text:
Why do the ancestors of birds still exist?
If I am not mistaken, scientists believe that birds are evolved from reptiles. Why do the ancestors of birds (that is, reptiles) still exist?

Does this answer clear it up? Species don't evolve into other species. They evolve from them.

Birds evolved to use different environments than reptiles.  Reptiles are still better adapted for their own environments, so birds haven't displaced them.  There are so many problems with your question's assumptions that this ultra-simplified answer is barely a start; I suggest you learn more about evolution.

You appear to have several (rather common) misunderstandings about how evolution works. I strongly suggest reading through Understanding Evolution from the University of California, Berkeley. It is a short but thorough and easily-understood introduction to the topic that should address your misconceptions.

Reptiles are not ancestors of birds. There are many answers in this site (including the one here by Remi.b) that have clarified it. I am putting this question on hold as a "homework" because you have some misconceptions regarding the concept of evolution properly and any answer would simply be a crash course on evolution. Moreover, since your assumption itself is incorrect, the question gets invalidated.

As this type of question results from a common misconception, I think we should make sure to keep this post around to be able to link to it. I am voting to reopen.

Introduction to phylogeny
Short Intro to Speciation
Let's talk about speciation. Speciation is the process by which a single lineage split into two. This happens in a number of ways (allopatric vs sympatric vs parapatric, BDM model and others). I will consider a simple case of allopatric speciation below as it is the simplest one to understand (although not necessarily the process causing most speciation events).
Following the story of a lineage through its speciation events
Think of a population at time $t=0$. Let's call this species A (for Ancestor). Imagine that an ecological change brings a barrier right in the middle of the range of this population of A. Such a barrier could be originally caused by a fire, or a river that has changed direction or a mountain range "popping up". The two now isolated populations are free to diverge randomly through time. This is what we call a speciation event. Note that under this model, there is no necessary need for selection to explain speciation. Let's call the two diverging population B and C which exist at time $t=1$.
Now, imagine C goes under another speciation event and split into the populations D and E. In the same time, population B may have changed quite a bit so that we might want to call them F. Here is a diagram of the situation
  F           D ----- E     t=2
  |               |
  B ------------- C         t=1
          |
          A                 t=0

A is an ancestor of B,C,D,E and F and does not exist today. B is an ancestor of F but does not exist today. C is an ancestor to both D and E and does not exist today. Let some more time pass by and you may eventually end up with the following tree
  G ----- H       K   I ----- J t=3
      |           |       |
      F           D ----- E     t=2
      |               |
      B ------------- C         t=1
              |
              A                 t=0

At time $t=3$, only species G, H, I, K and J exist today, the other are ancestors of current species. Let's expand this tree even further.
  L ----- M   N       O       P ----- Q      t=4
      |       |       |           |
      G ----- H       K   I ----- J          t=3
          |           |       |
          F           D ----- E              t=2
          |               |
          B ------------- C                  t=1
                  |
                  A                          t=0

You will note that lineage I went extinct at some point between $t=3$ and $t=4$.
Naming subsets of the tree
Reptilia
I am now suggesting to give a generic name for all the lineages present in the tree we drew (which we call a phylogenetic tree by the way). Let's call them Reptilia. So all the species A,B,C,D,E,F,J,I,J,K,L,M,N,O,P and Q are Reptilia.
Birds and Mammals
Now let's consider a subset of this tree. Let's consider the subset made of the species J, P and Q only. Let's call them birds. Let's also call mammals the subset composed by the species G,L and M.
Lizards (and others)
Finally let's call lizards all reptilia that are not birds, nor mammals (in reality it would be more correct to call this group lizard_crocodile_turtles_snake_amphibians_tuatura). Of course, the right tree is much bigger! By the way, you can explore the tree of life yourself on OneZoom.org.
What is a taxon
By the way, a group of species is called a taxon (plur. taxa).
Monophyletic taxa
It might be straight forward to you that there is something fundamentally different between the groups that we called mammals, birds and reptilia to the one that we called lizards. Indeed mammals, birds and reptilia are called monophyletic as they are composed of a given ancestor and all its descendants. lizard on the other way is not monophyletic. A monophyletic taxon is also called a clade. Below is a graph representing what a monophyletic taxon is. It also uses the terms polyphyletic and paraphyletic to describe different types of non-monophyletic taxa

Concept of species
You might want to learn more about the issues behind the concept of species in the post How could humans have interbred with Neanderthals if we're a different species?
Concept of taxonomic ranks
What we decide to call a class, an order or a family is also somewhat arbitrary too. For example, we generally consider the monophyletic taxon Mammalia is a class. However, there is no non-arbitrary reason for calling Mammalia a class rather than Eutheria (eutheria = placental mammal).

Online resources
I suppose the above answered a big part of your question. You will be able to read all of what I just wrote (and much more) on any good introductory course to evolutionary biology. Consider having a quick look at Understanding Evolution by UC Berkeley for example as @MattDMo suggested in the comments.
Issues in your post
There are issues in your post that cannot be addressed in a single post (another reason for you to follow a quick intro course to evolution). Below I consider your post piece by piece mainly to point to some issues

Scientists believe

Terrible statement. By belief, we often refer to a non-justified belief, that is a belief about the world that is not justified (in science, the method of justification is called "the scientific method"). The statement, therefore, suggests that non-justified beliefs have a place in science while they don't. By being a little lose on the semantic, one could say that scientists "know" or they don't know but they don't believe without good reasons to believe.

that birds are evolved from reptiles

This is misleading (and it mislead you) because by "reptile" you think of a lineage that currently exists. Also, the expression "are evolved from" sounds very wrong. The expression "has evolved from" would be more correct.

evolution occur so that the organism can survive in the environment by developing new characters

This is wrong both in terms of the semantic (issue of causality when saying so that) and in term of the definition of evolution. You seem to confound evolution with natural selection.

According to natural selection

Natural selection is a process, not an explanation. It is like saying "according to gravity". The semantic is wrong, you should say "according to the theory of gravity" or "according to the theory of evolution" (or eventually "according to the theory of natural selection").

According to natural selection, those with favourable variations will survive and those with unfavourable die

You seem to apply that statement to population-level fitness (which would be mainly wrong) rather than to fitness variance within a population.

Why do the ancestors of birds (that is, reptiles) still exist?

The ancestors of birds don't exist anymore. I hope that was made clear from the above explanations.

Why didn't they get eliminated by natural selection?

This sentence suggests that you do not really understand what natural selection is but this is a story for another time. You can learn about natural selection on Understanding Evolution by UC Berkeley.

+1 Thank you for the extremely clear answer here (as well as on my question)

Reptiles evolving from birds is an example of divergent evolution. This wiki article has more information. Essentially both birds and reptiles are still around because they both fill a niche. That is, birds and reptiles separated have a common ancestor, and at some point their evolution diverged. At that point, birdoids which better filled the "bird" niche had higher fitness, and reptiloids which better filled the "reptile" niche had higher fitness, so birds evolved to be more like birds, and reptiles evolved to stay reptiles.

This answer is not fully accurate either, and shares some misconceptions with the original question. Reptiles did not evolve from birds, nor did birds evolve from reptiles; both evolved from a common ancestor, which we may today think of as more "reptilian" but is not a modern reptile. It is possible for species to be thought of as more "ancient" if they have not changed in gross structure over long time periods (i.e., crocodilians are often described in these terms), but those species still spent just as much time "evolving" as have humans, for example.

It is surprising to see an upvote on this answer. The answer is in between misleading and wrong.

Reptiles did not evolve from birds as Bryan said.


text:
What is this spider

What is this spider? Is it poisonous?

What is the location and climate? What is the approximative size?

The eyes (and other structure of the head) are key for spider identification. Can you take a picture of the dorsal side of the spider?

This is unambiguously a female Araneus, and judging from coloration pattern of the legs and ventrum — very likely the common cross spider Araneus diadematus: see ventral view photos, or some other very similar species. A better photo of the specimen from the dorsal side and some information on the location would be very helpful.
And no, these spiders are not poisonous.

Photo: Michael Gäbler, via Wikimedia Commons

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
What is this creature? Where can it be found?
I recently received the picture below from a friend and began to worry. Does it really exist? What type of creature is it? What habitat does t live in and what is its range?

A probability always depends on a priori such as typically where do you live, do you often drink from rivers, etc...? You should probably just ask "Is this a real thing?", "what is it?" and "where does it live?" Note that you can  improve the post by removing unnecessary informations such as how many people liked the post or what time it was when you took the screenshot.

Thanks for the comment, I've edited the question and the picture to suit your request.

The creature in the man's hand is a baby eel. Giveaways: it has fish eyes and the flattening of the tail. The lower right picture suggests it's a vertebrate (i.e. not a worm.)

Exactly which eel it is is unclear, but you can read more about it in the linked article. Indeed, your first picture appears in the article.

These transparent wonders are not a species, but rather they are the second stage in the life cycle of a number of eel species in the family Anguillidae. This particular specimen is an American eel, Anguilla rostrata. For the rest of the post I'll focus on the life cycle of this species for simplicity's sake.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Are the transverse septum in sharks and the diaphragm in mammals homologous structures?
Are the transverse septum in sharks and the diaphragm in mammals homologous structures?
I have searched on Google Scholar and Web of Science, but haven't found substantial evidence to prove or falsify the claim.

What is your reasoning one way or the other? Let us know your reasoning. What are the two structures made of?

