text:
Reason behind selection of sites of administration of pituitary extracts?
There are two ways by which pituitary extracts are administered in a fish's body during induced breeding of fish.

Intramuscular injection is the most common practice in India and it is less risky in comparison with the other methods.The extract is injected into the muscle near the tail above the lateral line.
Intra-peritoneal injections are given through the soft regions of the body, generally at the base of the pelvic fin or sometimes at the base of the pectoral fin.

Why are these sites chosen? What physiological effects arise as a result of administration that these sites got chosen ?

maybe to avoid injecting nerves as it may cause paralysis due to damaged nerves.

Intramuscular injections are usually preferred because they result in a more constant delivery of hormone and there is less chance of injuring the fish. The preferred site for an intramuscular injection is into the thick muscle of the back. This is because it is mostly used for fish movement and therefore has the most intensive blood circulation. Thus, injected hormone will be transferred thought the body quickly. Additionally, as this muscle is big, there is smaller chance to injure internal organs by the needle.

Source: assignmentexpert.com

Melatonin is an evolutionary highly conserved molecule that plays an important role in conveying the clock and calendar information to all living organisms, including man. The hormone is synthesized mainly by the pineal gland, and, to a lesser extent, by extrapineal tissues--such as the retina, Harderian gland, and gastrointestinal tract.
It is a standard slow acting hormone injection. Once the injection is in the animal, it just propagates throughout the animal's physiology and takes the normal melatonin chemical and physiological pathways that it does in vertebrates, it prompts the pituitary gland to produce a lot of different hormones including sex and serotonin.
It doesn't act instantaneously if you overdose (humans have tried), OD negative effects occur after 1-2 days and thereafter. It doesn't react as violently as some other hormones such as Adrenaline, which is absorbed fast and dissipates fast and can give you a heart attack. Melatonin has a physiological effect that is more extended, for example steroids for inflammation.
The aim of intramuscular injection of the fish is that it is effective and safe, If you read the guides, they are concerned with the safety of the fish, it's nerves and vital organs... The tail is mostly muscle and the injection is IM. Once the hormone is injected, its absorbed by the animal over an extended period. There have been many experiments of pineal injection in rodents so refer to them to know the time frame of absorption.

For your kind information the question is about injection of pituitary extract and not pineal extract.        P.S. I didn't read the entire answer but up till the second paragraph.


text:
How does rho-dependent termination occur?
Rho-dependent termination is not fully understood but there’s a brief description in almost every concerned book about it.
In Snustard and Instant notes-Molecular Biology it is written that, the rho protein binds a stretch of 72 nucleotides at the 3' end of the nascent RNA, which could be a recognition site and then moves along 5' -> 3' direction separating the DNA-RNA hybrid.
But how's it possible, rho binding to 3' end (which is not free) and moving in 5'-> 3' (if so it is sure to fall off!)?
Diagram from Berg showing something opposite, i.e. it has attached to the 5' end and is moving in 5' -> 3' direction.

What is the right thing?

There is no dichotomy in the two sources you have described. The text book you linked to says, exactly (emphasis added):

Rho appears to bind to a stretch of 72 nucleotides near the 3'-end of the nascent RNA...

It doesn't say at the 3'-end, which is obviously impossible since the 3'-end forms a double-stranded hybrid within the transcription bubble.
Rho is not loaded at the 5'-end of RNA, either, but rather binds internally at cytidine-rich Rho utilization (rut) sites, which will be somewhere 5' of the actual point of transcription termination. As you mentioned, there is a lot of uncertainty in the process and, while a lot is known about rut sites, as far as I can tell there is no consensus sequence, thus making it difficult to systematically identify rut sites throughout the genome. I have found papers which identify rut sites in the 5'-UTR (1) as well as within the 3'-UTR, intercistronic regions and coding sequences (2, 3, 4).

Mechanism of internal Rho loading:

Koslover DJ, Fazal FM, Mooney RA, Landick R, Block SM. 2012. Binding and Translocation of Termination Factor Rho Studied at the Single-Molecule Level. J Mol Biol 423:664-676

Your diagram is correct. Rho protein binds at the 5' end and "chases" RNA Polymerase. It's not possible for Rho protein to bind at the 3' end, as this hasn't been transcribed by RNA Polymerase yet.

can you add some references to your answer?

source: Stack Exchange

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text:
How do both autotrophic and heterotrophic successions end up having Gross Production = Respiration?
I was reading Information theory by Eleith, Odum and Golley  from different sources, one of which was Funfamentals of ecology by Odum:

... autogenic succession usually begins with an unbalanced community metabolism, where gross production, P, is either greater than or less than community respiration, R, and proceeds towards a more balanced condition, where P=R. The rate of biomass production (B/P ) increases during sucession until a stabilised system is achieved, in which a maximum of biomass (or high information content) and symbiosis between organisms are maintained per unit of available energy flow.
The succession begins with P>R in autotrophic sucession and P<R in heterotrophic sucession.

I have tried to find explanatory texts both in this and other books without any success so my question is how's this balanced state achieved in both types of successions (the answer is hinted in the first paragraph which I don't quite understand)?
Related to my last post.

The author is saying that 1) Mature ecosystems tend to have a balance between production (=P) and use (=R, respiration) of biomass. This is actually tautological because the author would probably define a mature ecosystem as one where this is true (P=R).
If it starts out P > R, the autotrophs are dominant: more biomass is being produced than used up. It is possible, for a time, that P will increase as, for example, plants grow more leaves, but R is growing too, and there is an eventual limit on P, which at maximum depends on the light available to the ecosystem. As biomass grows, so does the amount of biomass to potentially decay, so eventually R will always catch up to P, until there is balance.
If it starts out P < R, that means you are using up biomass faster than you are creating it. This case is even simpler: you will gradually run out of biomass, and R will decrease.
In either case, when the author is talking about P = R, this is going to be in relative terms; there might still be variations between them, for example seasonal variation, but on average over years or decades you would expect P = R in a mature, stable ecosystem.

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text:
What is Tandem repeat?
After reading -

(wikipedia) Tandem repeats occur in DNA when a pattern of one or more nucleotides is repeated and the repetitions are directly adjacent to each other.
( a paper) A tandem repeat in DNA is two or more contiguous, approximate copies of a pattern of nucleotides.

I deduced that the portion of oriC containing all four 9mer-s
was to be called a tandem repeat and it together with all three 13 mer-s, two tandem repeats.
But again while reading Principles of genetics by Simmons I stumbled upon the following-

The single ori in E.coli has been characterised in considerable detail. It is 245 nucleotide pair long and contains two repeated sequences. One 13-bp is present in three tandem repeats. The three repeats are rich in ...

So here it says that each 9-mer in the series is a tandem repeat actually.
Which meaning is more accepted?

I don't know much about Simmons, but the definition by wikipedia is seemingly more accepted.

The DNA sequence "TATATATA" contains 4 repeats of the 2-mer "TA" and because these repeats are adjacent to each other, they are tandem repeats. The pattern of  nucleotides is repeated and the repetitions are next to each other.
This is what both the Wikipedia and the Simmons definitions are trying to communicate.  The statement you quote from Benson'a paper can be taken to mean the same thing (except for "approximate"), but might also be construed as saying the collection of all contiguous repeats is one tandem repeat, but that is not what was intended.
So, the oriC sequence has 4 tandem repeats of one kind (9-mers) and 3 tandem repeats of another pattern (13-mers).


text:
Identification of Sunbirds

Location: Asansol-Durgapur region, West Bengal, India
Question:
Do they belong to the same species?
Note:

I presume the bird in Pic-1 is a male  Purple-rumped sunbird (Leptocoma zeylonica).
I think the birds in Pictures : 2-5 could be non breeding male Purple sunbird (Nectarinia asiatica) because they match very much with the Wikipedia description though the bird in Pic-2 has a short tail.
Pic-4 and Pic-5 capture the same bird.

The bird in Picture-1 is  Purple-rumped sunbird (Leptocoma zeylonica) according to this decription from wikipedia:

The males have a dark maroon upperside with a blue-green crown that glistens at some angles, bright green shoulder patch and violet/purple rump patch which is generally hidden under the wings. The underparts are whitish with dark throat, maroon breast band and purple/violet patch in the throat which is visible in some angles.

The birds in Pictures 2-5 is a single species, non-breeding male of purple sunbird (Cinnyris asiaticus) according to this description:

The male is glossy metallic purplish black on the upper parts with the wings appearing dark brown. The breeding male has the underparts also of the same purplish black, but non-breeding males may show a central streak of black on yellow underparts.

References:

Wikipedia
r/whatsthisbird


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Why do some people burn and others tan?
Connected to What is happening when we get a tan? - Why do some people burn while other people tan?
Very pale people tend to just burn while other people tan very nicely, what causes this difference?
I assume it has something to do with pigmentation - so what is the pigmentation in our skin actually doing in order to protect us from getting a sunburn?

Also have a look at this post. It is not directly related but addresses some points on UV damage.

There are two things happening: First melanin absorbs the energy from the UV radiation and releases it as infrared energy and thus protects the cells in the skin. This happens in all people, the deeper the skin color is, the better is the protection.
What is different between people is the amount of pigment they produce, the number of melanocytes is approximately the same. This depends on their genetic backgroud and is influenced by mutations in the pigment production pathway. As this is relatively complex, there are numerous positions which can influence the ability to tan, so I will only name a few.
The rate limiting enzyme for the pigmentation is Tyrosinase which catalyzes the first step of the melanin biosynthesis and oxidizes the amino acid tyrosine into DOPA. Without tyrosinase humans are not able to make any pigment at all which causes albinism. This is pretty drastic and doesn't happen too often. See reference 1.
Other possibilities are mutation in the signalling towards pigmentation, more specifically mutations in the MC1R gene which encodes on of the receptors. These mutations affect the ability to tan and are associated with red hair color, pale skin and freckles (most of the red-haired people carry at least one mutation in their MC1R gene). See reference 2.
Then there are mutations in the tyrosinase gene, which results in an enzyme with a lower processing rate. Because of this, less pigment can be made as the amount of materials is limited. See references 3 and 4.
The diversity of the human pigmentation is influenced by all these (and much more) genes. Have a look at references 5 and 6 for details.
References:

Analysis of tyrosinase mutations associated with tyrosinase-related
oculocutaneous albinism (OCA1).
Red hair is the null phenotype of MC1R.
Mutations at Critical N-Glycosylation Sites Reduce Tyrosinase
Activity by Altering Folding and Quality Control
Mutational mapping of the catalytic activities of human tyrosinase.
Molecular genetics of human pigmentation diversity
The genetic architecture of normal variation in human pigmentation:
an evolutionary perspective and model


text:
What is happening when we get a tan?
Almost everyone nowadays wants that nice summer tan, but what exactly is going on beneath the skin? I've heard a few different theories about tanning - such as a tan is nothing but the pigmentation in your cells burning, but is this true?
My questions:

What exactly is happening to our skin as we tan?
Are pigments being burned (like I was told in school), or is pigment being produced by the cells. ?

