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How can a nucleotide falling *outside* a binding site affect a transcription factor's ability to bind to said site?
In this paper regarding a polymorphism within the AQP7 gene and its potential effects on one's metabolic profile, the authors use a luciferase assay to confirm that the alleles of this SNP have a definite impact on the expression of AQP7 in the presence of CEBPB, but the SNP itself falls outside the predicted CEBPB binding sequence:

The only thing I can imagine is a second transcription factor that cooperates with CEBPB has a binding sequence that overlaps this SNP, but I see no mention of such a thing in this paper. If this SNP truly affects the binding of CEBPB, then wouldn't the corresponding binding sequence have to extend through this SNP?
Edit:
To quote the paper, "A gel shift assay was then performed to investigate whether the A-953G SNP affects C/EBP binding. Compared with the radiolabeled oligonucleotide carrying the 953A, the one carrying the -953G variant showed a 30+/-7% reduced binding to C/EBP"
And here is the gel shift assay:

As far as I can tell, even if the scientists had reason to believe that this SNP affected CEBP binding in this region, it shouldn't be beyond science for someone to hypothesize how that is.

The authors of the paper presumably do not say — I assume you have read the discussion and this is the case — because they have no experimental evidence that bears on the question. They are professional scientists and are behaving as such. We can all think of possibilities, but it is hardly fruitful to discuss them without evidence.

Did they assess binding of CEBPB to the two different promoter sequences? Have you looked up what other factors are known to bind this promoter? There isn't enough information here to give a non-speculative answer without doing a lot of extra research, but the short answer to your question at the end is 'no' — there are many ways that SNP could affect expression, only some of which involve altered binding of CEBPB.

@David they state, "measurement of mRNA content in
adipose tissue and functional studies in transfected cells
clearly support a biological role of the -953G variant in
negatively modulating AQP7 expression by reducing
C/EBP-DNA binding" so apparently they had reason to believe that this SNP affected CEBP binding despite not falling within their predicted binding site, so that doesn't really follow what you're saying

@David You say that a scientist wouldn't extrapolate beyond the evidence and yet seemingly thats exactly what is happening here unless you can give we an alternative explanation

@tyersome see edit

No. They are just stating what their experiment shows. A results in B. Their experiments do not show WHY A result s in B, and so they leave it at that.  Some authors might present possibilities in the discussion. For whatever reason, these authors do not. It could be that they don’t want to appear foolish suggesting something that turns out to be wrong, or they didn’t want the referees of the paper to ask why they didn’t do experiments to test a suggestion, or they have an idea and don’t want to be scooped. But in professional science, if you stick out your neck…

@David Well even if these scientists didn't wish to include any postulations in their publication concerning this, I still wish to know what can be said outside of the paper. When I said "I see no mention of such a thing in this paper" it wasn't to imply that the authors left something out or that they had an obligation to speak on it, my question stands regardless of whatever is or isn't in the paper I cited.

If you have a question about the indirect influence of DNA regions on transcription factor binding, I think it would be better to pose in general terms, rather than relate it to a particular paper, which in any case few members of this list are likely to read. But you need to show evidence that you have thought about it yourself first.

@David from your very first comment you had no interest in actually answering my question, but rather you would much rather talk down to me as though I don't know what a scientific paper is. This is neither my first time reading a paper, nor my first time asking a question on stackexchange. "You need to show evidence that you have thought about it yourself first" yea thats exactly what I've done here. If I may ask, what to you merits "showing you've thought about it" if not citing exactly where the question arose? Additionally, the question has been answered, do not reply to me again.

I think the question is fine as-is. The question title asks about a general concept; the body of the question shows what motivated OP to ask the question and demonstrates that they've thought about it enough to rule out some obvious counter possibilities. I think it's fine that OP doesn't quite gather on their own the importance of structure in binding to DNA sequences, because a lot of general textbooks gloss over or fail to mention this when talking about recognized sequences, hence the question and resulting answer.

