothesis which is falsifiable and fits the data. (Note that "god made everything" is not a falsifiable hypothesis, since it makes no testable predictions, and therefore not relevant to science.) If you come up with anything, let us know!
$^*$ As pointed out in comments, a priori one could imagine other rearrangements between the ancestor genome and the chimpanzee/human genomes that give the same result, but I believe this is the simplest hypothesis.

Just to clarify, we "don't know" in the same sense you can't know whether it's better to leave an apartment through the front door, or the window on the second floor...

"We don't find any old fossils of modern-day animals" -- but when you do find a coelacanth, MOST IMPORTANT PRESERVE SKELETON AND GILLS ;-)

@SteveJessop, All right, there are some current species that have changed little in recent evolutionary history and so we do find fossils of them. I was trying to describe the general trend.

@Cephalopod  Not sure what you mean. I meant "we don't know" in the sense that the scientific method (within Karl Popper's paradigm) does not prove hypotheses, it only disproves. Those hypotheses that are still not disproven after lots and lots of testing are accepted as theories. Like evolution, for example.

Nitpick: why couldn't it have been that the common ancestor of humans and chimps had 23 chromosomes, but in the chimp lineage, one of them split?

@zwol, Very good point! I didn't mention it, but we know the chromosome did not split because human chromosome 2 has an extra centromere, derived from the other ancestral chromosome. This centromere is no longer functional in humans, but clearly recognizable from sequence data. So there must have been a chromosome fusion event.

But we didn't know this before, did we? So we didn't have to find "exactly this arrangement". Could have been any number of fusions and splits of chromosomes. Also, I don't see why our last common ancestor needs to have had 24 chromosomes.

@BlindKungFuMaster, If you consider additional fusions/splits, they would have to happen independently in the same way in both the homo and pan lineages to generate two genomes that look like they are just separated by a single fusion event. That's very unlikely to occur by chance. So by far the most likely hypothesis is a fusion in the homo lineage, which implies the ancestor must have had 24 chromosomes.

@Roland you haven't explained why we would expect to find a fusion in homo rather than a split in pan, without already having looked

In your answer you derive the prediction based on the number of chromosomes alone. To me the numbers would only imply that the difference between fusion and split events in the homo lineage is one higher than in the pan lineage. If more information went into the prediction, like "the look" of chromosomes, maybe you could expand on that.

"Note that 'god made everything' is not a falsifiable hypothesis, since it makes no testable predictions, and therefore not an option." What do you mean by "not an option"? I'm confident you're not saying it is necessarily untrue, but I could easily see someone unfamiliar with the logic misunderstanding what you mean here.

@OrangeDog I guess a split chromosome in pan is a possibility a priori. Although it would somehow have to duplicate the centrosome, I'm not sure if that possible. But regardless, the observation of a fusion chromosome (with an extra centromere) is vastly more likely under the evolution hypothesis than under any alternative that I know of.

@jmpc  I mean that "god made everything" is by definition not a scientific hypothesis since it is not falsifiable. You may still choose to believe it, of course, but it's outside the realm of science.

One alternative, falsifiable, false hypothesis is that multiple species evolved in niches so narrow that there was no alternative which could lead to survival. Of course, that didn't happen (and would require an implausible transfer of this restriction from phen. to gen.; also environmental conservation of "junk", which you DON'T see in cases like convergent evolution of eyes). But it's interesting as an academic recreation to think of such things. On a small scale, though, you do get SNPs which multiply arise with no common ancestor (eg adult human lactose tolerance without common ancestry).

To be fair, the bible and religion in general provides plenty of falsifiable hypotheses. It's just that believers keep moving the goal posts and if that doesn't work anymore, they do the intellectual equivalent of sticking fingers in their ears and shouting "lalala" at the top of their lungs.

Coming back to this question after years, there’s a simpler way to look at evolution: It’s a model

If you look at a scatter plot and roughly see a line, you might deduce a linear relationship. This relationship could easily not be linear (or even not exist) but given the data in front of you, a linear relationship is the simplest explanation, and by Occam’s razor, the best.

It is vanishingly unlikely that when DNA sequences which are thousands and thousands of bases long are identical between two creatures, that those sequences have no common origin.
That's like saying, "Your Honor, I didn't pirate that Justin Bieber track; I generated random 16 bit audio samples which just happen to match!"
That is less likely than the proposition that Melania Trump's speech wasn't plagiarized from Michelle Obama's, which already sits at a laugh-inducingly low probability level.
It's not a question of what we know, but of eliminating vanishingly improbable, time-wasting hypotheses.
Not only do we have the statistical argument that even a vast number of monkeys typing on typewriters are not going to reproduce the text of Macbeth, but there is the observable fact that DNA replicates.  We can almost literally see identical pieces of DNA being reproduced from a common origin.  The replication from a common origin hypothesis to explain sameness is overwhelmingly probable, whereas independent origin is vastly improbable.
It's not a question of how do we know, but rather what is the most plausible hypothesis from among those that are consistent with our observations.
Knowing is reserved for pure facts, like consistency between logical and mathematical propositions. We can know that some theorem in mathematics proceeds from some axioms. We can also "know" the content of an observation, in some sense. We cannot know whether an explanation for it is true.
We can know when an explanation is false and we can gradually repair our understanding by identifying these failing situations and improving the explanations.
A final remark. Just because two creatures have some common DNA doesn't mean that those creatures got that DNA from a common ancestor at the time when they diverged. DNA can be introduced by vectors such as viruses. So that is to say, two creatures that diverged, say, a hundred million years ago could have some common DNA that they acquired more recently, like a million years ago. It is practically certain, though, that this same DNA itself has a common origin.
Unless you regard viruses as your ancestors, then some common strand of DNA is in fact not necessarily evidence of common ancestry per se.

