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Is evolution theory falsifiable by whether mutations result in a loss or gain of genetic information?
If I understand the theory correctly, evolution revolves around the process of adaptation of a being to its environment which results in the increment of survival and reproduction chances for that being.
But I constantly hear debates around whether the mutations that trigger these evolutionary changes result in the loss of genetic information or acquisition of new genetic information. The existence of these discussions gives the impression that if genetic mutations only resulted in the loss of information, evolution, as understood today, wouldn't work.
Is this a valid way to falsify evolution theory?

Can you point to one of these debates that you hear? I most often see this sort of arguments put up as some misguided critique of evolution, to make wrong arguments like "evolution can't result in gain of information."

Your representation of the theory of evolution (that we call the modern evolutionary synthesis) is very biased and very lacking. You might want to have a look at a very short intro to evolutionary biology such as evo101 for example.

@BryanKrause Well I watch (and read) a lot of internet debates between creationists and scientists, but the recent one I'd like to refer to is this one between AronRa and Grady McMurtry. Almost right out of the gate the discussion revolves around the question I'm posting here. This is the video: https://www.youtube.com/watch?v=cvnW6N3oy5k

@Remi.b Usually people ask these questions when they actually don't know and want to see if more knowledgeable people can provide valuable insight. If my position seems to be biased in some way, it's probably because I'm not a scientist and therefore I came here looking for help by asking the question. But thank you very much for the link. I will for sure go through it. Thanks!

It would be so amazing if downvoters were required to express why they are downvoting a question. People come genuinely looking for an answer to a site that's populated with a lot of learned individuals. It's rather disappointing that genuine questions just get stepped on instead of answered.

The issue with the question is that the concept of information of a sequence is very much undefined (see Calculating Shannon Entropy for DNA sequence?). If you'd wish to offer a good working definition for the amount of information of a genetic sequence, we could talk about whether new mutations tend to increase of decrease it.

On a sidenote: I have no downvoted but I can picture why it has been downvoted from the comments you have received. I agree that forcing commenting when down voting would be a somewhat pleasant policy.

@Remi.b I have rephrased my question just to clarify that I'm not trying to push a bias. I've sincerely googled for quite some time and I haven't found an answer. I would think that evolution theory works whether the mutations are only losses of information or not. But I don't know for sure. Any ideas? Thanks you!

@sergeidave Don't worry, I meant that your representation of the theory of evolution is quite wrong but never did I mean that you had bad intentions.

I'm voting to close this question as off-topic because the concept of information content is very much undefined (see for example Calculating Shannon Entropy for DNA sequence?). If the OP can offer a working definition (a metric) for quantifying information from a genetic sequence, then the question would be on-topic.

As @Remi.b says, you have to first clarify what you mean by information otherwise your question would be considered unclear.

Does "information", presumably as encoded in DNA, even make that much sense in evolutionary terms?  Say you have the complete genome of a creature, for instance a mammoth: can you use that alone to create a new mammoth?  Or do you need a female mammoth?  And if you did somehow create a baby mammoth, would it be able to survive without being taught by other mammoths?

You also need to define what you mean by Evolution theory.   Evolution is just a change in the genetic composition of a population during successive generations, its is an observation a factual statement not a theory. There are mechanistic theories explaining how it works (such as the theory of evolution Via natural selection) but no "Evolution theory"

This question may already answer your question, https://biology.stackexchange.com/questions/16106/how-does-the-creative-process-of-biological-evolution-work

This is parroting the claims in Behe's latest book. They have been refuted many times. Rich Lenski has recently put up a series of blog posts starting here, with extensive references, further refuting Behe's claims, and clearly showing how dishonest Behe is in continuing toput forward these claims that he must know are lies.

This might not have a purely objective answer. For example:

Most people lose the ability to digest milk by their teens. A few thousand years ago, however, after the domestication of cattle, several groups of people in Europe and Africa independently acquired mutations that allow them to continue digesting milk into adulthood. Genetic studies show there has been very strong selection for these mutations, so they were clearly very beneficial.
Most biologists would see this as a gain in information: a change in environment (the availability of cow’s milk as food) is reflected by a genetic mutation that lets people exploit that change (gaining the ability to digest milk as an adult). Creationists, however, dismiss this as a malfunction, as the loss of the ability to switch off the production of the milk-digesting enzyme after childhood.

And if you go read a review paper on beneficial mutations (as opposed to a popsci article), it never gets to the topic of information loss/gain. The latter seems to be most a concern for creationists (and those debunking their silly claims).
The closest thing that is of concern to biologists is whether a mutation causes a loss or gain of function of the affected protein. There exist ways to score a mutation as gain-, loss-, or switch of function.

I also note that you've substantially edited your question (toward an emphasis on  whether that issues invalidates the theory of evolution) after I answered it. As a brief and obvious addendum: no, the argument doesn't  invalidate the theory of evolution.
After some searching I found that the argument in question has been put forth by Lee Spetner. Dembski has a somewhat similar argument but not exactly this one. Anyway there seems to be countless variations to it:

An especially good example of silliness is the ID assertion that natural processes cannot create new genetic information. ID advocates have recently been pushing this line heavily as of late (Meyer 2009), even in the science standards of some states (see Matzke and Gross 2006, for discussion and refutation of the information argument), and in the ID movement’s new textbook, Explore Evolution (Meyer et al. 2007). Interestingly, this talking point, at least in the form of a seemingly technical chemical/mathematical conclusion (there are older, more informal versions throughout the creationist literature), was invented in the 1984 proto-ID book The Mystery of Life’s Origins (Thaxton et al. 1984), as a modified version of the creation scientists’ Second Law argument (Matzke 2009). It has since grown into one of the top two or three arguments made by ID advocates.

Thank you for your answer. You are correct, I modified the question because from the comments I received, it seemed it wasn't clear enough. Hopefully I left the essence of the question still intact. Thank you very much for your answer.


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Why can we hear above 8 kHz
Why have humans developed ears capable of hearing sounds that are (never?) heard in nature.
Is it known why humans developed the ability to hear up to 20 kHz when all the relevant noises are below 8 kHz? (at least in my experience) Or why was it beneficial to hear in that range?

Your question seems to be based on a false premise, because indeed there are sounds in nature >8kHz, including sounds at higher frequency than human hearing (for example, mice vocalize up to 60 kHz or so).

@BryanKrause Yes of course there are some sounds but why would it be beneficial for us to hear them?

@user1136 How does that help with sounds that aren't in high frequency ranges? Doesn't this only work with very high frequencies? How is it helpful for a human to localize mice and other small animals?

Sounds in nature aren't usually pure tones.  They have overtones at higher frequencies, and these are very important in distinguishing between sounds.  Think of several musical instruments all playing the same note: you can readily tell the difference between a piano, a violin, and a trumpet, can't you?

@jamesqf But why don't you hear the tone that's over 8 kHz only the part of the tone that is deeper? Or do you?

You do hear those tones - that is, the ear reacts to them.  But the brain interprets them as a single sound instead of separating them into pure tones.  Similarly, the eye has just 3 color receptors (for most people): the brain combines signals from them to produce the 10 million or so different colors that a human can distinguish, but you don't see the separate RGB signals.

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How is it possible for phosphate to form two ester bonds in DNA replication?
I understand that in phosphodiester bond formation, two hydroxl groups on the phosphate molecule bind to the 3' and 5' OH groups on two independent pentose sugars. This is a condensation reaction, so two molecules of water are released.
I am just confused about the hydroxl groups on the phosphate. From what I know, the phosphate molecule looks like this.

How is phosphate able to do a condensation reaction with two pentose sugars if it has no hydroxide groups?
Thanks a  lot

It's catalyzed by a ligase, e.g. DNA ligase It's not a one-step process.

Orthophosphate is not involved in phosophodiester bond formation, but deoxynucleotide triphosphates and the 3'-OH on a deoxyribose of a growing polynucleotide chain. Consult a text book to see the actual reaction, as you are expected to do before posting here.

@David I read this resource https://teaching.ncl.ac.uk/bms/wiki/index.php/Phosphodiester_bond which stated that "In phosphodiester formation, two hydroxyl (OH) groups on the phosphate molecule bind to the 3’ and 5’ carbons on two independent pentose sugars." But isn't there only one hydroxide on each phosphate? Thanks

I said a text book. Berg et al. on NCBI Bookshelf is a reputable source. Read about the DNA Ligase reaction there, especially Figure 27.28 and 27.29. The DNA polymerase reaction (which forms most of the phosphodiester bonds) is described in terms of the enzyme mechanism, but the reacting species are shown correctly in Figure 27.12. Explore the rest of this book if you need more context.

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Sulforaphane vs. Hyperthermic conditioning (sauna use) which would induce a greater heat shock response in the human body?
I’m curious to know which would induce a greater upregulation of heat shock proteins, consuming sulforaphane or putting the body through heat stress such as using the sauna.
Sulforaphane reference- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975177/#!po=79.7872
Hyperthermic conditioning reference-
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3418130/
There are many more articles/studies done on these two subjects, these are just 2 references of the many.

Could you please edit your post add the references you are referring to regarding the upregulation of heat shock proteins by sulforaphane? This might not be common knowledge. I addition, the answer to your question might depend on the concentration of sulforaphane and the temperature/humidity/duration of the sauna use.