Bonus related question:
Why do some people burn and others tan?
Bonus related question: https://biology.stackexchange.com/questions/35719/how-does-our-tan-disappear

When our skin is exposed to the sun, this can cause some damage in the upper layers of skin. This activates DNA damage repair and also induces signalling towards the melanocytes (which produce the pigment). Signalling means the excretion of signalling molecules (mostly alpha-Melanocyte stimulating hormone, aMSH) which binds to the MC1R receptor (melanocortin 1 receptor) on the surface of the melanocyte (the cell which produces the pigment) and induces (or increases) the production of melanin. The melanin is then transferred in the melanosomes to the adjacent keratinocytes, which are then better protected from the sun. This figure (from this article) illustrates this process nicely:

Short term tans (the fast reaction) are based on the changed distribution of melanosomes (granules containing pigment) from the melanocytes to keratinocytes. Longer term suntans are caused by increased pigmentation in the skin as a reaction to the UV exposure by the accumulation of melanin and by the burning of cells. So it is no wonder that it looks like increased pigmentation, it really is. People tan differently because of their genetic background. This influences their ability to react to sun exposure.
There is relatively little known about the degradation of the melanosomes (the granules containing the melanin). What is known is that they are degraded in the lysosome, and that the melanin is most likely degraded through oxidation. There happens to be a permanent turnover of the melanosomes, and when the body is producing fewer new melanosomes than are degraded, your skin will get lighter again.
References:

Shining light on skin pigmentation: the darker and the brighter side
of effects of UV radiation.
Melanocyte biology and skin pigmentation.
Melanosome Degradation: Fact or Fiction

I have a doubt. As keratinocytes are shed off from stratum corneum then will the melanosomes that they contain also be lost with them?

@WYSIWYG This is true for the dead cells in the stratum corneum. And there will be some pigment in them. But there has to be some degradation mechanism, as freckles also get weaker in the winter (with less UV exposure) and these don't get lost generally.

Some additional details on the same lines as Chris' answer:
Coelho et al. have studied the short and long term effects of UV on human skin and they report that there are different stages of tanning:

Immediate pigment darkening: happens in a few minutes and persists for some hours. It is most probably due to melanosome redistribution and melanin oxidation by UV.
Persistent pigment darkening: happens in a few hours and can persist for days. It happens because of new melanin synthesis in the epidermis.
Delayed pigmentation: happens in a few days and persists for weeks. It results from "prolonged increases in melanin content".
Long-lasting pigmentation:  persists fore more than 9 months after the first UV exposure. The mechanisms underlying this response are not very clear.

IFN$\gamma$ signalling is involved in inhibition of melanogenesis and apoptosis of melanocytes [1,2]. This is one possible pathway of detanning. This happens in the order of days.

First, one should mention types of skin: skin type defines how the person will tan -

Second, the solar radiation (UV) absorbed by sun defines the amount of melanin produced by melanocytes of the skin to protect the skin = melanogenesis (which in turn depends on skin type).
When the solar exposure diminish, the natural repair processes causes melanocytes to remove excessive amounts of melanin.
As mention by WYSIWYG, the question too broad, you can continue your education via wiki.


text:
Is sigma factor a transcription factor?
After I googled 'sigma TF' I stumbled upon two papers(only).
From a paper:

Sigma factors (sigmas) are bacterial transcription factors that bind core RNA polymerase (RNAP) and direct transcription initiation at cognate promoter sites.

and another paper had the title -

Specific binding of the transcription factor sigma-54 to promoter DNA.

However this contradicts with my book- Principle of Genetics Snustard and Simmons:

Unlike their prokaryotic counterparts, eukaryotic RNAPs cannot initiate transcription by themselves .... require the assistance of protein transcription factors to start synthesis.

Is it a TF?
Note: From what TFs are, sigma factor seems to be a TF to me.

As far as I know, a sigma factor is an initiation factor that must be connected to the RNA-Polymerase in order to bind to a specific sequence in the DNA and initiate the transcription. A TF in the other hand, is for the regulation of transcription..

Having read @loolipop’s answer, you should realize that this is a semantic question, with no right or wrong answer. If you define it in terms of the known characteristics of eukaryotic transcription factors, prokaryotic sigma factors clearly do not conform. However, if you define transcription factor as a protein that is required for transcription (by analogy to the terminology for translation factors), or even as a protein that confers specificity on the initiation of transcription, then the sigma factors can be called transcription factors.
Because of the differences between the prokaryotic and eukaryotic systems, I think it more useful to maintain the historic terminology* (check Berg et al., for example) for prokaryotic transcription and, unlike the authors you quote, just refer to the sigma proteins as ‘sigma factors’. This allows you to discuss the similarities and differences between prokaryotic sigma factors and eukaryotic transcription factors without confusion.
*Historic Terminology.
The prokaryotic transcription system was worked out in detail at a time that almost the only thing that was known about eukaryotic transcription was the existence of different RNA polymerases for mRNA and rRNA. The term transcription factor was never used for the sigma factors. The index of the 5th edition of Berg et al. (2001) contains no entry for transcription factor, and focuses on prokaryotic transcription. The index of the 11th edition of The Biochemistry of the Nucleic Acids (Adams et al.), about ten years earlier, does have entries, but almost exclusively for eukaryotes. The only entries that refer to prokaryotes actually relate to termination of transcription, and the term is used to distinguish between (rho) factor-dependent and factor-independent termination.

Prokaryotic sigma factors confer specific promoter recognition to RNAP via Sigma subunit σ1.1, which acts as a DNA 'mimic' - occupying the downstream DNA binding site. This interaction is displaced only when the promoter region is bound, hence conferring the specificity.
Note that Sigma factor on its own cannot bind DNA, as σ1.1 binds σ4 in the unbound form, preventing binding to any sequence.
Source: Section 2. Structural Organisation of σ70 and Other Group 1 σ Factors in this paper
This is in contrast to eukaryotic transcription factors, which can bind to the DNA on their own - indeed the assembly of the general transcriptional machinery in eukaryotes (read: In Yeast) is stepwise and involves first the binding of TFIID to the DNA, then TFIIA, then TFIIB, before finally the Polymerase is incorporated into the growing complex. Source: Molecular Biology of the Gene - James D. Watson, p.g.449-454
In prokaryotes, the sigma factor needs to be bound to the core enzyme (forming the holoenzyme) in order for this promoter specificity to be achieved. Your book 'Principle of Genetics - Snustard and Simmons' is referring to the core RNAP, not the holoenzyme with the Sigma factor bound.
This is why sigma factors are often not included under the umbrella term of 'transcription factor' - they achieve the same functionality as eukaryotic TFs, but are fundamentally different in terms of their binding to the polymerase.
Often authors note that eukaryotes need TFs whereas prokaryotes don't because the point they want to convey is that eukaryotes use huge multiprotein complexes bound to the Polymerase, whereas prokaryotes just use the RNAP holoenzyme, giving Sigma factors a somewhat 'special' place among the transcription factors.

Please add some references to your answer.


text:
Denaturation of protein

Exposure of native protein to heat leads to partial denaturation of the protein due to breaking of-
a. S-S bonds
b. H-bonds
c. Hydrophobic interactions
d. Peptide bonds

After a bit of surface googling I understand peptide bonds are not broken in the process of denaturation and di-sulphide bonds are not broken either (by heat) but by reducers like $\beta$- Mercaptoethanol. These reducers are added in experiments to ensure that the bonds which contribute largely to the tertiary structure are broken.
So either H-bonds or hydrophobic interactions are affected. I cannot make out which one would be the most affected/first one to be affected since the question says partial denaturation, meaning, it was not heated for long.

If you think about the boiling of water, I'm sure you can understand that heat breaks hydrogen bonds. Next consider that the hydrophobic effect is driven entropically and so, by the equation $\Delta G=\Delta H-T\Delta S$, its strength increases with temperature (to a point). See here and here for further explanation. Also, this paper for a more empirical view.

So as the temp. increases the hydrophobic interactions become stronger /are favoured until it is high enough to be disturbed. In the latter is it due to high KE that the hydrophobes are unable to maintain their interaction(closeness)?

@Tytoalba Thanks, I'll add the link (and some others) to the answer. I don't like some of their wording, but overall it's pretty intuitive. I think the first link should answer your question in the comment.

Protein found in a biological system with a unique three-dimensional
  structure and biological activity is called a native protein. When a
  protein in its native form, is subjected to physical change like change
  in temperature or chemical change like change in pH, the hydrogen
  bonds are disturbed. Due to this, globules unfold and helix get uncoiled
  and protein loses its biological activity. This is called denaturation of protein. During denaturation secondary and tertiary structures are destroyed but
  1º structure remains intact. The coagulation of egg white on boiling is
  a common example of denaturation. Another example is curdling of
  milk which is caused due to the formation of lactic acid by the bacteria
  present in milk.

According to the above paragraph, denaturation occurs due to disruption of hydrogen bonds. The answer should be option (B). Note that the energy of hydrogen bonds are 3 - 10kcal/mol. Therefore, hydrogen bonds can be broken and formed easily. You can imagine the process of replication, transcription, etc. where H-bonds are broken and formed easily.
NCERT XII CHEMISTRY (PART II) Chp.Biomolecules 14.2.4 Pg. 141 of that PDF, but in actual book Pg. 416

Thank you :) for putting an effort at writing an answer.