It is like finding crap in your backyard and thinking about what animal must have laid it. You don’t have a camera in your backyard, but you do have reason to believe it’s your dog.

You didn’t find any other animal footprints and the DNA test matches your dog’s DNA with DNA found on the crap.
So either some animal snuck into your backyard without leaving a trace and took a crap that was then painted with your dog’s DNA, or the crap was your dog’s.

I think one very fundamental fact that you are overlooking, which we pretty much take for granted, is that DNA is the mechanism of inheritance of traits.
What I mean is that my DNA is very similar to my parents' and siblings. It's also similar, but slightly less so, to my grandparents, my cousins, aunts and uncles, etc. The further you go from my known relatives, the less similar our DNA becomes.
This is also true for all living organisms. For everything from bacteria, to plants, to flies, we can look at their DNA, and that of their relatives, and the more closely related (in the familial sense, as in parents, siblings, etc., not in the evolutionary sense, although I'll speak to that in a moment), the more similar the DNA.
So that is demonstrably true for every living thing we can observe today. But what about the past? Well, if this theory of DNA and familial relationship is true, then we can predict that, for instance, my DNA is more similar to the DNA of present-day people in the countries where my ancestors came from than from other countries, even though we have no historical/genealogical evidence of relationship. And this bears out-- a commercial DNA ancestry test shows I share genes with the general populations of the countries my recent ancestors are documented to have immigrated from.
This idea that familial relationship are biological relationship should seem at once obvious but also surprisingly insightful. If I am related to my human cousins because of the mechanism of DNA inheritance and the sharing of a common ancestor (our common grandparents), then it also stands to reason that chimpanzees are literally our familial cousins, very distant, from a common ancestor a long long time ago. Biological relatedness is in fact the same thing as familial relatedness.
If you don't buy that, then you have to explain why it's true that all observable organisms today share familial relatedness through DNA, but for some reason, this isn't true going back into the far past. What changed in the past? When did this start happening?
The only reason we get tripped up in this line of reasoning is because chimpanzees look very different from humans, and we cannot mate. In the past, people thought this was because different species were fundamentally different types of beings. But biological insights, specifically the understanding of DNA, shows that we are all fundamentally the same type of creature, with reproductive incompatibilities developing over time. The tree of life is literally a family tree.
Also, from biochemical understanding, we know generally how long mutations take to arise. Combined with fossil evidence, we can create a pretty good model of how far back divergences arose.

"Also, from biochemical understanding, we know generally how long mutations take to arise. Combined with fossil evidence, we can create a pretty good model of how far back divergences arose." I am not sure about how good those models are, given the opaque nature of mutation rates ... ;) Good answer, though!

There are some good answers here already but they mostly focus on whether similarities in the DNA sequence of organisms imply common ancestry. This misses something much more fundamental that is very strong evidence for this particular question: we all use essentially the same configuration of machinery to store genetic information and turn it into proteins.

All organisms on Earth use nucleic acids with a ribose/deoxyribose backbone and not other chemistries like XNA, PNA or other alternatives.

"There is nothing Goldilocks about DNA and RNA," Holliger told
  Science. "There is no overwhelming functional imperative for genetic
  systems or biology to be based on these two nucleic acids."

All organisms on Earth use the same nucleobases (G, C, A, T, U), even though alternatives exist that can apparently replicate perfectly well.
All organisms on Earth use the same genetic code for protein synthesis (with a few slight variations) even though the matches between codons and amino acids are probably largely arbitrary.


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Real-world examples of Darwinian extinction
Darwinian extinction (also known as "evolutionary suicide") refers to processes of selection-driven self-extinction, i.e. the cases where natural selection causes the extinction of an evolving population.
In the literature, there are many models of life-history evolution and (to a lesser extent) experiments with bacteria in which Darwinian extinction has been demonstrated. However, I couldn't find anywhere real-world examples (i.e. not from models or experiments) of Darwinian extinction of complex organisms within more or less constant environment.
Do we know of such examples?
And if we do, could you please refer me to them?
Edit: A mechanism of the Darwinian extinction could be, for example, the emergence of ”selfish” strategies w.r.t frequency-dependent selection, which are beneficial to individuals when rare, but may result in a deteriorating environment and smaller population size once they become common.

I think the OP is looking for something like an example of mutational meltdown or an example of a selfish genetic element driving extinction. In short an example of extinction that is of particular interest to evolutionary and conservation geneticists. I think the current answers (despite one being generously upvoted) do not answer the question.

Although you don't mention it in your question, I guess you'd like examples of extinction in (more or less) constant environment? Then I guess you'd like cases of extinction due to the introduction of an overseas species out-competing the original one.
Red squirrel is not extinct yet, but its sharp population decrease is mostly linked with competition with newly introduced grey squirrel, although habitat loss and concurrent introduction of a virus are also part of the causes. Read at https://en.wikipedia.org/wiki/Red_squirrel

It could be worth noting that the most important component of the decline is actually squirrelpox virus, which causes subclinical infection in greys but kills reds.