Do the references added suffice for you?  @Arsak


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The space of all human DNAs
This is both a math and biology question but I think it makes more sense for a biologist to answer it. My question is: what can be said, if anything, about the space of all possible human DNAs (for a suitable definition of "human" in the context of this question)? Is it open or closed with respect to a suitable topology?
EDIT: To fix ideas and make it less a matter of opinion, one (admittedly incomplete, this is for the sake of making the question more precise) definition to use might be "those who can reproduce with existing fertile human beings"?
EDIT 2: To be clear, I am not a biologist but a computer scientist and maybe my question is guided by assumptions that simply do not hold. My naive vision of someone's DNA is a string of A,T,G,C which, when "interpreted", becomes that person. I am also under the impression that a single mutation of a letter may render them nonviable. On the other hand, other mutations may produce an individual with altered characteristics, who may or may not be able to reproduce with other human beings. So I was wondering if there is an interesting way to think of the space (in a mathematical sense) of all strings of DNA which produce a viable human being in this sense. If my assumption that a single mutation can render one nonviable, I would expect that this space would be "closed" for some topology.
I'm totally ready to accept that this way of thinking about DNA is flawed and/or unrealistic, and in that case I'd be happy to learn why, if possible in layman's terms.

The question is entirely dependent upon the definition of "human" you are willing to use. There is no obvious "suitable definition", there are only definition each person might want to come up with. I am VTC because an answer will necessarily be opinion-based.

I think the definition of human is less of a problem (one can probably assume we are mostly interested in healthy human cells, preferably in vivo) than the definition of open and closed topology of DNA: DNA chromatin status (which what's usually used as a proxy for the overall DNA topology) is VERY hard to measure directly and is therefore mostly assessd by indirect methods (ChiP, Acetylation state, occupancy by proteins &/ RNA-pol)

I hope I'm interpreting your question correctly; you are asking how large the possible conformation space is for DNA contained within 23 pairs of human chromosomes. The answer is very very large, since there are countless ways to arrange it, loop them, tangle them. Evolution has certainly sampled many ways to do this, but the number of possibilities unsampled is probably much astronomically higher. It's a bit like asking how many ways you can tangle a single, very long string, or 46 of them, for that matter, not including mitochondrial DNA. (cont...)

(...cont) Each cell in your body is unique in this respect, although cells of similar type share similar features that may distinguish it from other cell types. Chromosome conformation is difficult to determine, and the best ways currently we have of looking at it involves looking at the modification of histones (methylation, acetylation, etc.), looking at which transregulatory elements are bound at specific locations (polymerases, cohesins that hold loops in place, which portions of DNA are accessible to DNA-cutting enzymes, etc.), and methods like chromosome conformation capture ("3C").

@user3078439 if you'd like a super simplified explanation of the role of DNA in "creating" a person, see here and then here for 2 quick video explanations (< 5 minutes). It's a very basic (and relatively non-biological) approach to explaining things, but the videos should confirm for you the conceptual role of DNA in a human (cont...)

(...cont) ... Note, though, that I put "create" in quotes, b/c really DNA codes for the production of proteins that either make-up or generate the parts necessary for a body to form and function. In other words, DNA doesn't "become" a person; but rather, DNA provides the instructions for creating the various parts needed to assemble the various cellular and intercellular components in an organism (such as a human).

The best way to answer this question may be to root the answer in data.  We now have human genome sequences for a sizeable sample of humans.These sequences, and the variations between them, already define a sample of what it means to be a human.  We might assume that as the size of the sample grows, it will eventually converge on a definition of the entire genome-space of what it means to be a human.  We can only speculate about whether a genome configuration outside that space could give rise to an individual we would regard as human, but I think this is moot.

To add an opinion of the answer to your question, it seems to me that the space is closed but unimaginably large.


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Confusion regarding Lindeman's law
I came across Lindeman's 10% law at school. It states that 10% of the total energy entering a trophic level is available for transfer to the next trophic level.
I was reading Ecology: Principles and Applications
By J. L. Chapman, M. J. Reiss and they mentioned two contradictory statements:

The 10% law, i.e. the trophic efficiency is always 10%
The trophic efficiency increases with trophic level (which was substantiated by data).

This is the statistics:

What is right? Is Lindeman's 10% law actually valid?

Lindeman's "law" is not a true "law" like the laws of thermodynamics, it's more of a catchphrase for a concept.
The true, valid concept from Lindeman is that "lots of energy is typically lost as you go to the next trophic level, especially at early stages...but there might be exceptions." This is characteristic of most of the "laws" of biology: there is always a lot of flexibility and leeway in biology.
The data in the chart you provide support this generalized version of the law: namely, most of the energy is lost at each trophic level, and a rough average or rule-of-thumb is that it's about 10%.
The usefulness of the 10% number is that it presents a nice benchmark: when you look at these data, you should notice and remark on the relatively high 22.3% level for secondary consumers on the Cedar Bog Lake: you should wonder "what features of this ecosystem or these consumers mark the relatively high energy transfer here?" Without the "10% law" you wouldn't know which numbers should stand out and which are unremarkable.

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Explanation of universal model of energy flow
I am trying to understand the Universal model of energy flow by Odum.

In this linked diagram I is the input energy(the amount of energy present in the food consumed by this tropic level, say its, the 2nd tropic level, the herbivores), part of this food is excreted as undigested food (the NU) , the rest is digested, absorbed and assimilated reaching the cells and then the energy accumulated at cellular level is called the assimilated energy (A). Now part of A is utilised to make ATPs that are being used to fuel the metabolisms occurring in the organisms which is represented by R and the rest is available to the next tropic level(?) as P ?
Then what makes the standing biomass? The organisms the are not eaten up?
Besides I don't understand the Energy Storage part. What physiological process corresponds to this?

If you were to take a snapshot of the biomass present for a species at an instant of time, that would be its standing biomass. So, in a way you are correct with "the organisms not eaten up". But this can be quite misleading when used to attempt to explain pyramids of production up trophic levels. For example, in some aquatic ecosystems the standing biomass of primary consumers is greater than that of primary producers. On study in the English Channel showed 21 g/m3 of zooplankton but only 4 g/m3 of phytoplankton. This is due to the rapid proliferation of the phytoplankton and the rapid consumption by the zooplankton.
Typically it is preferable to describe the energy flow through ecosystems in terms of energy units, Joules for example. However, you could do this with biomass if you summed the biomass produced over time. When done like this, the English Channel example would look like a proper pyramid with the producers out-massing the consumers over a meaningful period of time.
Energy storage is simply the energy stored in the chemical bonds of the molecules created during growth that add to biomass.
My example, and context, is from Biology, Campbell & Reece, 7th edition.

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Why is mutation rate high in introns?
Principle of genetics mentions

The fact that introns accumulate new mutations much more rapidly than exons indicates that many of the specific nucleotide-pair sequences of introns,excluding the ends, are not very important.

Though 'are not very important' is not true as introns do have a number of functions (both discovered and undiscovered).
But why is DNA polymerase less efficient at replicating introns? Is it known?

Note it doesn't say polymerase is less efficient; rather that mutations accumulate. This could be because of things other than different rates of new mutation creation.

Some introns might contain functional parts is very different from all introns are functional. The web site you linked is no proof. Indeed, it seems to be written by someone supporting the intelligent design hypothesis for the human genome (which of course, IMO, is wrong). So it is an opinion-based site containing also some information about biological facts. I would stick to more neutral references including standard Biology books.

"Accumulates" is the key term, the mutation rate is not higher, mutations are just less likely to be removed, which makes sense if the area is non-functional, most of the mutation will have no effect thus are unaffected by selection.

Is there any evidence that the mutation rate is higher in introns than exons? Isn't it the fixation rate that is higher in introns than in exons?

Not less efficient, but introns are under less selective pressure than exons. Exons actually encode the protein. A single bp insertion will ruin a mRNA encoding a protein by causing a frame shift in how the sequence is read.
However the same is not true for introns. 1bp insertion even if the intron has function such as transcription or translation factor regulation has a higher chance of not damaging anything important. Simply because such factors are spaced apart and the space is not really important.
http://www.nature.com/scitable/topicpage/rna-splicing-introns-exons-and-spliceosome-12375
https://www.ncbi.nlm.nih.gov/pubmed/17570818

This is not completely true. Insertions in introns also cause frame shifts which may render splice acceptor sites non-functional. This also affects the protein coding sequence.

Only the very terminal ends of an intron are involve in splicing and the branch point can tolerate fair amount of change as long as the 'A' branching point is unchanged. So only a few bp of an intron in constrain by splicing requirements. And given that mammalian intron are large, most of the intron is just space.

@JayCkat It would be great if you can add some references.

@JayCkat It is OP's job to clarify the question but is there any evidence that the mutation rate is higher in introns than exons? Your answer seem to rather tackle the question "why is fixation rate higher in introns than in exons?" and not "why is mutation rate higher in introns than in exons?"

If you ask the question "Do intron have a higher replication error than exons during DNA replication", the answer is maybe. Longer answer is DNA polymerase have difficulty accurately replicating nucleotide repeats (mono, di, tri). Such repeats are more likely to appear in Introns compared to exons. These repeats do expend and shrink during DNA replication, independent of homologous recombination. However accurate sequencing of such repeats is difficult, so in vivo occurrence is next to impossible to verify. Only real solution is to wait for minion seq tech to mature.

One paper after this question was asked indicates that it might be both stronger purifying selection in exons and a higher basal mutation rate in introns, likely due to the different accessibility of the DNA.
You are correct that introns play an important role in regulation (perhaps both timing and overall expression, in addition to the presence of enhancers and the potential for alternative splicing that affect the actual protein produced).

