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Which plasmid can express T7 RNA polymerase in mammalian cells?
Does anyone know what plasmid could express T7 RNA polymerase in mammalian cells, I would like to transfect it with other plasmid containing Gene Of Interest under control of T7 promoter. Thanks a lot!


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What to do with this Araucaria sprout
I live in Santiago, Chile, and I see this Araucaria frequently:

For what I have read, it seems to be a female A. angustifolia individual (leaves are 2-3 cm long and a few mm wide, with a very sharp point; it gives round-ish cones with nuts, about 15 cm in diameter). Am I right?
Two days ago I found a nut in the ground, which I took without thinking about it too much. It was laying superficially and it took me no effort. Only when I had it in my hand I realized that it was a sprout, and become interested in knowing more.

Only then I learned Araucarias reproduced sexually, and understood the unlikeliness of my finding. It is possible that the sprout is A. angustifolia x A. araucana, since there are individuals of both species in the vicinity. (not very close, though!)
Considering the IUCN status of both species, I'm interested in raising it. I put it in a pot.
Q: How can I identify the child? Can I save it? How should I care for it? (especially, watering, temperature, lighting, and the like)

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From stem cells to fully differentiated cells
I'd like to understand better how stem cells produce fully differentiated cells via progenitor cells. I assume the following:

Only cells that are not fully differentiated do divide at all.
When a stem cell divides (at least) one copy remains a stem cell (and remains at its place), the other one starts to differentiate and to travel away.
Between the stem cell and the fully differentiated cell there may be one or a few progenitor cells.

My questions are:

How many cell generations are there between the stem cell and the fully differentiated cell? Any answer from "zero" or "one" (with one progenitor cell inbetween) to "quite a few" seems possible, but  maybe "zero generations" do never occur, i.e. no copy of a stem cell fully differentiates at once, i.e. without an intermediate progenitor cell.
How many cell generations are there between the stem cell and the last progenitor cell in the lineage from stem cell to fully differentiated cell?
How many cell generations are there between the last progenitor cell and the fully differentiated cell? By definition there should be zero, because when there is another not fully differentiated cell between them, then this would be another progenitor cell.

The questions are for somehow typical numbers (of generations), but the answers may depend on the tissue (resp. the type of the stem cell), so it would be interesting to know how strongly (this depends).

The answer may depend quite a bit on the boundary between stem cells and progenitor cells, which is a bit artificial and not entirely settled upon. Also "There are essentially three or four types of adult stem cells, one for each of the three germ layers, plus one for the neural crest, possibly" is false - even a source like Wikipedia would show you that with a very cursory attempt.

@BryanKrause: Thanks for the hint on adult stem cell types. I deleted the remark, since it is not crucial for the question.

I don't think it will be possible to give a general answer to this question, because the number(s) you are looking for will be different for almost every cell type. Also note that some fully differentiated cells (i.e. B-cells) can & will divide under special circumstances.

From this answer to a similar question one can derive that between a hematopoeitic stem cell and a mature blood cell there may be up to 16 generations (with 216 ≈ 70,000).

To the downvoter: What's wrong with this argument? (I changed it a bit.)

I didn't downvote, but it may be because you answered your own question on the same day you asked it by quoting an archived answer. And as you can probably agree, the answer itself is incomplete and doesn't really answer your own question adequately and contextually. That'd be my guess. On that rather reasonable basis I'd hazard to say both you and others would consider down-voting such answers.

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What is the function of dreaming? Does a particular hormone secretion interfere with dreaming? Why do some people dream more?
I'm really interested to know when we are sleeping how a series of stories come to our mind that we called this process dreaming. If you know a useful article on this topic, please tell me thanks.

Welcome. I see 3 different questions in the title, and a 4th in the main body. We encourage clear, focused questions, preferably 1 question per post. We also ask you to provide us with some background to narrow down the scope of the question and give us a lead in which direction you are seeking answers. So could you tell us your findings or thoughts so far investigating this topic? Have a look at the section on asking questions in the help center. Cheers.

Relevant xkcd. Researching & understanding sleep is hard, even without going into dreams. I'm not an expert, but my best guess is that a lot of this is just not currently known.

Hi @Zahra - normally we strongly encourage edits to improve questions, and I like many that you've made, however they change your question a little too much for one that already has an answer. I'd strongly encourage you to both A) Edit this question along the lines of AliceD's suggestions, without disrupting the central point of the original question, and B) Ask a new question along the lines of your edits - I think that second question will be a good one. Thanks!

Thanks for your guidance AliceD .I will regard these points in my future questions and in this case l tried to explain more in the body and I have changed my question too.

Thanks Bryan for your points. I changed my question . whats your idea about this new one?

@Zahra Hi, sorry for the confusion - I've rolled your question back to a previous state, because the edits you made invalidate an existing answer - it changes the meaning of the question too much. I think your new question can be a good question but you should ask it as a new question please.

Dreams are hallucinations that occur during certain stages of sleep. They’re strongest during REM sleep, or the rapid eye movement stage, when you may be less likely to recall your dream.
Research is yet to reveal the true reason of dreams. But we know for sure it is not one reason.
Speculated Reasons:
1. Dreams as fight-or-flight training
One of the areas of the brain that’s most active during dreaming is the amygdala. The amygdala is the part of the brain associated with the survival instinct and the fight-or-flight response.
One theory suggests that because the amygdala is more active during sleep than in your waking life, it may be the brain’s way of getting you ready to deal with a threat.
2. Dreams as memory aides
One widely held theory about the purpose of dreams is that they help you store important memories and things you’ve learned, get rid of unimportant memories, and sort through complicated thoughts and feelings.
Research shows that sleep helps store memories. If you learn new information and sleep on it, you’ll be able to recall it better than if asked to remember that information without the benefit of sleep.
How dreams affect memory storage and recall isn’t clearly understood yet.
3. Creative times!
One theory for why we dream is that it helps facilitate our creative tendencies. Artists of all kinds credit dreams with inspiring some of their most creative work. You may have awakened at times in your life with a great idea for a movie or a song, too.
Without the logical part of the brain working, emotional and illogical thoughts take over your mind!
Eectroencephalography (EEG), electro-oculography (EOG), and
electromyography (EMG) are used to monitor neurological data from the brain to reveal information about neurological activities in the sleeping brain.
Here is a scientific literature (pdf) you can go through for in-depth study ( this link leads to ResearchGate page, you can read it there or download the pdf) :
https://www.researchgate.net/publication/281071308_The_Role_of_Dreams_in_the_Evolution_of_the_Human_Mind

Thanks alot Navoneel.


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Can a Chihuahua and a Great Dane breed the "old fashioned way?"
I saw this vid:
https://youtu.be/eu2qe-FNtjg
And this question crossed my mind.  The dog in the video seems to be boxer sized... And I wonder if that strategy would work with something a little bigger....
Also, this is obvious, but let me clarify: 'I'm thinking about  a FEMALE Great Dane and a MALE Chihuahua. (The other way arround, we would get a Chihuahuaburger before anything even happened... And would be animal cruelty. ) Since they're the same species ( a dog, aka Canis lupus familiaris) that means they can make  viable offspring, rigth?

I'm not watching this video but yes, it is possible with artificial insemination or if you support the small dog during mating. Chihuahua and Great Dane might be a bit ambitious for the latter, though.

I don't think artificial insemination is very "old fashioned" ;) lol.  But thanks. What sort of support? like... putting the chihuahua on the Great Dane's back? (that's the way the chihuahua does it in the video, it jumps on top of the boxer, on it's own...)


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How do bees help flowering trees survive?
I have often heard a vague claim that bees help flowering tree populations survive.
As far as I know, bees take nectar and pollen concentrations from the flowers of flowering trees and use at least the nectar as a food source, but they don't take seeds out of these trees, so it's unclear to me how they help these trees survive in that regard.
Given that bees don't take seeds of flowering trees (and drop some when they fly) How do bees help flowering trees survive?
How does the taking of nectar and pollen away from flowering trees make bees symbiotically help such tree populations to survive and endeavor?