Well, wouldn't resistance to pathogens be part of Darwinian fitness? Although it is true that the virus is reported to have been introduced along with grey squirrels, thus it's difficult to decouple the population reduction due to its introduction and the interspecies competition.

Yes, constant environment. And thank you for the example, looks promising. But I was more interested in ”selfish” strategies w.r.t frequency-dependent selection, if you know of any such examples. I'll edit my question.

@Joce Differential pathogen resistance is part off interspecies competition.

Yes, but what I meant is that if the pathogen is introduced (or exposition increased) at a given time, this is modifying the fitness of the species independently of interspecies competition. Thus part of the adjustment in population size may be a response of this new environment only (and would be obtained for same exposure to virus w/o the competing species presence)

@joce it would, yes. 'Competition' is a broad description of what is happening; I'm just suggesting this answer might be improved by a more specific description of the mechanism.

@Joce ''this is modifying the fitness of the species independently of interspecies competition'. No, the differential response to the same pathogen between species is not independent from interspecies competition but part of interspecies competition. -1

@AlexDeLarge: have you read my comment? If the introduction of the pathogen is concurrent to the introduction of the competing species, then you could have extinction of gray squirrel without any competition, simply by epidemics. If the pathogen was already present, then you are right that the population diminution can be read as the outcome of the interspecies competition.

@AlexDeLarge: As this is not appropriate for a comment, I have started a new question to discuss this. See http://biology.stackexchange.com/questions/49246/interspecies-competition-and-pathogen

It hard to find example like that because evolutionary suicide does not mean it must end with extinction
I think this 2 words is not equal. Member of every specie would evolve into something disadvantage to specie as a whole, but then it would rapidly lead to equilibrium and/or evolution arm race before extinct
I could say most predator evolve to starve their specie, if they have many offspring then the prey would all gone and they will starve to death as a whole. But before all prey die the predator would gradually fall and the prey member will rise up again into equilibrium
There are also specie that develop infanticide or cannibalism. But before that specie gone extinct the group that develop those trait would have decrease, those group would gone extinct before the whole specie, or at least some group without those trait would have better chance to survive

This doesn't really answer the question. And by definition, Darwinian extinction results in extinction.

@101010111100 Darwinian extinction is extinction but evolutionary suicide is not the same word

The loss of self-incompatibility (gaining the ability to breed with oneself) in the Nightshade family has been demonstrated to result in both a higher diversification rate and an even higher extinction rate, overall leading to a lower diversification rate in self-compatible lineages.
http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.702.1437&rep=rep1&type=pdf


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Why my proteins are migrating like this on SDS-page?
I'm trying to make a SDS-page of total proteins extracted from algae but I'm encountering two problems. First, when I depose my proteins in the wells the sample goes down and then it starts to move up the sides of the well. Second the result of my run looks like this:

so my bands are not visible and I have like a vertical smear on the sides of the lane.
The buffer used to extract proteins contains Tris, NaCl, EDTA DTT and Glycerol and my loading buffer is a 5x commercial dye with B-mer.
Thank you!

What did you expect? Single bands clearly visible? How much total protein did you load?

I loaded 10 ug of total protein extract and I expected to see at least some neat bands. Honestly I don't know if the "smear" effect is normal (but I've never seen that with bacterial protein extract), or if it can be related to the degradation of my sample or if it is just a problem in the migration.

10ug is not very much - you could load more (20-30). Simply do this as a side by side comparison. Additionally: This is pretty much how I would expext a raw cell extract stained with coomassie to look like. There are hundreds of different proteins of different sizes in there, you would only see bands for really strongly expressed ones. Or for ones which you can enrich for. Otherwise I woud use Western blot to stain for specific proteins, which usually gives very nice bands even from raw extracts.

Indeed my goal is to perform a western blot but I'm not seeing a nice band where it should be, that's why I tried to compare my samples with a coomassie staining.  :-)
Ok, I'll try to load a bit more protein and I also tried to change the extraction buffer to solve the "moving up" problem.

You don't have to see a nice band on the coomassie stained gels to get nice bands in western blots. I do this all the time (doing whole cell extracts and use them for western), I can post the protocol I am using later today as an answer.

I'm running a gel right now and with the new buffer I solved the problem of the sample moving up the wells. Later I will see if I also have sharper bands.

what is your solution for this problem?I am have the same situation. Any more suggestions?

@Ying Zeng  In the end I changed the protein extraction buffer with a new one, I really don't know why the other one wasn't working. In this moment I don't remember the recipe and what is different from the previous buffer but I can post it here if you want.

It's a guess, as I haven't run a algae sample on SDS-PAGE, but your migration problems might be due the algal polysaccharides that are present in your sample. Check if your protein purification protocol is specific for algal proteins and see if there is any step dealing with the algal polysaccharides.


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What reason that land vertebrate evolve keratin while other animal use chitin
I don't know why there are evolutionary split in material. Why we evolve keratin and lose chitin? What the advantage and disadvantage for each material? Is it because the size or there are other biological reason?