Thank you for the edit — that makes the question much clearer and helps it conform to the expectation that questions will be self-contained (not requiring users to visit other sites). However, please read the sites Code of Conduct — you may find David's approach frustrating and feel insulted, but he made no personal comments. Your last response is crossing that line and I encourage you to delete it. ——— David holds questioners to very high standards, but he has contributed many answers and they have been consistently excellent.

This is an answer to the general question posed in the title and not what is happening in the specific case of C/EBPβ.

How can a nucleotide falling outside a binding site affect a transcription factor's ability to bind to said site?

Transcription factors (TFs) associate with a specific shape of DNA. Two binding motifs that are identical at the sequence level may have different helical conformations due to torsional strain associated with flanking sequence context or proximal protein binding. See Figure 1 of Inukai et al. 2017 1 for an overview of the factors that affect TF-DNA interactions beyond primary DNA sequence:

TF-level features: (A) Several TFs can display binding specificity for multiple, distinct nucleotide sequence motifs. Motifs shown are examples of two motifs bound by the bispecific human forkhead TF FOXN2: FHL (red box) and FkhP (blue box) binding site motifs; motifs were obtained from UniPROBE (Accession Number UP00521). Interactions between (B) TFs and (C) TFs and non-DNA-binding cofactors can specify distinct binding site motifs from the monomeric TF motif.
DNA-level features: (D) DNA modifications, such as 5-methylcytosine (left), can modulate TF binding. (E) Numerous TFs use DNA shape readout, such as minor groove width (depicted by red arrows), and rotational parameters such as helix twist, propeller twist, and roll, as part of TF–DNA recognition. (F) Sequences and features outside of the binding site motif (depicted by blue box), such as GC content and / or DNA shape, can modulate TF– DNA binding. These features may immediately flank the core binding site, or may extend more distally from the motif. (G) Genetic variation in either the TF protein sequence (depicted by orange star, middle) or the DNA binding site (depicted by X, right) can alter TF–DNA binding.

References

Inukai S, Kock KH, Bulyk ML. Transcription factor-DNA binding: beyond binding site motifs. Curr Opin Genet Dev. 2017 Apr;43:110-119.

Thank you, situation B was essentially what I had imagined might be the case but this does broaden my horizons


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Is there any animal known to produce structures of both keratin and chitin?
I began with thinking about the similarities between keratin in its hardest form (fingernails, horn sheaths) and the chitin that composes the exoskeletons of some few beetles I've seen in my life. To my eye the two materials seem to have comparable properties. Then I found out that tarantula hair is also made out of chitin, so in more aspects than one it seems that chitin and keratin have convergently evolved.
I understand that chitin is a carbohydrate while keratin is a protein, so there's no commonality regarding the origin of the two, but I am curious as to whether an animal has ever been demonstrated to produce both compounds in some capacity?

Some fish and some salamanders are capable of making chitin.

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Ion Chromatography System For Extracting Aminoacids from Microalgae
I am interested in extracting aminoacids from microalgae after having ruptured its membrane and carried out proteolysis. After some research, I came to the conclusion that ion exchange chromatography is the best for a medium scaled extraction of aminoacids. However, considering that the tool is quite prohibitive, I was wondering if it were possible to make a small scale DIY version of it, in order to, get a feeling of how it works and what parameters it needs. Even though, I am not sure this question can be asked here, I do wonder how I could make a DIY ion-exchange chromatography system. Even though, a straight-forward answer would be appreciated, I would really value just to hear small tips on it.
Other "side" doubts:

How can I "stick" the ionic resin to the tube's wall?
Do you know of any online sources that will help me give the system the correct pH parameters in order to achieve optimum net charge?
Am I not approaching this correctly, is ion exchange chromatography not the solution?

I do apologize if this question isn't meant to be here. If that is the case, I would be grateful to have the question migrated elsewhere. I will only need to extract these 20 aminoacids (which are, basically, the 20 aminoacids in human metabolism).