It is OP's job to clarify the question but is there any evidence that the mutation rate is higher in introns than exons? Your answer seem to rather tackle the question "why is fixation rate higher in introns than in exons?" and not "why is mutation rate higher in introns than in exons?"

Please see the first linked paper (someone else chose the link location, and maybe I should change this). The other answer addresses fixation rate and it's well established so I didn't link anything about that. Perhaps you meant to add this comment to that thread?


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Mechanism of RNA synthesis by RNA polymerase
I want to study the mechanism involved in RNA polymerase's catalysis in E.coli. Things like:

How does it bind to the promoter?
How does it unwind the DNA?
How does each component of the enzyme contribute to this synthesis?

I have looked into books like, Berg, Snustard Simmons, Lehninger, Alberts, Lodish and Google.Scholar, found information like:

After σ binds to the core the holoenzyme binds to duplex DNA and moves along the double helix in search of a promoter, forming transient hydrogen bonds with exposed hydrogen-donor and -acceptor groups on the base pairs. (Without σ the core enzyme can bind to DNA but unspecifically.)
After the RNA polymerase binds tightly to the promoter DNA in this way, it opens up the double helix to expose a short stretch of nucleotides on each strand . Unlike a DNA helicase reaction , this limited opening of the helix does not require the energy of ATP hydrolysis. Instead, the polymerase and DNA both undergo reversible structural changes that result in a more energetically favorable state.
Interaction of the σ subunit with a promoter signals the polymerase to initiate transcription at a specific sequence in template DNA.
The β and β′ subunits polymerize ribonucleoside triphosphates (NTPs) as directed by the template strand.
The α subunits interact with regulatory proteins and, in some cases, with DNA to control how frequently RNA polymerase initiates transcription from a specific promoter.

But that's all that I have found. Where can I find a full length explanation about this with proper diagrams(if possible)?
P.S. Has the mechanism not been fully discovered?

Almost everything in this world has something additional to be known. For what you are asking you have to go through different papers. I don't think there is a book dedicated to the mechanics of RNA-polymerase. You may find some extensive reviews but the likelihood of finding a recent one, despite its importance, is low. Considering all this, your question appears to be too broad.

This site is a good start, https://pdb101.rcsb.org/motm/40 as is this one http://mol-biol4masters.masters.grkraj.org/html/Gene_Expression_I2-RNA_Polymerases.htm

I have found an article which describes all the major steps of the mechanism of working of RNA polymerase II. Since the article is too long, I'd rather put the main points here. You can read the complete article here. Since putting the whole answer under blockquote would be inappropriate, I am just putting the main points with the reference at the bottom. Remember, this is not the complete article, this is just the summary for the ones who can't read the full article from NCBI or who don't have time or access to do so.
THE RNA POL II TRANSCRIPTION CYCLE
Pol II transcription typically begins with the binding of gene-specific regulatory factors near the site of transcription initiation. The core promoter serves to position Pol II in a state termed the Preinitiation Complex (PIC) analogous to the bacterial Closed Complex. In this state, Pol II and the general factors are all bound to the promoter but are not in an active conformation to begin transcription. Next, a dramatic conformational change occurs in which 11–15 base pairs of DNA surrounding the transcription start site are melted and the template strand of the promoter is positioned within the active site cleft of Pol to form the Open Complex. After synthesis of about 30 bases of RNA, Pol is thought to release its contacts with the core promoter and the rest of the transcription machinery and enter the stage of transcription elongation. Factors that promote productive RNA chain synthesis, RNA processing, RNA export, and chromatin modification can all be recruited to elongating Pol II.

PROMOTER RECOGNITION USING MULTIPLE LOW AFFINITY INTERACTIONS
Sequence elements found in core promoters include the TATA element (TBP binding site), BRE (TFIIB recognition element), Inr (initiator element), and DPE (downstream promoter element). The core domain of TBP consists of two imperfect repeats forming a saddle shaped molecule that binds the widened minor groove of an 8-bp TATA element, unwinding about a third of a helical turn and bending the DNA about 80 degrees toward the major groove. Biochemical studies elegantly showed that TBP does not bind to TATA elements with high orientation specificity, leading to the finding that other promoter elements in combination with TATA determine the orientation of transcription machinery assembly at a promoter. The other two core promoter elements with proven function, Inr and DPE likely serve as binding sites for the TAF (TBP Associated Factor) subunits of the general factor TFIID.
The role of TBP at TATA-less promoters: From biochemical studies of the yeast HIS4 promoter, mutation of the TATA to a GC-rich sequence allowed recruitment of the transcription machinery to a promoter at a reduced level, but transcription initiation was completely abolished. These results demonstrate that at one class of promoter, assembly of the transcription machinery into a productive complex requires that TBP bind the TATA element as seen in the crystal structure. Although TBP has tremendous flexibility in the ability to bind variants of the TATA sequence, not all sequences are compatible with TBP binding.
GENERAL FACTORS INTERACTING DIRECTLY WITH TBP
TFIIA and TFIIB are the two general factors that interact specifically and independently with TBP. TFIIA stabilizes TBP-DNA binding and strongly promotes binding of TFIID to DNA through an anti repression mechanism by competing with the TAF1 N-terminal domain (TAND) that occludes the DNA binding surface of TBP when TFIID is not bound to DNA. TFIIA can also compete with the negative regulatory factors Mot1 and NC2 to promote TBP binding in vitro.
TAFS ARE SHARED SUBUNITS OF TWO LARGE COMPLEXES
The TAFs function in promoter recognition as well as in positive and negative regulation of transcription. A subset of TAFs has DNA binding activity and at least one TAF has the ability to bind acetylated nucleosomes, protein acetylase, and ubiquitylation activity. A core of 5 TAFs are found in both TFIID and the acetylase/coactivator complexes.
POL II THE CENTER OF ATTENTION
Pol II subunits can be classified into three overlapping categories: subunits of the core domain having homologous counterparts in bacterial Pol (Rpb1, 2, 3, and 11), subunits shared between all three nuclear polymerases (Rpb5, 6, 8, 10, and 12), and subunits specific to Pol II but not essential for transcription elongation (rpb4, 7, and 9).
Pol II structure: Pol II is composed of four mobile elements termed Core, Clamp, Shelf, and Jaw Lobe that move relative to each other. The Core element  accounts for about half the mass of Pol II and is comprised mainly of subunits common to all cellular Pols. At the center of the enzyme is a deep cleft where incoming DNA enters from one side and the active site is buried at the base. This cleft is formed by all four mobile elements and has been observed in both closed and open conformations in the 10 subunit enzyme. The Shelf and Jaw Lobe elements move relatively little and can rotate parallel to the active site cleft. The Clamp element, connected to the Core through a set of flexible switches, moves with a large swinging motion of up to 30 Å to open and close the cleft.

The Pol II CTD molds itself to a binding partner: Pol II undergoes regulatory phosphorylation and dephosphorylation as part of the transcription cycle with the Rpb1 C-terminal domain (CTD) the target of this modification. The CTD, which is unique to Pol II, contains 25–52 repeats of the tandemly repeated heptad sequence YSPTSPS, with both Ser2 and Ser5 the sites of phosphorylation. The CTD acts as a platform for assembly of factors that regulate transcription initiation, elongation, termination, and mRNA processing. New structures of CTD interactions with two different binding partners have revealed that the CTD appears to mold itself to its binding partner, adopting different conformations. In one study, a complex of a single copy of the CTD with Ser2, 5-P bound to the Pin1 peptidylproline isomerase was solved.
ASSEMBLY OF POL II WITH THE TRANSCRIPTION MACHINERY
These studies showed that the transcription machinery makes extensive interactions with promoter DNA between positions −43 and +24 with respect to the transcription start site. Two RNA Pol II subunits (Rpb1 and 2) make extensive DNA interactions over 60 bp. TFIIB and the small subunit of TFIIF (TFIIF$\beta$) both interact with DNA on either side of the TATA and the large TFIIF subunit interacts with DNA downstream of TATA. TFIIE interacts with promoter DNA just upstream of the transcription start site while the TFIIH helicase subunit interacts downstream and possibly upstream of the transcription start.
Pol II and TFIIF interact over an extended surface: TFIIF binds Pol II as a heteromer and contains two subunits that are conserved among human, insects and yeast, termed Tfg1 and Tfg2 in yeast (Rap74 and Rap30 in humans). The N-termini of both conserved subunits form a dimerization domain and the C-termini of both subunits are winged helix domains. The structure of Pol II with the Tfg2 subunit alone implicated Tfg2 binding to the extended clamp region and Tfg1 binding to Rpb4/7.
OPEN COMPLEX FORMATION AND THE TRANSCRIPTION START SITE
Transcription start site selection: At TATA-containing promoters in vertebrates and Drosophila, the transcription start site is located about 30 bp downstream from the beginning of the TATA sequence. A model to explain the transcription initiation site in higher eukaryotes would be that TFIIB binding to both Pol II and promoter DNA sets the distance needed for the DNA to travel from the TFIIB binding site on Pol II to the active site of the enzyme.
REFERENCE
Structure and mechanism of the RNA Polymerase II transcription machinery: Steven Hahn, 2005 Aug 24

@SanjuktaGhosh maybe you don't need a book after reading this :)

@SanjuktaGhosh if you are focused at only the initiation phase, then this might be helpful. If you want, I can post it as a separate answer.

No, it's alright. I'll follow the link.