A beginning of answer here below, I hope. Please first consider that many structures are involved in the question here, the diaphragm (UBERON:0001103), the diaphragmaticus muscle (UBERON:0036071) and the septum transversum (UBERON:0004161). At Bgee (bgee.org) we aim annotating relations of similarity between anatomical structures, please have a look at our GitHub
https://github.com/BgeeDB/anatomical-similarity-annotations
We already annotated 'diaphragm' as a mammalian structure, not homologous in Amniota (please see https://raw.githubusercontent.com/BgeeDB/anatomical-similarity-annotations/master/release/similarity.tsv). In our next release, you will see the annotation for the 'diaphragmaticus muscle' which is an analog organ in Crocodylians (and Turtles) but not homologous to the mammalian diaphragm either. See here for more details about this new Uberon class:
https://github.com/obophenotype/uberon/issues/1229.
Based on the comments here above, I would say that currently we can argue that there is no evidence for a homologous relationship between the 'septum transversum' in sharks and the mammalian diaphragm. Please note that UBERON:0004161 septum transversum describes the (mammalian) embryonic structure that will give rise to the central tendon of the diaphragm, while here you are talking about a adult structure closer to a 'diaphragmaticus muscle'-like septum, as far as I understand.
But anyway thank you for your interesting question that points out a very exciting and rapidly evolving evo-devo field, as this recent paper also suggests
https://www.ncbi.nlm.nih.gov/pubmed/?term=27859325


text:
Can two half-cut potatoes fuse back together?
If I cut a potato in half, then I hold the two parts together, will the two halves fuse back into a single potato?

I'm voting to close this question as off-topic because it could easily be answered by running a very simple experiment.

I'm voting to close this question, it can be answered by a small practical. Also it's off-topic.

I do not agree. While the experiment can be done easily, it does not explain the underlying process. Will it hold together because it is glued by the starch, or do the cells regrow, or is there something that make it really impossible? As a novice in biology, I really thing this deserves a detailed answer.

A question does not become off topic simply because it can be easily answered using a simple experiment. It looks on topic (may be a bit funny but still related to biology) and can have a scientific answer.

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


text:
What is this colourful insect?
Found this colourful  insect in our garden. It measures about 1.5cm. I am from Kuching, Sarawak, Malaysiai

Not that colourful IMO! What do you think it could be? Look like some hymenoptera with its apocrita to me

The short orange antennae and the round eyes are those of a Diptera, although I can't tell the family

Check on from yr response i.e. Diptera order, I think it is from Family:Micropezidae.

This looks to me like a stilt-legged fly from the family Micropezidae.
https://www.singaporegeographic.com/insects/insect/stilt-legged-fly-micropezidae
Perhaps, more specifically:  Mimegralla albimana

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


text:
Is evolution of gametangia in land plants and charophyceae convergent?
Is the presence of gametangia in both land plants and charophyceae a result of convergent evolution or are they of the same origin (and have been lost in other types of algea)?


text:
How to selectively breed a plant?
Let's say I ordered seeds of a plant online. Then, I plant the seeds and grow a few plants. Then I take the seeds that the plants produced and separate them based on each plant.
Is it possible that I could then use those seeds to continue growing plants that have a desired characteristic? For example, if I wanted to grow taller and taller plants could I just keep planting seeds from the tallest plant? Or would I need to use a different method or technology to do this?

Yes, just planting seeds from the tallest plants would already do great. You could just chose an arbitrary size threshold under which you discard the seeds and above which you plant the seeds. Or you could plant all the seeds of the largest plant, almost all the seeds of the second to largest plant, all the seeds of the third largest plant etc... If plant height is a heritable characteristic (and it certainly is) then you will see a result after a few generations only.
You might want to ensure you understand the definition of heritability and the basics of quantitative genetics by reading the post Why is a heritability coefficient not an index of “how genetic” something is?.
Now instead of picking a random threshold for selection, you could be smarter and make some calculations. If you were to perform too a strong selection pressure (such as growing the seeds of the tallest individual only), then you will very quickly reduce genetic variation for height to zero and therefore remove all heritability. If you are using not a strong enough selection pressure, then you might barely see any changes even if you go on for many generations. Estimating the right type of selection pressure depends on the specific population you are facing (typically population size) and to its evolutionary history (typically previous selection on height or correlated traits and past population size).

Just a quibble: if the seeds are commercial varieties, they may be hybrids, and could be sterile or not capable of breeding true.  Also for commercial or hobby breeding, other techniques such as hybridizing between species or inducing chromosome polyploidy are used.


text:
Can upper motor neuron lesions cause hypotonia?
I have been taught that hypotonia is always caused by lower motor neuron lesions while hypertonia is by upper motor neuron lesions. However, I recently learned of an entity called central hypotonia, which means hypotonia caused by a central nervous system lesion. This makes it so confusing.

UML leads to disuse, this can also cause disuse atrophy and hense hypotonia.


text:
What is the difference between vegetable and fruit?
Is there any exact definition of vegetable and fruit? How can new plant be classified?

A true fruit is a ripened ovary that usually starts ripening when it is fertilized. And vegetable is any vegetative part of the plant which is edible and contains stored food probably in the form of starch.
These definitions are not exact as there are a lot of fruits which are fruits but do not strictly follow the given definition. See Syconus, Composite fruits, Sorosis.etc
Classification is based on several different criteria, for example the mode of reproduction, arrangement and design of flowering parts and flowers and also on the basis of habitat and habit.

From a culinary point of view, the difference between a vegetable and fruit is are they sweet or not.
Hence eggplant, tomatoes and bell peppers which are biologically fruits are considered vegetables.
Potatoes which are tubes, are considered vegetable. Kale which are leaves are considered vegetable. And cauliflower which are flowers are considered vegetables.
The question of fruit and vegetable would be might be tested if somebody made a very sweet and soft carrot, at which point I am not sure what the master chefs of the world might say. Could a soft and sugary sweet carrot be able to graduate into the word of fruits and leave the world of vegetables behind?

Please always make sure to include sources in your answers. See here for tips in writing good answers. This answer, which describes [biologically improper] culinary definitions, is inappropriate here (a biology site). Also, half your answer is proposing a new question -- which is further inappropriate within an answer. Please drastically improve this answer or it will likely be downvoted and/or deleted. Thanks.

I am answering the missing part of the question because somebody will then ask... but wait why is an eggplant called a vegetable? The phasing of the question vegetable or fruit... indicates this question. And really.. vegetable... that is not a biological category. A vegetable is a culinary category.

Then please provide that context and structure to your answer to make that clear. As written, your answer is off-topic. Regardless, you need to provide sources to back up all of your claims.


text:
Can I control my dreams?
Is it possible to completely realize that I am only dreaming and to completely manage my dream?
Thank you.


text:
Do animals also dream?
By "dream", I mean:

Dreaming while sleeping.
Dreaming about their future life while being awake.

Thank you in advance.

I think this question is useful and clear even if it shows little research effort (+1). IMO dreaming is an interesting biological phenomenon. I wish that those who gave the two downvotes gave justifications.

There have been experiments with cats whose brains were leisioned to eliminate sleep paralysis. These cats exhibited behaviors like hunting I imaginary  prey, grooming, etc. this was interpreted as a cat dreaming

You might be interested by this post

Yes, they do!

Dreams are simulations created by the brain in order to train us to cope with challenging situations. Most of the dreams present situations where the individual is confronted with challenges or risks he/she might face during the life. Evolutionary concept of dream suggests that its a way by which brain try to notify some risks and train us to invade through it. The evolutionary acceptance of dreams is due to the "threat simulation" feature it possess. By which an individual can gain advantage of several situations he/she confronts in life.

Finnish psychologist Antti Revonsuo posits that dreams have evolved
  for "threat simulation" exclusively. According to the Threat
  Simulation Theory he proposes, during much of human evolution physical
  and interpersonal threats were serious, giving reproductive advantage
  to those who survived them. Therefore dreaming evolved to replicate
  these threats and continually practice dealing with them. In support
  of this theory, Revonsuo shows that contemporary dreams comprise much
  more threatening events than people meet in daily non-dream life, and
  the dreamer usually engages appropriately with them. It is suggested
  by this theory that dreams serve the purpose of allowing for the
  rehearsal of threatening scenarios in order to better prepare an
  individual for real-life threats.

Question 1

Yes they do. Studies suggests that animals can dream while sleeping, entire  human dreams occur during the REM sleep period. Most of the mammals do have the REM sleep period and it suggests that they do dream in this time of sleep.

Dreams occur during REM sleep. We typically have 3 to 5 periods of REM
  sleep per night. They occur at intervals of 1-2 hours and are quite
  variable in length. An episode of REM sleep may last 5 minutes or over
  an hour. About 20% of sleep is REM sleep. If you sleep 7-8 hours a
  night, perhaps an hour and half of that time, 90 minutes, is REM
  sleep.
REM sleep is characterized by a number of other features including
  rapid, low-voltage brain waves detectable on the
  electroencephalographic (EEG) recording, irregular breathing and heart
  rate and involuntary muscle jerks.
  Reference

This link provides much more examples.
According to the studies of MIT,

Wilson, associate professor of brain and cognitive sciences at MIT,
  and biology graduate student Kenway Louie trained rats to run along a
  circular track for a food reward.
They monitored the animals' brain activity during the task and while
  they were asleep. While the animal ran, its brain created a
  distinctive pattern of neurons firing in the hippocampus, a brain area
  known to be involved in memory.
Like us, rats go through multiple stages of sleep, from slow-wave
  sleep to REM sleep. In humans, it is during REM sleep that most
  dreaming occurs.
The researchers then examined more than 40 REM episodes recorded while
  the rats slept. About half repeated the unique signature of brain
  activity that was created as the animal ran. The correlation was so
  close that the researchers found that as the animal dreamed, they
  could reconstruct where it would be in the maze if it were awake and
  whether the animal was dreaming of running or standing still.
These memories were replayed at about the same speed that the animal
  had experienced them while awake.
  Reference

Question 2

Dreaming about their future life while being awake, good question. If they do so then it will be a contradiction to our long held view of animal thought process. Most of the animal thought process that we try to reveal is through the firing of particular areas in their brain with the association of certain hormones. By this process we can find that which all neural pathways are used while dreaming and which are not.
As we can find that animals also have dreams, then it is obvious that they could recollect it (some what vague) and can prepare mentally to face those particular situations. This doesn't mean that they do have plans about events coming for them in future, but researchers states that dreams are their only offline experience with those events. The memory of those dreams help them to ensure little advantage over those future events. While in the case of humans, we have a highly complex brain which is so good at simulating events by which we can plan our future, but other animals lack this complex structure(complex but not as much as ours), so they entirely rely on dreams for that purpose.