I think this is too broad a question. Chitin and keratin are completely unrelated -- chitin is a sugar polymer found in exoskeletons and scales, keratin is a protein forming intracellular filaments. They are hardly comparable.

exoskeletons and cell walls are hard... keratinized skin is more flexy...


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house keeping gene variation under treatment
I am injecting BCG in mice ears to measure the local inflamation response in the infection side, one ear in the same mouse is kept as control by injecting PBS, in the other one, BCG is injected. When I do a qPCR the house keeping gene comes out later in the BCG ears compared to PBS control (even I measure RNA and DNA concentrations to have the same amount of materia). Does it means I have less amount of material in the PBS injected ear? or could it be the expression of the house-keeping gene is afected by BCG infection? Any other ideas?
Thanks

What house keeping gene are you using as a control?

I tried 3, Gapdh, bactin and hprt, and always appears the same problem, the ears infected with BCG all the house keeping genes is shown to appear at less cycles compares to the ears injected with PBS.


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Finding diploid neanderthal alignment data, looking for ambiguity codes
I'm using Neanderthal alignment data from here: http://www.eva.mpg.de/neandertal/draft-neandertal-genome/data.html
Specifically, the .bam files. I would like to find alignments for neanderthal sequences to human genomes that state ambiguities (such as M or R). However, the data from that site does not have the ambiguities. Is there a way to find such information? Or are there no ambiguity codes in neanderthal alignments?
My goal is to compare diploid neanderthal sequences to diploid human sequences. How do researchers typically deal with this given the limited data they have for neanderthals?

Why would you use the draft genome instead of the high coverage Altai genome?

Is there more than 1 whole genome sequence (besides Altai) for neanderthals? I'm looking for at least 5.

Oh, ok. There is the Denisova genome (a close relative of Neandertals), but other than that, you really have to stick to low coverage (it was not clear from the question how many genomes you need). But if you use low coverage, you should avoid using Altai or Denisova genomes for the sake of comparability.

Ah ok, thanks. I'm looking for at least 5 or more Neanderthal genomes. I guess I'd have to stick to low coverage then if I want that many.


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Do experiences shape actions of insects? Animals?
Would an insect behave differently to stimuli depending on what stimuli occurred to them earlier (that only affects them cognitively or their conscience)?

Are you asking about any non-human animal? Because I would think it's pretty obvious that animals like trained dogs are behaving according to what has happened to them before. There has also been several studies of insects that you can find if you search for "conditioning". example: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000529

Not to be picky, but insects are animals  :)

"Simple" insects like fruit flies can learn to associate odors with food, e.g. see here for a pretty classic example. Drosophila even show some kind of depression which is acquired. Their sexual experiences even shape their alcohol intake.
You will find similar examples for other model organisms as well.
So, yes, simple animals behave differently in response to previous experiences.

You say depending on what happened to them. The expression "what happened to them" is so broad that the answer is necessarily yes. I am giving a few very obvious examples.

If you give royal jelly to a bee larvea, it will drastically affect its morphology and behaviour. So yes, presence of royal jelly will affect their future behaviour.
If you cut all the legs of an ant than it will not run toward a smell of food! So yes, depending on what happened to an ant, the response to a food smell stimuli will vary.
If you kill a beetle, it won't react the same way to future simuli either than if you don't kill it!

So yes, even in insects the past affects the present. The same is true for any other living organisms. You might even go on an argue the same for a stone although it might take some consideration of semantic in order to apply the concept of reaction to a stimulus for a stone.

You can't really think that that's what I mean? :/ If you do, can you help me word my question better?

I realized you might have expected something else (although I hoped you would liked the first example) but strictly speaking this is a correct answer for the question as currently phrased :). You should think about what kind of events that may have happened in the past you are willing to consider. Make sure then to correctly define the set of events that you are willing to consider.


text:
Is our genetic evolution driven by what we catch?
When an environment changes, a multi celled organism can lose some cells without it producing an equal evolutionary change. But when a single cell organism experiences the same environmental pressure change, its life or death.
So single celled populations should evolve in direct relation to the environmental changes, while multi celled populations would evolve only in response to large scale environment changes.
If we are infected by the single cell organism, and it manages to insert highly evolved genes into one of our stem cells, then is it possible for these genes to insert in the correct place and upgrade our genetic code with new adaptions to the minor environmental changes?

Welcome to Biology.SE. The question is unclear to me. It is a little hard to pinpoint to what is unclear and there's little I understand. Here are two points. (1) lose some cells without it producing an equal evolutionary change I don't understand what you mean by evolutionary change here. (2) what do you mean by highly evolved genes. I think the start by saying that organisms of different size often face environmental variations at different scale (which is true). Then you seem to talk about parasitology but I am not sure what your question is.

As you are using terms and expression that are never used within the field of evolution biology (such as upgrade our genetic code or evolved genes), I think you might want to follow an introductory course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.

If the question is "do populations evolve in response to parasites", then the short answer is "yes".

But when a single cell organism experiences the same environmental
  pressure change, its life or death.

Do you understand that evolution is not about changes to individual organisms?  It's about changes to populations of organisms

So single celled populations should evolve in direct relation to the
  environmental changes, while multi celled populations would evolve
  only in response to large scale environment changes.