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Does a brown Pieris brassicae chrysalis indicate it is dead?
I have been breeding Pieris brassicae larvae in a glass tank indoors for my own personal observation. One of them, after the fifth instar, has moulted into a chrysalis. After 5 days of development in which the pupa changed colour accordingly to the information I had researched, going from a vibrant green to a paler green with black, white and yellow dots, the chrysalis has turned light brown on the sixth day.
I have found no correspondence of this in any of the sources, articles and videos I have studied. Does it indicate that the pupa is dead / stressed? (I am keeping the larvae at room temperature, i.e. 22°C and under a bright led light that is used to light up the whole room)

Did you do a google image search? I found this and others like it.  But time will tell. When my chrysalises die (different butterflies), they do turn brown, but they also appear dehydrated. IOW, they look dead.

Thanks! Do you think I should move them to a cooler space, (e.g. outside)? Or perhaps the bright led lighting I am using has a role in all of this?

I can't help you with that. I can tell you that most of the chrysalises that die for me were unrelated to the conditions in which metamorphosis was occurring. The caterpillar could have been stressed into pupating early or infected/parasitized (it's pretty awful to see a wasp come out of a Monarch chrysalis.) As I said, time will tell, and it's more likely than not that it would have died anyway.


text:
How do eukaryotes terminate transcription? (clarification on Campbell Biology)
I'm having trouble understanding how eukaryotes terminate transcription. Studying Campbell Biology (pg. 342, 10th ed.), I read:

In eukaryotes, RNA polymerase II transcribes the polyadenylation signal sequence on DNA, which specifies a polyadenylation signal (AAUAAA) in the pre-mRNA. This is is called a "signal" because once this stretch of six RNA nucleotides appears, it is immediately bound by certain proteins in the nucleus.

The text continues with:

Then, at a point about 10-35 nucleotides downstream from the AAUAA, these proteins cut it free from the polymerase, releasing the pre-mRNA.

Does this mean pre-mRNA continues to be synthesized for 10-35 nucleotides after AAUAA is transcribed before finally being cut off?
Thanks so much.

According to Lewin's Genes XI - Krebs et. al on Eukaryotic Transcription, RNA Splicing, and Processing

It is not clear whether RNA polymerase II actually engages in a termination event at a specific site. It is possible that its termination is only loosely specified. In some transcription units, termination occurs more than 1000 bp downstream of the site, corresponding to the mature 3' end of the mRNA (which is generated by cleavage at a specific sequence) Instead of using specific terminator sequences, the enzyme ceases RNA synthesis within multiple sites located in rather long "terminator regions." The nature of the individual termination sites is largely unknown.

It does go on to say,

The site of cleavage/polyadenylation in most pre-mRNAs is flanked by two cis-acting signals: an upstream AAUAAA motif, which is located 11 to 30 nucleotides from the site, and a downstream U-rich or GU-rich element. The AAUAAA is needed for cleavage and polyadenylation because deletion or mutation of the AAUAAA hexamer prevents generation of the polyadenylated 3' end (though in plants and fungi there can be considerable variation from the AAUAAA motif).

I should add that the significance of 11 to 30, or as you said 10 to 35 nucleotides is that it is telling you the approximate size of the protein complex that is sitting on the RNA and where the active site of the protein is. The domain that recognizes the termination sequence is about 10 to 35 bases wide. It is likely that the variation is due to the RNA sequence following the termination sequence ability to form a stem loop structure.
Campbell takes a necessarily basic and less nuanced approach to the information that they provide on molecular biology. The approach is to provide some details and show the evolutionary commonalities between a diverse range of biological systems. The approach is okay as it gets you into the frame of mind of thinking about the interconnectedness of biological systems.
As you progress in your studies you will see that the reality and specifics are far more complex and exception based than was presented in introductory courses. But the more advanced courses spend an entire semester focused on what Campbell covers in one chapter. Campbell is accurate but incomplete out of necessity.


text:
Do spinal cord reflexes (such as the knee-jerk reflex) continue to function under general anaesthesia?
The knee-jerk reflex (patellar reflex) is an example of a stretch reflex (myotatic reflex). Stretch reflexes are monosynaptic reflexes happening in the spinal cord without involvement of the brain.
Does it mean that this reflex will continue to function in an unconscious person, e.g. under general anaesthesia? Does it depend on the "deepness" of anaesthesia? Does it depend on a specific drug? I would also be interested to know if spinal reflexes keep working in unconscious states such as e.g. alcohol poisoning or a knockout.

The issue is complicated. In general it depends on the specific spinal reflex and on the specific anaesthetic. But it seems that the modern general anaesthetics usually do NOT block monosynaptic spinal reflexes (such as knee-jerk).
Here are two figures from Baars et al. 2009  that show that propofol and sevoflurane strongly inhibit withdrawal reflex (spinal two-synaptic reflex) but have almost no effect on the H-reflex (spinal monosynaptic reflex closely connected to the stretch reflex):

See below for many more details. Disclaimer: I know very little about anaesthesia and am simply writing down what I found after a couple of days searching and reading.

Withdrawal reflex
As @AliceD wrote, withdrawal reflex (a two-synaptic spinal cord reflex) usually disappears under any anaesthesia and this disappearance is used as a clinical sign of anaesthesia being deep enough for the surgery. As an example, this handout on monitoring anaesthetic depth in rodents has the following entry on the list of criteria for surgical anesthesia:

Withdrawal    reflexes    are absent! Try at  least   2   toes    and the ears    so  that    you are  sure   that    this    reflex  is  absent.

Knee-jerk reflex: early history
On the other hand, it is known from the XIX century that stretch reflexes such as knee-jerk (note that they are monosynaptic) are very persistent. They can be abolished under some drugs (such as e.g. chloroform and ether) that act directly on the spine, but keep working under others. I am quoting from three old papers on the topic (here and below emphasis is mine).
Horsley, 1883, Note on the patellar knee-jerk:

In 1881, while experimenting (on myself) with this gas [nitrous oxide] for
a different purpose, it occurred to me to contrast the conditions of the superficial and deep "reflexes," taking the
plantar reflex as an example of the former, and the patellar
phenomenon to illustrate the latter. Being aware of the fact
that deep chloroform-narcosis abolishes all the "reflexes,"
superficial and deep, and yet that with ether-narcosis, however deep, ankle-clonus frequently, appears, I was scarcely
surprised to find that the knee-jerk persisted in the deepest
anaesthesia from nitrous oxide, while the superficial reflexes
all disappeared.

Sherrington, 1892, Notes on the arrangement of some motor fibres in the lumbo-sacral plexus (p 671):

With regard to the effect of anaesthetics on the "jerk," a better proof of
the action of chloroform being rapid and direct on the nervous mechanisms of
the cord itself could hardly be found than in the speedy abolition of the
"jerk" by chloroform inhalation when the cord has been previously divided
in the thoracic region.

Simpson & Herring, 1905, The effect of cold narcosis on reflex action in warm-blooded animals:

The knee-jerk is a very persistent phenomenon. It is known to disappear in deep anesthesia produced by ether or chloroform [Sherrington 1892]. [...] The knee-jerk is as a rule easily elicited, and we find it present when
all the reflexes have disappeared. [...] The lower the
temperature the smaller the jerk. [...] In several animals that died at a low temperature the disappearance of the knee-jerk was simultaneous with death [...] The lowest temperature at which we found the knee-jerk present was 15° C., and this
was also the lowest temperature at which any of our animals were
still alive. [...] Pinching the skin does not provoke any response till the temperature is 25° C. [...] We have compared these results with similar ones obtained from
cats in recovery from deep ether anesthesia and find that the order of
reappearance agrees very closely.

Modern studies in animals
Hara & Harris, 2002, The Anesthetic Mechanism of Urethane: The Effects on
Neurotransmitter-Gated Ion Channels mention in the abstract that

Urethane is widely used as an anesthetic for animal studies because of its minimal effects on cardiovascular and respiratory systems and maintenance of spinal reflexes.

(they don't specify which reflexes specifically).
Ho & Waite, 2002, Effects of Different Anesthetics on the Paired-Pulse Depression of the H Reflex in Adult Rat study the effect of five different anaesthetics (ketamine, halothane, etomidate, saffan, and nembutal) on the Hoffman reflex (H-reflex), a monosynaptic reflex similar to the stretch reflex. They report that it keeps working under all five drugs, but the drugs modulate the decrease of the reflex under repeated stimulation (this decrease depends on the descending controls and is affected differently by different drugs):

The  results  suggest  a  preferential
action  of  some  anesthetics  on  descending  pathways
involved in reflex modulation [...]

Strangely, Ho & Waite do not describe how anaesthesia affects the reflex strength following an unrepeated stimulation, but in any case it is clear the the reflex keeps functioning.
Propofol etc.
What about the anaesthetics widely used in humans, such as e.g. propofol? Matute et al., 2004, Effects of propofol and sevoflurane on the excitability of rat spinal motoneurones and nociceptive reflexes in vitro:

We used an isolated spinal cord in vitro preparation from rat pups and superfused the anaesthetics at known concentrations. [...] Applied at anaesthetic concentrations, [...] sevoflurane produced a large depressant effect on the monosynaptic reflex whereas propofol was ineffective. [...] Sevoflurane produces large inhibitory effects on nociceptive and non-nociceptive reflexes which are likely to contribute to immobility during surgery. Compared with sevoflurane, propofol appears to have much weaker effects on spinal reflexes such as those recorded in an isolated preparation.

Kerz et al., 2001, Effects of Propofol on H-reflex in Humans:

Previous studies of motoneuron excitability using H-reflexes or F-waves during general anesthesia found significant depression after administration of halothane,  enflurane, isoflurane, desflurane, or nitrous oxide. [...]
Recommended propofol doses for induction and maintenance only had a transient effect on the H-reflex and were no longer demonstrable after 10 min of propofol anesthesia. [...] Immobility during propofol anesthesia [...] does not seem to be caused by a depression of spinal motoneuron circuit excitability.