It is my first answer on this site and you are welcome.


text:
Simpson's index
Simpson’s index is a diversity index which is the summation of the square of the probabilities of the species in a community.

The value varies between 0-1.
here, pi=n/N where ni=number of individual of species i in the community and N=total no. of individuals.
S=total number of species.
It is the measure that equals the probability that two individuals taken at random from a community belongs to the same species.The probability decreases if the species richness and evenness increase. It is strongly influenced by the most abundant species.
From:

Wikipedia
Fundamentals of ecology, Odum
Biodiversity of fungi

What is meant by 'It is strongly influenced by the most abundant species'?

I'm assuming that term is meant as a critique/limitation or at least a point to note when taking the index as a measure of diversity. They just mean that the value for D in that equation is affected strongly by how abundant the most abundant species is. So, if you have one species that is very abundant, you might get a high value for D (=low diversity, strangely) even if there are hundreds of other, less abundant species, because adding 1 more species with low abundance does little to the measure.

I don't know whether this math will be clarifying forr you, but it might help you understand why "It is strongly influenced by the most abundant species." It is all about finding the best p's that does the minimization for $D$. You can skip to conclusion if you feel like skipping all the math.
You want to find the critical point (where the function attains its minimum and maximum) of:
$$D = p_{1}^2+p_{2}^2+...+p_{n}^2$$
given ${p_{1}+p_{2}+...+p_{n}=1}$, for $p_{i}$ of species.
Lagrange Multiplier method is one of the techniques to find the values given to $p_{1}, p_{2}, ...p_{n}$ to make $p_{1}^2+p_{2}^2+...+p_{n}^2$  go to maximum or minimum given some constraint on this.
Assume:
$$f = p_{1}^2+p_{2}^2+...+p_{n}^2$$
$$g = p_{1}+p_{2}+...p_{n}$$
According to Lagrange multiplier:
$$\partial_{p_{1},..p_{n}} f = \lambda \partial_{p_{1},..p_{n}} g$$
We have to find the value of $\lambda$.
So after partial fractions step, we will end up with these equations:
$$np_{1} = \lambda ; np_{2} = \lambda;  ... np_{n} = \lambda$$
and we already know that $p_{1}+p_{2}+...+p_{n} = 1$
From above, we know that:
$$p_{1} = p_{2} = ... = p_{n} = \lambda/n$$ we get $\lambda = 2/n$ and from this the minimum values of the function:
$$f = D =  p_{1}^2+p_{2}^2+...+p_{n}^2$$
is when all $p_{i} = 1/n $ for i is denoting each species in ${1,...,n}$
Conclusion:
So $D$ value attains its minimum when all terms $p_{i}$ are equal. As any value goes away from $1/n$ ('n' is the total number of individuals of species you got)the value increases drastically as it is being squared in $D$.
Sample example will be like $0.5^2 + 0.5^2 = 0.25$ but a change from this say $0.6,0.4$ increases $0.5$ term by $0.11$ but decreases $0.4$ term by only $0.09$.
Hope this helps.


text:
What is sense RNA?
I heard my professor use this term.He said that it is a RNA that has the sense of synthesising the protein. But there's no authentic online source to verify it, except this one (biology-pages.info) which says:

Messenger RNA (mRNA) is single-stranded. Its sequence of nucleotides is called "sense" because it results in a gene product (protein). Normally, its unpaired nucleotides are "read" by transfer RNA anticodons as the ribosome proceeds to translate the message.

So my question , is mRNA or the pre-mRNA called the sense RNA ?

I suppose it could be, considering that things like siRNA use "anti-sense" sequences to form double-stranded RNA, targeting it to the degradation pathway, but I've never heard the term before. It's kind of like we hear the term "disgruntled" all the time, but no one is ever described as being "gruntled".

When I see this it seems logical to call every mRNA sense RNA.

Both mRNA and pre-mRNA would be considered "sense"
The term "sense" means that the strand is the direct coding strand. That is, the strand that has the proper codons to be translated into the protein of interest. This term can be applied to both DNA and RNA.
The term "anti-sense" means that the strand is Watson-Crick complementary to the "sense" strand. Likewise, the term can be applied to both DNA and RNA.
The "anti-sense" strand of DNA is used as the template to create an RNA transcript that copies the "sense" strand of DNA. Therefore, the mRNA is always "sense" regardless of its stage of maturity.


text:
What is the difference between Crossbreeding, Outbreeding and Outcrossing?
I only found one book which isn't a textbook  named Storey's Illustrated Guide to 96 Horse Breeds of North America By Judith Dutson (not sure if it is good enough to follow) that defined these terms.

Outbreeding/ outcrossing is deliberately crossing one line of horse within a breed to a very distant or unrelated line. The term is also occasionally used as a synonym for crossbreeding.
Crossbreeding is the deliberate crossing of horses of different breeds.

My understanding:
Outbreeding or Outcrossing is the mating between two individuals of a  breed but different varieties/sub-varieties.
Crossbreeding is the mating between two individuals of different breeds (could be intraspecific or interspecific as well).
Are these definitions correct?

The term cross breeding is a bit broader term , whereas outbreeding is more specific.

Answer in keywords
Inbreeding : related individual,same breed
Outbreeding

Cross breeding : between different breeds
Outcrossing : unrelated individual,same breed,no common ancestor

Detailed answer
Inbreeding it is a mating within the same breed between different superior male and superior female. Inbreeding between close relatives can cause inbreeding depression like decreased Vigour , fertility and productivity. It is therefore advisable to mte superior animals of different population of the same breed .
Outbreeding is mating between unrelated animals of same or different breeds.
Outcrossing is mating between unrelated animals of same breed with no common ancestor for at least 4 to 6 generation. Offspring formed from such a cross is called out cross .
Cross breeding is mating between superior animals of different breeds for raising new breeds for improving local breeds.
Please note: Outcrossing and
cross breeding are two types of Outbreeding.
If you have any further doubts please ask .
Hope it helps!!

Welcome. If you can add the definition of Outcrossing, and add appropriate resources (wikipedia would suffice here I guess, given the textbook-question-like-nature of this post) this would make a great answer (imho - I'm not an expert on this topic). For now, no upvote and just a banner.

The link is broken. Also, please do not post a link only answer. Link only should better be posted as comments.

I have updated my answer as suggested.

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text:
MCQ - Independent assortment or Incomplete linkage

Two flies were crossed one wildtype another double mutant sepia(se) and vestigial(vg) yielding 40% wild type 40% se vg, 10% se and 10% vg. The genes show-
a.Complete linkage b.Incomplete linkage c.Independent assortment d. epistasis

My attempt at a solution
Since no. of combination of phenotypes appeared =/= 2 ( there are non-parental traits so) it is not complete linkage.
It is neither epistasis because two genes are controlling two diffrenet phenotypes, not one.
It can be independent assortment or incomplete linkage.
Since the question says double mutant sepia(se) and vestigial(vg) (I am getting the idea that) it is a female and the wildtype individual (with no genotype concerned hint) is a male. The genes are likely on X chromosome.
So..... it is incomplete linkage.
But I'm not sure why not independent assortment.

@GerardoFurtado Could you elaborate why it is not correct?

@GerardoFurtado Nothing much about the wild type flies has been mentioned to determine it's genotype so considering it male would be right- was the thought behind my assumption.

It doesn't really matter on which chromosomes the where concerned genes are located, Now coming to your question.
A> Complete linkage > Complete linkage says that the concerned genes are right next to each other and no crossingover is possible so the expected genotype of the offspring would be 100% parental type. 50% Wild (se+ vg+) and 50% Mutated (se vg)
B> Incomplete linkage > This is the correct answer. According to incomplete linkage, the genes are close but not right next to each other so there is space for crossingover to take place. However, they are still close, close enough to be considered as linked and thus chance of obtaining recombinant offspring would always be less than that of the offspring with parental genotype, parental type always remains over 50% and here the parental type offspring is 80% (40% wild type parental genotype + 40% mutated parental genotype) and 20% recombinant genotype [(10% se & wild type vg+) + (10%vg & wild type se+)]
C> Independent assortment says that there is no linkage and thus no crossingover, this is possible only when the concerned genes are located on different chromosomes but here in the obtained data of offspring it is clear that crossingover did take place and 20% of the offspring is result of the crossingover so this option is not correct
D> Epistasis : In your attempt you mentioned that it is not epistasis because two genes are controlling separate phenotype thus it is not epistasis. your explanation is wrong. Don't get me wrong, the answer is not epistatsis, I am just saying your explanation is wrong, epistasis is the phenomenon where one gene interferes with the expression of another gene, look at the term carefully. I am calling them as genes not alleles. Alleles are different version of the same gene that control the same phenotypic character. In epistasis two different gene that control completely different phenotypic expression are interacting. One gene if expressed prevents the other gene from getting expressed, this not about the dominant alleles where if the dominant allele expresses recessive allele wont express. For example, assume gene A codes for white flower colour and gene B codes for sweet smell. If B gene expresses then A gene wont express. This is epistasis


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Hodgin-Huxley model for a single neuron - continuation
As  continuation to This question I have posted. Another set of questions is given for the same model :

This time it is also given that for $t<0$ the membrane potential is $u_0$, and at $t=0$ it is instantaneusly jumps to $u'$, and that $u_0,u',u_2,u_{ion}$ are maintained for $t \geq 0$.
So, with this additional data I could actually compute $r(t)$ and $s(t)$ for $t \geq 0$ in the following way:
For $t \geq 0$, $u(t)=u'$
so $r_0(0)=r_0(u') \approx 1$ and $s_0(0)=s_0(u') \approx 0$.
Also, $\tau_r(0)=\tau_r(u') = 1$ and $\tau_s(0)=\tau_2(u') = 15$.
So, we get:
$r' = -\frac{r-1}{1}$ and $s'=-\frac{s-0}{15}$ $\Rightarrow$
$r' + r = 1$ and $s' + \frac{s}{15} = 0$.
These are a first order linear diff. equation of the form:

$y'(x)+p(x)y=q(x)$

So their solution is of the form:

$e^{-\int{p(x)dx}}(\int{q(x)^{\int{p(x)d(x)}}}+C)$ ($C$ is a constant)

So I get:
$r(t)=C_1e^{-t}+1$ and $s(t)=C_2e^{-t/15}$.
I think that we have no way of knowing our initial conditions $r(t=0)$ and $s(t=0)$ (am I right?)
So for simplisity let's assume that $C_1=C_2=1$ and we get:

$r(t)=e^{-t}+1$ and $s(t)=e^{-t/15}$.