Do you know what pollen is?

@John hello ; I know it is a powder like material scattered by flowering trees to defend themselves (for example, causes allergy to humans in some situations) and as food for symbiotic relations; I think I have heard it does also with reproduction but I am not sure about that.

I read this in the opener in Wikipedia article "Pollen" Pollen in plants is used for transferring haploid male genetic material from the anther of a single flower to the stigma of another in cross-pollination but it is unclear to me what it means.

One of the goals of every living organism (including plants), thus it seems, is to create offspring for the next generation. This is the way plants (angiosperms) have sex.
That said; I personally define pollination as:

The act of transferring pollen grains from the male anther of a flower
  to the female stigma.

It should be noted that not only Bees play a very important role in pollination, but also other insects like wasps, beetles, mosquitoes etc.

When a bee sits on the flowers to collect nectar, its feet pick up pollen grains ( the powdery stuff) from the anthers and transfer it to the female stigma (which is sticky to hold the pollens).
Michigan State University:

When a bee lands on a flower, the hairs all over the bees' body attract pollen grains through electrostatic forces. Stiff hairs on their legs enable them to groom the pollen into specialized brushes or pockets on their legs or body, and then carry it back to their nest. Individual bees tend to focus on one kind of flower at a time, which means it is more likely that pollen from one flower will be transferred to another flower of the same species by a particular bee.

Then the pollen grain makes its way into the ovary of the flower through the long stalk (style) and fertilizes the egg. Then the flower matures to for a fruit and the ovules become it's seeds.
It's a symbiotic relationship where the plant provides food and the bees pollinate them in turn.
Also, certain bright colouration of flowers and their sweet smell attract more insects.
A declining population of pollinating insects signal the decline of the whole ecosystem including plants and trees.
Entomologists keep a check on various insect populations. They have found a decline in the population of bees world wide! This is an alarming situation. This will cause huge damage to fruit industries including kiwifruit, watermelon, squash and many others. It's time we take the environmental issues seriously.The reports aren't vague!
Penn State College of Agricultural Science:

Historically, managed honey bee populations in the US and Europe have been monitored due to their vital role in providing pollination services in agricultural systems.  Several studies indicate that American and European beekeepers are suffering large annual losses.  In the US, beekeepers have lost ~30% of their colonies every year since 2006, with total annual losses sometimes reaching as high as 42%

Edit
Citations:
https://en.m.wikipedia.org/wiki/Pollinator#Honey_bees
https://en.m.wikipedia.org/wiki/List_of_crop_plants_pollinated_by_bees
A brochure from FAO on importance of bees as pollinators :
http://www.fao.org/3/I9527EN/i9527en.PDF
Penn State College of Agricultural Science on declining population of pollinators :
https://ento.psu.edu/pollinators/resources-and-outreach/globally-pollinators-are-in-decline
Wikipedia on the same issue:
https://en.m.wikipedia.org/wiki/Pollinator_decline

This answer is a good start, but does not answer how increased pollination by bees leads to increased plant survival.  I think a more complete answer would include a discussion of the relative efficiencies of cross-pollination and self-pollination, as well as the consequences of these different strategies on genetic heterogeneity in plant populations (e.g. variation in resistance to pests and disease)

@Dirigible Ok, so you have used the words " increased pollination by bees lead to increased plant survival ". The more accurate picture is that Bees do not increase pollination. If they aren't present there would be no pollination for certain plant species in certain geological places, this would lead to the collapse of the ecosystem. They pollinate a major section of plants, and not just " increase pollination ".

Hello @NavoneelKarmakar ; I thank you for the great answer ; I have recently suggested an edit of primarily markdown, HTML and web accessibility; please go through my edit suggestion and it's description. Again thank you, in great appreciation; John,

Navoneel Karmakar's answer is correct -- there are many plant species for which bees are crucial or necessary pollinators because of self-incompatibility.  Indeed, the disappearance of bees would lead to the collapse of these plant populations if no other mechanism of pollination (e.g. wind) was available.
But there are many plants that do not rely on insect pollination, and can self-pollinate to reproduce as well as exchange gametes by insect cross-pollination.  Would the disappearance of bees (or the preferred insect pollinator) lead to reduced survival of such a plant population, by a mechanism other than drastic population collapse?
From a population genetics perspective, variation is a good thing.  If a geographically isolated population of plants reproduces exclusively by pollination between genetically homogenous neighbors, the genetic diversity of that population is limited to the genes of individuals in that population (plus mutagenesis, though beneficial mutations are generally a consideration only in the long term).  If a pest or pathogen is introduced to this population, and no individuals in that population carry the genetic determinants of resistance, that population will be threatened, barring some rare mutagenesis leading to resilience.  Even outside the threat of disease, any isolated population is subject to inbreeding depression by propagation of deleterious alleles.
Now, introduce an insect pollinator.  This organism can ferry plant gametes between geographically isolated populations, expanding the existing genetic space of each population to include the other.  This pollinator is an agent of outcrossing, which combats the effects of inbreeding depression by the introduction of new alleles.

Take, for example, Chamaecrista fasciculata, a species of bee-pollinated legume.  Mannouris and Byers discuss the effect of habitat fragmentation on this plant, which has led to smaller populations resulting in reduced genetic variation and increased genetic drift load, defined here:

In small populations, genetic drift is likely to play a stronger role in changes in allele frequencies than natural selection. Random loss of alleles through drift is more likely to leave behind deleterious recessive alleles than selection would do. The result is an enhanced level of genetic load in small populations due to the effects of drift, known as ‘genetic drift load’.

This species can be selfed, but relies heavily on bee pollination to maintain genetic diversity.

Chamaecrista fasciculata is 80% outcrossed by bumblebee pollinators and the populations have been found to be very spatially structured due to limited seed and pollen dispersal.

Moreover, fragmentation of the prairie habitats has led to populations that are too isolated for bee cross-pollination.

All of the prairies listed as isolated on Table 1 were at least 30 km from another known prairie with C. fasciculata, which is beyond the distance bumblebee pollinators are expected to forage.

All of this to say, while C. fasciculata does not exclusively rely on bee pollination to reproduce, there is a deleterious effect of the loss of cross-population pollination evident in reduced population genetic diversity.

Also note that there are many plants that pollenate via the wind, but for wind pollenation, the plants have to grow where there's wind, and have to produce lots of pollen.  Insect (or bird, bat &c) pollenation doesn't require wind, and can be more specific if your pollenators evolve to prefer your kind of tree.  https://northernwoodlands.org/articles/article/why_are_some_trees_pollinated_by_wind_and_some_by_insects


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design and assessment of qPCR primers for COVID19
I read the False Negative of qPCR test for COVID19 is high compare to CT scans.
https://pubs.rsna.org/doi/10.1148/radiol.2020200642
I was curious if experts can comment on why and what makes it difficult to design more accurate PCR given the genomes is out there.

The WHO's primers are compatible with every sequences found so far, when the PCR fails it is because the sample doesn't contain enough viral genomes (here the probe https://blast.ncbi.nlm.nih.gov/Blast.cgi?CMD=Get&RID=607FNKGR01R )

what do you mean by compatible ? every test as sensitivity and specificity. here is the question, given the high match on blast - what makes it to have low specificity ? it is clear in the paper and other papers these pcr tests suffer from high false negative :)

Compatible means the forward and reverse primer (20 nt each) bind to the ends of the target 100 nucleotides subsequence of the viral genome (and its minus sense copy) and this subsequence contains the probe (25 nt). When extended by the TaQ polymerase the probe releases its quencher so that its fluorescent end produces light which is detected by the fluorometer. If some mutations appear in those three 20 nucleotides subsequences the PCR will stop working or it will be much less efficient and the WHO will have to make new primers with more diversity


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L-system rule for different plant types
I have coded an implementation of L-systems (Lindenmayer systems) and would like to use it to generate realistic looking trees. Is there a reference list that shows which rules are most appropriate for different types of trees? For instance, which rules are best for an oak tree, which are best for cherry trees, etc.?