So why is then the withdrawal reflex so easily abolished and the stretch reflex is so persistent (e.g. under propofol)? This does not seem to be well understood. Baars et al., 2009, Effects of Sevoflurane and Propofol on the Nociceptive Withdrawal Reflex and on the H Reflex write

Both H reflex and nociceptive withdrawal reflexes are reduced dose-dependently by propofol and sevoflurane in humans. [...] We have shown a striking difference of the degree to which both reflexes are reduced by the two anesthetics. The relative reduction of the polysynaptic RIII reflex amplitude was more than four times higher than that of the H reflex. This difference can probably be attributed to the higher number of neurons interposed in the RIII reflex pathway in comparison to the H reflex.

Note that the last sentence is very vague; it says that the difference is "probably" due to monosynaptic vs. polysynaptic mechanisms of these two reflexes but does not offer any explanation. Withdrawal reflex is mediated by an excitatory interneuron and propofol acts on GABA (which is inhibitory transmitter), so it remains unclear. This study is from 2009 and I did not find anything relevant in the papers that cite it.

From an animal-experimentation perspective, the absence of functional reflex arches are often used to assess adequate anesthetic depth. For example, in rodents  a toe-pinch is often used to assess whether the animal is sufficiently anesthetized to commence surgery. The absence of a withdrawal reflex marks the point to proceed after initiation of general anesthesia. Hence, in these cases, pain-induced muscle reflex arches are suppressed. Note it is a two-synaptic process (nociceptor to spinal chord, spinal chord to muscle).

Thanks, Alice! +1. This is interesting; withdrawal reflex is polysynaptic, but nevertheless a spinal reflex. So what is your intuition then: would a knee-jerk also disappear under similar anesthesia? By the way, by now I think that the answer might depend on the specific drug and dosage, but I am actually not interested in anesthesia per se. I will now update my question to specify that I am rather asking about any "unconscious" state, such as e.g. after an alcohol intoxication or after being knocked out.

My intuition is that these reflexes will be absent. I will try to ping @anongoodnurse here in the hopes she can shed light on this. After your edits it is outside the realm of my expertise. Note that alcohol, being quite related to ether, may be considered a general anesthetic, in a way. I think that the question is becoming quite broad as of now and I'll not attempt another answer. Good luck and nice question nonetheless, +1'd.

I guess you are right to say that the question becomes quite broad because "unconscious states" can (I presume) be quite different and can have distinct properties. I am not asking for a lot of details here and would be happy to accept any answer that gives a short overview. Also, I have just updated my question with some quotes from several XIX - early XX century papers that I found on the topic, I think you might like them.

I have posted my own answer with a lot of citations; it seems that modern anaesthetics such as e.g. propofol do eliminate the withdrawal (as you say) but do NOT affect the stretch reflex (contrary to your intuition). Even though the effect seems to depend strongly on the specific drug. I have no idea at all why the withdrawal is so much more susceptible than the stretch. Neither can I make any general claim across various anaesthetics, because I only found some isolated information about several specific ones.

I am not a surgeon.
However, I might have some insight:

General anesthesia often (most of the time ?) include curare derivated drugs (such as pancuronium) that will effectively block any muscular response (by interfering in the neuromuscular junction: they block nicotinic Acetylcholine receptors). So this will effectively inhibate any reflex by blocking the final effector.
Spinal anesthesia might also inhibit reflex arc, for the same reasons, but only for a specific zone.
Other kind of anesthesia might be conservative regarding reflex arc.

You will find informations on wikipedia:
https://en.wikipedia.org/wiki/Neuromuscular-blocking_drug
https://en.wikipedia.org/wiki/Spinal_anaesthesia
If you want me to give you a more elaborate answer, just say so, I will try to improve a little bit.

Thank you for your answer! +1. As far as I understood, neuromuscular blockers such as pancuronium are often used in anaesthesia (to prevent possible movements) but do not have an anaesthetic effect themselves. I guess you are right, and neuromuscular blockers would block spinal reflexes too, but my question was rather about unconsciousness/anaesthesia without an additional muscle paralysis. Your third bullet suggests that spinal reflexes will be unaffected in this situation (and I agree that it sounds plausible) but I would like to have some direct evidence or reference.

My intuition is that, if there is no neurological lesions, or muscular pathologies, and you're just in presence of a person that is under anesthesia, spinal involving reflex won't be affected. But I will ask to the folks at the hospital tomorrow, whether this is true or false and get back to you.

Maybe that will also interest you: https://en.wikipedia.org/wiki/Lazarus_sign

General anesthesia is not induced by muscle blockers. They are given to block muscle activity to enhance ease of operation.

I couldn't get anyone at the hospital to answer me.

I cannot add commentaries for other posts, but inhibition of withdrawal reflexes is kinda logical speaking of anesthesia. You are aiming to block nociception signal and responses as well as to provoke unconsciousness. I think if you do not administer morphine, or any other kind of analgesic and only use propofol to knock someone down, this will not abolish reflexes.

Abolition of all reflexes necessitates blocking every signaling way involved in those. This can be achieved either by drugs, which have either a broad or narrow spectrum, either by nerve damage (either by some mechanism I wouldn't be aware of, like brain inhibition of reflexes if that exists)

Thanks, @OvoiDs. I have just updated my answer, putting my earlier update to the question in there (to have it everything together). It seems that you are right, and propofol does not abolish stretch reflexes. My remaining confusion about withdrawal reflexes is that those are also entirely spinal, so I don't understand why a drug (such as propofol) would affect two-synapatic withdrawal reflexes but leave monosynaptic stretch reflex unaffected. Does it have anything to do with the number of synapses? Or is it just that the modern drugs are selected to abolish specifically withdrawal?

So, I've looked a little bit on pubmed. Propofol acts by linking to GABAa receptors (so it tends to inhibit neuronal signals). In the case of a monosynaptic reflex, there is little to no regulation (this is purely hypothetical). In case of polysynaptic reflexes, regulation can occur. For withdrawal reflex, if there are inhibitory GABAergic neurons, these will be affected by Propofol and this inhibit the signal leading to reflex abolition.

I haven't read the entire paper, but at least the introduction of this paper might be of interest for you: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.325.4279&rep=rep1&type=pdf

The more neurons you have, the bigger the chances of regulatory systems, either with an excitation cascade, either with inhibition. Inhibitory neurons are for most part GABAergic or Glycinergic neurons, and those are widely spread in the spine's dorsal horn. However, I wasn't able to find a clear answer in any book i've looked, so I guess this should all be considered as hypothesis. Sorry !

Thanks for your replies! Withdrawal reflect seems to be meditated by an excitatory interneuron, not an inhibitory one... I found this paper from 2009 that explicitly measures the effect of propofol on withdrawal/stretch in humans and reaches the same conclusions. In the discussion they say that "This difference can probably be attributed to the higher number of neurons interposed in the RIII reflex pathway in comparison to the H reflex". Note the word "probably"... I have updated my answer to include this study.


text:
How is curcumin effective in fighting cancer?
Can you explain the mechanisms of how curcumin affects cancer cells and how effective it is?
More reading:
http://www.ncbi.nlm.nih.gov/pubmed/25667441
http://link.springer.com/article/10.1208/s12248-009-9128-x

Can you please add some references to this research?

http://www.ncbi.nlm.nih.gov/pubmed/25667441

Since I cannot post more links with my reputation I will post them here  http://www.cancerletters.info/article/S0304-3835(07)00105-X/abstract
http://europepmc.org/abstract/med/1578097
http://www.tandfonline.com/doi/pdf/10.4161/cbt.7.9.6659
http://europepmc.org/abstract/med/16521985

Inflammation is a promoting factor in tumor progression.Curcumin has been proven to be a potent anti-inflammatory agent.
A warning:
There has been considerable amount of bogus research in "miracle natural" compounds, including curcumin. I vouch personally for the study (PMID: 19793800) where curcumin has been studied in inflammation/tumor progression mouse model.

I did not check curcumin in depth, but I think its mechanism is similar to resveratrol's. Both activate SIRT1, which suppress tumors.

Activation of SIRT1 by curcumin blocks the neurotoxicity of amyloid-β25-35 in rat cortical neurons.
SIRT1, Is It a Tumor Promoter or Tumor Suppressor?

I threw a reference in the OPs comments. May also inhibit SP-1, STAT3 and NF-kß pathways.


text:
How to find the concentration of an enzyme?
I need to know the concentration of pectinase enzyme (sigma aldrich) which has stated 5KU, 5U/mg protein (lowry) and lot result 20U/mg protein in the label of the enzyme bottle. This is all it has mentioned. How do I calculate the concentration from this information?
hey everyone, sorry for not been straight forward with the question. I'm asking for U/ml.I think I can find it if the label has mentioned the total volume of enzyme solution. Then I know how much mg in 5KU which is 5000/5=1000mg which I can easily get mg/ml or U/ml which is more appropriate. But the question is pointless if it hasn't mentioned the total volume. Thanks for the replies.
PS My supervisor asked me to prepare a standard graph of enzyme concentration (U/ml) against absorbance(O.D value) for DNS assay instead of a Galacturonic acid standard/glucose standard.(galacturonic acid is not available so he thinks it is better to you this graph than a standard glucose graph)
PS I checked the bottle again.On the bottom side of the bottle it has stated 10 ml.