Why do animals dream about one experience and not another? "This work
  allows us to evaluate the content of dreams and create tests to see
  which awake patterns create patterns when the animal is asleep,"
  Wilson said. "If we are able to evaluate the content of the dreaming
  state, we may be able to find out why certain events get replayed and
  others don't."
This work also raises questions about long-held assumptions about
  animals' thought processes. Only a handful of species — among them
  chimps and dolphins — were thought to have any ability at all to
  recall and evaluate detailed sequences of events after they occurred.
  Wilson points out that "dreams are the ultimate off-line experience.
  This work demonstrates that animals are capable of re-evaluating their
  experiences when they are not in the midst of them."
  Reference

+1 you say that " rapid, low-voltage brain waves [are] detectable on the electroencephalographic (EEG) recording". Unfortunately your [Reference] link doesn't work, whether they give amplitudes (voltages) and frequencies of the brain waves there. Can you tell? Does this apply to humans or animals?

@draks...: These low voltage brain waves are called "delta waves". Delta waves, like all brain waves, are detected by electroencephalography (EEG). Delta waves were originally defined as having a frequency between 1-4 Hz, although more recent classifications put the boundaries at between 0.5 and 2 Hz. Delta waves occur in all mammals, and potentially all animals as well.

From the ScientificAmerican

Yet, given the vast documentation of realistic aspects to human dreaming as well as indirect experimental evidence that other mammals such as cats also dream, evolutionary psychologists have theorized that dreaming really does serve a purpose.

Although the linked article doesn't look like they were talking about animals. But I wont purchase the article to check that...
As for your second question, I would say yes, when you would say, making a plan is equivalent to dream of the future. Crows are smarter than you think...

@fileunderwater OK I included it, but why do you think my edit is not an answer to the second question?

Mostly because it wasn't a full answer on its own, and only hinted at a possible answer. As a small addition to your first answer it might useful, but it would be much better if you expanded and explained what you actually mean. At the moment, the addition is only an empty proposition and a link.

@fileunderwater why protecting this question?

It has received 6 comment-like answers that are now deleted. The protection only serves to discourage comments/answers from users that are not familiar with the site (<10 rep), and it has no other effect.


text:
Can we change one's genome into the genome of somebody else
If I (grown-up individual and not just an egg after fertilization) wanted your exact genome, would we be able with today's technology to change my genome into yours?

Do you mean if all genetic material in a grown-up person can be modified?

No, that would be practically impossible with modern technology. The explanation is pretty lengthy, but do you have specific questions or a certain method you were thinking of that could be more concretely addressed?

@Tusky - The future doesn't necessarily mean centuries from now... the future is also tomorrow ; )

@gstestso I am trying to save your posts today $\ddot \smile$. I rewrote your post to clarify it. It still is a very introductory question but at least it gets rid of the feeling it gave that your question mixed philosophy and science (the definition of a "person" goes way beyond its DNA and the question of identity is a question of philosophy not biology). Feel free to roll back if you don't like my edits.

@Gstestso If you think your question has been answered (which is my feeling), then please check the answer you prefer below (same for your other posts). Thanks

There are 3.72x1013 (37 trillion) cells in the average adult human body. It would be essentially impossible to target every single cell just to change a single base pair, let alone the massive genetic and epigenetic changes that would be necessary to change someone into a clone of another.

I am going to go one step further than Matt and say it would be impossible even if we had the technology.
And here is why.
Lymphocytes, B-Cells and T-cells, through V-J and V-D-J joining actually recombine their DNA as they are maturing, they cut out long stretches of DNA, so each and every one of those cells has regions of DNA that are different from every other cell in your body.
Then even when they get selected and go through clonal expansion those regions of DNA go through a process called somatic hypermutation which deletes and replaces nucleotides in the hyper variable regions of those genes, in the hopes of making them better binders.
So you would then have to account for every single one of those unique genomes, and the only way to do that would be to destroy the cells, so in the Biological equivalent of the Heisenberg uncertainty principle, the act of observing effects the outcome because you would be changing the other person as well. So you will never ever be able take on the complete genetic make-up of someone else.


text:
Will moths evolve to become blue if we paint walls in blue?
I know dark moths are more frequent than white moths when the environment is full of dirty (dark) walls/trees; it is a consequence of natural selection. Will moths evolve to become blue if walls/trees are painted in blue?

There were a few languages issues in your post. I rewrote it (Note, btw that english is not my mother tongue). Feel free to roll back if you don't like my edits. Note that my edits will likely make future readers think you have a better understanding of evolutionary processes that you actually do.

I think the question was poorly formulated (mainly for language issues) and is quite introductory but I think it can still be answered. I don't vote to close.

Note that the following answer is an over simplification. For example, I don't consider cases of balancing selection.
What is Natural Selection?
Definition
Natural selection is the process that yield to a change in allele (≈variant of a gene) at a given locus (=position on a chromosome) frequency in a population due to a differential in fitness (≈reproductive success) between individuals carrying the different alleles.
What Natural selection does
By selecting some alleles over others, natural selection ultimately causes a decrease in the genetic variance to the extreme point where only the beneficial allele is left in the population. Of course, in the absence of genetic variance (that is if there is only one allele at a given locus), natural selection cannot act.
Where does genetic variance come from then?
If natural selection decreases genetic variance, how come there is some genetic variance left in population then. The answer is mutations.
Will the moth population become blue if you pain all walls (or trees) in blue?
Intro
The moths could vary from white to dark because there is genetic variance for the level of pigmentation in their population.
Note of course that for the blue variant to be beneficial (=to have a higher fitness) when the walls are painted in blue, you will need predators (as the moth colour evolve first as a camouflage to hide from predators) and you will need to assume that it is not too costly to produce the blue pigments.
If there is no "blue" allele
If there is a few alleles coding for being blue, then if you paint walls in blue, you will see a change in the frequency of blue individuals in the population just as we saw changes in the frequency of white/black individuals in the population.
If there are "blue" alleles
If there is no allele coding for being blue in the population, then you will need to wait for a mutation (or a series of mutations) to give the ability to produce blue pigments. This may take a very long time (can be approximated by a sum of exponential distribution) with parameters that depend on the exact developmental processes of the moth.
Why down votes and close votes
I think (but I might miss the some reasons) you receive them because...

there are a few english mistakes and that makes the question a bit difficult to understand. I tried to fix that issue.
The question is quite introductory and I think that having a look at an introductory course to evolutionary biology (such as Understanding Evolution for example) will help you.


text:
dominance coefficient, why (1+k)?
I'm trying to get a better understanding of quantitative genetics by reading Lynch and Hill 1986. I'm getting stuck with some notation that's used right at the beginning referring to the mutant and WT alleles at a given loci.
2ai is the genotypic value for WT homozygous
(k+1)ai is the genotypic value of the F1 heterozygous
 0 genotypic value for the non-existent "mutant" homozygous
From my understanding, a is the additive genetic effect and k is the dominance coefficient. I understand that 2ai is the additive genetic effect at this particular loci which moves this trait away from the population mean for this trait.
Can someone explain the (1+k)? I understand that there could be dominance between the new and old allele, but I don't understand why 1 needs to be added to the dominance coefficient.

Without digging into the paper to be sure, it seems to just be a definitional thing.  Including the "+1"  would allow the dominance coefficient (k) to scale between -1 for perfectly recessive to +1 for perfectly dominant.


text:
Does mass spectrometry data have units?
I am reading some journal papers about the proteome of certain brain structures. In these papers, they used mass spectrometry to identify the proteins that were present in the brain structure as well as their abundance. In one paper, they performed high-performance liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis. In another paper, they performed nanoLC-high resolution mass spectrometry and used a tandem mass tags (TMT)-based labelling approach.
I am interested in finding out whether certain proteins are expressed in these brain structures. I have downloaded the supplementary tables from the papers that gives information about average level (as they had several samples of the brain structure) of each protein found in that brain structure. However, I am new to analysing mass spectrometry data and I unsure about what are the units of mass spectrometry data. I could not find anything regarding the units of the data in the papers or their supplementary tables.
In general, I was wondering for mass spectrometry data, what are the units used to describe the abundance of a protein in a sample? For example, in RNA-Seq data when quantifying the number of gene transcripts you have normalised read counts such as RPKM/TPM. These values can be averaged across samples such that you get the average RPKM/TPM value for a gene.

Can't you just weigh the sample first?

You really need to refer to either a concrete example in a paper that we can interpret, or state precisely what it is you want to do — compare proteins in one experiment, from different experiments, determine absolute concentrations or what? The “data” is obviously a spectrometries trace in which you can measure the height of a peak, or the area under it. This obviously has no units as such.

@David I am trying to interpret the data from this paper (https://www.sciencedirect.com/science/article/pii/S2211124721012572). In Supplementary Table 1 of this paper (where they show the average levels of each protein in the synaptosomes), I am trying to figure out what the unit of protein abundance is.

@ceno980 — I see you have accepted an answer, but I'll have a look at it tomorrow and add any additional comments I may have.

@David Thank you

As far as I can see from the paper they mention "the availability of lipid standards for quantification" so I imagine that quantification (in standard units of concentration) is  based on comparison of the area under the curves of standards and unknowns.