I d search for procedural trees... i.e. https://amp.reddit.com/r/proceduralgeneration/comments/6mpthc/procedural_tree_generation_incl_code/

There are many good papers by Karl J. Niklas where he models tree growth. I'm not sure if he used L-systems in particular, but I'm sure his work can inform you about the 'rules'. You can find out more here and here.


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Combining MAOIs with Stimulants
Is it dangerous to combine MAOIs with stimulants? According to wikpedia, Parnate, for example, "leads to an increase in the availability of monoamines, such as serotonin, norepinephrine, and dopamine, as well as a marked increase in the availability of trace amines, such as tryptamine, octopamine, and phenethylamine." A stimulant like Vyvanse, for example releases dopamine but doesn't act significantly on serotonin. So would combining the two be dangerous?

This question is closed, but I want to comment for the sake of future readers: yes, this may be dangerous. MAOs are one (of several) ways the body has to remove monoamines. If you simoultaneously increase the availability of monoamines and decrease one of its elimination pathways there may be an excess of monoamines, which may be dangerous.


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Does the genetic sequence of SARS-CoV-2 end with 33 A's?
Looking at the DNA (or RNA?) sequence of the Covid-19 virus here: https://www.ncbi.nlm.nih.gov/nuccore/MN908947.3
I notice it ends in 33 a's. Does the virus really look like that, or is it some artifact of the sequencing process, or some sort of padding to round out numbers?
Here's the last few lines:
29761 acagtgaaca atgctaggga gagctgccta tatggaagag ccctaatgtg taaaattaat
29821 tttagtagtg ctatccccat gtgattttaa tagcttctta ggagaatgac aaaaaaaaaa
29881 aaaaaaaaaa aaaaaaaaaa aaa

Related: https://bioinformatics.stackexchange.com/questions/11227/why-does-the-wuhan-coronavirus-genome-end-in-aaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaa

@jpa is that not a duplicate?

@MCMastery That's the issue with having overlaps between Stack Exchange websites and not allowing“crossover questions” between sites.

This is a poly(A) tail, which is a feature found in the majority of eukaryotic RNAs (especially mRNA) and is also not uncommon in RNA viruses (which essentially mimic endogenous mRNA for their own replication). As with mRNA, this poly(A) tail in coronaviruses is bound by poly(A) binding protein in the cytoplasm [1], which is involved in translation initiation. In coronaviruses, this poly(A) tail is also necessary for replication independent of its role in translation [2].
[1] Lin Y-J, Liao C-L, Lai MM. 1994. Identification of the cis-acting signal for minus-strand RNA synthesis of a murine coronavirus: implications for the role of minus-strand RNA in RNA replication and transcription. J Virol 68(12):8131-8140.
[2] Spagnolo JF, Hogue BG. 2000. Host protein interactions with the 3′ end of bovine coronavirus RNA and the requirement of the poly (A) tail for coronavirus defective genome replication. J Virol 74(11):5053-5065.


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Why might long telomeres be selected for in laboratory mice?
In a recent episode of The Portal, Eric Weinstein sits down with his brother Bret Weinstein to discuss Bret's Reserve-Capacity Hypothesis. It's an incredible story of scientific discovery and academic injustice.
One prediction of the hypothesis was that laboratory mice, known at the time to have abnormally long telomeres for their lifespan, were not a representative sample of the wild mouse population because the environment the lab mice were being bred in was selecting for longer telomeres. This had serious implications for drug safety testing.
My surface level understanding as a non-biologist from listening to the Podcast goes like this. Please point out any misunderstandings.
Antagonistic Pleiotropy Hypothesis for Senescence
George Williams predicted that pleiotropic (multi-purpose) genes which are advantageous early in life but detrimental later in life will be selected for in nature since organisms often die or reproduce long before the disadvantageous effects manifest themselves. This is an evolutionary theory for aging, which argues that trade-offs exist between early life and later life fitness. This effect was observed, but no gene had been known to be the cause. This was the "missing pleiotropy".
The Hayflick Limit
Telomeres are repeating, non-coding regions of DNA at the end of each chromosome which aid in cell division. Each division, the telomeres shorten. Telomeres are counters of sorts, which provide a hard limit (the Hayflick limit) to the number of divisions a cell can undergo. Any cell that started dividing uncontrollably (cancer) would eventually reach its Hayflick limit and die. Aging (senescence) is the manifestation of cells in an organism reaching their Hayflick limit.
The Reserve-Capacity Hypothesis
This is Bret Weinstein's work. The way I understand it is that Weinstein pointed out that the missing pleiotropy was not a gene at all, but telomeres. Weinstein observed that there existed a trade-off which was reflected in telomere length. Long telomeres allow cells to repair themselves many more times, slowing the effects of aging, but simultaneously leave the organism vulnerable to cancer, as cells which begin to divide uncontrollably will never reach their Hayflick limit. The length of telomeres is the result of a trade-off between dying of cancer, or dying of old age.
The JAX Lab Scandal
One critical prediction of the Reserve-Capacity Hypothesis was that mice (which were at the time thought to have abnormally long telomeres for their lifespan) don't naturally have long telomeres. Instead, it was specifically the mice coming from the Jackson (JAX) Laboratory (which supplied a significant percentage of North America with mice) which had abnormally long telomeres. Since JAX Lab had economic incentive to breed as many mice as possible as quickly as possible, they were artificially introducing selective pressures on the mice. Namely, the pressure of breeding the mice early in their lives. This meant that any late-life disadvantages, such as susceptibility to cancer as a result of longer telomeres, were not playing an important role since the mice were bred well before they were likely to develop cancer. Since telomeres are a non-coding region of the chromosome, variation can happen very rapidly (no need for the traditional timescales of Darwinian selection). Over time, long telomeres became dominant in the mice population, and so research being done on mice purchased from JAX lab concluded that mice had very long telomeres.
The primary gap in my understanding is the following. Why was it that longer telomeres were selected for? It is unclear to me how discounting the late-life disadvantages of long telomeres would result in long telomeres becoming dominant in the population. If anything, telomere length should become irrelevant. If so, we'd see a wide distribution of telomere length. That is, unless longer telomeres provide benefits to organisms early in life. Is that the case? If not, how can we explain long telomeres becoming not just common, but dominant?

That is a very good and well-stated question, outside my knowledge set.

Their arguments for increased telomere length in lab mice are:

Rate of tumour formation is dependent on the number of cells within an organism. Additionally, tumours take time to form. Therefore, small animals that only need to reproduce early in life, like lab mice, are less prone to tumours and there is then less selective pressure favouring telomere shortening.
Senescence has a negative effect on reproductive success, even early in life, and there is therefore selective pressure favouring increased telomere length that reduces senescence.
While the lack of selection on senescence due to the short window for reproduction could have the opposite effect of reducing telomere length, point 2 is the dominant factor.

To be frank, this all sounds extremely speculative to me and the supporting evidence they did provide was not entirely convincing (though I am far from an expert in the field). Keep in mind that it’s a hypothesis only.
In case you don’t have access to their article, I quoted the relevant section below:

The unusual telomere system of lab mice may be an unintended consequence of captive breeding. Retirement of breeders after 8 months eliminates selection on late-life effects. Tumor-forming mutations take time to occur, tumors take time to become lethal, and the likelihood of tumor initiation is presumably a function of the number of cells in the body, so in small bodied animals like mice, tumors may be rare and inflict minimal cost in the first eight months of life, even absent a telomeric fail-safe. Further, selection for sustained high reproductive output (beginning early and maintained for 8 months) should strongly favor a reduction in senescent effects occurring in that window. Selection acting to eliminate senescent effects and increase early reproductive output may tend to elongate telomeres. Because of the inextricable connection between tumor suppression and somatic maintenance, telomere elongation should dramatically increase the risk of eventual tumor formation, but any effects manifesting after the breeding cut-off will be selectively irrelevant. By our model, selection for early high rates of reproduction in the absence of selection for longevity or tumor suppression should produce long telomeres and a strong propensity for eventual tumor incidence. Despite diminished senescence, we expect these mice to have reduced maximum longevity compared to wild conspecifics. At all ages, lab mice (with elongated telomeres) should be more likely to die of tumors than wild mice. These mice should also be unusually resilient to somatic damage and show few signs of aging other than tumor formation.
...
The hypothesis that an 8 month breeding cut-off should select for non-senescent, tumor prone mice seems paradoxical. One might expect the elimination of selection on late life effects to accelerate senescence, not retard it. But in lab mice, selection for high, sustained rates of breeding appears to be the dominant factor. The tumor fail-safe has effectively been turned off, condemning these animals to form tumors, but leaving an early-life window of reproduction within which there is minimal senescent decline.