Are you trying to extract free amino acids or proteins? I'm afraid free amino acids would be a very small fraction of the total content of the cells, and you'd have to get rid of a lot of junk before doing ion exchange chromatography. You're definitely going to need some sort of pH meter to ensure the mobile phase is at the correct pH. Salt concentration will also be an issue. The beads which are the stationary phase are just packed into a column, you don't have to adhere them in any way - there's a frit at the bottom that keeps them from falling out, but allows fluid to pass.

@MattDMo Free amino acids though I will first add some hydrochloric acid in order to break the proteins. Lipids are also going to be a problem.

HCl may help break some proteins up a bit, but it won't digest them down to amino acids alone, if that's what you're trying to do. To prepare your sample, I would first lyse the cells using an appropriate lysis buffer (with protease inhibitors if you wish), then centrifuge the lysate and only analyze the supernatant. That will help get rid of some of the cell walls, DNA, lipids, etc.

@MattDMo Yes, I did forget to mention centrifugation. What would you suggest for the chromatography system? ion exchange systems are too expensive ...

I've never purchased a system, so I honestly don't have the slightest idea what they even cost.

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Help ID snake near Deming NM
This snake is in our yard, south of Deming NM, in Luna County.
Approximate length is about 3 1/2 feet.
It moved slowly at the time, but was being picked on by a couple of medium-sized birds.
It is basically black with a black, narrow head.
The body and snout have pale yellowish markings.  On the body, the yellow is individual scales, so almost spotted.  And on the snout, more like lines or stripes.
I have some good photos, and even videos, but it says the files are too big - need to be under 2 giggleburps or something and I don't know how to do that.

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

Though a full body image would help a lot, I feel certain that it is the desert king snake scientifically known as Lampropeltis getula splendida. This species is seen in most parts of New Mexico and is not venomous. It primarily feeds on rodents, lizards, birds, snakes and eggs.
Here's a link to a website with more details on this species and other snake species of New Mexico: http://www.nmherpsociety.org/reptiles/snakes/lampropeltisgetulasplendida/index.html
Here's a variety of different photos of the desert king snake from different angles (but different ages, sizes and pattern varieties of the same species).


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Summation on muscles
I am learning myology and encountered 2 problems in tetanus and summation:

Unfused tetanus is just a continual summation of twitches if I am not mistaken. However, is it a MUST for summation / unfused tetanus to constantly increasing muscle tension from the photo (the graph) i.e. is this the definition?

Since we are in unfused tetanus when we hold something, and I can’t feel my biceps are constantly increasing in contraction / tension. (to my understanding, complete tetanus is when we are lifting up very heavy things only as it utilizes too much ATP)

Can I say the muscles are in tetanus during contracting (lifting), and also in tetanus during constantly contracted state (keep the thing holding up) Since tetanus is just a frequent action of sliding filaments, which is common in both actions?

Also, during tetanus, I don’t need to shorten my muscles anymore (just holding something still), but myosin heads are still power-stroking to shorten the sarcomere/muscle, may I ask how to explain this?
Thank you very much.


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Where are neurotransmitters secreted?
As far as I know, neurotransmitters are proteins, so they should be secreted from the cell body of the neurons.
However, when I checked online, they say neurotransmitters are secreted in the axon terminal (pre-synaptic terminal). This is due to the incoming nerve impulse to the axon terminal, hence 'exciting' something to secrete the neurotransmitters with the help of ATP (abundant in mitochondria).
May I know what is the true location in which neurotransmitters are secreted?

It's usually helpful to include a link to where you found a particular piece of information, so other users can decide whether it is valid or not. This is better than 'checked online, they say....'.

There are proteins (in truth, small peptides) released by neurons, but these are not the most typical or canonical type so I don't know where you got that information. Wikipedia has a list. Most are amino acids or derived from amino acids. They are transported into vesicles and then released when these vesicles fuse with the plasma membrane.
Neurotransmitters have to be released in the axon terminal. That doesn't mean that neurons can't also release growth factors and such in the vicinity of their cell body, but the entire function of a neuron is to transmit a message from one place to another (after some processing that occurs based on received input). Neurotransmitters are the way that message is released for most neurons, and axons are the typical "output" structures of a neuron.