What kind of concentration do you need? A mg/ml number? For enzymes this is relatively meaningless, since the activity is more important here (you can have a lot of dead protein in your preparation which is of no use for the enzyme reaction). So usually you get a U/ml (or whatever) concentration and you have a definition for the unit.

Is it just me or anyone else find ironic that OP's name k.m and he/she is asking for enzyme concentration :P

Welcome to BioSE! Please include a bit more information on how you have tried to solve the problem yourself.

If you want to know the concentration in moles/litre then you need the molecular weight of the protein molecule--you did not provide this information. You would also need the volume of the solution in the bottle--you did not provide this information. moles = weight (in grams) / molecular weight.

The enzyme unit U is not a measure of enzyme concentration but its activity, defined as the conversion of 1 micro mole ($\mu$mol) of substrate per minute (under a specified condition such as pH and T)
Absorbance (O.D. at a specific wavelength) of the enzyme is a measure of enzyme concentration, regardless of its activity. Depending on the unit of the extinction coefficient, Absorbance can be converted directly by Beer's Law to enzyme concentration, typically in mg/mL or in the standard mM.
5U/mg is the specific activity of pectinase, and the bottle contains a total of 5 kilo U (KU), meaning that there is a equivalent of 1g of active enzyme inside (often in powder). If you assume all pectinase molecules inside the bottle are active, when dissolved in 10mL water, you have a pectinase concentration of 100mg/mL. If the molecular weight of pectinase is 31kDa (31000 g/mol), then 100mg/mL is the same as 3.2mM in concentration.
By the way, Lowry protein assay measures enzyme concentration, not activity in U while DNS assay measures activity (of enzyme that produces reducing sugars), not enzyme concentration.


text:
A basic example of the interactions of 2 or more non-identical alleles leading to an advantageous outcome for an individual organism
Could someone help me out with a basic example of the interactions of 2 or more non-identical alleles leading to an advantageous outcome for an individual organism? Based on empirical research OR on a theoretical model.
An example of 2 or more non-identical alleles cooperating across replication iterations/generations between individual organisms would be even beter. I somehow find this more spectacular :)
Please let me know if I'm not mentioning enough elements to answer the question. It's a very broad question and I accept very broad answers - semantically and across scientific branches.
All the best,
Flo
Personal background: I am new to the scientific field of biology. I think I caught up on some of the basic principles of genetics, allellomorphs, loci and DNA replication and I've gotten interested in the workings of alleles.

I don't fully understand your question for two reasons. 1) When you say an example do you mean an empirical observation or do you mean a theoretical (mathematical and/or logic/intuitive) model? 2) You're interested about a case where 2 alleles cooperate. You mean, you have two bi-allelic (to keep it as simple as possible) genes and for each gene one allele is causing the individual carrying it to produce a helping behavior?

Or a helping behavior only restricted toward individuals that carry the right allele of the other gene? Or do you mean, if two genes, A and B which alleles are A1, A2, B1 and B2. If one individual is A1B1 then this individual has a high fitness advantage. Any other combination does not provide any fitness advantage. Something like this? Or do you mean anything else? Could you please give a better description of what you mean by "allele that cooperate".

Thank you for revealing some of the ambiguities of my question to me. I admit my question is open to different interpretations and not well specified. I have edited the question to address your comments, although not to the full extent.

Reading your updated question, I think you are interested about epistasis. Let me know if I am mistaken.
The concept of epistasis might be confused with the one of pleyotropy, so I will define both terms.
Pleyotropy occurs when one gene influences multiple phenotypic traits. Note: the phenotype, to make it simply is what a living things look like (its cells, proteins, shape of the face, size of the leaves, etc…). It is often thought in duality with the genotype which is the total genetic information contained in an individual that codes for the phenotype (Be careful, the environment is also an important factor influencing the phenotype, if you make sports you will have big muscles!)
Epistasis is when the effect on the phenotype of one gene depends on the presence of several (or only one) other genes. Wikipedia gives this (simplistic) example:

Here, two bi-allelic genes are involved. One gene that determines the hair color. The two alleles influence the phenotype such: one allele gives red hair and the other allele gives blond hair. Now There's another bi-allelic gene coding for baldness. One allele causes the bearer to be hairy and the other one causes the bearer to be bald. Therefore, if an individual carries the allele "Bald" in the "Baldness" loci, what this individual carries on the other loci is not important because it will result into the same phenotype anyway, he is bald. Now if in the baldness loci, the allele is "Hairy", then the expression of the other gene "Hair color" matters and therefore if the allele is "blond", the bearer has blond hair and if the allele is "red" the bearer has red hair.
The "Baldness" gene is called a modifier. One can also say that the expression the "Hair color" gene depends on the genetic background of the individual.
Now cases of epistasis are not always that easy and if they influence the fitness, this kind of epistatic interaction might have implications for their evolution.

awesome - it looks like a fitting example - I'll study epistasis and pleyotropy in the near future (added to my to do list)

;) Great! I would recommend to avoid using the word "cooperation" for such interaction. Cooperation in evolutionary biology is linked to the concept of altruistic behavior. Therefore, cooperation is a word that mostly stand for relations at higher level, between individuals (or between cells) and not between genes. The evolution of altruism is a big field of evolutionary biology (social evolution, evolution of multicellularity, level of selection,…) that is still on debate.


text:
Does a phenotype include the presence of a recessive gene
I am trying to understand what exactly a phenotype is to try and understand a genetics database. (Ie I don't really know very much about genetics at all)
I've been reading through wikipedia on what a phenotype is and from what I can gather it is an observable trait which may be impacted by a specific gene.
What I would like to know is if you were looking for the presence of a phenotype such as red hair, would characteristics like not red hair and carrier of red hair also be phenotypes?
For example the following table is named Phenotype,
+------+------------------+
| Code |   Description    |
+------+------------------+
| RR   | Red Hair         | this makes sense with my understanding of phenotype
| RN   | Red Hair Carrier | this doesnt
| NR   | Red Hair Carrier | this doesnt
| NN   | No Red Hair      | this doesnt
+------+------------------+

The whole code column looks like it represents a gene not a phenotype

I agree with one of Alan's comments when he says:
"I think this comes down to whether you include being a carrier of a genetic "condition" a part of your phenotype. It's almost a question of semantics"
To expand on this, I would say there are two major definitions of phenotype, and both are employed by geneticists depending on the context.  Definition one is a bit more naive, and I tend to use it when teaching or trying to explain phenotype to a layman: anything you can observe is a phenotype.  Under this definition, having red hair is a phenotype, not having red hair (or, more directly, having black, brown, blonde, etc. hair) is a phenotype, but carrying the recessive gene for red hair is not a phenotype.  I can observe without checking your genome that you do or don't have red hair, I cannot tell without checking your genome that you have one copy of the recessive gene for red hair.
Definition two is more complete, and I tend to use it more in a lab research setting: anything that is the OUTCOME of a genotype can be defined as a phenotype.  Again, red hair and not red hair (meaning brown, black, blonde, etc) are outcomes defined by the genotype.  However, depending on the context (let's say I'm interested in understanding heritable potential and not the color of hair) I'd say that the phenotypes would be 1) the ability to pass on red hair to progeny (outcomes of genotypes RR, RN, RN in your example), and 2) lack of ability to pass on red hair to progeny (outcome of genotype NN in your example).  In both cases, the phenotype is the outcome of the underlying genes, I just have to make sure I frame my scientific context appropriately.

I think you are correct, "phenotype" really should be what you observe, or measure in the organism, and genotype is what the underlying genetics is, either inferred, or experimentally determined.
Keep in mind, Mendelian genetics makes for great homework exercises, but there are a million more phenotypes that don't fit the Mendelian paradigm than there are ones that do.  Hair color is a phenotype, but it has a lot more genetic components than the simple "one gene, two alleles, one completely dominant over the other" model that Mendel found applied to his 7 phenotypes.

Thanks that's what I though, obviously the data is a little different to what's above but it demonstrates the point.

You say it yourself: The phenotype is the observable trait. So this means if you have red hairs, your hair phenotype is red. The most likely reason for it, the mutation of the melanocortin-1-receptor, is the underlying genotype.
Or: The phenotype of mouse coat color is black, white, brown, speckled, whatever. That what you see, the reasons for that can be (and are) completely different between different mouse strains.
The first column of the table is the genotype and showing that red hair is a recessive trait (without naming a gene, but this doesn't matter), the second only is a representation of the first and makes actually no statement about the actual phenotype.

Thanks that half answers what i was after, im really interested in the counter case, what shouldn't be a phenotype. I have a table in a database called phenotype which has things like carrier of red hair and no red hair these dont really match what i have read and understand a phenotype to be but its really hard to tell as ive only just read some wikipedia articles. are these phenotypes?

I am not sure, if I understand your problem: You are thinking about comparing red hair carrier to not red hair? Simply speaking: Hair color is a phenotype, as is skin color (or the color of your eyes). The reason for it (the genes underlying and causing your hair, eyes, skin to have the color it has) is the genotype. Can you show this table?

i added the table into the question, does this make a bit more sense?

I think this comes down to whether you include being a carrier of a genetic "condition" a part of your phenotype. It's almost a question of semantics.

I depends on the definition. I learned a quite strict one (actually what you see), so this doesn't fall under phenotype.