So for example: $r(t=100) = e^{-100}+1 \approx 1$ and $s(t=100) = e^{-100/15} = 0.0013$ and $r(t=3) = e^{-3}+1 = 1.0498$ and $s(t=3) = e^{-3/15} = 0.8187$
So my question is:
How come answers 4 and 7 below denoted as true?

Actually there is a way to determine the initial conditions for this problem.
We assume that the gating variables $r$ and $s$ are at a steady state before the membrane potential jump from$u_0$ to $u'$.
If we look at the first graph(the steady state relation versus membrane potential) we can see that at the membrane potential $u_0$ that $r(t=0)\approx 0$ and $s(t=0)\approx 1$.
Then we make our jump in voltage from$u_0$ to $u'$ and now our $r(t)$ and $s(t)$ will change towards their new steady values $r'=1$ $s'=0$ with time constants given by the second graph.
Your equations $r(t) =C_1 e^{-t}+1$ and $s(t)=0+C_2 e^{-t/15}$ are correct, but using the information from the graphs we can se that $C_1= -1$ and $C_2= 1$.
From these equations we can see that $r(3)=1-e^{-3}\approx .9502$ and $s(3)= e^{\frac{-1}{5}}\approx .81$ (note that .81 is close enough to 1 for this particular problem). This means that the channel is mostly open as statement 4 asserts.
Now for statement 7 we have $t= 100$ and while $r(100)= 1-e^{-100}\approx1$, and $s(100)=e^{\frac{-100}{15}}\approx 0$. This means the product $r(100)^2* s(100)\approx 1^2 * 0 \approx 0$ thus the channel is mostly closed.
Hope this helps.

All true. Just remember that a particular channel is pretty much either open or closed (as verified by single-channel electrical recordings), so 0.81 open means that 81% of channels are open at $t=3$.


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Which of the three is true for insulin receptors?
I have seen the following question in a Cell Biology exam:
Which of the following is true"

Insulin has an hydrophobic Signal Peptide and the insulin receptor does not have an hydrophobic Signal Peptide

The insulin is coded by two genes, the insulin receptor has an hydrophobic sequence in the middle of the protein.

Receptors in the ER bound the SRP that is bounded to the insulin receptor, SRP is made of RNA and proteins.

I think that (1) is the right answer. However, people I talked with thought (3) is the right one.
I think 1 is right because I have never seen anywhere that insulin receptor has a signal peptide so I assumed it does not have.
I also think that SRP is a part of the insulin receptor, which is located on the ER (and not bounded to the ER by receptors), this is why I thought (3) is not the right answer.
Am I right, or did I miss anything?

Eeeeh, if you meant insulin receptor has a signal peptide which is removed during receptor maturation, then you are correct. http://www.uniprot.org/uniprot/P06213

Signal recognition particle (SRP) receptor, also called docking protein, is a dimer composed of 2 different subunits that are associated exclusively with the rough ER in mammalian cells. The surface of the rough endoplasmic reticulum (often abbreviated RER or Rough ER) (also called granular endoplasmic reticulum) is studded with protein-manufacturing ribosomes giving it a "rough" appearance. so i don't think (3) is the right statement.
the insulin receptors is made up of two hormones, insulin and glucagon, are at the center of this signaling system. there is no such things as hydrophobic sequence in the middle of the protein i believe.
also, Insulin is a peptide hormone produced by beta cells of the pancreatic islets and and insulin receptors doesn't have an hydrophobic signal peptide. so i think (1) is the correct answer.
Edit :
https://en.wikipedia.org/wiki/Signal_recognition_particle_receptor
https://www.healthline.com/health/type-2-diabetes/insulin#Function1
www.news-medical.net/health/What-is-Insulin.aspx


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What is the meaning of "Rb is in the active state"?
I am reading about cyclins, cdks and Rb (Retinoblastoma) and some of the terminology is not clear to me.
I understand that when CDK phosphorylates Rb, it disconnects from E2F, and E2F can act as a transcription factor. My question is about the terminology.
My questions are:

When people say "Rb is active", do they mean "active = phosphorylated state" (where E2F is free from Rb) or do they mean "active = not phosphorylated state"?

Does "active cyclin" means cyclin is going to join CDK and cell cycle proceeds? or is "active cyclin = cyclin is not activating CDK and cell cycle paused"?

Active CDK means CDK is activated by cyclin and cell cycle can proceed?

In general, Maybe one can say that binding (Rb with E2F or Cyclin with CKD) means activation and disconnecting means inactivation?

Thanks!

(Image source: Kolch, Walter, et al. "The role of Raf kinases in malignant transformation." Expert reviews in molecular medicine 4.8 (2002): 1-18.)

The terminology of "Rb is active/inactive" refers to the activity of inhibiting E2F.
So active Rb inhibits E2F, while inactive Rb doesn't inhibit E2F.
With regard to Rb and phosphorylation - the story seems to be more complex ([1] describes Rb as an enigma).
According to [2] (this quote is from the summary of the paper by eLife):

Narasimha, Kaulich, Shapiro et al. now present biochemical analyses of
  Rb proteins that show— completely unexpectedly—that the cyclin D
  complex adds just one phosphate group to Rb during the G1 phase,
  although this group can be added to one of fourteen different sites.
  The resulting 'mono-phosphorylated' Rb varieties can each sequester
  different transcription factors and stop them working.At the
  restriction point, many more phosphate groups are then rapidly added,
  and the Rb protein is inactivated by a different cyclin. This
  cyclin—called Cyclin E—then drives cells into the next phase of the
  cell cycle. Establishing how cyclin E is activated is a priority for
  future research.

+ 3. Wikipedia's Cyclin-dependent kinase (CDK) page says:

By definition, a CDK binds a regulatory protein called a cyclin. Without cyclin, CDK has little kinase activity; only the cyclin-CDK complex is an active kinase.

Wikipedia's Protein kinase page says:

A protein kinase is a kinase enzyme that modifies other molecules, mostly proteins, by chemically adding phosphate groups to them (phosphorylation).

And here is a nice visual explanation from Life: The Science of Biology (10th edition):

So both "active CDK" and "active cyclin-CDK complex" (and according to the other answer, also "active cyclin") refer to the case in which a cyclin is bound to a CDK to form a cyclin-CDK complex, such that the CDK might phosphorylate some substrate.
(I didn't mention the cell cycle here on purpose, as I am not an expert, and so I am wary of claiming that an active CDK always pushes the cell cycle forward. If I understand correctly, we still don't know exactly how each cyclin-CDK complex affects the cell cycle.)

As for your last question:

In general, Maybe one can say that binding (Rb with E2F or Cyclin with
  CKD) means activation and disconnecting means inactivation?

As mentioned above, you could say that about a cyclin and its CDK.
Unfortunately, you can't say that in general. E2F here is a counter example (it is inhibited when Rb binds to it and activated when Rb disconnects from it).
However, you could say that in general, when something binds to a protein, the protein might change its shape, which might lead to activating or inhibiting some function.

[1] Dyson, Nicholas J. "RB1: a prototype tumor suppressor and an enigma." Genes & development 30.13 (2016): 1492-1502.
[2] Narasimha, Anil M., et al. "Cyclin D activates the Rb tumor suppressor by mono-phosphorylation." Elife 3 (2014): e02872.

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


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Why inhbition of RTK will not help in a case of mutant EGF?
I was given the following as an example for a quiz question but i don't understand the answer. Any help will be most welcome:

Question: Iressa is a Tyrosine Kinase Inhibitor. As a young oncologe, to whome of the patients will you recommand not to take this treatment:
a. Biopsia has shown that the EGF receptor is mutant
b. Biopsia has shown that the RAS protein is mutant
c. Biopsia has shown that the MAP Kinase stays in the nucleuous permanently
d. The treatment can help each of a,b,c, cases.

The right answer should be a. Can someone see why and help here?
I know that tyrosine kinase receptor is the inside part of the EGF receptor (where the two monomeres become a dimer and phosphorelate each other).
So, if the EGF receptor is mutant, shuldn't it help inhibiting it's continuation inside the cell and thus prevent to many EGF cascades?
Thanks!

Have they given more information how the receptor is mutant?

The right answer should be A? Patients with EGFR-positive lung cancer who are also positive for mutant K-Ras don't respond to erlotinib, a common EGFR-TKI (example). This is directly because the bulk of Ras mutations are activating, which would naturally subvert the need for EGFR-RTK signaling to begin with. Thus, for mutant Ras patients I wouldn't recommend TKIs.


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Do the two catalytic cores of DNA polymerase III operate in the same direction?
This diagram is from Molecular Cell Biology by Lodish, 2000 which states:

The other core-polymerase molecule, which elongates the lagging strand, moves with its β-subunit clamp in the direction opposite to that of the fork movement.

Again the images provided in Principle of genetics by Simmons, 2015 and Cell Biology by Karp, indicate that the catalytic cores are directed in the same direction. The following diagram is from former book.

Which one is correct and why(please provide citations)?

The DNA polymerase-III holoenzyme moves in one direction (along the fork). One of the DNA polymerases works on the lagging strand but the enzyme is oriented in the same direction as the one that is working on the leading strand. For details see this review (it is old but this fact is also old enough).
The second diagram shown in your question is an accurate representation of what happens. This, statement is confusing (and misleading):

The other core-polymerase molecule, which elongates the lagging
  strand, moves with its β-subunit clamp in the direction opposite to
  that of the fork movement.