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what powers power strokes
I am wondering what really powers the myosin head to undergo the power stroke to push the actin filaments towards the M-line. I have 2 thoughts:

when ATP in the myosin head gets hydrolyzed, the energy released is stored in the head. This energy powers for the power stroke.

when ATP is hydrolyzed, inorganic phosphate and ADP leave accordingly (90deg--> 50deg --> 45deg), the conformational changes of myosin head proteins cause the power stroke.

I think (2) is more plausible as the order of actions (moving actin filaments by 6.7nm + 1.3nm in order) is more 'conventional'(wiki), rather than a single action (using energy by ATP hydrolysis, a 1-step boost of energy).
However, if (2) is really correct, then may I ask what is the energy released in (1) used for in the myosin head, does it just simply fade away as heat energy?
thank you very much.


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What is the name of this sea creature?
I found this creature on the beach in San Diego. It is 8cm long and the end to the right is the mouth. The underside is exactly the same as what is visible. What is the name of this species.

This animal is a sea cucumber. It is probably a "sweet potato" sea cucumber (Molpadia arenicola). Here is a useful link describing this animal with pictures quite similar to yours:
https://mexican-fish.com/sweet-potato-sea-cucumber/

Welcome to Biology.SE! You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

@tyersome I have a question about the accepted behaviour in this site. If an answer is correct but very short like this one are we supposed to edit the answer with photos and references or should we write a new answer?

@trinitrotoluene — I'm not sure there is a clear standard, but anything that results in a better answer is good. Constructive editing is always acceptable (and your suggestions will be reviewed). I would personally give the original answerer a day or so to respond and then post a better supported answer if they don't. You could also ask about the etiquette for this in the [chat] or post a question on [meta]. I had a quick look in the latter and didn't find anything related, but I could easily have missed something ...

@tyersome thank you for the insight. This was the most relevant answer i could find on meta. It seems it is best to discuss such changes with op in comments before editing.

@trinitrotoluene For an answer as short as this one, don't feel bad about adding a proper separate answer that includes citations and an explanation. For a longer answer that's just missing a citation you could comment or edit first, but it's also not a problem to write a new answer. We expect most answers here to be cited (some very basic biology that you would find in a "bio 101-like" freshman textbook probably doesn't need a citation, but I usually add a note to answers of mine like that to check a basic textbook, or at least link to wikipedia).

Thank you for editing, but please add a discussion of the features that lead you to this conclusion and upload at least one supporting image. If you do this, the banner can be removed from your answer and you will receive at least one upvote (mine). Thanks!


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What is the modern state of the theory of evolution?
When I studied biology at my medical school, we used to learn topics around a century old: the famous Darwin's voyage on "Beagle" to the Galapagos Islands, the classical triad of his Theory of Evolution, etc.
At the same time we were told that there is no evidence found in nature for many of these statements of his evolutional theory. For example, people studied wildlife around Chernobyl and found that no new species emerged due to much higher mutation rate as a consequence of radiation. On the contrary, there were no significant differences between the species living under elevated radiation level and those living in "normal" conditions.
Do these facts somehow influence our understanding of the theory of evolution? Are there any breakthrough findings which happened in the last 20 years that prove or disprove it?

Similar to http://skeptics.stackexchange.com/questions/2057/demonstrable-and-repeatable-examples-of-evolution, and probably a better match for that site.

Some books may be written on this topic.
Evolution is not only speciation and boundaries of species are more or less arbitrary. About Chernobyl - read also this paper.

Wow, you were told complete BS. :-(

I think that BS is a mild word for that sort of total deceit (ie. LIES).

These sound like the sort of things you'd learn at Oral Roberts University (being a total caricature of what the theory of evolution actually says...).