I have no idea what you mean here.  If you mean "A little DDT won't cause any changes to DDT resistance in a population of mosquitos", you are just wrong.  If you mean "A global climate temperature increase of 1 degree won't affect polar bear populations at all", that's wrong.

If we are infected by the single cell organism, and it manages to
  insert highly evolved genes into one of our stem cells,

Can you start with some evidence that this every happens?  Or any evidence that it happens often enough to be a common driver of evolution?  (Note that viruses are not organisms)


text:
Does xylitol kill all kinds of bacteria?
Xylitol is known as a bad bacteria killer in human's mouth.
But I am curious about one thing.
Does xylitol kill all kinds of bacteria regardless of good or bad?
If so, Does xylitol kill bad bacteria more than good ones at least in human's mouth?

Toxic compounds do not differentiate between good or bad.

Xylitol does not kill any bacteria.
Xylitol is a sugar alcohol that bacteria happen to not be able to use as an energy source. In the absence of other sugars, bacterial growth slows. Therefore, its antimicrobial mechanism is bacteriostatic rather than bactericidal.
No antibiotic exists, or will ever exist, that kills or inhibits all kinds of bacteria.
One thing xylitol can kill is a dog – keep xylitol-containing products such as gum well out of their reach.

Your answer is punctual, thanks. It does not kill bacteria directly. But does xylitol make all bad bacteria starving while it doesn't much affect to good bacteria? To understand my question, vice versa, if there's much sugar in human body, which bacteria grow faster, bad bacteria or good bacteria?

In one study, using xylitol-sweetened chewing gum reduced levels of the bad bacteria by 27-75%, while it had no effect on the friendly bacteria. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3434645/


text:
Crick’s Central Dogma — Counter Cases
I was recently reading about non-coding RNAs being a counter example to Central Dogma of Biology. Can someone add more cases which violate the Central Dogma? Thanks!
UPDATE - Reference of lncRNAs violating Central Dogma:

Although the central dogma remains a core tenet of cellular and
   molecular biology, the appreciation of lncRNAs as functional genomic
   elements that defy the central dogma may be essential for fully under-
   standing biology and disease. [Iyer et al. Nature, 2015]

No, neither of those are counterexamples to the central dogma, as stated by Francis Crick: the dogma only says that information does not flow from protein back to DNA and RNA. Crick was well aware of RNA viruses. See his paper http://www.nature.com/nature/focus/crick/pdf/crick227.pdf

@Roland Thanks for highlighting the virus thing. Please have a look at updated question (with reference of statement)

Well, I guess Iyer et al never looked up the original definition of the central dogma :)  I know many textbooks have simplified / corrupted the concept to mean "DNA --> RNA --> protein", but that's a strawman ... In a sense it's just arguing about definitions, but to be correct, lincRNAs do not violate Crick's statement of the dogma. I suggest you read Crick's 1970 paper to get some context.

Do not take it too seriously. Biologists - as most scientists - tend to find definitions for themselves and those are not always compatible with other definitions. And this also makes sense in the scientific progress, as otherwise you would have a hard time adapting theories and, as a consequence, definitions. Crick's definition is as far as I know not the common textbook definition most biologists might have in mind and therefore this is just an ongoing scientific debate, rather than an oathbreaker. ;) Make sure to use the definition you want to promote in publications. ;)

I have changed your title of "Central Dogma of Biology" to "Crick's Central Dogma". Crick proposed this in an article on protein synthesis, which you can read here. Crick had a training in physics and I would be surprised if he described himself as a biologist at that time. His Central Dogma died (or had to be modified) with the discovery of the reverse transcriptases of retroviruses, over 40 years ago.

@David "Central Dogma died by reverse transcriptase of retroviruses" Wasn't Crick already well aware of viruses (as mentioned in his paper and thanks to Roland for highlighting it)? I think majority of us overlook this part in his paper

Talha. I've changed my view on that as I mention in my updated answer. I think there was a general misinterpretation of Crick's Central Dogma when Temin and Baltimore discovered reverse transcriptase, which evoked the reaction I expressed. (I was there at the time. Presumably there is a Nature News and Views article about it.)

Crick’s Central Dogma was actually:

The Central Dogma
  This states that once ‘information’ has passed into protein it cannot get out again. In more detail, the transfer of information from nucleic acid to nucleic acid, or from nucleic acid to protein may be possible, but transfer from protein to protein, or from protein to nucleic acid is impossible. Information means here the precise determination of sequence, either of basesin the nucleic acid or of amino acid residues in the protein.

So, although in my comment I stated that the discovery of reverse transcriptase was the first violation of this — as was generally regarded — this turns out not to be the case.
I remember that the case of reverse transcriptase was felt to be different from the existence of RNA viruses because it involved the flow of information from RNA to genomic DNA, which were generally represented by a unidirectional arrow in the opposite direction in diagrams of the dogma. The following is a typical illustration of that, taken from some University lecture notes that I found on-line and which are described as:

These diagrams ..., created originally by Crick, summarize the basic processes of information transfer within cells.

But the NCBI collection of facimilies of Crick’s documents include a 1956 diagram that is quite different and much more sophisticated:

And, so the central dogma has not been violated (certainly not by lncRNAs), unless you consider that it has by prions, where information of sorts is transfered from protein to protein.
Morals

It’s amazing what you can find on the internet.
Never believe what you find on the internet.