I think MS data, like other spectroscopy and chromatography data, is usually quantified by comparing peak areas (in arbitrary units) to those of a quantitative standard. So the Y axis is just the intensity of the signal, often which doesn't display its direct experiment readout units  (like current or voltage). In other words, you need the results of control or calibration experiments extraneous to the raw MS data.

I don't think the units are 'arbitrary' per se, but rather are the units that result from integrating the signal with respect to time. If the units of the variables are not arbitrary, which for physical units they are not, then the definite integral's units are not arbitrary either. For someone interested in the concentration of an analyt, it is true that the (usually linear) calibration converts this area measure into units of concentration (or similar) such as Molar. That aside, I think your answer cuts pretty cleanly to the point (+1).


text:
Why do bacteria denitrify?
Denitrification is the microbial respiration in anoxic condition. If the process is complete we have :
$$2 \text{NO}_3^{-} + 10 \text{e}^{-} +12\text{H}^+ \rightarrow \text{N}_2 + 6 \text{H}_2\text{O}$$
In this series of reactions, nitrate and hydrogen are transformed into nitrogen and water with bacteria's energy. All the elements are given back to the environment. So why do bacteria denitrify? What do they take for themselves in this process?

The same thing they get from aerobic respiration, just less of it.

Need water? Need to lower pH? Remove excess nitrogen to something relatively inert?  These questions might serve to hypothesize about the 'biological function' that this chemical reaction serves in the metabolism of an organism.

nitrate is energy you can even use it to make explosives so it contains a lot of energy for bacterial growth.

Welcome to SE Biology. One of the things we ask people who ask questions to do is to research their question themselves before posting, and tell us what they found and how it was insufficient for their purposes. One obvious resource is WIkipedia which gave me the answer. Did you try that and understand the page? You say that this process uses energy — but that is not correct. Have you learned about energy generation in living organisms?

I said 'lower pH' above, but rather it would be 'raise the pH'. I meant lower the hydronium concentration rather than lower the pH.

On the topic of energy, "Denitrifying bacteria use denitrification to generate ATP." is suggestive.

Notice that the reverse process, biological nitrogen fixation, requires lots of energy.


text:
Receptors and their distribution over the human population
For humans it has been reported that there are three vasopressin receptors (AVPR1a) and four dopamine receptors (DRD2). (Source: UNIPROT)
Question: Does every human contain all three variants of AVPR1a? Or is it the case that some individuals contain fewer than the three variants found in the total population?

do you mean variation in one gene or presence and absence of multiple paralogs/copies of these genes? I don't see where you are getting this info in uniprot, directly linking/screenshotting would be helpful.

Short answer: my database search yielded different results: Three receptors were identified with different names: AVPR1A, AVPR1B, AVPR2.
I have actually never heard of a distinct human population completely lacking one gene (I might be mistaken). Usually, only single nucleotide polymorphisms vary between populations. I also do not think that this matters, unless your project addresses specifically that question.
I find three paralogues of the vasopressin receptor (homologous copies of a "similar" receptor found on different chromosomes): AVPR1A, AVPR1B, AVPR2 (might have missed one though)
If these receptors pop up in a search in a human database, their mRNA (cDNA) was sequenced at some point from human tissue and annotated to the genome.
Protein Atlas shows two splice variants ("number of transcripts") of AVPR1A.
NCBI shows one splice variant of AVPR1a from three different databases (MANE, NCBI, Ensembl). (please see this tutorial to use the NCBI-genome viewer)


text:
What determines whether I will have any dream or not?
Sometimes I have many consecutive "dreamfull" nights but sometimes there is no dream during week. Why? What determines whether I will have any dream or not?


text:
Color van der waals bonds in swiss PdbViewer
I'm trying to color certain amino acid's van der waals bonds as in the following picture:

can anybody please describe the steps to accomplish that?

Use Photoshop? Please clarify, I assume you want to do this using the same program that produced the image, so tell us what you're using!

If I'm right in assuming you are trying to get colouring like the purple AA VDW bonds then I can only specifically colour VDW bonds in solid 3D view (under display, Render in solid 3D) in SPDBV but not when solid 3D view is not activated, as in the example in your picture. One option is to use POV-Ray but I haven't worked with it.

@Bez thank you, so I guess it's possible only via 3d mode, please consider writing your comment as an answer so I could mark it as the right one

If I'm right in assuming you are trying to get colouring like the purple AA VDW bonds then I can only specifically colour VDW bonds in solid 3D view (under display, Render in solid 3D) in SPDBV but not when solid 3D view is not activated, as in the example in your picture. One option is to use POV-Ray but I haven't worked with it.
If the purple colouring is not photoshoped by the authors of the paper you got the picture from, then the chances are they have written a custom script for it in the software, which allows them to do this. So I would just contact the corresponding author and ask them how they managed it and if they have done it through a script or some other software. Most of the time people are happy to share their methodology once they have published it!
Also have you tried the Jalview software? Although it's designed primarily as an alignment tool but it has a nice 3D Jmol view. You can load up your sequence and the associated PDB file and you can play around with it. The graphics output are quite publication friendly. I'm not an expert at it and I've only been playing around with it for a bit but when you get the hang of it, it's quite nice graphically. Although the VDW view is still space fill 3D but it's a bit nicer as it has opacity etc etc. Just download it and as soon as you open it up, you are presented with an example alignment and Jmol view. Just play around with the alignment section and the Jmol view and see if you like the aesthetics. The only tricky part in the software is getting the residues you want selected but once you manage that, you can get the program to display VDW only for the selected residues.
Hope this helps.

You might also want to look at which version of SPDBV was used to generate that image. It's not uncommon that certain features of applications get disabled in new versions for whatever reason.


text:
Why is neutralizing important when carrying out the Benedict test?
When testing for non-reducing sugars, acid is added, then the solution is boiled, then it is neutralized, benedict solution is added and then it is boiled again. Why is neutralizing the solution important?

Benedict's reagent is used mainly to test the presence of reducing sugars.
However, it can also be used to test non-reducing sugars indirectly. For that to happen, non-reducing sugars are first converted to reducing sugars by breaking glycosidic bonds in the presence of acid (ex: HCl).
Now, the next step is to check for the presence of reducing sugars using Benedict's reagent. Before adding our reagent, neutralization is done because the benedict's reagent requires an alkaline environment to work properly.
After neutralization only, the benedict's test proceeds further.
Note -> Since, Benedict's reagent is an alkaline solution, so the test solution is only neutralized and not made alkaline in nature.
For more info -- https://www.enotes.com/homework-help/what-steps-testing-non-reducing-sugar-704998


text:
Why isn't the Ramachandran plot symmetric?
Since only relative position of groups along a bond is considered while calculating torsional strain and considering "+" and "-" means clockwise and anti clock wise rotation, shouldn't any set of $\phi$ and $\psi$ angle say (x, y) satisfying the energy consideration have correspondingly (-x,-y) since they are relatively the same configuration? But only the Ramachandran plot for glycine shows this symmetry, see below, why doesn't this show for all the proteins?

Not what you are looking for per se, but note that the Ramachandran plot is a field over a subset of $\mathbb{R}^2$. Such a field will have a parity decomposition which relates to reflection invariance (symmetry) and reflection equivariance (i.e. odd "symmetry").

Welcome to SE Biology. However . I can't understand your question as it stands, and I've published papers with Ramachandran plots in them. To explain something like this you absolutely need a diagram and you need to explain exactly what Ramachandran plot you are referring to. (And please do not give links to common terms from Wikipedia — we don't need to know what glycine is, but a plot of glycine in some context showing symmetry would help.)

Wikipedia has a Rama plot of glycine. Is that representative of the symmetry you mentioned?

@AgnesianOperator yes

but only the Ramachandran plot for glycine shows this symmetry

With the exception of glycine, all the common amino acids exhibit chirality at the carbon atom adjacent to the carboxyl group.

Except for glycine, the amino acids exist as chiral molecules in two forms, the L- and D-enantiomers. Although the two enantiomers exhibit identical physical and chemical properties, living organisms use only amino acids of L-chirality.

Jeong, Y., Kim, H.W., Ku, J. et al. Breakdown of chiral recognition of amino acids in reduced dimensions. Sci Rep 10, 16166 (2020).

+1 I thought of this but wasn't confident. In principle if we switched the left-right handedness of each chiral center, would we expect to see the reflection of the original Rama plot on the Rama plot of the reflected molecule?

That sounds correct to me.

It's awkward answering your own question, but I think I have now realized where my misconception arose from.
If we look at the 3 dimensional structure of a protein

and consider the third alpha carbon to visualize. Let us take phi and psi as (x, y) and (-x, -y), then the groups associated with nitrogen and carbonyl carbon attached to alpha carbon are relatively in same configuration for both (x, y) and (-x, -y) but here we are missing to consider the relative configuration of groups attached to carbonyl carbon and nitrogen with respect to the group attached to the alpha carbon, since if a clockwise rotation of psi brings the oxygen attached to the nitrogen closer to hydrogen, then the anticlockwise rotation will bring the oxygen closer to the side group, thus clockwise rotation and anticlockwise rotation of phi or psi is not symmetric when considering it with respect to the alpha carbon. Since the alpha carbon of glycine has another hydrogen attached to it instead of a side chain both clockwise and anticlockwise rotation become equivalent leading to a symmetric graph.
If we say that (x, y) is stable for an L- amino acid chain then (-x, -y) will be stable for D- amino acid chain (we can imagine this as R and H on alpha carbon switching places for L and D amino acids, thus the once stable counter clockwise orientation for L- amino acids will now have to be clockwise for D-amino acids for it to be stable again)

It's awkward answering your own question - actually it's encouraged! If you find an answer to your own question otherwise, please include it as an answer.


text:
Photolysis of water
Photolysis of water releases $\text{O}_2$, $\text{H}^+$ ions and $\text{e}^-$.
$\text{Mn}$ in the $\text{O}_2$ evolving complex also produces $\text{e}^-$.
What provides $\text{e}^-$ to P680:$\text{Mn}$ and water?