I think the question as it stands currently is too broad. The "fact" about animals around Chernobyl is also pretty much a giant straw-man, radiation certainly increases the mutation rate for exposed animals, but you still wouldn't expect that to cause new species to develop in those extremely short timespans. Evolution takes a lot of time, it doesn't happen over night.

I wanted to have it a little bit broader than usual to get a nice answer and to have a good search entry for Google :)

My friend Brightblades is right in one thing.  It seems your teacher was working off a caricature of what the theory of evolution actually says.  First of all, you should read Sklivvz's excellent answer at this question.  Now to address the elephant in the room, the accident at Chernobyl only happened in 1986.  That was only 26 years ago.  In that timeframe, noticeable effects in an animal population really would not be at all noticeable.  Furthermore, the paper cited by Marta Cz-C actually shows that there have been some changes (in fungi though, not animals).

fungi seem to interact with the ionizing radiation differently from other Earth’s inhabitants. Recent data show that melanized fungal species like those from Chernobyl’s reactor respond to ionizing radiation with enhanced growth. Fungi colonize space stations and adapt morphologically to extreme conditions. Radiation exposure causes upregulation of many key genes, and an inducible microhomology-mediated recombination pathway could be a potential mechanism of adaptive evolution in eukaryotes.

Read the rest of the paper for more information on how there have been some other slight changes to fungi at Chernobyl as well as other locations throughout the world.
Now I am going to repeat a bunch of stuff from one of my web pages that talks about evolution.  This web page is set up mostly to deal with creationist arguments, however, the caricature is so severe as to warrant this.  As I said earlier, evolution is a population phenomenon.
Evolution acts upon heritable variation of characteristics, and you can only have variation of this sort within a population. A single individual organism, at least if its a multicellular eukaryote, has a fixed genome. It can't change what it has inherited. But a large number of organisms can all have different genomes, and can disseminate variation via inheritance to the next generation. It is upon the population as a whole that evolution acts, with various mechanisms coming into play to remove some variations from the population, and propel other variations to numerical dominance within the population. The organisms in question remain part of that population, and within a generation, those organisms don't change. But the moment a new generation is produced, dissemination of variation can result in the appearance of a new feature in one or more members of that population. If that new feature leads to greater reproductive success for the organism possessing it, that feature spreads through the population, as more and more future offspring inherit it. Over time, the population changes, and more and more organisms with new features appear within that population.
Understanding inheritance basics and mechanisms for changes (genes), we have all that is needed for the appearance of cladogenesis events. Split a decent sized population of living organisms into two, and let's call these new, separate populations A and B. Now let a barrier be erected between population A and population B, so that individuals from one cannot reproduce with individuals from the other. This barrier can be an insurmountable physical obstacle, for example, but this need not be the only form such a barrier can take. Now, first of all, there is no reason whatsoever to think that population A and population B will start off in identical states to begin with. After all, those two populations were derived from an original population comprising lots of organisms with different genomes, and the likelihood of population A and population B being identical at the start of this process is vanishingly small. Then, once our barrier is erected, and our populations are allowed to reproduce separately from that point on, there is no reason to think that those populations will move in the same direction in the long term. Indeed, it is far more likely that they will be subject to different environmental and ecosystem influences, and those different environmental and ecosystem influences will shape the long term heredity of those populations. Indeed, that's all that natural selection IS - it's a single, concise term used to encapsulate all of those environmental and ecosystem influences succinctly, and additionally to encapsulate the fact that those influences affect the inheritance of characteristics within a population over the long term.
As a consequence, any two separated populations of living organisms, that originated from a single population, will diverge from each other. If the extant influences on those two populations are sufficiently different, that divergence will take place more rapidly. Eventually, we will arrive at a point where those two populations become sufficiently diverged from each other that individuals from population A can no longer produce viable offspring with individuals from population B, and vice versa. When this happens, we have a speciation event. Indeed, this has been observed taking place in the wild AND in the laboratory, and has been documented in the relevant scientific papers. So, if anyone wishes to assert that there are 'magic barriers' to speciation or other cladogenesis events, then reality doesn't agree.
You will not have any animals giving birth to any radically different animals as a result of radiation.  Most changed sue to radiation will not provide any particular advantage to an animal anyway.  Also, a change may also be dependent on a previous change and require many generations to fully manifest.  All this was demonstrated by the long term evolution experiment led by Richard Lenski at Michigan State University.
So in essence, your teacher was just plain wrong.  As for the findings of the past 20 years, we are always learning more and more.  For instance, there has been an explosive capability in DNA analysis and sequencing, which has only provided more support for the theory of evolution.  A mechanism that Charles Darwin could not have had any idea about in his day and age, yet it perfectly supports his conclusions.  Again, read the answer provided at Skeptics.