Both polymerases move in the same direction but elongate DNA in opposite directions. The opposite elongation direction, as shown in the second figure, is facilitated by looping of the lagging strand.
You can simply google "DNA polymerase-III holoenzyme" and you'll get many sources that will corroborate this.


text:
What is meant by increase in information embodied in the system?
From Ecosystem Ecology
edited by Sven Erik Jørgensen

After the initial capture of energy across a boundary, ecosystem growth and development is possible by

an increae of the physical structure(biomass),
an increase of the network (more cycling)
an increase in the information embodied in the system.

What is meant by increase in information embodied in the system?
Does it mean increase in diversity of the genes (genetic information)?

Doesn't the book explain it? We could speculate on this, but I think it will be difficult if not impossible to give a final answer.

@RHA No, it doesn't.

Table 1 on the next page (p. 36) lists a number of properties for each of the three "growth forms".
For information, properties include:

Life history types
Diversity (taxonomic & ecological)
Body size
Stability

I have to admit that some of these properties doesn't really make sense to me under these headings (at least from the common use of these terms). However, I suspect that they are used in a very specific sense that might make sense if you read the entire book. And systems ecology isn't really my thing.
Note also that exergy (which is used in relation to these three growth forms in the book) is a term borrowed from thermodynamics (ie physics), and it describes potential/available work. Exergy is also negatively related to entropy, so when exergy decreases, entropy increases. Since higher entropy is related to disorder, the opposite goes for exergy, so high exergy means a higher amount of order (within the system), which can be translated into "structural information". I suspect that this is the form of information that the book is referring to, as one of the "growth forms".

I'd also add that "information" can be closely related to "complexity" in many contexts outside of contexts where "information" has its usual colloquial meaning (e.g., application of Shannon information/Shannon entropy outside of communication systems). I suspect that's what this author is referring to, the complexity of the ecosystem, such as the number of hierarchical levels that the energy passes through.

@BryanKrause I agree, and the "structural information" that I mention is clearly a way of expressing system/structual complexity. To me, one slightly confusing aspect of how information is used here (in the book/question) is that high entropy (so low exergy) is equivalent to high information (see Shannon entropy), which is kind of the opposite of the  complex, ordered system that the question describes. Random or chaotic systems have high information but are disordered.


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What is the best way to clean immersion oil from the microscope lens?
My job is to photograph mushroom spores at x100 using immersion oil.
What is the best practice for cleaning the oil from the lens?
Right now I am just wiping it with a cotton swab.

If you want to remove oil from anything, you need an appropriate solvent. Detergent and water would likely work best, and is less hazardous than working with organic solvents like hexane.

In my experience, any microscope worth using has a minder. I would strongly suggest finding that minder, their opinions about cleaning practice should be respected. Objective lenses can be very pricey so they should be handled with care.
Detergent or water are inappropriate for an oil immersion lens. Detergent is likely to damage anti-reflective coatings on the lens. Water doesn't mix with oil.
My standard procedure with oil objective lenses is to wipe oil off with a good quality lens tissue (Kodak). Do not use facial tissues or a lab tissues, such as kimwipes. They are too abrasive and may sractch the lens. If someone has allowed oil to dry on the lens, I take care to know what solvents are correct for the lens and oil that are being used.

A lens tissue - you mean like those soft cloths used to clean your touch-tablet screen?  I never thought of that.  Seems better than a q-tip (which is what my "minder" recommended to me).

No, they are tissues rather than a cloth. Whatman, Lens Cleaning Tissue 105 lens tissues or these.

The least possible amount of cleaning naphtha, pharmaceutical quality (in German: "wundbenzin") and high grade lens cleaning paper. In the ol' days microscopists used some saliva on a piece of cloth, but that was in the pre-coated optics era.

Welcome to BiologySE... can you add some references or additional information so that others can read more about your answer in the context of this question? We always appreciate referencing answers on the site so that all users can follow along if interested. Thanks

Clean immersion oil from a lens by first pulling a fresh piece of lens paper slowly across the lens, like a bath towel across the back, to absorb the oil; shift to a fresh area of the sheet as required, and use more than one sheet if necessary (although that suggests you my have used too much oil).  Then gently wipe the lens with fresh lens paper with a bit of solvent on it; for the most common Cargille type A and B oils, use a high grade of naptha or xylene (xylol).  Finish by wiping with dry paper.
If a residue persists, and it will at least part of the time, clean the lens with lens tissue after gently breathing on the lens to fog it up:  you want condensed moisture, not saliva.  So it is a gentle, long h-a-a-a-a.  Wipe in concentric circling motion, drifting in or out.  Repeat. This method assures you will not wet and possibly harm the lens.  Dried up oil can be softened with a trace of new oil, or better yet, one of these solvents.  So yes, Always Confused, you still are; you need to remove that final trace of xylol. Don't use detergent. Or water. Ever.  Use Xylol or naptha!
The range of answers here shows the dangers of soliciting online advice.  Look at the online microscope "universities" put up by Zeiss and others, specifically, if possible by whomever made YOUR microscope.  That's where to get the right answer.  Today,even"minders" may not know!


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What evidence is there that common PCR DNA purification kits can isolate DNA from pathogens engulfed in macrophages?
I have previously asked a more general question about how PCR sequencing reaches all possible DNA targets here. I want to ask more specifically now: what evidence is there that common PCR DNA purification kits can isolate DNA from pathogens engulfed in macrophages?
Specifically what such a KIT would have to achieve is to destroy the double lipid cell membrane of a macrophage and destroy the cell walls of engulfed bacteria or fungi. (The latter of which even contain chitin)
I am looking for as specific evidence as possible proving that if one takes a whole blood sample and employs a purification KIT, any microorganism's DNA engulfed in a macrophage should be isolated. Please allow me to say that I am looking for evidence beyond just the manufacturers specifications. I would like to find publications, book chapters or other written statements that specifically show and discuss how isolation techniques work on the barriers I mentioned or even better how they work on intra-cellular micro organisms. Thank you!

What do you mean by a "PCR DNA purification kit" ? Can you link to such a kit?

Also, colony PCRs routinely work on either colonies of bacteria or isolated mammalian cell culture, so there is no reason bacteria inside mammalian cells won't work. I can't say the same for fungi, since I have not worked with yeast.

@March Ho: the link you asked for, https://www.qiagen.com/de/shop/sample-technologies/dna-sample-technologies/genomic-dna/qiaamp-ucp-pathogen-mini-kit/

@March Ho: so your reasoning ist that since isolation techniques work on mammalian cells and on bacteria, they should also work on one inside the other? That might be the case but does not follow by pure logic! The kit you use on one (bacteria/mammalian cells) might not work on the other and even if you use the same kit for both it might not isolate the dna of bacteria inside mammalian cells for reasons of: too short exposure time or not enough reactants or competitive binding or unforseen reactions or altered cell wall of intracellular bacteria or...

I didn't use a kit, but merely ran a PCR using the cells instead of purified DNA as the template.

@MarchHo : From the manufacturer of the KIT you have linked in my other question I quote: With colony PCR, an initial 5 minute denaturation at 95°C is recommended and Use of high quality, purified DNA templates greatly enhances the success of PCR.
http://www.neb.sg/protocols/1/01/01/taq-dna-polymerase-with-standard-taq-mg-free-buffer-m0320

Of course purified DNA works better, but the point is that it is not necessary for PCR to work

For this problem, I would generate the evidence myself taking the following approach:
Apply the DNA extraction kit to the macrophages with pathogens engulfed. As controls, also use the DNA extraction kit on the macrophages alone (negative control), and the pathogen alone (positive control 1). Additionally get purified genomic DNA of the pathogen for a better positive control.
Now, design primers which specifically amplify pathogen DNA. You should test the primers against the independently purified pathogen gDNA to ensure they are working. I would focus on generating 200 bp fragments, so that your primers can be used for qPCR later. Since it seems you are interested in potentially a high throughput sequencing, you may want to target multiple genes to see if there is a difference in efficiency.
Now use your kit on all the samples (Macrophage + pathogen, Pathogen alone, Macrophage alone) and then run PCR on those purified samples. If you detect pathogen DNA from the macrophage + pathogen sample, this would give you strong evidence that the kit is capable of simultaneously purifying both DNA sequences. Otherwise, it would confirm that this co-purification does not work. You can make the technique better by incorporating qPCR to see if the efficiency of extraction is significantly reduced by having the pathogens inside the macrophages.

This does not provide an answer to the question. Once you have sufficient reputation you will be able to comment on any post; instead, provide answers that don't require clarification from the asker. - From Review

@tyersome I am a new user with a Ph.D. in synthetic biology. Can you elaborate on why your feel this does not answer the question? My procedure would help this user to generate the answer to this question, which I feel would be very valuable to a practicing academic. Additionally, this post had no answer for half a decade. My answer provides something versus nothing. Please let me know why this is inappropriate for Biology Stack exchange.


text:
Minichromosome maintenance protein structure and function
I am having difficulty answering three homework questions which relate directly to Chong et al. (2000).
Questions

The authors have determined that MtMCM is able to bind both ssDNA and dsDNA (see Figure 1). However, they don’t mention whether it is the same or a different site on the protein that is involved in binding the two forms of DNA.
Question #1: Propose an experiment that would help to distinguish between these two possibilities and what result would you expect?
Question #2: If ssDNA and dsDNA do share the same MtMCM binding site, what part of the DNA do you suppose is involved in stimulating the ATPase activity? In a helicase assay, the authors show that MtMCM can displace large ssDNA fragments (up to 500 bases) from a circular substrate (p. 1533).
Question #3: Explain why this is, or is not, a suitable assay for MtMCM processivity?

My Answers
Question 1:
One possible method to determine whether the MtMCM complex uses two different sites to bind ssDNA and dsDNA is through the identification and blockage (i.e. by using a ligand) of a single specific binding site on the MtMCM. If the blockage of this site prevents the binding of MtMCM to both ssDNA and dsDNA, this would suggest that the same site is used for both. The research paper suggests that ssDNA and dsDNA do share the same binding site because chelation of magnesium ions prevented the protein from binding to DNA.
Question 2:
No ATP hydrolysis was detected in reaction mixtures containing the K341E or delta-N mutant proteins, however, both wt and K341E protein still formed complexes with the DNA. If ssDNA and dsDNA do share the same MtMCM binding site, then perhaps it’s the delta-N portion of the DNA that is involved in stimulating ATPase activity.
Question 3:
I found it hard to start this question. This is what I have so far: This is a suitable assay for MtMCM processivity because a population of substrates possessing displaceable strands of increasing length was used. This allowed the researchers to compare the displacement of the different strands and quantify the processivity of the MCM complex.
Let me know if I should provide more information. Any help or guidance would be greaetly appreciated!