Can you clarify your sources and where this information derives from? Even though this is related to fundamental biochemistry that every undergraduate learns, it's still good for us to understand what your materials are.

Consider this diagram from Wikipedia.


text:
What are the (evolutionary) advantages of secondary transport?
Secondary active transport uses electrochemical gradients as a source of energy for the uphill transport of substrates (coupled to downhill transport of the ion).
However except for in a few cases (e.g. Electron transport chains) the electrochemical gradient is formed by ATPase pumps which use energy from ATP to pump the ions.
So why not just use ATP in the first place (and not have to set up the gradient). (I do understand that the gradients are useful for signalling, action potentials etc. but that is a seperate issue.) i.e. What is the advantage of secondary transport.
My (complete) speculation:
Is secondary transport perhaps used because it allows a sort of inherent regulation. Stop the gradient forming pump and you immediately stop all the secondary transport using that particular gradient? If that is the case are secondary transport proteins in groups with similar functions/pathways utilising the same gradient?

I'm not sure if I understand the question properly. Essentially, it seems like you are asking why the protein network is one way compared to another simpler design. The answer to that is likely to be speculative; something to do with evolutionary ancestry of the proteins and possible functional redundancy built into the network. These types of questions at the organism level are often closed as duplicates of "Why do some bad traits evolve, and good ones don't?"

@James, I was actually presuming that there is an evolutionary reason for secondary transport, i.e. it has some sort of advantage and thus is so pervasive. My question is whether there are any hypothesises (preferably with evidence) as to what that advantage may be? I've tried to make the question more explicit.

I have not read the post but the title question (Why have secondary transport?) is grammatically wrong and does not mean anything. You should edit that.

I think an easy analogy for why this approach evolves is to think of how humans use electricity (or energy more broadly).
Although it is feasible to have localized electricity generators (for example, a solar panel on a simple calculator), it's typically more efficient to have centralized electricity production. With that organization, changes to the electricity generating machinery can proceed without any changes needed at the end user. If the power plant improves efficiency by 10%, that improves the efficiency of the entire system without a change needed in every lightbulb, refrigerator, and phone charger.
Once an ion gradient is established, different independent systems can use it to perform otherwise energetically unfavorable tasks. Of course this is not the only way evolution could proceed: as linked in a comment there are several general explanations for why evolution doesn't produce every possible combination. There are in fact a lot of proteins that use ATP directly.
The sodium-potassium ATPase that powers one of the major secondary transport systems is particularly interesting because it moves 5 ions at a time, making it very efficient. It would waste ATP if it only exchanged 2 ions at a time. By producing that gradient, other proteins can then evolve to use this gradient at an appropriate energy level rather than needing to work on a "1 ATP = 1 cycle" basis.

also keep in mind a common active ion being transported out that drives it is sodium and it is easy to see why the transport of sodium out of the cell would evolve by itself in some environments. once it exists it can be exploited for other purposes. the other common ion is H+ which can be used on it own to regulate PH.


text:
Is complete dominance actually a genotypic process?
An example often stated for codominance is blood groups, where both alleles version of the protein is expressed and can be found in the cell membrane.
An example of incomplete dominance often given is of red and white flowered snapdragons giving pink flowered offspring because enzymes for both pigments are transcribed and translated and the mixing of these pigments gives the intermediate phenotype.
In both these examples both alleles are transcribed and translated.
In the text-book mendelian situation of a dominant and recessive allele are there actually a cellular mechanisms by which a 'dominant' allele silences the 'recessive' allele and inhibits it's translation, transcription or both? If so are there any well characterised examples?
Or are all alleles actually codominant at the transcription/protein level? e.g like in many recessive gentic diseases where both the mutant and the normal protein are present (cystic fibrosis, sickle cell anemia etc) but the activity of the normal protein gives the 'healthy' phenotype.

Related: Evolution of dominance of alleles

I don't think dominance is subjective at all. Do you have any references for the claims you made? For example "for a physician the healthy allele is dominant".

As @Cell said, you seem to confound dominance with fitness. Make sure to clarify that. Many people also confound dominance and frequency. Make sure to understand that these concepts are very different.

@Cell I'll reword the question but I am paraphrasing from an example in my undergrad lectures

@Mirte It is a good question +1. Can you please make sure to cite your source (what text-book are you referring to) and eventually give a direct quote (although you don't necessarily have to).

"Or are all alleles actually codominant at the transcription/protein level?"
Yes this is the right idea. Generally all alleles are transcribed independently (with some exceptions like in females where one X chromosome is inactivated). And the dominant and recessive phenotypes are in a sense extreme cases of codominance. The terms are used for describing phenotypes and depend on thresholds of activity. In the snapdragons example we can associate 2 functional enzymes EE with the red phenotype and white (lack of red pigment) associated with 2 nonfunctional enzymes ee. But one E is not enough to make the red pigment so we see some red pigment and a pink phenotype.
Now consider a yeast cell with 2 hexokinase genes (H). With two inactive proteins (h/h), the cell will grow slowly. Now let's say that H is a very efficient protein and that glucose transport into the cell is rate limiting so one active H has the same phenotype as having 2 H/H, so H/H is the same as H/h thus H is a dominant allele and h is recessive because one H is past the threshold of activity for fast growth on glucose. h is recessive because h/h genotype is needed to see the h phenotype. Hope that helps.

An example of incomplete dominance often given is of red and white
  flowered snapdragons giving pink flowered offspring because enzymes
  for both pigments are transcribed and translated and the mixing of
  these pigments gives the intermediate phenotype.

White snapdragons are not making a white pigment.  A step in the pigment-making pathway fails, because a needed gene is broken.  A snapdragon with one working pigment enzyme allele makes some pigment, but not as much as one with two working enzyme alleles.
https://en.wikipedia.org/wiki/Haploinsufficiency
A blood does not react to A blood.  B blood does not react to B blood.  AB blood doesn't react to A or B blood.
One copy of the A allele does all the same stuff as having two copies.  One copy of a working pigment enzyme does not make as much pigment as two working copies.

In both these examples both alleles are transcribed and translated.

It is not at all clear to me that the broken pigment enzyme is necessarily translated at the same rate as the working one.  There are cellular mechanisms to clear away non-functional transcripts, the broken enzyme transcript might be subject to those processes.
https://en.wikipedia.org/wiki/Nonsense-mediated_decay
Or the defect in the broken allele might be in its promoter, preventing it from being transcribed at all.


text:
How can there be a one-to-one correspondence between RNA and genes?
From what I know, multiple strands of DNA make up a gene, so how can for each gene there can only be one RNA corresponding to it and vice versa? Is my knowledge incorrect?

how are you defining "gene"?

By multiple strands do you mean two strands of DNA ? By what I have understood from your question you seem to ask how can a single RNA be formed when a gene is a fragment of a DNA (ds DNA) . Isn't it?

No, I mean doesn't a combination of DNA molecules form a gene?

No. Each gene is on a single molecule of DNA.

Very few things are that clear cut in biology. There are three main things to consider here.
1. Gene to RNA
Most eukaryotic genes are spliced. This is basically a process by which a single gene can be transcribed to multiple, different, mRNAs each of which will then be translated to a different protein.
Therefore, there is usually (some genes aren't spliced) not a one-to-one correspondance between a gene and the mRNAs it can produce.
2. RNA to Gene
The next issue is that some genes exist in multiple, similar copies in the genome. For such genes, it is not always possible to know which of the duplicates was actually read to produce a given mRNA.
There is, therefore, not always a direct one-to-one correspondance between an mRNA and the gene it was transcribed from. This, however, is far less common than the splicing issue mentioned above and can, in most cases, be ignored.
3. Each gene is only on a single strand
Each gene is only on a single strand of DNA. Yes, DNA is double stranded, but each gene resides on only one of the two strands (the other strand will be the reverse complement of the gene).

Despite the points made above, it is actually usually possible to map an mRNA molecule to the gene that produced it. In the case of duplicate genes you'll just get multiple hits. The programs that exist to do this sort of analysis can mostly deal with splicing. So, for example, if you have the sequence of the human chromosome 21 and the mRNA sequence of the ERG gene, you can do (on a *nix system with exonerate installed):
exonerate -m coding2genome -t chr21.fasta -q dscam.fasta > out

Which will produce:
Command line: [exonerate -m est2genome -n 1 -t chr21.fasta -q erg.fasta]
Hostname: [oregano]

C4 Alignment:
------------
         Query: gi|609878487|ref|NM_001291391.1| Homo sapiens ERG, ETS transcription factor (ERG), transcript variant 8, mRNA
        Target: gi|528476536|ref|NC_018932.2| Homo sapiens chromosome 21, alternate assembly CHM1_1.1, whole genome shotgun sequence:[revcomp]
         Model: est2genome
     Raw score: 7669
   Query range: 0 -> 1546
  Target range: 39594417 -> 39332536

        1 : GTTTTCACTTGGTCGGAATGGGGAGAGTGTGCAAGAGATCGCTGCGGGACAGGT :       54
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39594417 : GTTTTCACTTGGTCGGAATGGGGAGAGTGTGCAAGAGATCGCTGCGGGACAGGT : 39594364

       55 : TCCTAGAGATCGCTCCGGGACGGTCGTGACGGCCCCCGAGGGACATGAGAGAAG :      108
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39594363 : TCCTAGAGATCGCTCCGGGACGGTCGTGACGGCCCCCGAGGGACATGAGAGAAG : 39594310

      109 : AGGAGCGGCGCTCAG  >>>> Target Intron 1 >>>>  GTTATTCCAG :      133
            |||||||||||||||++         76685 bp        ++||||||||||
 39594309 : AGGAGCGGCGCTCAGgt.........................agGTTATTCCAG : 39517600