Thanks. A couple of follow up questions: How does senescence negatively effect reproductive success early in life? How might the elimination of selection on late life effects accelerate senescence, assuming no other factors were at play?

@aRockStr (1) This may warrant a separate question, or a better answer to this question. Either way, I don’t have a good answer. Check out this paper and specifically the section titled “Cellular senescence and ovarian aging”; it might give some insight. (2) I think their idea is that without selection on late life effects, selection against tumour formation would be dominant and therefore favour shorter telomeres, which would accelerate senescence.

(2) is the argument that if aging is a non-issue, the telomere trade-off is dominated by tumour defense?

Yes that’s my understanding of it.

I think I understand then. The whole argument relies on the existence of a trade-off between defence against cancer and 'defence' against aging. If one of these factors are removed from the system, the other will dominate. This was Bret Weinstein's contribution.


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Melanistic Snow Leopards?
Are there any confirmed cases of melanism in snow leopards? I am aware that melanism is much more common in Jaguars and Leopards, both often called black panthers, but I cannot seem to find any info on melanism in snow leopards.

I'm not aware of any confirmed cases of melanism in snow leopards either.
There are some relevant studies on the evolution of melanism on Felidae. Melanism seems to occur only in two extant species of the genus Panthera (Panthera onca and Panthera pardus). There is a direct correlation between melanistic colorations and enviroment (especially humidity):

Moist forests (especially in Southeast Asia) presented very high
  frequencies of melanistic leopards (e.g., 39 of 71 individuals [55%]
  in Southeast Asia), and more than 80% of the black animals in our
  database, a fivefold increase relative to the expected number based on
  the overall number of records. Furthermore, we found no confirmed
  melanistic leopards in the Middle East, Arabian Peninsula, Central
  China, and Russian Far East, nor any mention in the literature as to
  the presence of melanism in these regions, indicating that this
  polymorphism is really absent from these areas. Overall, there was a
  significant reduction in the frequency of melanism in some biomes that
  consist of open habitats or temperate forests. There thus is a clear
  pattern in which melanism tends to increase in tropical/subtropical
  moist forests and decrease in open/dry or temperate habitats

References:

https://www.sciencedirect.com/science/article/pii/S0960982203001283
https://www.intechopen.com/books/big-cats/ecology-and-evolution-of-melanism-in-big-cats-case-study-with-black-leopards-and-jaguars


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Why does it take so long for the human brain to develop from an evolutionary point of view?

I have read that it takes about 25 years for the brain to be fully developed.
  Coincidentally, humans from the Neolithic and Bronze Age had a very short life expectancy, in fact most of their life their brain wasn't fully developed.

My question is:
from an evolutionary point of view, is there a reason why humans spend so much of their life not being fully developed even long after being sexually fully developed?

You are asking about the phenomenon of neoteny, the delay of development well into adulthood. You will not get a better answer than this comprehensive wiki on neoteny in humans. You will find a rather impressive list of reasons and arguments throughout the entire page, especially under the Human Evolution section.

We can say that brain and our nerve system is the first system in embryo that starts to develop and as you said this system is continuing to develop until after birth.
So here is a question that why our brain don't develop completely before the birth ?  Evolution has gone so far as to limit the development of the brain in the human embryonic phase and to allow it to continue into the postnatal phase. This helps the infant to be born and ease the birth both for mother and the new born because if the brain had fully grown, the size of the head would have made problem in birth. Now, after birth, the brain continues to grow and develop majorly between ages 2-3 and becomes more mature after that . The ability of the brain to grow over the years gives us the ability to adapt to different environments , learnings and new issues and other capabilities That happens with the subsequent creation and pruning of dendritic spines.

This partially explains why we're not born with fully mature brains, but doesn't at all answer the question of why it takes so long for the brain to fully mature, long past when the rest of our organs and systems are fully functioning.

At the end of the paragraph I mentioned the one point that why our brain developing takes too long

Being born with a fully-developed brain would still give us those same capabilities, although one could argue that language acquisition is uniquely easier during childhood (due to the characteristics of the brain during that time) than it is in adulthood. As it is, I'm not going to downvote the answer, but I'm not going to upvote it either. I think you could go a lot farther in explaining the evolutionary biology of neoteny.


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Genes and proteins with a significantly inbalanced composition
According to Wikipedia, the median size of a protein-coding gene is 26,288 bp which makes it possible (from statistical considerations) that the nucleotides C, G, A, T appear in roughly equal amounts in one strand. But maybe this is wrong so I want to ask:

Are there and which specific protein-coding genes have a significant inbalance
  of amounts of C, G, A, T in one strand?

Related to this is the question if there are larger proteins (containing up to 27,000 amino acids as the titins do) with a significant inbalance of amounts of the 20 different amino acids?
Might it be the case that from an inbalance of the gene an inbalance of the protein may follow?

I don't know about the base usage/(im)balance, but using the transcriptome sequences, that would be relatively easy to check. For amino acid usage, I think there is a bias for evolutionary older proteins (especially mitochondrial ones related to bacteria) to not use certain amino acids as much (mostly the aromatic ones I think)

Tangential to the topic of protein, but related to the "strandedness" mentioned in your question, is the phenomenon of GC skew (not to be confused with GC content).  Differences in strand composition may be explained by asymmetric mutational pressures between the leading and lagging strands during transcription and replication.


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Which proteins are part of the most different protein complexes?
Let n be the number of different protein complexes (as defined here) that a protein may be a stable part of for a considerable amount of time (and not only transiently). Which proteins have the largest n?
An answer should include the number of different protein complexes  the protein is part of.
Or where should I start doing my own research? I have no clue.

Can you better define "protein complex"?  Are you asking which proteins have the greatest number of distinct binding partners?  Are you asking which proteins are most promiscuous in their binding to other proteins?  While I appreciate your thought-provoking questions, Hans-Peter, I feel that you've made no attempt at research for this one.

@Dirigible, thanks for asking. But are your paraphrases more unambiguous than my "simple" question? I agree that "of the most different protein complexes" doesn't sound perfectly right. I'll try to do better.

@Hans-PeterStricker As an example of what Dirigible might mean: all proteins are translated by ribosomes, along with a bunch of accessory proteins and chaperones to assist in properly folding proteins. Therefore, the ribosomal proteins (and associates) may be said to be complexed with every other protein. I haven't checked but this almost certainly gives them the highest degree in a protein-protein interaction network. This is a trivially true answer to your question, but it's almost certainly not what you mean.

Also: I would suggest reading a little bit more about protein-protein interaction networks, which I'm pretty sure are what you are interested in: https://www.ebi.ac.uk/training/online/course/network-analysis-protein-interaction-data-introduction/protein-protein-interaction-networks

This answer does not address the number of complexes that a protein participates in, but rather a related question -- With how many proteins does a protein interact?  I acknowledge this  is a fundamentally different question, though I think it's a good starting point on which other people can build a better answer.