The table in your question is a derivative of a punnett square, which shows how different dominant Vs recessive alleles go on to inform phenotype in a logical way; In this case R is dominant red and r is recessive red.
RR = red : rr = not red :  rR / Rr = carrier of red. Red is the phenotype expression (for red hair).
A carrier can pass on either the (R)ed or the (r)ed during meiosis, whereas a totally dominant (R) or totally recessive (r) will pass on just one type, to be combined with the other contributing parent chromosomes during meiosis 1.
I hope this helps.

Hmmmm... no, that is not what a Punnet square does. A Punnet square gives you the expected outcome of a specific crossing. In any case the table in the question has nothing to do with it, aside from having some genotypes written in it...


text:
iodine: how did they manage without it in old ages? (People who were living far from the sea)
Knowing that today iodine comes either from fish products or (artificially) enriched table salt, how did people who lived far from the sea survive before (especially during the the Middle Ages)?
Edit 1: nowadays we could find some iodine in cow milk, cheese and eggs but those sources are artificial

(Increased iodine content in food due to greater use in: food
  processing, animal rations, antimicrobial agents...)

source
Edit 2

A small amount of iodine enters the atmosphere and, through rain,
  enters ground water and soil near the sea

source
Summarized of the comments: thanks to  ddiez this question has been partially answered. But as vsz pointed out the the mystery remains:

areas with iodine deficiency didn't get completely depopulated during the Middle Ages
  seems to suggest that it does not affect all people that severely.

So the question remains: could humans survive and reproduce without any iodine source?
Edit 3:

“If all women in the UK took iodine supplements while pregnant, IQ
  would rise by 1.2 points per child” but some says "Some observational studies suggest supplements could even lower IQ, perhaps because excess iodine might harm the thyroid gland." (Newscientist, August 2015)

They had problems - strumae were pretty common in old ages.

@Chris, I would like to suggest tagging this question with "iodine" and/or maybe "thyroid hormones". None currently exist. No experience so far with tagging and its rules.

@ddiez I think iodine is a bit too specific to warrant a tag and thyroid hormones as a tag only indirectly describes this question; I think it's prefectly appropriately tagged

@Armatus I understand, and agree, with your arguments. Thanks for the explanation.

@GuillaumeCombot, I am afraid you have misunderstood my answer/comments. Iodine appears naturally in food (although certainly can be added). Iodine deficiency has not been an issue at all in the Middle Ages in places where the water or soil was iodine-rich. Iodine deficiency is still an issue today in many parts of the world. I have updated my answer to make things more clear.

Iodine is naturally found in sea water and soil but it is not evenly distributed, with many areas in the world with low levels of iodine. Iodine accumulates naturally in fish, and plants growing in iodine-rich soil. Mammals that eat these plants get iodine from them, which then accumulates in the milk, making dairy and its products (e.g. cheese) another natural source of iodine. Table 1 from the Iodine deficiency section at the American Thyroid Association web page contains a brief list of iodine-rich food.
Quoting the web site:

What are the sources of iodine?
Iodine is present naturally in soil and seawater. The availability of iodine in foods differs in various regions of the world. Individuals in the United States can maintain adequate iodine in their diet by using iodized table salt (unless they have to restrict the amount of salt in their diet), by eating foods high in iodine, particularly dairy products, seafood, meat, some breads, and eggs, and by taking a multivitamin containing iodine (see below). However, the amount of iodine in foods is not listed on food packaging in the U.S., and it can be difficult to identify sources of iodine in foods.

As mentioned, the amount of iodine in some food depends on how much iodine is present in the water or soil. For example, in the International Council for the Control of Iodine Deficiency Disorders (ICCIDD) there is some mention about the natural sources of iodine and its limitations:

Most of the iodine we consume comes from what we eat and drink. Seafood is usually a good source because the ocean contains considerable iodine. Freshwater fish reflect the iodine content of the water where they swim, which may be deficient. Other foods vary tremendously in iodine content, depending on their source and what may have been added. Plants grown in iodine-deficient soil do not have much iodine, nor do meat or other products from animals fed on iodine-deficient plants. Because the breast concentrates iodine, dairy products are usually a good source, but only if the cows get enough iodine.

Iodine deficiency causes important health problems. Iodine is necessary to produce thyroid hormones. Lack of thyroid hormones causes hypothyroidism, cretinism and goiter. However, iodine deficiency is not mortal per se.
Conclusion
As a consequence, in the Middle Ages iodine deficiency was not an issue in places where water and/or soil was rich in iodine. In other places they would suffer of iodine deficiency, leading to a higher impact of the related diseases.
Nowadays, iodine is added artificially to food in order to prevent iodine deficiency. This practice has diminished the impact of iodine deficiency-related diseases. However, iodine deficiency is still an important issue today, as reported by the World Health Organization in its map describing the Degree of Public Health Significance of Iodine Nutrition. As shown in the map, in many places in the world there is still risk of severe iodine deficiency.

Sources:

Iodine deficiency - Wikipedia
American Thyroid Association
World Health Organization
International Council for the Control of Iodine Deficiency Disorders (ICCIDD)

thank for your detailed response! I added more details in my question, it's more tricky that it sound.

@GuillaumeCombot I am sorry but cannot see how your edits change my answer. Is your question different? Basically in the Middle Ages people got iodine from food, wether it be sea food or other food (e.g. vegetables and dairy) from places with iodine rich soil. Iodine deficiency does not typically cause death - but some (very serious though) diseases. During the Middle Ages those diseases were more prevalent.

I suppose they could have eaten thyroids, that's where the most iodine would have been. But most people at that time probably couldn't get much meat anyway, and they probably wouldn't know enough to associate thyroid consumption with preventing iodine deficiency, or even knew about iodine deficiency. And I have no evidence to say whether or not anyone actually ever ate thyroid.

@user137 certainly in the Middle Ages they did not know about iodine deficiency and eating thyroids would, very likely, not be extended. Iodine deficiency appeared in places with iodine deficiency in soil or water, or (and that is a fair comment) in places where people didn't have access to food or water. However in those places starvation and malnutrition would probably be a much more serious issue than iodine deficiency.

@ddiez the things is that unless they were living near and not too far from the sea they could not get it from food (iodine can only be fund in the soil near the sea since it comes from the sea so for instance around Paris or Berlin or Moscow you would logically not have fund anything is the soil, and thus the food).

@@user137 eating  thyroids (even by chance) makes sense but the problem remains the same: where would this animal iodine would come from at 500 km from the sea? Asteroids, who knows!  Yes could people did die before by starvation, but can human reproduce without iodine? Still looking for an answer...

The fact that those areas with iodine deficiency didn't got completely depopulated during the Middle Ages seems to suggest that it does not affect all people that severely. Are there people who can have good health with much less iodine that can cause others to suffer severe symptoms?

That was behind my question! Could humans survive and reproduce without any iodine source. Updated my question with vsz comment!


text:
Has anyone ever sucessfully translated xRNA or yRNA?
I've recently been researching the subject of size-expanded nucleobases in alternative genetic sets. Many papers describe the, at least, partial success in replicating xDNA and yDNA, as well as transcribing them, as suggested here.

At the same time, studies on polymerase replication and transcription of oligonucleotide sequences reveal that chemical entities other than the typical nucleoside triphosphates can be tolerated to varying degrees.

My question is can the cell's molecular machinery, including ribosomes and tRNA, possibly lead to translation of xRNA or yRNA? Would the translation product yield the traditional 20 amino acids? Have this ever been attempted?
References to original papers would be appreciated. Thanks!


text:
How do I find a protein from this DNA sequence?
I have a DNA sequence from a sequencer. How can I determine what protein is it? I tried some translator but it didn't help. What protein is this and how can I determine it?
The sequence: CGTTCTATAGATACGCGATGACGGTATACCATCCGCAAAGT
Thank you very much!

Have you tried to blast the sequence?

Translation would fail on this sequence since it’s not a complete open reading frame (doesn’t start with a start codon, doesn’t stop with a stop codon, and length not divisible by three). As such, we don’t even know whether it’s in frame, or maybe shifted by a nucleotide.

Entering fragment in BLASTX helped

Enter it in BLASTX. This will give you any protein sequence matches as well as likely homologues given a nucleotide sequence.

Great, I hope that was good news for you!

You might want to try searching against NR/NT database using BLAST. This way you will get to know what this sequence might be similar too. The length of the sequence is too short to code for any meaningful protein.


text:
What recovers normal polarisation after hyperpolarisation?
I have been taught that a $\ce{Na+/~K+}$  pump helps to recover normal polarisation after-hyperpolarisation in neurones. I could not find out how it does that, since I've also been taught that such a pump moves $\ce{3Na+}$  out of the cell and $\ce{2K+}$  into the cell. That implies that the potential can only get more negative. How does this work?
My hypothesis was that the potential 'leaks' out and recovers the 70 mV that way. I couldn't verify that, however.

Can't give a full comment at the moment, but... Na+ and K+ have different electrochemical equilibriums, and in addition to the Sodium-Potassium Pump there are many porins that act as passive diffusion routes to re-establish the cell's preferred equilibrium.

Na/K ATPase will pump as long as it is energetically favourable. At about -70mV ATPase work is balanced by leackage

Remember that the action potential gets more positive in the first place, so increasing positivity is achievable. Net Na+ movement into the cell makes the potential more positive. This occurs as the Na+ gate (right on the image below) are open. The key message is that the membrane can move charge to cause an increase in either positive and negative potential.

Imagine one side becomes more negative. The Na+ diffusion will correct this to reach an equilibrium around 3 to 4 milliseconds (ms) after the stimulus to reach the resting potential
 (as alluded to my @MCM in the comments).
There are some great animations demonstrating this principle on the University of Bristol's website. They clearly show how positive charge can be conferred over the membrane.
A (now deleted) comment linked to the below image that shows the potential and when the gates are opened and closed. I would still go to the bristol website too to see it in action, but this figure is a quick go to once you get your head around the timing of ion flux.