Footnote
I’ve seen the DNA → Protein arrow repeated as if it were fact in diagrams, although Crick only said ‘may’. I know of no example of this.

This is really enlightening, both biologically and philosophically (in terms of history of science). +1

Loved the moral part, but David its Nature – not an XYZ sitting on internet and writing blogs. I have wrote the author email in this regard. Awaiting his [never coming] reply

@TalhaIrfan — You're right to feel aggrieved, but a little explanation of how things work may help. When a paper submitted to Nature is sent out for review it will be because the authors claim to have made some substantial scientific progress. This will be expressed in the Title and the Summary of the paper, and the referees will be most concerned with whether the work is really important and whether it is correct. That is their main job. Hyperbole that only appears in the final paragraph of the discussion will often be ignored with a shrug of the shoulders.

The "Central Dogma" is an obsolete concept.  It has no biological significance today. It's been outdated for decades since the discovery of reverse transcriptase, but it was never intended to be taken particularly seriously anyway; Crick deliberately gave it its portentous name as a provocative approach, to drive people to think more about the topic and look for the counterexamples he presumed were there.
Unfortunately, it seems that in some places -- notably India -- shoddy, ignorant teachers don't understand anything about modern biology and still believe that the Central Dogma has more than historical interest.  It does not; it should not be taught in biology course, let alone treated as a testable concept, and any mention of it should be limited to History of Science courses.
Because it is an outdated concept that no longer matches modern biology, and because these ignorant teachers still try to squeeze it into their courses and tests, many students (again, especially from India) are very confused, thinking that their understanding is wrong because it contradicts the Central Dogma.
If you need to parrot something for an exam, I sympathize with you, but don't make the mistake of thinking that the Central Dogma is a real, relevant, modern biological concept.

I agree that there is no particular reason to mention the Central Dogma in teaching (and I never have myself), but it turns out that you are wrong about it being wrong in the way you say. I'm not criticising you, because I've only just discovered what Crick actually said and drew, as shown in my updated answer.

Kind of makes the situation in India worse.  Not only are these pedagogues insisting on teaching an outdated, irrelevant, biologically meaningless concept, they're not even teaching it correctly in the first place.

— I don’t know about Indian universities but a comment by Anurag Chaurasia you may have seen in Nature recently would seem to express similar sentiments. I have been fortunate enought to have come in contact with students from India who have been most capable of critical thinking.

That's my point.  The people (often from India) who come to StackExchange with questions about the Central Dogma are obviously capable of critical thinking, because they are baffled by the useless, stupid garbage they're being taught.  They usually don't understand that they're being taught garbage, but they do understand that it doesn't make sense, and they blame themselves for missing something.  It's incredibly frustrating to see baffled question after question about the same thing, actively harming the understanding of clearly smart, clear-thinking people.

The central dog is an old 1950s concept that is obsolete and should be removed from the text box of the 2010s. It states that the flow of information from DNA->RNA->protein is unidirectional
Examples that goes against this idea are
Reverse transcriptase which transcribes RNA -> DNA. Reverse transcriptase was originally found in RNA viruses. But has since been found in transposons which can be though of viruses that permanently resides in the host cell.
Telomerase... uses to elongate the ends of chromosomes from becoming shorter (something that occurs on the lagging strand of DNA during DNA synthesis) the shRNA used by this enzyme only encodes a few base pairs (6-8bp depending on kingdom)... but it is an example of RNA->DNA
RNA dependent RNA polymerase RNA-> RNA (No DNA is required to make more RNA). has been found in yeast.. with the role of maintaining the centromere... and likely will be found in humans too, since centromeric structure is believed to  be conserved in the broad sense.
Prions. Where a prion serves as the template to cause a normal protein prion protein (PrPc) to undergo a change in folding and become the infectious prion (PrPsc). An example information in propagating between protein molecules. Protein-> protein
Then there is epigenetics... where proteins can leave methylation marks on genes (DNA)... changing the expression of the gene in an inheritable way. So information from proteins can flow upwards. While not DNA bases are changed, the DNA is modified. Protein -> DNA
There is also histone modification.. which can be inheritable depending on gene. But it is regulation of DNA by controlling how available that DNA is to being read by transcription machinery.
Then there is siRNA... which can and does modify gene activity. A weaker example of how information can flow from RNA -> DNA.
Next are proteins called cytidine deaminases. These proteins naturally convert cytidine to uracil. APOBEC modifies RNA.. creating a premature stop and thus a shorter APO-B protein with lower activity.. regulating lipid metabolism. So mRNA editing by APOBEC proteins changing the information in RNA aka Protein -> RNA. Next is AID, another cytidine deaminase but one that targets DNA. It used by the immune system to cause hypermutation and thus variation in the antibodies. A poor example of protein inducing genetic changes. Not controlled unlike the DNA methylation example.
Lastly there are ribozymes. RNA that have catalytic activity. So no need for the protein to catalyses a reaction.. RNA can do it on its own.

Jay - can you add some references to the terms you use in your answer? It would help other users follow along with what you are saying and definitely strengthen it.


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A creature from Mediterranean
I have recently encountered this red thing on one of the beaches of east Sardinia. It was pretty close to the coast (around 20 meters) and has sticked to one of my fins.

My question is: how is this creature called? Is it dangerous to have skin contact with it?