Since an organism isn't specified in the question or tags, this answer focuses on a simple and extensively studied model: E. coli. Taking the data from STRING v11 1 for all protein-protein interactions (PPIs) in Escherichia coli str. K-12 substr. MG1655, we can subset these PPIs to include only those of action type "binding".  This database provides PPI scores between 0 and 1 based upon experiments (co-purification, co-crystallization, Y2H), textmining, co-occurence, co-expression, and co-localization of coding genes across genomes.
If we set no cutoff for the confidence in these binding interactions, we see that 2585 proteins have ≥1 binding partner, and one protein has an astonishing 273 binding partners (pfo, a putative pyruvate-flavodoxin oxidoreductase).  Also, this database states this E. coli strain has 4127 distinct protein-coding genes, so approximately 63% (2585/4127) of genes encode a protein that interacts with at least one other distinct protein.
If we limit the interactions to those with a "high confidence" score (≥0.900), only 656 proteins (~16%) are seen to have ≥1 binding partner, with a maximum of 55 binding partners seen for 4 proteins.  Unsurprisingly, and consistent with the comment from Maximilian Press, these proteins are all associated with the ribosome (sra, rpsP, rpsI, and rpsR).  The spike in the graph below at 54 interacting partners for the high-confidence PPIs is a group of of ribosomal proteins, most of which are annotated as co-interactors.

Two important notes on interpretation of interactions in this database:

splice variants and post-transcriptionally modified proteins are collapsed into single nodes in the interaction network, so all gene product variants are represented by one coding sequence
self-interactions (e.g. dimerization) are not counted, which are a valid type of protein complex per the question

References

Szklarczyk D, Morris JH, Cook H, Kuhn M, Wyder S, Simonovic M, Santos A, Doncheva NT, Roth A, Bork P, Jensen LJ, von Mering C. The STRING database in 2017: quality-controlled protein-protein association networks, made broadly accessible. Nucleic Acids Res. 2017 Jan 4;45(D1):D362-D368.


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Open Reading Frames vs Coding Sequences (CDS), are they different?
The two terms confuse me for a long time. What is the difference between ORF and CDS. Some people say ORF could contain intron and CDS does not. The wikipedia definition of ORF does not contains intron. Could someone define the two terms and point out their differences? Thanks!

I (mostly) like the definitions given on this page.

An ORF is a sequence of DNA that starts with start codon “ATG” (not always) and ends with any of the three termination codons (TAA, TAG, TGA). Depending on the starting point, there are six possible ways (three on forward strand and three on complementary strand) of translating any nucleotide sequence into amino acid sequence according to the genetic code. These are called reading frames.
The Coding Sequence (CDS) is the actual region of DNA that is translated to form proteins. While the ORF may contain introns as well, the CDS refers to those nucleotides (concatenated exons) that can be divided into codons which are actually translated into amino acids by the ribosomal translation machinery.

However, I do not entirely agree with this statement:

In Prokaryotes the ORF and the CDS are the same.

While it’s true that all CDSs are within ORFs, not all ORFs are CDSs. You can have ORFs that are transcribed as noncoding RNA elements, and ORFs that are not transcribed at all. CDS refers specifically to the ORFs whose post-transcriptional fate is to be translated.

I just found a post on biostar with the same question and lots of discussions: https://www.biostars.org/p/47022/


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Is downregulation of neurological receptors fully reversible, i.e. complete upregulation and resensitization?
Are down/upregulation truly reciprocal mechanisms? After a binding ligand or agonist is removed, such as a prescription medication, is upregulation and resensitization able to occur to a level that exactly equates to and completely reverse and fully make up for any loss of receptors, bonding affinity, etc? Could anything theoretically be permanent? Does time/length of prescription play any role in this, including when prescribed a benzodiazepine (Clonazepam)?


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Is COVID-19 claimed to get less deadly over time? If so, why?
From a TV news report of a press conference from (I think) the German Robert Koch Institute, I remember hearing an expert declare that he was expecting COVID-19 to get less deadly over time.  Unfortunately, I don't know what press conference it was (I'm not sure if it was the Robert Koch Institute — it might also have been the Charité university hospital) and cannot find such a stated expectation on the internet.
Why would an expert express this expectation?
Is it because we're heading toward summer (at least where most COVID-19 cases have been reported), or is it a standard pattern, perhaps either due to people's immune systems or due to the virus evolving and becoming weaker?

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

While the data are much too sparse and noisy to give an answer about what is happening to COVID-19's virulence (the technical term for the "deadliness" of an infectious disease), or to forecast what will happen to its virulence in the future, there are indeed theoretical reasons that one might expect the virulence to decline in the future.
There is an entire theoretical literature on the evolution of virulence (e.g. see Read 1994, or see Wikipedia); Robert May and Paul Ewald are two researchers who contributed seminal ideas. The basic idea is that infectious 'organisms' (including viruses) may face a tradeoff between their ability to produce lots of infectious particles (e.g. by replicating faster within the host) and the length of time that they can stay in the host before it dies or activates immune defenses sufficiently to end the infection. In this case, some intermediate level of virulence may evolve.
Evolution of virulence in ways predicted by the theory has been observed in the real world in such diseases as myxomatosis (a viral disease of rabbits). The theory has also been suggested to apply in HIV and syphilis.
The actual forecast can depend on many details of the biology and epidemiology of a particular organism. If COVID-19 happened to have a higher-than-optimal virulence in humans at the time of emergence, we could expect its virulence to decline over time. It could also decline if epidemic control was applied in such as way as to differentially affect more-virulent strains; this has been suggested by Tang et al. on the basis of the pattern of mutations in different strains, although their logic has also been criticized on Twitter by an expert in genetic epidemiology, and now by a more official rebuttal by McLean et al. (with some back-and-forth discussion between the authors and critics).
This explanation doesn't include the possibility of host evolution, which is theoretically important but not really relevant to COVID-19 — it would only happen over many generations, and only if the epidemic was so severe that it was a significant overall cause of death or failure to reproduce ...

Tang et al. "On the origin and continuing evolution of SARS-CoV-2", National Science Review, nwaa036, https://doi.org/10.1093/nsr/nwaa036 .
Read, Andrew F. "The evolution of virulence." Trends in microbiology 2.3 (1994): 73-76.

To summarize, the most performant virus is the one that keeps the hosts well enough and socializing for the most time with the highest output of virus to others in their vicinity.

There's a theory that a highly deadly virus kills its hosts and therefore replicates less. With Covid killing somewhere between 0.1% and 1% of infected people, that seems to be completely irrelevant.
There's a better theory that when a virus is very deadly then people will do whatever they can to stay away. Boris Johnson wouldn't have shaken hands with Ebola patients. A virus same as Covid but 50% lethal would have massive voluntary lockdown and fights for vaccines. For those reasons, it would spread less than Covid. With 50% lethality you could expect 99% of people to lock themselves up out of fear, and the 1% in the streets shot on sight.
I am told that the current Omicron variant has changes which body parts it affects (throat instead of lungs). And these changes make it at the same time less lethal and more infectious. This sounds reasonable, but not necessarily true. So you may try to think of something that makes the virus both more lethal and more infectious at the same time.
But fact is that the virus has no advantage from killing people. No evolutionary gain. However, it has an advantage from being more infectious. On the other hand, Covid is very infectious already, so a random change is very unlikely to make it more infectious. The "better" it is at infecting people, the harder it is to improve.


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Does the composition of a meal play a big, or small, role in food's thermogenic effect on the body?
Reading in: "Diet and Health: Implications for Reducing Chronic Disease Risk /  Calories: Total Macronutrient Intake, Energy Expenditure, and Net Energy Stores" [NCBI Resources]:

"The thermogenic effect of a meal usually amounts to approximately 10% of the caloric value of the ingested food, and is higher for carbohydrates and protein than for fats".