I edited the post to try to improve the format. Feel free to roll back if you don't like it.

I don't know if anybody will be willing to read through the article and answer all three question. It is not my field so I don't quite realize are familiar is the average molecular geneticist to this article.

Thanks for the edit. I realize it's quite a specific topic and quite a bit of reading but I thought I'd put it out here, perhaps someone knowledgeable on this topic will come across it :p


text:
Why is uracil, rather than thymine, used in RNA?
This question was posed on SE Biology some time ago, but all the answers, including the accepted one, answered a different question instead: “Why is thymine, rather than uracil, used in DNA?”. I therefore changed the title to match the answers, giving notice that, if the change were approved, I’d post the original separately question myself (and answer it, if necessary). Here it is:

It is believed that thymine replaced uracil (the RNA base) in DNA because of the deleterious effects of slow spontaneous deamination of cytosine to uracil: by employing thymine instead of uracil, any uracil in DNA would clearly be aberrant, allowing a specific mechanism of repair (involving uracil DNA glycosylase) to evolve with impunity. As this was clearly advantageous, why didn’t RNA also evolve to use thymine instead of uracil?

N.B. By “why?” I mean “how can one rationalize the fact that?”. Obviously, the answer to this type of question is not, and probably cannot be, known with certainty.

I have now accepted my own answer to this question. However comments and criticism are still welcome as the answer should not be regarded as necessarily final.

Regardless of the question† of which came first*, RNA or DNA, it is possible to rationalize the absence of thymine in RNA by a cost–benefit analysis. There is a cost to using thymine, so there must be sufficient benefits to make this worth while.
Cost of using thymine rather than uracil
The most obvious cost of using thymine is the energy requirement for its synthesis (in terms of reducing power — NADPH).

An analogous conversion of rUMP to rTMP (if it existed) would incur similar costs. (There may be additional costs, but they may be contentious and this is indisputable, so it will suffice.)
Benefit of using thymine rather than uracil
For DNA the benefit is clear and stated in the question. By not using uracil as the complement to adenine, uracil produced by spontaneous deamination of cytosine can be recognized as abberant and removed by the DNA proof-reading repair systems. This presumably gives the organism an advantage (benefit) by reducing harmful mutations to DNA — the genetic material.
RNA is not the genetic material of contemporary autonomous organisms. Hence unrepaired C to U deaminations will not affect that aspect of the viability of an organism. How serious will they be for the cell, though? The largest and most long-lived RNAs are the structural ribosomal RNAs. Such mutations in the cells rRNA might have no effect on ribosome function as much of the RNA is thought to be structural. However, even if they did, the inactivation of a small percentage of the ribosomes of a cell would have little impact on protein synthesis. Likewise for the small tRNA molecules.
Messenger RNA poses a different problem as we can conclude that abberant proteins made from mutant mRNA are dangerous to the cell from the fact that a proof-reading mechanism exists to correct errors in the charging (aminoacylation) of tRNAs. I would argue that the relatively short half-life of mRNA compared with the frequency of deamination of cytosine means that the latter process is not responsible for a significant amount of mutant mRNA.
Conclusion
The benefits of using thymine — together with a repair system — in RNA would be marginal, and hence not worth the energetic cost this would entail.
†Footnote: We don’t need to argue about which nucleic acid came first
The current metabolic pathways for formation of dTTP from dUTP and the reduction of ribose to deoxyribose are strongly suggestive to me that RNA preceeded DNA in evolution. (They suggest nothing about whether RNA preceeded protein.) However, the rationalization presented here does not require this assumption. If DNA came first and RNA initially had T instead of U, the rationale could be used to argue why RNA changed bases from T to U. Indeed, the rationale can be employed by those who do not even believe in evolution — they could argue (and probably do) that some deity created things that way because it was more efficient in terms of cost–benefit.

In the absence of answers I consider satisfactory, I have answered my own question, as I 'promised'. Comments are welcome, and may be included in the answer if I think fit.

Answering this question accurately is difficult as it touches on the origin of life hypothesis. In the RNA World Hypothesis, RNA is the original "life" that is able to catalyze its own self-replication. There are various evidences of support for this hypothesis. Uracil's structure is relatively easy to synthesize in reactions that plausibly could take place on early Earth conditions. It could be that RNA used Uracil simply because of Uracil's abundance in nature. This seems to be the case for the use of Adenine in ATP. Guanine can also be used in an energy carrying molecule GTP, but those instances are vastly outnumbered by ATP.
However, there's no set in stone theory as to why either RNA uses Uracil instead of Thymine, or DNA uses Thymine instead of Uracil. Only a lot of circumstantial evidence. The inverse argument for DNA's use of Thymine could also support RNA's use of Uracil. In a competitive environment, a higher mutation rate afforded by the deamination of Cytosine to Uracil may have been an advantage to quickly promote change.


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Why is duck fat less saturated than cow fat?
Why does the composition of fat in animals vary?  Is there an evolutionary advantage to producing fat that is less or more saturated?

I can't reply in-full at the moment, but yes. There are plenty of advantages. Saturated fat is (slightly) more energy-dense, makes cell walls more rigid (bad in a cold environment - like polar waters), and have higher melting points (which also means they can insulate better).

Because ducks need to float and cows don't. If there was a densely fat duck it wouldn't float or fly very well and it wouldn't survive to reproduce.
To answer your question, the composition of fat varies because of the different conditions in which the organism needs to thrive. Fur is different as well. Bear in mind nature is a cruel place and any tiny edge you can get is vital for your survival.
My answer is a bit general but I hope it addresses the question.


text:
Can "human exclusion zones" in national parks for preserving Wolves and Grizzlies be a good idea?
There are National Preserves in the National Parks where some human activities are permitted. But can it make sense to create "exclusion zones" so no human would be permitted in a certain area, not even scientists or researchers just so Grizzlies and Wolves can have a whole world to themselves ?
I know we won't be able to find out how those species are doing, but would there be any benefit ? Has any country ever tried that ?

Good idea from what perspective/for whom? For species conservation, the ecosystem, the individual animals ("..a whole world to themselves"), humans (having untouched ecosystems), Gaia?


text:
Can two humans with 44 chromosomes produce viable offspring?
It is known that there are very few individuals having 44 chromosomes, not the usual 46 chromosomes.
One example is a male in China: the first article, the second article.
The other is a female in Turkey, unfortunately the article is in Turkish.
It is claimed in the links that they might reproduce and make healthy children if they mate. So I wonder if this already happened and such a couple is living, or if it would be theoretically possible?
Edit: As requested, here is the Karyotype of Turkish female, which the professor in the video call her HomoNeoSapiens, with Robertsonian translocation between 13 and 14 chromosomes. So, this translocation is different from Chinese Man's translocation, which is between 14 and 15 chromosomes. So in this case they can't breed a healthy children? Gosh, I was about to create a new species :((

I migrated the question to Biology and also rewrote it to include the question if it is at all possible, not only if it already happened, please correct it if I did misinterpret something.

"both his chromosome 14s are stuck to his chromosome 15s" - means both his mom and his dad had a Robertsonian Translocation which doesn't really result in the loss of any genetic material.

The article says "both his chromosome 14s are stuck to his chromosome 15s" - meaning both his mom and his dad (46,XX,rob(14,15) and 46,XY,rob(14,15) had a Robertsonian Translocation which doesn't really result in the loss of any genetic material. The very small chance occurred which one sperm carrying the translocation chromosome fused with an oocyte carrying the other translocation chromosome.
So the genotype of the dude is 44,XY,rob(14,15)(14,15), meaning he's normal because he technically has all the genomic information of a normal human.
If he mates with a normal woman (46,XX), then the resulting progeny will have an extra copy of chromosome 15, resulting in trisomy 15, which is non-viable.
If one such 44 chromosome individual mates with another person of the same chromosomal arrangement, then probably a viable fetus would be produced if a translocation chromosome ends up with the same translocation chromosome from the mother. I wouldn't call it a new species per se because it still contains the genetic material from a human. For example, there are many humans with chromosomal abnormalities (I.e trisomy 21, XXY, etc...). Also the background rate of translocations and chromosomal aberrations in somatic cells is notable, so I wouldn't use this as a new species definition.

same Robertsonian Translocation is claimed to have happened for us the human. and This translocation might have created a few new genes that separated us from Chimpanzee. I mean, although that 44 chromozomed guy have the same genetic codes, he might have additional genes as well which lead him to be a different species, right? http://www.thetech.org/genetics/news.php?id=124

I don't see where additional genes may come from. Also, speciation is a very gradual process that takes tens of thousands of years so I doubt the appearance of this 44 chromosome man is the defining point of a new organism.

If he did have 22 chromosome children sounds like they could start a new species!  exciting if you like science fiction.

Interesting question. You refer to aneuploidy.
I don't have idea, but I loved to make some calculations. Feel free to edit because there are some very approximative assumptions.
Aneuploidy, the loss or gain of a chromosome, is estimated to occur in 13-25% of oocytes, 1-4% of sperm, 20% conceptuses and 0.3% of newborns. (reference)
The 46 chromosomes are made of 23 pairs, if the chromosome loss is evenly distributed, we have 0.3% / 23 newborns with the same chromosome loss (0.013 %).
Now, consider that the lost chromosome is likely not really lost, but just translocated on another of the 22 chromosomes. For instance, the individual you refer was having two chromosomes (the 14 and the 15) fused together.
So individuals with the same chromosome loss (0.013%) should have also the same translocation on one of the remaining 22 chromosomes (0.013% / 22 = 0.00059%).**
Chances are now that two of the 0.00059% newborns with exactly the same chromosome loss, will mate together.
Assuming random mating between humans, we have 0.00059% x 0.00059% = 0.0000003 % of possibilities, which is 1 possibility every 333,333,333 human beings.
We are now 7 billions on the Earth, so assume 3.5 billion couples all fertile despite of the age. If we assume also no spatial constraints, so that everyone could mate with every else one on the Earth, there could be no more than 10 couples with the same aneuploid mutation.
Provided the mutation does not affect genes important for reproduction, for instance genes between the two chromosome junctions that get interrupted, this couple could reproduce I guess.
To find that child, chances are now that he/she will have a kariotype done. Quite difficult to find isn'it?