      134 : GATCTTTGGAGACCCGAGGAAAGCCGTGTTGACCAAAAGCAAGACAAATGACTC :      187
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39517599 : GATCTTTGGAGACCCGAGGAAAGCCGTGTTGACCAAAAGCAAGACAAATGACTC : 39517546

      188 : ACAGAGAAAAAAGATGGCAGAACCAAGGGCAACTAAAG  >>>> Target In :      226
            ||||||||||||||||||||||||||||||||||||||++         9093
 39517545 : ACAGAGAAAAAAGATGGCAGAACCAAGGGCAACTAAAGgt.............. : 39517505

      227 : tron 2 >>>>  CCGTCAGGTTCTGAACAGCTGGTAGATGGGCTGGCTTACTG :      266
            bp         ++|||||||||||||||||||||||||||||||||||||||||
 39517504 : ...........agCCGTCAGGTTCTGAACAGCTGGTAGATGGGCTGGCTTACTG : 39508374

      267 : AAGGACATGATTCAGACTGTCCCGGACCCAGCAGCTCATATCAAG  >>>> Ta :      312
            |||||||||||||||||||||||||||||||||||||||||||||++
 39508373 : AAGGACATGATTCAGACTGTCCCGGACCCAGCAGCTCATATCAAGgt....... : 39508326

      313 : rget Intron 3 >>>>  GAAGCCTTATCAGTTGTGAGTGAGGACCAGTCGT :      345
             130340 bp        ++||||||||||||||||||||||||||||||||||
 39508325 : ..................agGAAGCCTTATCAGTTGTGAGTGAGGACCAGTCGT : 39377955

      346 : TGTTTGAGTGTGCCTACGGAACGCCACACCTGGCTAAGACAGAGATGACCGCGT :      399
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39377954 : TGTTTGAGTGTGCCTACGGAACGCCACACCTGGCTAAGACAGAGATGACCGCGT : 39377901

      400 : CCTCCTCCAGCGACTATGGACAGACTTCCAAGATGAGCCCACGCGTCCCTCAGC :      453
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39377900 : CCTCCTCCAGCGACTATGGACAGACTTCCAAGATGAGCCCACGCGTCCCTCAGC : 39377847

      454 : AGGATTGGCTGTCTCAACCCCCAGCCAGGGTCACCATCAAAATGGAATGTAACC :      507
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39377846 : AGGATTGGCTGTCTCAACCCCCAGCCAGGGTCACCATCAAAATGGAATGTAACC : 39377793

      508 : CTAGCCAGGTGAATGGCTCAAG  >>>> Target Intron 4 >>>>  GAA :      532
            ||||||||||||||||||||||++         21741 bp        ++|||
 39377792 : CTAGCCAGGTGAATGGCTCAAGgt.........................agGAA : 39356027

      533 : CTCTCCTGATGAATGCAGTGTGGCCAAAGGCGGGAAGATGGTGGGCAGCCCAGA :      586
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39356026 : CTCTCCTGATGAATGCAGTGTGGCCAAAGGCGGGAAGATGGTGGGCAGCCCAGA : 39355973

      587 : CACCGTTGGGATGAACTACGGCAGCTACATGGAGGAGAAGCACATGCCACCCCC :      640
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39355972 : CACCGTTGGGATGAACTACGGCAGCTACATGGAGGAGAAGCACATGCCACCCCC : 39355919

      641 : AAACATGACCACGAACGAGCGCAGAGTTATCGTGCCAGCAG  >>>> Target :      682
            |||||||||||||||||||||||||||||||||||||||||++         19
 39355918 : AAACATGACCACGAACGAGCGCAGAGTTATCGTGCCAGCAGgt........... : 39355875

      683 :  Intron 5 >>>>  ATCCTACGCTATGGAGTACAGACCATGTGCGGCAGTGG :      719
            698 bp        ++||||||||||||||||||||||||||||||||||||||
 39355874 : ..............agATCCTACGCTATGGAGTACAGACCATGTGCGGCAGTGG : 39336142

      720 : CTGGAGTGGGCGGTGAAAGAATATGGCCTTCCAGACGTCAACATCTTGTTATTC :      773
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39336141 : CTGGAGTGGGCGGTGAAAGAATATGGCCTTCCAGACGTCAACATCTTGTTATTC : 39336088

      774 : CAGAACATCGATGGGAAGGAACTGTGCAAGATGACCAAGGACGACTTCCAGAGG :      827
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39336087 : CAGAACATCGATGGGAAGGAACTGTGCAAGATGACCAAGGACGACTTCCAGAGG : 39336034

      828 : CTCACCCCCAGCTACAACGCCGACATCCTTCTCTCACATCTCCACTACCTCAGA :      881
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39336033 : CTCACCCCCAGCTACAACGCCGACATCCTTCTCTCACATCTCCACTACCTCAGA : 39335980

      882 : GAGA  >>>> Target Intron 6 >>>>  CTCCTCTTCCACATTTGACTT :      906
            ||||++          867 bp         ++|||||||||||||||||||||
 39335979 : GAGAgt.........................agCTCCTCTTCCACATTTGACTT : 39335088

      907 : CAGATGATGTTGATAAAGCCTTACAAAACTCTCCACGGTTAATGCATGCTAGAA :      960
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39335087 : CAGATGATGTTGATAAAGCCTTACAAAACTCTCCACGGTTAATGCATGCTAGAA : 39335034

      961 : ACACAG  >>>> Target Intron 7 >>>>  GGGGTGCAGCTTTTATTTT :      985
            ||||||++         1911 bp         ++|||||||||||||||||||
 39335033 : ACACAGgt.........................agGGGGTGCAGCTTTTATTTT : 39333098

      986 : CCCAAATACTTCAGTATATCCTGAAGCTACGCAAAGAATTACAACTAGGCCAGG :     1039
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39333097 : CCCAAATACTTCAGTATATCCTGAAGCTACGCAAAGAATTACAACTAGGCCAGG : 39333044

     1040 : TACGAAAACACCCCTGTGTGATCTCTTCATTGAGAGACATCCCAGATGTCCTGC :     1093
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39333043 : TACGAAAACACCCCTGTGTGATCTCTTCATTGAGAGACATCCCAGATGTCCTGC : 39332990

     1094 : TGAGATCCGTGCCCTAAGTCACGTGATACAAAGAGAGCTGATCCCGGAGCTGAA :     1147
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332989 : TGAGATCCGTGCCCTAAGTCACGTGATACAAAGAGAGCTGATCCCGGAGCTGAA : 39332936

     1148 : GCCAGTCCCAGACAGTCTTATTCTGCCTCTGTTGATTTGGAGACTAAATCCACT :     1201
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332935 : GCCAGTCCCAGACAGTCTTATTCTGCCTCTGTTGATTTGGAGACTAAATCCACT : 39332882

     1202 : CAAACCATTTCATTCAAAGACCACACTAAAGGAATTAAGAGCAGATTAGCCCTT :     1255
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332881 : CAAACCATTTCATTCAAAGACCACACTAAAGGAATTAAGAGCAGATTAGCCCTT : 39332828

     1256 : TAACTAGCTTTTCAGAAAGACAGATGGGCAAAGAAGGCATCCTGGATGCCTGGC :     1309
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332827 : TAACTAGCTTTTCAGAAAGACAGATGGGCAAAGAAGGCATCCTGGATGCCTGGC : 39332774

     1310 : AGTTAGGAATAGGCCGACTTTTGAACTAACAGAAGGATCTGTCCCTCCTCGGGG :     1363
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332773 : AGTTAGGAATAGGCCGACTTTTGAACTAACAGAAGGATCTGTCCCTCCTCGGGG : 39332720

     1364 : GAAGAGCACAAAACAAGGACACTCCCCAGATTCACAGTGACCGATTATCAGTAT :     1417
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332719 : GAAGAGCACAAAACAAGGACACTCCCCAGATTCACAGTGACCGATTATCAGTAT : 39332666

     1418 : GTCACAAGAAGCCAGTCTTGCAGAGCAGAAGCATGCAACCAGTAGTATTTACAT :     1471
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332665 : GTCACAAGAAGCCAGTCTTGCAGAGCAGAAGCATGCAACCAGTAGTATTTACAT : 39332612

     1472 : CTGAATCTTACTGCCTGTCCTCCAAATGATTTAATTAGGTAATAAATTTACATG :     1525
            ||||||||||||||||||||||||||||||||||||||||||||||||||||||
 39332611 : CTGAATCTTACTGCCTGTCCTCCAAATGATTTAATTAGGTAATAAATTTACATG : 39332558

     1526 : CCATTCATGCAAAAAAAAAAA :     1546
            ||||||||||||||| ||| |
 39332557 : CCATTCATGCAAAAATAAACA : 39332537

vulgar: gi|609878487|ref|NM_001291391.1| 0 1546 + gi|528476536|ref|NC_018932.2| 39594417 39332536 - 7669 M 123 123 5 0 2 I 0 76681 3 0 2 M 102 102 5 0 2 I 0 9089 3 0 2 M 86 86 5 0 2 I 0 130336 3 0 2 M 218 218 5 0 2 I 0 21737 3 0 2 M 152 152 5 0 2 I 0 19694 3 0 2 M 204 204 5 0 2 I 0 863 3 0 2 M 81 81 5 0 2 I 0 1907 3 0 2 M 580 580
-- completed exonerate analysis

Alternatively, you can use an online resource like the UCSC's BLAT page to align the mRNA against the genome. You can see the results here and in the image below:

As you can see, our query mRNA sequence (NM_001291391.1) overlaps perfectly with the ERC gene.

There is no one-to-one correspondance between RNA and genes but not so much for the reason you seem to have in mind (although I am not sure what you have in mind).
You should read the wikipedia article on RNA splicing, it will teach you a lot of what you will need to get to the answer you might be looking for.
You might also want to follow an introductory course such as the series DNA to RNA to protein from Khan Academy.