Does that mean that the thermogenic effect of a meal fluctuates between 9% and 11%, depending on it's composition? If so, the thermogenic impact on the body by a meal's composition would be quite small in comparison with the impact of a meal's calorie content. Or, does food's composition play a bigger role than that? Looking for information from reputable sources.
Calories: Total Macronutrient Intake, Energy Expenditure, and Net Energy Stores

"It only takes 2.5 calories to convert 100 calories of fatty acids into body fat. It takes 23 calories (10 times as much energy) to convert 100 calories of protein or glucose into body fat." (Sweet Poison: David Gillespie)

According to Diet Induced Thermogenesis (Nutrition & Metabolism, 2004), the percent of calories converted to heat depends on a nutrient:

Proteins: 15-30%
Alcohol: 10-30%
Carbohydrates: 5-10%
Fats: 1-3%
A mixed meal: ~10% (this is an estimated average)

The thermic effect of nutrients is not a fixed value and can vary greatly within a person and from person to person:

Reported intra-individual variability in DIT, determined with
  ventilated-hood systems, is 6 to 30% [7,8]. Reported within-subject
  variability in DIT, determined with a respiration chamber, is 43 to
  48%.


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Are these spinach leaves?
I often buy baby spinach from the store, and sometimes, in a few bags of spinach I also find these leaves:

They have a different shape than the spinach leaves, they are a lighter green, and they taste differently. The bag doesn't say that "it may contain traces of" other plants, so are these some part of the spinach plant? Or are they something different? Why do they often come together with the spinach leaves? I haven't found any other kind of leaves (besides spinach) in the bags except those in the picture.

Those are the cotyledons (seed leaves) of spinach.
For comparison, here's a picture of what spinach sprouts look like:

Source: https://wimastergardener.org/article/spinach-spinacia-oleracea/


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Probabilities in calculating the kinship coefficient
I've been reading up to try to understand how the kinship coefficient (or coefficient of coancestry) is calculated. https://brainder.org/2015/06/13/genetic-resemblance-between-relatives/ this is the best explanation I've been able to find so far. However, I've not been able to find an explanation that makes a clear distinction between genes and alleles.
In my initial reading of the above I factored in this fact and assumed that often when the author wrote gene he/she meant allele (an assumption which I now think is incorrect), and thus that identity by descent of a single allele between individuals would be enough to satisfy kinship in the context of the definition of the kinship coefficient. This lead me to confusion upon reading the kinship coefficient as mathematically defined from the condensed coefficients of identity:
D1 + 1/2(D3+D5+D7) + 1/4(D8)
Surely, I thought, the kinship coefficient should merely be the sum of the probabilities of all the possible ways in which the two individuals may share the same allele. And thus there is no reason to multiply the sum of D3, D5, and D7 by 1/2 and D8 by 1/4.
Finally to my question; Kinship coefficient is defined as the probability that two individuals are identical by descent at a single randomly selected gene. Remembering this, is the reason it is calculated in this way because in order for the gene between individuals to be fully identical in the case of D3, D5, and D7, an additional identical allele is required from one parent (an event with a probability of 1/2), and in the case of D8 additional identical alleles are required from both parents (an event with a probability of 1/4)?
I'd be very grateful if someone could clarify for me why it's calculated in this way.

You might want to read "Relatedness in the post-genomic era: is it still useful?" by Speed and Balding.

If anyone is interested in a rigorous formulation of the kinship coefficient, please check out the answer https://biology.stackexchange.com/a/95775/8344.


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Does animal based food contain molecules that behave like dietary fiber for humans?
I have read that dietary fiber is beneficial to human health in many ways, for example that it can help to reduce risk of colorectal cancer. However, when I look at nutrition labels on food it seems that only plant based food contains fiber; animal based food (meat) contains none.
What exactly is meant by fiber? I looked it up and found that there are actually a variety of definitions. The CODEX Alimentarius Commission has recently come up with an updated definition described in a paper by Jones. The definition states that “dietary fiber means carbohydrate (CHO) polymers with ten or more monomeric units, which are not hydrolyzed by the endogenous enzymes in the small intestine (SI) of humans”. Further more their definition "includes resistant oligosaccharides, resistant starch and resistant maltodextrins" when a footnote of the definition is included.
Jones points out that some definitions of dietary fiber do not explicitly rule out dietary fiber from animal sources. So does meat or animal based food contain any carbohydrate (CHO) polymers that are not hydrolyzed by the endogenous enzymes of the small intestine in humans?
An earlier version of this question was posted in my blog.

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). In particular, your question is based on an assumption — I suggest you find references that support that assumption, which will almost certainly lead you to an answer for this question. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

Definitely prior research needed.  For instance, why would digestibility by humans matter to microbes?  It would mean they would just have to get to (some of) the human-digestable stuff before the human uses it.  Also, I think the idea of dietary fiber is that it is not digested by either humans or gut microbes, and thus adds bulk to the stool,

Thanks @jamesqf for your feedback. I overhauled the question and provided a reference for my assumption. I focused only on the definition of dietary fiber, and left off the discussion about gut bacteria since that was just confusing things.


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Why is Ibuprofen contraindicated in asthma patients?
So yesterday a patient showed up at the clinic with a massive swelling in his left face region. Upon examination it was found to be due to infected first premolar. Dentist recommended him to get the tooth extracted as the patient also had generalized attrition and abrasion. The patient was an asthmatic and diabetic on Ecosprin. The dentist while prescribing him medicines said that he won't prescribe him Ibuprofen as the patient was asthmatic. I have been looking for an explanation since then and Rang and DaLe have something to say about the isomers of COX enzyme. I am looking for a simple explanation.

Yes. Since am under observation at a dental clinic, it counts as a homework question for me.

More a personal medical question, but on-topic as it involves biological mechanisms of drugs, not advice on taking them (which you already have.)

Ibuprofen is an NSAID. So it acts by inhibiting COX (Cyclooxygenase) enzyme. What it signifies is that, if COX enzyme has been blocked, the PUFA (say arachidonic acid, here) will be converted to leukotrienes through lipoxygenase pathway.

Leukotrienes (LT) are of different types and have several target receptors; one of which is CysLT-receptors on bronchial smooth muscle. Once they are activated through LTD$_4$,E$_4$,C$_4$ , bronchospasm will occur. For asthma patients this is really fatal. So for them Ibuprofen is contraindicated.

Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5072955/
Lo, P.C., Tsai, Y.T., Lin, S.K. and Lai, J.N., 2016. Risk of asthma exacerbation associated with nonsteroidal anti-inflammatory drugs in childhood asthma: a nationwide population-based cohort study in Taiwan. Medicine, 95(41).

Interestingly the patient insert for commercial ibuprofen doesn’t state this (at least not in such absolute terms): it only mentions that ibuprofen shouldn’t be taken if the patient has previously developed symptoms of asthma after taking it. That said, the RR in the cited study is quite impressive.

Understood. Thank you for explaining so well.


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Action potential: why called "depolarization" when polarity is reversed, not removed?
During an action potential, the voltage shifts from the resting potential of -70 mV, to +30  mV, to then fall return back to the resting potential again of -70 mV. This reverse of the polarity, what is the reason it came to be called "depolarization", as in, removed polarity?

While the cell is polarized (in the positive direction) at the height of the action potential, it has been depolarized from its resting, negatively charged state, meaning the original polarity has been lost or reversed. In my mind, the slight (30mV max) positive polarization for that brief period of time is kind of an "overshoot" of neutral charge, just like during recovery the potential exceeds -70mV for a period of time before coming back to the resting state.


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Expression of red and green fluorescences in the same tissue
In this article (https://jcs.biologists.org/content/122/14/2351), especially in Figures 1 and 2, they show the expression of GFP and red fluorescence in the same tissue, and I feel like that red fluorescence is present where GFP is expressed (though weaker than where GFP is absent), but I wonder why it's not yellow? Usually, when these two are expressed in the same cells (in this case, GFP is in cytoplasm and red indicates a membrane protein), the yellow color is observed, not like this. In this article, I feel like I see some red below green if that makes sense...
If anybody knows what this means, please give me some advice!
Thank you.

These images are not typically taken using color cameras. They are taken using grayscale cameras, using filters that allow the excitation wavelengths to hit the sample and the emission wavelengths to go to the camera.
For visualization, these black and white images are often put into the red or green channel in a digital image (TVs and computer monitors make color by mixing different amounts of red, green, and blue light: RGB). If you have red and green together that shows up yellow to a human eye, but that doesn't mean any yellow light is involved: it's just perception.
If you don't see yellow in these images it's because the red and green emission were not in the same place.