As with most biology, it is a little more complicated than that overly simple model. There are entire books on how neurones control their charges.

Note: The key terminology is somewhat muddled and there doesn't seem to be a standard term. I have seen this "recovery" phase called undershoot, overshoot (and overshoot rather unhelpfully also refers to another part of the action potential), the refractory period, and discussed as part of hyperpolarization. The go to term is afterpolarisation if you want to research this more thoroughly.


text:
If I buy a banana at the market, is there any chance that an insect is hiding inside it?
I watched this horrifying video on Youtube. It shows movement beneath the skin of a banana and then a spider pushes it's way out.
Suffice to say I'm too scared to eat bananas anymore!
I would like to know what is the probability that an insect is hiding inside a banana that I buy at the market? Even if there was just one chance in a million that an insect is hiding inside I would stop eating bananas forever.
I postulate that an insect could lay it's eggs in a banana and then the offsprings would be born inside the banana. Or perhaps an insect tries to eat a small chunk of the banana, it cuts his way out inside the banana, it gets trapped inside, and then someone buys the banana. Both of these ideas are troublesome since I'm not sure if there is air to breathe inside the banana.

The thing that comes out of the banana in the video is not an insect. Where do you plan buying a banana (where do you live?)? In a Wall-Mart at Fairbanks, Alaska or at a local market at Jakarta?

That video could be fake.

If you're scared of insects and insect eggs being in your food you're about to go VERY hungry. https://en.m.wikipedia.org/wiki/The_Food_Defect_Action_Levels

I like the question, but I think the reason you're getting so many down votes (and why I down voted) is because you link to a spider and ask about insects. Remember they are different and this is a pet peeve of entomologists! Did you actually mean to ask about insects, spiders, or anything in between?

That's not why I voted - I voted because I feel it's not on topic and primarily opinion based, and I've spent the last 7 years working with insects :)

Kaleb Lechowski, creator of that video, is a digital creator and animator of critters. I would propose that he did a very good job of rendering a CGI spider to burst from a banana.
Spiders (which are not insects remember) won't eat bananas. In fact, only one species is known to be mostly herbivorous: Bagheera kiplingi.
However, don't eat that banana just yet! The internet is littered with tales of horror about spiders in fruit. Like this Black Widow in a bunch of grapes. There is no bursting out of the fruit like Alien, but what has happened is the spider has unwittingly found itself being picked from its natural environment and transported with the fruit.
Fruit is good. Stay sceptical of internet rumours that are trying to get clicks with fear, and stay measured enough to remember that the benefits of eating (washed, clean) fruit far outweigh the extraordinarily low chance of finding a nasty bug hiding away.

Also I'd suggest many/most insects/spiders are edible, so there's no reason to be scared


text:
Longest lived land mammal when subtracting sleeping time?
Recently, it has been found that wild elephants only sleep two hours per night. Wild elephants also live quite long, the median life span is 56 years. Now, 56 years lived with 2 hours sleep per day amounts to about 51 years spent being awake, while a human being who dies at the age of 80 who sleeps 8 hours a day will have spent about 53 years being awake (here we ignore the larger sleep requirement during infancy, taking that into account may put the elephants ahead of us).
So, we see that taking sleeping time into account greatly affects the comparison between waking lifespans of animals. The question is then what land mammal has the longest lifespan when subtracting sleeping time i.e only counting the waking hours. Some sea mammals like whales are known to live for a very long time, but that may be due to very peculiar features of such mammals who have adapted to living in the oceans.

You cannot calculate it so mechanically. If you read just the Wikipedia article https://en.wikipedia.org/wiki/Sleep_in_non-human_animals#Sleep_duration, you'll find that the type of the sleep differs a lot between animals, so you cannot get comparable data just by "subtracting sleeping time". When you sleep and when an elephant sleeps, it's not the same experience :)


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Experimental Analysis: What are possible reasons for this increase in N₂O production?
My professor wanted us to each conduct an experiment for class on something we thought would interesting. My experiment was very simple, but I'm not sure how to interpret my results. (Please note that this is not for homework – I'm just genuinely confused and trying to understand the data.)
Basic method:
Take soil samples, add varying concentrations of Roundup and water equalling a total of 50ml, seal in airtight jars, incubate for 7 days, run through a Gas Chromatograph, and record the rates of production for CO2, CH4, and N2O. Overall, there was the Control and then three treatments, for a total 8 jars because each had a duplicate:

Control (Roundup: 0, H2O: 50ml),
T1 (Roundup: 10ml, H2O: 40ml),
T2 (Roundup: 25ml, H2O: 25ml),
T3 (Roundup: 50ml, H2O: 0).

I expected the Control to have the highest levels of production, followed with a decrease in production for T1, followed by T2, and then T3, with T3 being the lowest because all microbial activity was inhibited by the massive dose of Roundup.
However, the results were a bit surprising.
In general:

The Control rates were the highest, as expected.
T1 showed a decrease in production, as expected
T2, again, showed a decrease in production, as expected.
And then T3 showed a significant increase in production.

Here are some graphs to illustrate this in more detail:

This is a new field of science for me, so forgive me if I'm missing something obvious, but my natural intuition is certainly not helping me out on this one. What are some possible causes for this increase – in particular for the N2O/denitrification? Or at the minimum, are there any particular resources I can take a look at to better understand why this happened?

Edit
This is my brain on paper, so forgive me again for any ridiculous things I say. But, could it have something to do with the denitrification process such that more gas is given off as N2O because the microbes responsible for processing the N2O into N2 have died. So in the previous Treatments 1 and 2, the N2O was lower because the N2O was being converted into N2 (but we never recorded the N2), but in the final treatment, no conversion occurred, so the N2O appears to go up, even through the microbes are functioning even less.
Thoughts?

What was your process in collecting the soil samples? Prepackaged in any way, dug up by hand?

Dug up by hand, with gloves, placed in plastic bags temporarily for transportation, and then right into the jars. All were collected at the same time/day.

So, you have what could possibly be an outlier that's just due to that soil sample. It's a pain, but basically you would take more samples, have more replicates and data points, and you might see that the particular outlier point is just an artifact. The actual explanation why did that sample do that? would require a deeper investigation!

I am not a biologist so I have no idea. This said, the graphs do no show any error (actually incertainty) bars, which are needed to do any kind of interpretation.

This may have no correlation to your project but many insecticides, bacteriocides, and herbicides need a "solvent" or "transfer medium" such as water to be effective. Even when using ethanol in the laboratory against a variety of bacteria 100% ethanol becomes almost ineffective.
I would take a look at running round-up again by itself versus 95% roundup 5% water, and 90% roundup and 10% water and I am sure you may seem some results that will aid your experiment.
Good Luck!


text:
Concentration of a specific promoter in a cell?
I want to simulate transcription activation by a given transcription factor (TF) with known kinetics. The binding rate $k_{on}$ is given in $\mu M^{-1} s^{-1} $, describing a bimolecular reaction mechanism (second order reaction kinetics). However, what is the concentration of a specific promoter in a cell?

In a diploid organism there are two copies of DNA which means two copies or "molecules" of promoter in the entire cell. The volume of a typical eukaryotic cell (HeLa) would be 2.25×10-12 litres (Zhao et al. 2007, BioNumbers).
$$\text{Concentration }(M)=\frac{\text{Molecules per cell}}{\text{Avogadro No.} \times \text{Volume of the cell }(l)}$$
This comes to around 1.4758×10-12 M for 2 molecules of promoter. Accordingly, you can calculate for a haploid cell, multiple alleles or prokaryotic cell.
You can also assume a 2-compartment model with nucleus and cytoplasm as two different compartments. In this case, the DNA would be localized in the nucleus and therefore its effective concentration would be higher in the nucleus. You can look up nuclear volume in BioNumbers and plug that in the above formula to obtain the effective concentration.

Zhao, L., et al. "Intracellular water‐specific MR of microbead‐adherent cells: the HeLa cell intracellular water exchange lifetime." NMR in Biomedicine 21.2 (2008): 159-164.


text:
How does the splicing enzyme recognize where to splice the introns?
When the DNA from the nucleus is transcribed to an mRNA, the mRNA is spliced by an enzyme before it goes outside through the nuclear pore. What is the name of this enzyme and how does it recognize where to splice the DNA so only the introns remain inside? Would it not need an instruction set itself to recognize exactly where to cut so the sequence does not change?

There are two factors that involve the ability of enzymes to process RNA.
1) Structure see wikipedia
2) Binding affinitya
Let's take a look at the splicing process:

The active 'sites' (GU,A & AG) need to be in spatial proximity (point one), and the enzyme needs to be able to bind there, aka forming hydrogen bonds with the nucleotides, which is mostly the case if:
a) the nucleotides are 'free' as in they are not paired with other nucleotides
b) it is energetically favorable for the enzyme to bind and do its work, which factors like temperature, and of course on the correct nucleotides
If there were some mutations, the splicing might not work.

Comment for the enzyme: It's a complex, the splicosome. There is a cool movie about it: https://www.dnalc.org/resources/3d/rna-splicing.html

Simply add the additional information into the answer by using the edit function below it and do not put it in the comments.

There are several determinants. As you mentioned 5'-GU--//--[---]--//--AG-3' is the typical sequence of an intron.  There is also a polypyrimidine tract in the intron.