There could be more than 10 couples with the same mutation. Probability does not mean actuality. 10 is only the expected result.

I want to carry answers from soon-to-be-deleted forum to here (I also asked this in Coursera's Introduction to Evolution And Genetics), since I find them valuable. All of them belong to Andrew Wilmoth :
1st Answer:

The man has a Robertsonian whole-arm translocation which fuses
  chromosome 14 & chromosome 15. Essentially all of the genetic material
  is there, just packaged differently. He could have children whole are
  phenotypically normal regardless of whether his partner has a normal
  chromosome complement or a similar translocation.
My Turkish is inadequate to understand the karotype of the woman in
  the other link.
Persons with translaocations are well known. It is rare but hardly
  unique. The odds of two such persons randomly meeting each other and
  mating are probably pretty low. Depending upon each partner's exact
  karotype there may be no difficulty producing healthy offspring with
  unusual chromosome complements.
"If they will have make a new species, let's breed them!! Why doesn't
  science try that? :))"
Because they are people and they might not want to have a child
  together? Experiments on humans require informed consent. I cannot
  imagine conducting any such experiment to satisfy scientific
  curiosity.

2nd answer:

A child born of such a voluntary mating would not by itself be enough
  to be considered a new species. There are a wide variety of
  chromosomal rearrangements that are known and there is no serious
  speculation that persons with such karotypes are members of a
  different species.
It is quite possible that one of the many evolutionary changes that
  separate humans from chimpanzees evolutionarily is a translocation
  that fused chimpanzee ancestral chromosomes 2a and 2b to form human
  chromosome 2. There is strong genetic evidence for such a fusion.

3rd Answer:

As you surmised, every possible combination of gametes with those two
  karotypes will result in an aneuploidy... unless there is a mutation
  which "fixes" the problem.
But the gametes produced by these two individuals would not inherently
  be expected to result in a problem in an offspring. The F1 offspring
  would have only 44 chromosomes but likely be normal phenotypically.
  Any F2 generation produced by crossing two individuals from the F1
  would have a problem with possible trisomy 14 which would be expected
  to be fatal.

The man in China had both chromosomes 15 split and attached onto both chromosomes 14. If a male with 44 chromosomes wants to have children with a female with 46 chromosomes, this will not work. He won't be able to have viable offspring. During mitoses, he will have 22 chromatids and she will have 23. They will not match up and therefore no viable offspring. He'd have to meet someone who was his match and most likely that match is in his family, such as a sister or female cousin, who would have the same chromosomal arrangement as he has. In China, this man is from a family where a lot of miscarriages happened and other family members have variations on these fused chromosomes. They are very inbred for this to have happened. Only a close relative who matches identically to his arrangement would be able to have chromatids that could line up with his. His parents had chromosome abnormalities for this to have happened, so this is an inbred family. This family could go on to produce another species of humans with 44 chromosomes if they kept trying and future generations were stable with no odd arrangements that don't line up.
http://www.asiahealthcareblog.com/2011/07/03/chinas-44-chromosome-man-may-be-missing-link-between-us-and-the-chimp/


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Is there any genetic similarity that defy evolution theory?
For example,
say species A is common ancestor of B, and C. Species B is a common ancestor of D and E.
We would expect that there will be more genetic similarity between D and E than D and C. And those genetic similarity must exist in B.
In other word, we won't expect genetic similarity that don't "cross" the common ancestor or the evolutionary tree.
The exception is probably genetically engineered bacteria.
That being said, am I correct?
Some people say that we have similarity with pigs and chimps even though our common ancestors may be to far off. That won't happen right?
To summarize
I expect that evolutionary tree will form a well, tree. Genetic similarity would infect "nearby" trees and can't jump between trees without connectors, such as common ancestors.
Is that what we observe for ALL species?

There's a weird debate going on in the comments of dmm's answer and there were several downvotes that I don't understand on my answer. Do you think my answer answers your question? I thought you were interested in understanding whether or not D might be more genetically similar to C than to E, is it correct? Or were you mostly interested in a debate of what is "believing", or about a science-religion debate? Or something else...

Note: dmm's answer and the debate have been deleted.

A reader might also want to have a look to this post on the same subject

You have an excellent answer from Remi.b already but I just wanted to add/emphasise this (because there is always more than one way of explaining something and IMO the site benefits from having many answers to the questions)...
The tree we construct does not necessarily accurately reflect what happened in evolution. If B & C evolved from A, and D & E came from B, we would create this tree if we measured using the correct indicator. But the methods we have are not perfect. The first evolutionary trees were based on morphological descriptions etc. and clearly some of the classifications were going to be wrong. These days we use molecular methods, which are probably more accurate but could also be wrong some times. For example if we based our phylogeny on one SNP variant we could have some idea about the phylogeny between a few species, but if we based it on millions of SNPs we would have a much better idea - as technology & models improve that is becoming more realistic. The key point here being there is a difference between the trees we can draw from evidence, and the real evolutionary tree.
If, for example, D evolved from B but was more genetically similar to  C it could be due to convergent evolution (if the same mutations are selected for in C and D but neutrally or negatively in B). This is because, if there is a shared standing genetic variation at the point of speciation or the same mutations occur after speciation, and then C & D are imposed under similar selection and B is not, the allele favored in that environment will spread in C & D but not B (it may drift in B).
Imagine this with humans, where populations split off around the globe. Two populations spread from Africa (A) in to Southern Europe (SE) and Western Asia (WA). Population WA then derived two more populations - Central Asian (CA) and Eastern European (EE). If the Eastern European population developed a habit for drinking cow milk, and that information passed to the Southern Europeans, then selection would favor the ability to digest lactose in those two populations. If we then used the lactase persistence SNP (which had standing genetic variation at the time of divergence) to derive a phylogeny the populations SE and EE would appear related because the allele for lactase persistence is common, but in A WA & CA it would be rare (neutrally evolved). In this case the phylogeny we construct would be different to the true phylogenetic tree.
Basically if there is genetic variation at the point of divergence, or convergent selection, or any gene flow occurs after divergence it makes assessing the phylogeny more difficult and prone to error.

+1 Very good clarifications for important concepts I only wrote some lines about.

Very good point in deciding where my simple theory would go wrong.

Your question seems rather confused to me, I don't quite understand it. Below I try to explain some stuff, I am not quite sure it would help you finding the answer to your question. Let me know if it helps you and how I can improve this answer.
While natural selection selects for a given allele (gene variant), mutations create new variation. And because of this process of mutation there is genetic pattern in species D that would cannot be found in species B (assuming that we have the DNA of species D). But what is similar between B and D were probably also present in their common ancestor B. The exceptions are molecular convergent evolution and horizontal gene transfer (natural of artificial).
Because of common ancestry …

Humans have similarities with pigs

Example: endothermic amniotes

Humans have similarities with a bug

Example: bilaterial symmetry

Humans have similarities with jellyfish

Example: Heterotrophy

Humans have similarities with an oak tree

Example: We have mitochondrias

Humans have similarites with any living things on earth!

Example: Genetic information is hold into a DNA/RNA molecule.

If you might observe that D is genetically speaking more similar to C than to E… This can be due to:

Horizontal gene transfer (artifical or natural)
The mutation rate (or ability to fix mutations) in one lineage might be greater than in another lineage.

For example, if lineage E underwent many mutations, they might be genetically speaking have accumulated many difference compare to D, way more than the number of difference that D has with C.

The phylogeny might be wrong
There might have had some convergent evolution.

Think about fishes which opsins in the eyes need to be adapted to the amount of light which depends on the turbidity of the water. After the three lineages splitted, the change of envirronment might have occured the sequence AATGATCCT suddenly became beneficial. Only two lineages had the chance to produce the right mutation. Or maybe lineage E live at low depth and therefore it doesn't need this mutation because there is enough light at low depth anyway.

Therefore, one should not expect a common ancestor to be the arithmetic mean (supposing it means something) of the current species. And one should not expect that two closely related species on the tree of life should necessarily be more genetically similar to each other than any of the two to a third species.
Note that the phylogeny is constructed mostly based on genetic data. Which makes that two closely related species (on our tree which is not necessary the absolute tree of life) are (almost) necessarily more genetically similar (it is kind of a definition then).

I hope you don't mind, I added an image to make it easier to follow the discussion.

Are there genetic similarity between humans and pig that don't exist in chimps?

Yes there are. The reasons are found in the last part of my answer. The most important point concerns the mutation that occurred in the chimps lineage.

Note that if the rates of evolution are considerably different in different branches, taxa from slow-evolving lineages may have smaller genetic distances from each other than to their respective fast-evolving sister groups. Although this is not expected on the level of species.

Someone downvoted my answer. Please let us a comment when doing so.

@har-wradim Yes this is what I meant in the second point of the list of possible reasons. You're welcome to edit if you want to make it more understandable. Thank you.

O, I see. I'm not sure, the way you formulated this point is totally clear for everyone. What about adding another sketch for this case, supplied by a description in terms of distances?

Correct answer otherwise. Down-vote was definitely not from me :)

@har-wradim Ha ha no I didn't think you were the guy who downvoted. I updated my answer hoping to make it more understandable.


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What are samples of "Outlaw Genes"
I read this in a paper

Keller and Ross describe their greenbeard gene as an ‘outlaw’.
  Admittedly, the comment is only made in passing, but are they correct?
  In this context an outlaw is usually defined as a gene whose action
  favours itself, but opposes the reproductive interests of the
  individual organism. Where there are outlaws, natural selection at
  different loci is pulling the organism in different directions.
  Theoretically speaking, green-beard genes...

Yes: http://www.sciencedirect.com/science/article/pii/S0140175083901562
Basically loving your children is outlaw because it makes you sacrifice resources for your children. However, if your interest is defined as maximizing the number of children, then it's just your stuff working properly. Outlaw genes will be something that makes you die for a cause or stuff like that I suppose.