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Are mosquitoes attracted to blue lights in particular?
I've been confronting the fact since childhood that mosquitoes are attracted to lights, especially blue lights. Now I know that all insects including mosquitoes are attracted to bright light but I never got it verified that if they are specially attracted to blue light or not. Is it true or just another urban myth?

It is not an urban myth. UV and blue lamps are good insect attractants. They have been used for many decades in insect traps, and these too work for mosquitoes. These lamps are routinely used in ecology at insect sampling sites. In some cases, such as with diurnal moths, yellow lamps can also be good attractants. The reason why UV is applicable is because insects are equipped with three photoreceptors, namely the UV-, blue-, and green-sensitive photoreceptors. Below you can see the spectral sensitivity curves of the genus Apis, which is typical for many insects.

As to why they are good attractants is probably variable across species, because it would depend on the neurological encoding of this information. For instance, some species may use this information to determine night and day, or may be superstimuli for nectar as used by plants to advertise themselves for pollination. Or it may simply be for some other reason.

Nice answer. +1. However, it could address the OP's question about mosquitoes more directly. I'd suggest updating with some specific evidence about mosquitoes if you can find something.


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How difficult is it for wild birds to find food?
This question came to my mind when I was wondering if my parrots would have it better on the outside than with me. Also, is starvation a significant cause of death at different stages in a bird's life cycle? Obviously, this is an open ended question due to the many species and different habitats, but I wanted to know what the answer is in general.

If you live in the Costa Rica rainforest then your parrot may be better off living outside in the jungle.If you live in downtown New York City then your parrot is better off living inside with you.Starvation , predation and accidents(especially in urban areas) are three main causes of early death in many species.


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The new DNA study showing that we have two DNA codes and not only one unique code
I am looking for a study that i read maybe 2-3 years ago that i cant find at the moment.
Scientist has always believed that humans only have one unique DNA code that makes us who we are, but a couple of years ago scientist found that we actually have two DNA codes, something that the scientists called mysterious and that this changed what we always have belived regarding humans uniqe DNA code that makes us who we are, now this was not true anymore with this new finding, since we have two codes which means that who we are could be more complex and not only be information stored in one DNA code. I cant find this study when i look for it on google, do you know which study i am speaking of? i would like to find it again, so that i can see if there is any updates by the scientists, and i also think it is extremely interesting and don't want it to get lost, i forgot to save it in favorites before.

This is not about epigenetics is it? Defenitely know for longer than 2-3 years but otherwise might fit what you're looking for.

Perhaps you are referring to so-called "duons" (dual-use codons) discovered by Stergachis et al.. This paper was published a bit more than six years ago. A recent paper within the last 2-3 years references duons implicated in photosynthesis.
Duons essentially extend the idea that conserved coding DNA encodes proteins, but can in fact also preferentially encode sites which bind transcription factors, at the same time. DNA can code proteins as well as code that controls regulatory regions, which in turn are switches that control how proteins get made.
Disclaimer: I am a contributing author in the linked Science paper.

Thanks but thats not it, im talking about a whole new DNA code beside our orgiginal discovered DNA code. The author speaks about our individual traits not necessarily being defined by our original DNA code and the whole thing being mysterious.

I'm lost. But I hope you find the answer you're looking for.


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DNA methylation and the validity of the definition of epigenetics
I am currently studying a textbook that presents the following definition of epigenetics:

Epigenetics is defined as heritable changes in gene expression without changes in the DNA sequence.

The authors then claim the following:

DNA methylation is a stable and inheritable epigenetic mark. This genetically programmed modification is almost exclusively found on the 5' position of the pyrimidine ring of cytosines (5mC) adjacent to a guanine.

Given these two excerpts, it seems somewhat contradictory to define epigenetics as heritable changes in gene expression without changes in the DNA sequence. After all, the DNA sequence is comprised of nucleotides, and it is these nucleotides that are modified during methylation (for instance, the addition of the methyl group on the 5' position of the pyrimidine ring of cytosines adjacent to a guanine), right? So, is it not technically true that the DNA sequence is changed? Or is what they're saying that, although the nucleotide is changed (such as in DNA methylation), the base pairs are unchanged (I'm unsure if this is true, just hypothesising)?
I would greatly appreciate it if people would please take the time to clarify this.

A methylated nucleotide is the same nucleotide, for the purposes of base-pairing events. The methylated base will be paired with its Watson-Crick opposite after replication, for instance (and methylation will even persist after replication).

The Methylation will change the individual nucleotide(s) and persist after replication. However the order of the base pairs does not change, so the information in the DNA will still remain , and the base pairs remain with their same partners.For an analogy consider a hardcover book as the DNA . Then the author of the book signs the cover. The signature is like the methylated nucleotide. There is now more information on the book cover but the message inside remains the same.

Most of the DNA methylation in gametes is erased. However, not all the histone codes or DNA methylation patterns are completely erased and that may provide some transgenerational inheritance.


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Relationship between bacteria size and temperature?
I'm, doing a research in a TOC (total organic carbon) degradation in a BAC (biologically active carbon) filter for the grey-water treatment. Recently, I started to wonder if there is a relation between bacteria size and temperature. If anyone know any research paper or did a research by himself/herself where such relation has been checked, it would be of a great help.
Thanks in advance.

There is a negative correlation between growth temperature and genome size for prokaryotes, which may be driven by selection for smaller cell size overall in warmer environments. Sabath et al., 2013 provide a good discussion:

Smaller cells tend to have smaller genomes in both prokaryotes and unicellular eukaryotes (Shuter et al. 1983; Lynch 2007), for reasons that are not fully understood (but see Dill et al. 2011). This correlation suggests that cell and genome size are functionally related, such that an evolutionary change in one would induce an evolutionary change in the other. Previous studies have hypothesized that reduction in cell size could be advantageous, either to optimize surface-to-volume ratio for uptake of scarce nutrients (Dufresne et al. 2005; Giovannoni et al. 2005; Moya et al. 2009), or to decrease predation by bacterivores or bacteriophages (Yooseph et al. 2010). Similarly, we speculate that bacteria adapted to high temperature could be subject to selection favoring smaller cell size, which also requires smaller genome size—regardless of gene content.


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Understanding the ECG waveform with respect to Lead Positions
I am really confused about the Representation of potential in an ECG graph.
First i will ask what is on the vertical axis? (I guess it is electrical potential in millivolts)
But again it changes for various positions and the graph takes a different shape. These are called Lead positions ( correct me if i am wrong )
I don't understand why the waveform changes for different Lead positions. Basically I do not understand how the ECG machine works in relation to what happens in the heart ( i.e. the action potentials from SA nodes and so on...)
This diagram shows what I meant.
How am I supposed to interpret the data if it is different depending on direction.
I will be grateful if someone can also provide some information on the cardinal directions in these cases.
Thanks!


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Why are smaller mammals more prone to cancer and tumors
especially rats and mice usually develop cancer and tumors very fast, reducing their life expectancy.
From an evolutionary point of view, how come that these mammals are so prone to cancer and tumors even though they reproduce at a very fast pace?
Shouldn't they develop a resistance towards these illnesses through natural selection?
Source: https://www.thesprucepets.com/rat-tumors-1238498

Can you please add a source supporting your claim? Additionally both animals are not getting very old at all (a lot of mice for example only 2-3 years), so what do you mean by "in just a few years"?

Counterpoint: the naked mole rat is a small mammal that rarely gets cancer.

Here's some clues: https://www.researchgate.net/figure/An-illustration-of-Petos-Paradox-Cancer-is-a-disease-of-uncontrolled-cell-growth-and_fig1_318415292 and https://www.google.com/search?q=mammal+body+mass+cancer+frequency&sxsrf=ALeKk03Cg1u3LNP84BVSv3Z71LdGxNvdMA:1583687276279&source=lnms&tbm=isch&sa=X&ved=2ahUKEwiXxKbsrovoAhWo0eAKHehgDg0Q_AUoAXoECGEQAw&biw=1227&bih=646#imgrc=8T1PWiyWvtwtLM and try the web search for the same words.