So if I am given an RNA like MIR382, I would not be able to figure out which gene it corresponds to? Because that is what I am trying to do.

@Bob Just a thought: perhaps try posting your specific question as a separate question, and see if you can get a more specific answer for it. As it is, this current question might be a little too broad or different to get the answer you're looking for.

I'll guess that I'll do that, but I don't know if I can get a specific gene corresponding to a specific RNA molecule?

Yes, you can match an RNA to a gene. However, a given gene can yield to different RNAs and different alleles can yield to different or the same RNA. You should have a look at the sources of information I posted above. It is not very long and you'll understand a lot of what you are looking for.


text:
Effect of sleep deprivation on pupils and pupillary responses
What is the effect, if any, of sleep deprivation on pupils? Specifically:

Are pupils more dilated/constricted?
Is the pupillary response to light any different?
Anything else?

Are you referring to pupil measurements in passive subjects, or when engaged in cognitively demanding tasks? In other words, are you talking about pupil size as such, or to pupil responses during task performance?

Both, if possible. I was talking about effect on pupil size, and pupillary response to light, but if there is any other effect of sleep deprivation on pupils, such as a change in pupil responses during task performance, I would be grateful if I could know about that, too.

It's always best to ask specific questions. Broad inquiries like this question as it stands tend to result in open ended discussions.

Okay then, I am referring to pupil measurements in passive subjects.


text:
What is the difference between electrons and energy?
I'm studying microbiology right now and I have come across something confusing to me. I thought electrons provided energy to the cell by being incorporated into reducing powers and eventually driving the synthesis of ATP. However in classification of microbes energy sources (photo, chemo) and electron sources (litho, organo) are separate.
Is there a scenario in which the source of electrons and energy are different (besides phototrophy)?

This is not a biological question and if you are studying microbiology, then you would have also learnt basic physics. I am voting to close this question.

I'm voting to close this question as off-topic because it is not about biology but basic physics.

I think there is an interesting question hidden here, but the formulation is throwing us off. Something on the lines of which energy sources does the cell use other than redox reactions of ATP. We could try translating "what does energy do that electrons can't do" as "what do other cellular energy sources do that ATP synthesis/cleaving can't" or something similar.

@rumtscho I still cannot understand what the actual question is. I am interpretting it like this — how different sources of energy translate to ATP production?

You're basically confusing the fuel source with the energy it produces. For example, a car burns gasoline. That doesn't mean that gasoline is energy, only that gasoline can be used to produce energy. Similarly, a cell uses electrons in the production of ATP (source):

In the image above, electrons (symbolized by the flat arrow going from $\mathit{NADH}$ + $H^+$ to $\frac{1}{2}O_2$ + $2H^+$) flow from NADH-Q reductase (I) to cytochrome reductase (III), to cytochrome oxidase (IV). The electron flow across these complexes causes the pumping of hydrogen cations (protons) through the membrane to the extracellular space. This, in turn, produces a pH gradient and membrane potential which are used to drive the synthesis of ATP (by the $F_1F_0$ ATPase), which can be broken down to release energy (source):

So, electrons are needed1 to produce ATP and ATP can be thought of as energy storage. When ATP is broken down to produce AMP and Phosphate, energy is released in the form of heat. This is why ATP is considered as "energy currency". Neither ATP nor electrons, however, are "energy" themselves2. No more than gasoline is.

1 Are used, anyway. There are other choices.
2 No more than any other form of matter, at least. You can, actually, think of matter as condensed energy but that is really squarely in the realm of physics and not biology.


text:
Do cockroaches eat their shells after moulting?
I recently witnessed a cockroach eat its shell after it moulted. Do cockroaches always do this?

I have read that spiders eat their webs to re-spin them somewhere else. Eating a shell Might be some form of recycling

Yes, it's fairly common for insects to eat their egg casings, shed skin etc. where possible. In a similar vein, as Alex Stone mentions, spiders often eat their webs too. There's generally plenty of valuable protein and nutrients tied up in there, so why not recycle?

Thank you for the link! I thought along the line of recycling but I wasn't sure.


text:
What snake is this?

Just caught this snake today and he was really aggressive...tried to bite me but luckily I managed to kill him and I wonder what type of snake is this. If someone knows, help would be greatly appreciated.
Thanks!
Edit: the snake was found in Italy near Parma

It would be useful if you could update the question to include where the snake was found.

A zoom on the head might be useful. Scale patterns are used to identify snakes.

It looks like a Balkan Whip Snake (Hierophis gemonensis (syn. Coluber gemonensis)):

More images:

Reptiles of Crete
Reptile Database
Balcanica.info
Wikipedia image

According to iNaturalist.org:

The Balkan whip snake is a slender snake with smooth scales usually under a metre (yard) long but exceptionally reaching 130 cm (50 ins). The head is fairly distinct from the body and has prominent eyes with round pupils. The head and front of the body are olive-grey or yellowish-brown with dark spots separated by paler areas which may form irregular bars. There are often small white specks on some of the scales. Further back the dark spots are usually arranged in longitudinal lines giving a striped effect.

This snake is not endangered ("Least Concern") but there was no need to kill it, since it is non-venomous; you were certainly not "lucky" to kill this harmless animal.

I dont think so, iaork. The speckes of the snake in the question are black sploches on a light green background. The snake you have pictured has speckles which are more angular. Also, they are not in the same pattern as the ones in griffinwish's picture.They aren' on the same light green backgrown either. The colors of the individuals in many snake species  can vary a lot, I don't think that is the case here.

Considering the location and general shape/pattern I would say Green whip snake. The genus is the same as the one from the previous answer, but these inhabit the mentioned location. They can vary in the coloration from very patterned, as in the photo, to completely black.

Non venomous, not dangerous and usually only aggressive when provoked, but they do bite...
edit1: Don't kill snakes...


text:
Isolation of viruses and Koch's Postulates in connection with terrain theory and claims that viruses don't exist
If, as a physicist, I were to be told that quarks have never been isolated, and so they are not actually real particles, it would take some effort to respond.  I'd have to talk about the Standard Model and Asymptotic Freedom, and thus admit that they do have some properties that are not like other particles.
If faced with insistance that this proves the case, that they are actually some sort of epiphenomenon of particle accelerators, I might have some difficulty knowing how to proceed.  It's true that they manifest an as yet new characteristic, and so perhaps we have to expand our conceptualizaiton of what a particle is.
That may not be a perfect analogy for my question, but I have a medical friend who would like to tell me that no virus has ever been isolated, and that as opposed to some kind of transmissible, infectious organism, they are actually some kind of waste product of cells. I am told that any attempt to satisfy Koch's postulates involves the injection of materials in addition to the viruses at issue, and the claim is that it's these combination of materials that is making the animal sick.
I see a lot of varied "viruses don't exist" claims around the web, focused on HIV, measles, and CV19, and associated with names like Drs. Stefan Lanka, Andrew Kaufman, Tom Cowan, etc. Associated claims are that in any context that involves supposed exposure to a virus, less than 100% of the animals get sick, and so whatever may be going on, it's the animal itself at issue. In some quarters this is called "Terrain Theory." I would like to not have to dig too far into this.
How can I respond in a coherent way that doesn't require becoming a virologist?

Comments are not for extended discussion; this conversation has been moved to chat.

It is very easy to disprove their claims, but the burden of proof doesn't lie with you, it lies with the person making the claim. If they want to claim that there is a "cell waste product" that causes the widely varying symptoms and viral effects (in cells, model organisms etc) we see with different viruses (compare say chickenpox with SARS-CoV-2), then they need to prove that this is the case. They need to do the science and have it passed through peer review etc. Also remember that extraordinary claims require extraordinary proof - they need to prove the whole scientific consensus wrong in this case!
At its most simple, you can purify viruses via a range of methods (e.g. ultrafiltration, ultracentrifugation, chromatography etc) and resuspend in a simple salt solution of varying compositions (e.g. phosphate buffered saline, ringer's solution, tris buffered saline) and use that purified virus to infect. I would hope that even the most science-denying person would see that these solutions are very simple and don't contain anything special that could be "cell waste" or "its the fetal bovine serum" (another virus-denier claim). I would note that most of these denier people wouldn't understand the principles behind the above methods, but using them you can get pure preparations of viruses and other materials, down to separating out single molecule types from a crude solution.
You also run controls of the solution alone and easily see that the animals/cells don't infect at all with these controls, but do infect with the virus containing material. You can also run controls on your sample prep - for example, treat uninfected cells to the same virus preparative procedures as you did for the virus and show that this also doesn't result in infection.
If it were a product of cell waste you would expect to see these effects from all cells, not just virus infected ones.  For a cell waste you should also see some sort of dilution effect that is non-propagable (i.e. can't be passed on) - take your purified virus and dilute it in your solution of choice and it will still infect, but "purified" material from un-infected cells won't.
An additional note: You can also take the genetic material of the virus and use that to produce more virus. In some cases (as with positive sense RNA viruses and DNA viruses) you can use the genetic material directly and produce more viruses with the same characteristics as the source of the genetic material. Now, it doesn't work for some viruses - some genomes are too big, need special conditions, etc., but it does surpass some of Koch's postulates, as in you can synthesize this genetic material in the lab and using that material along with cells to produce a virus with exactly the characteristics of the original source of the genetic material.

The trouble is, the "burden of proof" claim may be formally correct but it is not necessarily rhetorically persuasive - and moreover it leaves any third parties to the dispute who are ignorant of the arguments on both sides hanging as to becoming better informed about what and why certain things should be believed. Someone could say, "sure, they haven't proven their case, but because xyz, why should I believe the 'mainstream' side either? "

@The_Sympathizer I totally agree - and it definitely is a problem, which is why the rest of the post is there...