It's a gene that motivate the host to kill individual that don't have that genes.

Okay, a good edit, but what is your actual question now?

Are there genes that survive well in the genepool in ways that hurt their hosts' gene pool survival. That is the definition of outlaw genes.

The t locus, which is described in detail in this book by Robert Trivers, is the classic 'outlaw' or 'selfish' gene.
If a heterozygous (single) t allele is present in the paternal mouse, the t locus is evident in sperm 95% of the time.  Talk about "Breakin' the Law"!  As a locus whose main phenotype seems to be for mitotic cheating, t seems to convey little or no benefit to the other genes by way of helping the host survive.  t/t homozygotes are sterile.  Nice summary here.


text:
What animals stop other members of their species from mating and why?
(In particular primates)
I know chimps do. Powerful alpha males chimp would beat up omega males that they caught mating.
I know gorillas do. Powerful alpha males gorillas would beat up omega males that they caught mating.
I know humans do. Politically powerful alpha males would jail or stone weaker omega "peasant" humans that they caught mating.
I know bonobo doesn't.
What about other primates/animals?
So what's the difference and why?
Reference:

The alpha animals are given preference to be the first to eat and the
  first to mate; among some species they are the only animals in the
  pack allowed to mate. Other animals in the community are usually
  killed or ousted if they violate this rule.

http://en.wikipedia.org/wiki/Alpha_%28ethology%29
How do preventing and punishing others from mate improve ones' own gene pool survival? Are there similarity between primates (including humans) in this regard?

You want list of animals that do this? if yes, then this is off topic.

@Ashu "So what's the difference and why?"

@RoryM as far as i know "list" questions are considered off topic on SE

Do you mean those that are caught mating with a desirable female are beaten up, or just in general?  As always, references would be great for these assertions.

I'd take issue with "just like humans."

You mean we're different? Very well, I remove just like humans phrase.
let me come up with references. Basically chimps would beat up weaker chimps. Basically chimps and gorillas cannot mate unless "allowed" by the ruling class.

@Ashu yep, they'd be considered Non-Constructive rather than off-topic but still closed, however this question is asking for the reasons behind the difference as shown in the quote I took out :-)

what does non-constructive mean anyway?

Possibly it could happen in mice through the Bruce effect, although its real advantage is quite debated.

@JimThio pretty much everything in this section of the FAQ =D

Thanks. I am just really puzzled. All those acts that are claimed to be unselfish are definitely selfish, but how?

As the comments suggest, I think a little basic reading so you understand the definitions involved here might be appropriate.  The questions are a bit anthocentric, and I think that's why folks with a bit more biological culture might be concerned about the answers.
Alpha type structures can be found in all sorts of animals.  Sperm competition, where many males simply mate with the female and let the sperm work it out are also v common from snakes to mice to primates.
Its hard to say without you asking a more specific question, but the essential question is whether the competition occurs between the animals themselves or between the intermixed sperm of the males inside the female.  If that sounds gross, that's a typical reaction if you are not a monkey, snake, duck or mouse to name a few.  Different species choose different social roles in mating and for reasons that may be difficult to divine.
For animals in an alpha troop modality, the alpha male will eventually get older or weaker and the younger ones will have their chance to mate.  There is always tomorrow.  That's my very brief answer.
It might be worthwhile to take some time to read some about this - a page of response to your questions is not going to really answer your questions.  (I say this having answered several of them :).  I would recommend "The woman that never evolved" by Sarah Hrdy.  As a feminist in the 70s Hrdy decided to do a survey of primate male/female roles in mating, to try understand how human men and women became who they are (and who has not wondered this?).  This book will give you an idea of how so many different animals have come to different roles and possibly why.
Since I have a little time today, I'm adding a couple of tangential references:  Mice sperm have responded to sperm competition so much by evolving hooks on their heads and chain up together and swim together which enhances the chances of paternity.  Ducks are quite different.  they have a lot of forced copulation, but female choice of mate is still quite influential.  Duck vaginas are very complicated, with corkscrews and dead ends to make it difficult to copulate without 'consent'.

@JimThio ...just a thought.   Feel free to contact me directly if you wish to chat about any reading.

Thanks Shigeta. So bonobo do not kill each other because their sperms fight (bravely) and humans and chimps kill, stone, and seize each others' car in civil forfeiture because their balls are much smaller and they, rather the sperms have to fight for more mates. That makes a lot of sense. Why are people concerned about the answers. Shouldn't they be exited to understand humans better? Don't we want to understand our species as well as we understand chimps.

@JimThio I'm sure it goes deeper than this, but its an okay short answer.  A common pattern for primates to live with nonexclusive mating, and just let it all come out in the wash so to speak.

@JimThio  Biology's such a sensitive issue as there are so many social ramifications.  I think the commenters just want to make sure that this is all kept on a scientific level.  Of course the only answer is for everyone to learn as much as they can about how biology really works.  Its very easy to personify these answers, but no worries really as far as I'm concerned.


text:
How does drinking 25 mg-50mg Viagra every night cure Erectile Disfunction permanently?
https://www.webmd.com/erectile-dysfunction/news/20040513/nightly-viagra-may-restore-normal-erections#2
This article says that people taking viagra once daily can have erection restored permanently again.
Those who take viagra only when they're about to have sex do not.
I do not understand their reasoning why?
They said it helps make Endothelial cells better.
If that's the case, how come people that take viagra only when they're about to have sex do not improve?

Hmmm... I am basically asking if that research is true. Somehow you think I ask for my personal self.

I don’t see anything personal about this medical question...


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Why E.Coli get bigger if they replicate faster?
When E. Coli divide faster, they tend to have larger volumes. If the same cells are grown in a poorer medium, they'll have longer replication cycles and shrink. What is the explanation of this phenomenon?
Refs.
http://book.bionumbers.org/how-many-ribosomes-are-in-a-cell/
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0023126

@Charles I don't think the answer is so simple. How do you justify the implication more nutrients --> larger matured cell? Faster growth might just mean that the cell divides faster, so the average volume need not change. There are other examples with mammalian cells, I'll post them here.

@Charles You are correct. I meant cell division rate, not growth rate.

Here's one way to think about this. The key question is "how does the cell decide when to divide"?
You can imagine there are two major mechanisms:

The cell needs to accomplish some task that takes more or less a constant amount of time (DNA replication may be a close example). After that's done it can divide
The cell needs to accumulate a certain amount of biomass to grow to a certain size (protein synthesis is closer to this). When it gets there, it can divide.

(1) is often called the "timer" hypothesis and (2) the "sizer" hypothesis.
If (1) was true, then cells would grow at the same rate regardless of the medium. If (2) was true, then all cells would always have the same size regardless of the medium. Neither statement is true, so the truth is some combination of both effects.
However, under the timer hypothesis, larger cell size with faster growth rate comes out naturally, since the cell size will be determined by the amount of biomass that can accumulate during the constant time. So as long as there is some aspect of "waiting for something that takes a certain amount of time", you will get a positive correlation between size and growth rate.
Now this is an extremely naive explanation. In fact, not all bacteria show this correlation. There are also models other than "timer" and "sizer" -- e.g. here's an "adder" model that also explains the size effect.
Google "cell size control in bacteria" for a ton more papers.

The timer model explains a correlation between biomass production per unit time (units of mass / time) and cell size. It does not explain the correlation between doubling time (units 1 / time) and cell size.

I think this is a misconception. Biomass production rate is also in units of 1/time (exponential growth). More biomass produces biomass faster. In your model (linear biomass, exponential cell number), cells would get smaller over time in constant conditions.


text:
Are there journals for theoretical models of protein-protein interactions?
Are there respectable scientific journals for publishing models of protein-protein interactions obtained by docking simulations? I would also discuss the biological significance of the particular mode of docking that I found through the simulations, and how it is consistent with available experimental evidence. The point is that my paper wouldn't have any new experimental evidence. Rather, I analyze existing experimental evidence in the literature and demonstrate that the model of interaction I propose explains this data. Are there respectable journals accepting this type of research? Can you post some example journals like this?
Also, can you post some references to good papers like these, hopefully highly cited, if there are any?

Several journals accept publications like this. The questions to ask are which biological audience would be most interested in the results and the expected impact of the results. Once you know these it is easier to narrow the journal search.

@Darwin Can you put some examples of journals? (And, if you have it, along with the impact points)

@becko Be careful about relying too much on journal impact factors (JIFs): yes, Nature Cell and Science do publish great research, but an article isn't necessarily great (or even decent) just because it's in one of those journals.

@DanielStandage Of course. But the impact factor does relate to the visibility of the paper.

@becko only very loosely. Many people regard it as a made up number that's doing more damage than good. Even the chief editors of cell and nature are wanting new bibliometrics.

please, move off-topic discussion in chat or elsewhere.

Protein-protein interactions is an area of biophysics, so certainly Biophysical Journal (published by Cell) is a nice place to look.
PNAS has a broad range of areas and they pay a lot of attention to nice biophysics and modeling. But also they require (seems to me) experimental evidence.
The Journal of computational chemistry certainly about a lot of simulations and modeling, so see for yourself.
As for publications, the fact that you are asking for references makes me think you haven't done your homework on literature review, as it is always first and foremost job in a research project.

I'd also recommend having a look which journals of the papers you have read and are citing have been published in. You will probably have to make a call whether you want to publish in a more methods-based journal (bioinformatics in your case) or in a more topic-based journal (biology/biochemistry/biomedicine...)

+1 Good answer. I am still deciding whether I'll begin this research project and which direction to take. I haven't found papers that are entirely "theoretical", in the way that I describe (although they support available experimental evidence published elsewhere). If you know any please post the reference.


text:
Kinetic mathematical model of glycolysis?
I am looking for papers containing kinetic mathematical models of glycolysis, hopefully in mammalian cells (or as close as possible, say yeast). The papers I have found do qualitative analysis (bifurcations, stability analysis, etc.), but do not actually fit the model to data, so you cannot be sure of the accuracy of the kinetic constants involved. The work I need to do depends critically on having reasonably accurate estimates of those kinetic constants.