Do we really have data on anything other than lab rats and mice, which are often bred to develop cancer, or have cancer given to them for experiments?  WRT the natural selection argument, almost everything in nature gets eaten by something else long before cancer or other age-related diseases develop.

The topic is called Peto's paradox, you can find references to studies on the wiki page, here's a summary:
A rat cell is more likely to get cancer than an elephant cell in the same time span. Mice have cancers in 2 years as often as humans have in 60 years.

Studies find that 4 ton elephants have only 4 times more blood cells than a 12 gram shrew. They have big mammal cells that divide at a slower rate. Rats can double their body weight every 10 days when they are teenagers, as if a puppy with a lot of appetite could become an adult dog in 30 days.

It is thought that the genetic safeguards that have evolved to protect large mammals against cancer would slow the growth and reproduction rates of small mammals. For example, an elephant has 14 copies of the cancer suppression gene TP53, humans have three copies, hyraxes and manatees have one copy.
Evidence for the paradox began to emerge in the 1970's. Studies from zoos on many mammal species have confirmed that big animals are protected from higher cancer rates.
https://en.wikipedia.org/wiki/Peto%27s_paradox

You could also look at it as a large slow growing animal had better be resistant to cancer or it is unlikely to live long enough to reproduce, simply due to the high turnover rate the impact of cancer on a small short  lived line of animals is much less.


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How can I make legal mature female Cannabis plants to Flower in home during March (springtime)?
In December 2019 I purchased 4 Cannabis seeds Legally in Canada.Two of my plants are now about 100 cm tall. I am using wide-spectrum LED grow lights and have fertilized them both. I started with 16 hours light per day and now have cut back to about 12 hours per day.I was told that these seeds were not auto-flowering.These seeds were from Tweed and were labeled "Baker Street Indica". The leaves are all healthy and dark green. Now I would like to stimulate flowering. As our days are getting longer I want to trick the plants into its Fall/Autumn flowering cycle. Any good ideas ?

This question should be asked at [gardening.se].

I'm voting to close this question as off-topic because it is about gardening rather than biology. It may be on-topic at gardening.stackexchange.com but please check their guidelines before re-posting there.

Keep the plants in dark night for 12 h , 13h then 14h per night.
Keep the plants well fertilized with lower N , higher P and K.
Keep well watered with a dry period in between watering.
Keep the plants protected until the plants are ready to flower.


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How do viruses die outside of host cells?
I am posting a question that a friend of mine has asked.  My friend wrongly assumes that SARS-CoV-2 virus can be transmitted through blood, although there is no such evidence.  However, his question remains a valid one.

With so much news about COVID-19 all around us, I have been doing some
      study on viruses.  I do understand that viruses are not really living
      creatures.  They just have some genetic information, which they can
      pass on to the host cell, causing the virus to proliferate, and in some
      cases interfere with the normal functioning of the cell.  Outside of a
      host cell they are completely inert.  In fact they show all the traits
      of a non-living entity.  I get that.
My question is based on the following scenario.  Imagine there are two
      doors, next to each other.  Let’s call them A and B.  There is a door
      knob on each.  A COVID-19 patient sneezes near the doors, and some SARS-
      CoV-2 viruses land on each door knob (i.e. door A and door B).
      Unfortunately within a few hours someone with a cut finger touches the
      knob of door A and gets infected.  So far no dispute.
Fast forward 5 years.  In the meantime the knob on door B never got
      cleaned/wiped.  In other words, the inert viruses are still on the door
      knob.  Again someone with a cut finger touches the knob of door B but
      in this case the person does not get infected.  Why?
Obviously something happened to the virus during these 5 years that
      caused it to lose the ability to pass on its genetic information to the
      host cell and replicate.  What exactly happened?

Addendum:
We received a response for the query that seemed reasonable to us but was voted down, and presumably deleted by the author.  Fortunately I was able to recover a screen capture.  To keep the discussion going, I would like to temporarily include the response here till a better response is posted.  Here it goes:

This isn't very professional, but there are the basics. Viruses are obligate parasites, which means they can't live outside a host (in this case, a cell) for long. Viruses get damaged as everything else, the damage taking many forms, such as hydrolysis, photolysis, free radical damage, reaction with other molecules (like detergent), conformation changes, dehydration, maillard reactions, and changes induced by heat of labile molecules (like decomposition). All types of damaging processes happen at an increased reaction rate with increasing light and heat. Viruses have rudimentary repair mechanisms if any, so it's a matter of time before they become inactivated. A damaged virus entering the body wouldn't be able to do much harm if any, as their genetic information would be damaged beyond repair, and so, not able to be replicated to make more viruses. Their proteins and genetic bits would still trigger an immune reaction and immunize against intact and not very damaged viruses (which is why damaged viruses are used in vaccines). Those damaged viruses that remained outside just become microbe food.

Yes, disputed. The virus is not circulating in the blood stream (as far as we know), it is replicating in the cells of the airways.

Any answer for the basic question: what causes (non-living) viruses to die outside of host cells?

They don't die since they are not alive.

Please do not post text as images as these cannot be indexed by the search and found.

I don’t think that including a deleted response in a question is appropriate. If the person deleted it you should respect that. And a question is a question, not a discussion to “keep going”. Finally, it is not acceptable to post text as images as it discriminates against those with visual difficulties.

What exactly are you looking for in an answer? As far as I can see, the response you received (and added a screenshot of) looks like a good enough answer to the question in your title. But if it doesn't answer the question in your mind, you should probably edit your question a bit.

A similar question has been answered here: https://biology.stackexchange.com/a/89953/55506


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Can I pellet DNA back from dissolved state?
I have a dissolved plasmid pellet in water. Can I pellet it again by centrifuging it at 13000 rpm? If not, why?

Only by centrifuging?

Is this a homework question? have you done any research on this? Could you share your findings here?

Hi Alex, It wasn't homework question. After centrifuging a while, the concentration of the plasmid reduced a bit.  (1.7 ug to 1.35 ug). Couldn't find a proper literature on it. So I thought it is worth asking.

No, you cannot pellet dissolved DNA with ultracentrifugation.
Yes, you can recover a pellet with additional treatments, similarly to how you got it in the first place; only instead of your input being homogenized cells, or tissue, or extract, or whatever you used to obtain your DNA, it would now just be your aqueous solution of DNA.
For instance, you may have performed a TRIzol extraction to separate your DNA into an aqueous phase, prior to spinning it through mini prep columns to elute your purified DNA in water. You could perform the procedure again and you'd have your pellet once more after the final alcohol (ethanol or isopropanol) precipitation step.
The key idea with pelleting DNA (or any nucleic acid) is to make it insoluble; this is achieved with by using alcohols and salts. If it is soluble, nucleic acids cannot 'come out of solution' to form a pellet.


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Why is gastrin not acing paracrine manner primarily, when it acts mainly on cells nearby its release?
Gastrin is released by G cells and stimulates Parietal cells to secrete hydrochloric acid. Why is it not acting in a paracrine fashion instead of endocrine?

Is this question based on the content of a course?

Nope, it is not.

Paracrine signalling would mean not merely that gastrin is signalling the same organ, but that it is signalling nearby cells in the same organ - so that a few parietal cells close by respond, while the others perhaps would ignore the signal because maybe the paracrine signal would be degraded.  While the distinction is not absolute - there are shades of gray in all these things - blood gastrin tests are commonly done and medically relevant ( https://medlineplus.gov/ency/article/003697.htm ).  Because you can look at gastrin level as a whole-body characteristic, it is certainly appropriate to call it an endocrine signal.
Though their role is less emphasized, bear in mind that there are gastrin-producing G cells in the duodenum as well, and gastrin affects other digestive organs.