Very good answer.  Much appreciated.  The various forms of "isolation" and the control methods are sufficient to what I was looking for.  Also, I've read some history of koch's postuatels, and see that they were criticized almost right away.

This may be too brief or simplistic, but a short discussion of electron microscopy might be in order; the different viruses are consistent in morphology in the diseases they cause (e.g. Ebola virus, smallpox, COVID, etc.)
It’s hard to argue with your own eyes (or a mental picture of what your eyes would see…)
To quote from a paper on the subject:

Using TEM, viruses can be differentiated by their ultrastructure: shape, size, intracellular location and for some viruses, by the ultrastructural cytopathic effects and/or specific structures forming in the host cell during their replication. Ultrastructural characteristics are usually sufficient for the identification of a virus to the family level.

And

For some viruses, TEM can be conducted on contents of skin lesions (e.g., poxviruses and herpesviruses) or on concentrated stool material (rotaviruses and noroviruses). For successful detection of viruses in ultrathin sections of infected cells, at least 70% of cells must be infected, so either high multiplicity of infection (MOI) or rapid virus multiplication is required.

If you know any cell biology. Viruses can’t be mistaken for cells or detritus.

What cell or piece thereof can the above be? Great picture of bacteriophages.

Ebola virus. Always present in Ebola, not present in other illnesses.
Electron Microscopy in Discovery of Novel and Emerging Viruses from the Collection of the World Reference Center for Emerging Viruses and Arboviruses

+1, best way to prove something exists is to go take a picture of it.

Excellent - the beauty of EM is that the capsids are so consistent with the species - and of course phages are only found in bacterial preps and look nothing like exosomes. I also really really wonder how the capsids of the filoviridae evolved, must be some significance to be so distinct.

@bob1  A bacteriophage is a wondrous thing, isn’t it? Such a tiny, ‘simple’ thing, but so elegant and dangerous to the bacteria it targets. Amazing!

@anongoodnurse absolutely, couldn't agree more. The diversity is incredible too, not to mention the abundance

At this point, anyone who doesn't accept the existence of viruses has reached flat-Earther levels of delusion and probably cannot be convinced otherwise by any evidence you would show them or any argument you can make. To believe that viruses are not the explanation for most diseases attributed to viruses, you have to believe in a vast conspiracy among government institutions, scientists, hospitals, pharmaceutical companies, and various commercial enterprises. If you think such a conspiracy is more likely than viruses doing what science says they do, then your method of weighing evidence is quite strange and, I'd say, wrong. There are many compelling sources of information that viruses are real. Even if you refuse to accept one of these sources, the others should be enough to convince you that the existence of viruses is more likely than such a massive conspiracy.

First-hand knowledge. Believing in a flat Earth requires rejection of evidence of an approximately spherical Earth that can be obtained firsthand (ships on the horizon, lunar eclipses, flights from Santiago to Auckland, flights from Johannesburg to Perth). Even more so (and unlike quarks), most people have first-hand experience with viruses, observing spread of colds, flu, chicken pox, and COVID-19 within families and people in close contact. It's pretty hard to explain this fact without proposing some kind of microscopic replicating organism-like thing that passes from person to person. Even if you don't believe that the viral particles are carrying these diseases, it should be clear to everyone that they are contagious diseases.

Changes in society in recent memory due to understanding how viruses work. Major early support for the existence of viruses came from the fact that vaccines work, which I am guessing virus-deniers don't accept. Vaccines are based on treated viral particles or components of viral particles (viral proteins, sometimes called toxoids). There are people living today who remember a time when people lived in fear of polio and measles was a common childhood illness. You can easily find history discussing the small pox and measles epidemics. What happened to those diseases if viruses aren't real and we don't understand how to combat them?

Pictures of viruses. If you think they are computer generated or something, you can probably talk to someone at your local university who has taken a picture of one. Taking pictures of viruses is easier than taking pictures of a round Earth. You only need a relatively low quality electron microscope, which you can get for less than $100,000.

Understanding viruses enables other technology. For many viruses, we understand the components that make them work. Besides vaccines, there are other technological uses of viral components. Retroviruses such as HIV must have a protein that copies RNA to DNA. You can buy such a reverse transcriptase to copy RNA yourself. Viruses are also used in gene therapy and you can contract with a large number of companies to create viral vectors with your custom gene. If we didn't understand viruses, why would people buy and sell this stuff?

Koch's postulates are only somewhat more relevant to modern medicine than insisting that electromagnetic waves must travel in some medium (luminiferous aether) is to modern physics. They do not describe necessary and sufficient conditions for proving that viruses cause disease, they're postulates that someone came up with over a century ago and were proven insufficient by subsequent investigation. They're not laws of nature, and any argument assuming that they are necessary and sufficient conditions to prove that a given pathogen causes a given illness is meaningless.

I'd argue that Koch's postulates are sufficient but not necessary to prove that a given pathogen causes a given illness: if you've got a pathogen that meets the criteria, it's reasonable to assume that it's the cause, but if you've got a pathogen that doesn't, you can't rule it out as the cause.

It's worth noting that Koch's postulates don't always apply to viruses, and that alternative postulates have existed for nearly a century to better identify putative viral pathogens. See Why did Rivers replace Koch's postulates?

I read about this, thanks @acvill .  Beyond Rivers, I also found Koch's Postulates in the 21st Century.


text:
Why does opening of the Ca-channels trigger the release of neurotransmitters?
I understand that the opening of the Calcium channels trigger the release of stored neurotransmitter in granules, but what is it about the flow of positive ions that makes the vesicles fuse with the cell membrane? Does the vesicle itself carry a charge or concentration gradient?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For example, have you looked at the related Khan Academy material? ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

I am not sure if this response is autogenerated, but I don't see how my question does not follow the guidelines. Synaptotagmin is not mentioned in any explainations I have read about action potential.

You'll note I didn't downvote (or flag) your question and I'm not claiming your question violates the guidelines. This was just intended as friendly encouragement to do some research on your own since this information is readily available online. ——— For example, when I did a search with keywords from your question ("neurotransmitter release calcium") one of the top hits was the Khan Academy video I linked to, another was this review, which does include details of the molecular mechanism ...

Ok I understand now, thank you for the clarification.

Synaptotagmin is a protein that is part of the synaptic release machinery. It binds calcium specifically, which leads to a conformational change that encourages vesicle fusion with the membrane, therefore the ultimate release mechanism is not via voltage or charge but by calcium itself.


text:
Decoding animal language (dolphins etc)
I have this idea about how we perhaps could decode animal vocabularies that I would like to have some input on.
The idea is to design an experiment/challenge where we could predict roughly what has to be communicated between two individuals of a species in order to succeed with the challenge, for instance two dolphins.
An example could be a colored button that one dolphin has to push to give both dolphins a treat, but where only the other dolphin (the one that can't push it) gets to know which is the correct one. This should encourage them to communicate what to do and specifically what colored button to press. And by doing this kind of experiment several times we could perhaps extract what sounds represent for instance "red". And so on we could build up a basic vocabulary. What do you think about that? =)
The main idea is to in some way encourage two individuals to communicate something that we by design can infer from the outcome of the experiment. If first training one individual in solving a challenge and then letting it observe another individual that has no clue how to solve it, it should encourage it to communicate the solution, if it's sufficient intelligent that is.
Could it be done you think? I wish I had the resources to try this out myself but alas I don't. I'm all out of dolphins. I have asked a few researchers for input but they don't seem to think this is possible since no animal are intelligent enough and have any kind of language in the way we think about it. But personally I don't fully buy that. I still think a few animals would be possible subjects for a test like this, such as dolphins.

You know what? You ought to give it a shot!

All my dolphins have escaped!

Then you don't need such mechanisms to understand why they did so ;)

The design of scientific experiments is an art!

No, that's not really a good design. First, it is more than unlikely that dolphins have a "word" for "red". It would sound like a very advanced vocabulary word already. Second, it is unclear how you would determine that whatever sound you're hearing aren't meaning "I am distressed" or "I am excited to get food" or "I want sex" or whatever other meaning such sound could have. You would at least need a control.

If it's useful for dolphins to communicate a color in some way I assume their "language" should include some "representation" for this? Or do you suggest that no animal except human can communicate anything other than basic needs and states of mind? Perhaps that's true but have we really looked for it? Perhaps we are blinded by our preconceptions. Also, my idea is to repeat the same experiment many times to filter out the sounds that always turn up, to be able to exclude all non-essential sounds.


text:
Can we define biological age?
How can we define ageing from a biological standpoint without making an appeal to chronological age?
Related, but less important, are there any metrics we can use to determine someone's biological age other than their chronological age?
Telomere length is an obvious candidate, but it is imperfect.

Basically, you're looking for some indices allowing to estimate the age of an organism, is it correct? If you meant estimating the "real biological age" rather than the "chronological age" then, the problem of finding indices is just the same as defining biological age. And just like any words, you can define them the way you want if you're the first to use them. Are you only interested in humans or can we talk about stuff like dendrochronology?

I guess what I had in mind was about humans. If something is correlated with chronological age, its not necessarily a part of ageing. What definitions of ageing are there to clarify when something is part of ageing and when something is just correlated but not causally related?


text:
The mechanism of the evolutionary rate hypothesis
There are several hypotheses for explaining the latitudinal gradients in species diversity (link). Of which, the evolutionary rate hypothesis states that warm temperature increases the rate of speciation. I want to know why warm temperature facilitates evolution.
This is not a question, but... some other hypotheses specifically discuss how a factor influences the rate of evolution (e.g., the size hypothesis discusses how large area can promote speciation). I think temperature hypothesis is a better name for the evolutionary rate hypothesis.

Related question: Is there a hypothesis that attempts to explain patterns of species richness along all three energy-related environmental gradients?