Nice picture! I do not know what it is, but I would not touch it.

How big is it? The perspective makes it hard to tell. (And I agree, very nice picture!)

It was about 15x15 cm.

This appears to be an anemone, with the pedal disc towards the camera. I can't offer a positive ID, but would hazard a guess at genus Actinia.
Anemones sting, and the stings of anemones range from completely harmless to humans to highly toxic. In the absence of a positive ID, I would avoid poking it.

Thank you! Based on your answer, for me it is mostly similar to this one. Some of the photos here look very similar too, although I didn't see those blue dots near the tentacles.


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How can evolution make such complicated beings?
So what I understand is, evolution is a mere mistake in the replication of DNA and this change is sometimes good and sometimes bad.
And the other day, in our biology class, we were told the functioning of the lungs and how the RBCs fetch the O2 from the alveoli and dump the CO2 out.
And I also know a little bit about some complicated processes in the body like, how the digestive system works, how the muscle cells switch to  anaerobic mode when we run out of O2 causing cramps, how the cells make ATPs in the mitochondrea.
And 1 more notable thing- the amount of complicatedness and all the neural networks in brain.
My question is- how can evolution(a mere mistake in copying a strand of DNA) make such a complicated machine, like our body. There are SO many organs, all working in collaboration to make the body work. And all of those organs are doing SO many things.
I know that this is a result of 3.8 billion years of evolution...but still... how can even a million "mistakes" make a body which is so well deisgned?
ALSO was the whitening of the polar bears a mistake too? Then what are the chances of such a mistake occuring in the replication of DNA? If it was evolution then why don't birds become the colour of the sky?

I'm afraid you need to learn a bit more about how evolution works. Evolution is not just a series of random mistakes, it also involves natural selection which is not random at all. A good starting point to learn about evolution is: http://evolution.berkeley.edu/evolibrary/home.php

@Roland I know about natural selection- its like the survival of the fittest right? Like if there are 5 species of dogs in an environment, then only the fittest species will survive.

@Roland im a 10th grade kid and all the knowledge that i have gathered about evolution is from 2 or 3 youtube videos

Yes, that's natural selection. It acts as a "force" directing evolution, which means that the way things evolve is not random at all. Many people have questioned how evolution can come up with such incredible complex structures, but it does happen over billions of years, with countless organisms alive and evolving at any moment. It's really hard to grasp the enormous scale of it all. But evolution is a large topic, and we can't provide textbook material on this site, so check out the Berkeley page I mentioned for more information!

@Roland ok, but 1 more question. Was there a species of animal with their brain not in their head? And maybe it went exist because the "brain in the heads" species was more fit? This is a silly question but it makes sense to me.

Well I'm no expert on evolution of the brain, but it doesn't sound silly to me. You might want to look at  https://en.wikipedia.org/wiki/Evolution_of_nervous_systems  If you don't find what you're looking for, you can post this as a separate question!

One example of an animal with a brain not in their head is the human species: http://www.scientificamerican.com/article/gut-second-brain/

Mistake is the wrong word. You want the word 'difference'.

@Adi, from my experience it is difficult to get an answer which is to the point in this web site. every entity will have (to a certain level) random mutation and it is very strange the barriers between species are very clear in this world.

We see many breeds of dogs, and cats but not something between. They are discrete. And the mutation that affects to evolution should occur to the germ(reproductive) cells before massive cell differentiation during embryo development(because after massive cell differentiation, mutation is minority and will be repaired, will not survive in the reproduction activity) and those period is very short term in an animal's life. So I think evolution is like a belief at the end deep inside people not thinking though it out.

Biologists talk about 64 mutations per generation in average (coincides with simple math by the way) and this should happen all in very early stage during embryo development. Do those 'believing' in evolution know about this? Is the probability a real measurement?

If this is a general question about how evolution works then Roland's comment is correct - you should start with one of the excellent resources available online, like http://evolution.berkeley.edu/evolibrary/home.php. However, this specific question sounds more like something we used to call the 'argument from personal incredulity' to me - you're willing to accept that evolution occurs, you're just not sure whether it is sufficient to create something as complex as the organisms you see around you. This is quite a common issue people have with evolution by natural selection, and it's a perfectly reasonable question to ask. Essentially, it originates in the difficulty of appreciating the sheer scale of the processes involved. To paraphrase Douglas Adams, "[life] is big. Really big. You just won't believe how vastly, hugely, mind-bogglingly big it is." But I'll do my best to try to help you understand this a bit better.
The number of single-celled organisms on the ocean floor is estimated at 2.9×10^29 - that's roughly three hundred billion billion billion. The current global human population is about seven billion - that's already effectively impossible to imagine. If every one of those people had seven billion tiny people living on them, and every one of those had seven billion people living on them, that's roughly the number of single-celled organisms on the ocean floor right now. Many of those appeared less than 24 hours ago and will be gone tomorrow. Natural selection is acting on every aspect of every one of those organisms simultaneously and has been doing for roughly 1.5 trillion generations. One-and-a-half thousand, thousand, thousand, thousand, thousand, thousand generations.
Natural selection is also a fantastic mechanism for homing in on solutions to complex problems - so good that we've started using it to solve mathematical and computational optimisation problems.
Essentially, it's one of the best approaches to solving complex problems we have been able to conceive of and it's had an insanely, mind-bogglingly long time to act on a planet-sized test tube. That's how we ended up with so much amazing stuff on our planet.

@arbrviral but still, like that complicated mechanics? Is the ability of the brain to switch itself off when we are hit on head also a mistake? Like I once saw in brain games that as light travels faster than sound, our brain perceives them both at the same time by lagging the light perception a little behind.  Now that is a really complicated process and I don't think that was caused by a mere mistake and natural selection. If it was caused by natural selection then wouldn't some organisms might have existed on the planet who lag behind the sound perception?

@Adi: It's not by mistake. It's by natural selection. And yes, there have existed many individuals that lagged behind in many aspects when you compare them to existent individuals. many of those did not contribute to future generations because of their lagging behind. And there are still individuals that lag behind and they will also more likely not contribute to future generations. You have to keep in mind that what we see on earth today is a very, very, very (...) short evolutionary time frame, say a glimpse or a snapshot, and therefore not very informative.

@Adi Some aspects of any organism's environment are highly unpredictable; one is contact with parasites and pathogens, one is social environment. In situations like this the optimal response can be to evolve a system which is itself adaptive, rather than a pre-programmed solution. The brain and the immune system are the most obvious (and most complex) examples of this. I'm not sure I follow your brain-switching-off example, but this partially explains how we learn to integrate sensory inputs. See also: https://www.theguardian.com/education/2012/nov/12/improbable-research-seeing-upside-down


text:
What would the presence of a hub metabolite in a metabolic pathway signify?
Say I have a metabolic pathway, consisting of multiple metabolites and reactions. On analyzing the pathway I find that among all the metabolite, one metabolite is the hub metabolite (hub metabolite is the metabolite such that maximum number of reactions involve that particular metabolite).
What is the significance of this metabolite or of this pathway?

It's hard to say without knowing what metabolite you're talking about -- all metabolites have different roles, and you won't learn much about it simply from network degrees. You have probably hit upon either a common cofactor like NAD or ATP, a small ion like H+, or a common group donor like glutamate.

@Roland isn't there any generalized perspective of it?

Not much, really ...  The "hub" metabolites of course give rise to many products, and they tend to be present in high concentrations (but not all are). But beyond that, you really need to look into the biochemistry. The examples I mentioned have completely different functions.

By your own definition you are talking about several pathways not just one. All you can say about the metabolite is that it's an important intermediate. What else would you imagine?

@David I am trying to figure out what else can be inferred from the hub metabolite... hence posted the question :)

Forgive me if I am wrong, but you sound like a computing science student who has been asked to perform some mathematical analysis on metabolism and is now wondering what the results mean and whether they are of any interest to biologists. I say this partly through experience and partly because I'd never heard the term 'metabolic hub', but on Googling find a paper from a computing science department using it. Note that paper refers to a metbolic network — as I said, several pathways.

@David you are absolutely correct. I am a computer science student. I have not been asked to do anything, but I am doing it on my own. And thanks a lot for the resource. Hope I will be able to get more insights regarding metabolic pathways :)

@Rishika — You were right to post, but try to make personal contact with biochemists. You need to find out whether there are real problems that your skills can solve. I know from experience that it can be difficult, and computing scientists have come up with things that are actually no use in the real world. In this case I would think you would just come up with things like ATP, NAD, glucose 6-phosphate, glutamate, the importance of which is already known. However if you can find a real problem, then your work can be worthwhile. Good luck.

@David would you mind if I could contact you somehow?

@Rishika — If you wish. You should be able to work out an email address from my profile.


text:
This Sequence Data (DNA) has very few Methionin-starts. How is that possible?
I'm working on my first sequencing related project and I'm trying to find proteins with a specific PFAM ID (PF11999). The project is called "MMETSP", I searched the annotations for that ID, identified signal peptides using SignalP and their target locations with a tool called MultiLoc2 (I was looking for extracellular targets only).
Out of the very few sequences that where left after all this filtering, none of the DNA-bits started with the basepair-code "ATG", for Methionine. How can this be?
I used the shell to calculate that only 1,83% of all the sequences start with ATG.
Any ideas on this?

Exactly what sequences are you searching?

I'm looking for Antifreeze proteins (PF11999) in marine diatoms, that are located in the extracellular region. Using the cleavage site provided by SignalP I can isolate the targeting peptide.
However, these peptides seem to have no "start"-code.
I got the sequences by looking up the protein IDs in the fasta files that I got from the annotation-search.

You're just looking at the cleaved peptide sequence then? There's no reason those need to start with a methionine unless they're type-I and don't receive further N-terminal processing.

Well, I'm looking at the DNA coding the peptide. The peptide is located in front of the "maternal" protein, so the ORF should start with a methionine, shouldn't it?

If there are no UTRs in this species and the CDS is annotated as full length then yes. Otherwise no.

Then it should be yes.. I'll talk to my Supervisor monday. Thanks for your time!

If anyone stumbles across this question, I found out what the problem was in the end:
contrarily to my assumption that the DNA sequences where all in proper 5'3'-direction, it turned out that we found the exact ORF on the complementary strand in the other direction and who knows where else. Luckily, the MMETSP-Data also featured a /pep directory, in which the needed sequences where found in a clean version.
Thanks for reading and good Luck.