+1 Great answer, but a minor technical note on the barriers part of your speciation example. These are not necessary, and sympatric speciation is a pretty active field of research right now. So the answer might mislead people into thinking that a physical barrier is necessary for speciation when it is not.

Perhaps the biggest advance since you studied evolution has been the sequencing of DNA and it's exhaustive analysis and decoding by computers and mathematicians.
Previously the proofs of evolution were geographical, anatomical, genetic, fossil, and a variety of other proofs.
Today there is also a vast library of genetic information.
You, judges. police, doctors and families all trust genetic tests for parentage, they provide incontrovertible proof of family relationships.
Here are 33000 sequenced species. https://www.ncbi.nlm.nih.gov/genome/browse/#!/overview/
If a single one of them showed that it had appeared spontaneously and was not related in an evolutionary tree, people would be amazed, evolution would have been disproved, 2+2 would make 7, people would be confused.
Fortunately all the 33000+ species sequenced recently since 2000 have proven an inherited relationship between all species in a very orderly and hyerarchical evolutionary tree. They find where many genes arise, how humans diversify and new genes appeared, what genes we share with mammals and lizards and fish.
It's a bit like having 33000 forensic pathology tests all in agreement that evolution is very real, it's like the block chain of bit torrent, DNA code is a very powerful method of understanding evolutionary relationships with massive precision and statistical depth.
Big surprises in evolution have happened too since 20 years, such as neanderthal DNA in humans, discovery of feathered dinosaurs and many flying dinosaurs species, 4,6 billion year old stromatolite fossils, and many others.

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Help in understanding a sentence about TCR-MHC interaction and immune synapse formation

T-cell co-stimulatory and co-inhibitory molecules (collectively named co-signaling molecules) play a crucial role in regulating T-cell activation, subset differentiation, effector function and survival. Following recognition of cognate peptide-MHC complexes on antigen-presenting cells by the T-cell receptor, co-signaling receptors co-localize with T-cell receptors at the immune synapse, where they synergize with TCR signaling to promote or inhibit T-cell activation and function.

I'm not sure I understand the second sentence. The language is a little confusing to me. Does it mean that after a TCR binds to a peptide-MHC complex, other TCRs present on the cell gather around that TCR? Does it mean that one TCR can bind more than one peptide-MHC complex (which, as far as I understand, isn't true)?
Here's my paraphrase of this sentence:

Following recognition of a cognate peptide-MHC complex on an antigen-presenting cell by a T-cell receptor, co-signaling receptors co-localize with (other) T-cell receptors at the immune synapse, where they synergize with TCR signaling to promote or inhibit T-cell activation and function.

Is it correct?

Does it mean that after a TCR binds to a peptide-MHC complex, other TCRs present on the cell gather around that TCR?

Yes. Other TCRs bind other MHC/antigen complexes and they all cluster together, forming an immunological synapse.

Does it mean that one TCR can bind more than one peptide-MHC complex (which, as far as I understand, isn't true)?

No. TCR:MHC bind 1:1.
Your final paraphrase is correct.


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What is the difference between fragmentation and true regeneration?
I read in my book that Planaria (flat worms) undergo true regeneration.
Fungi, filamentous algae and protonema of mosses multiply by fragmentation.
What is the exact difference between fragmentation and true regeneration ?

Regeneration is the ability of a creature to repair or regrow an organ after cutting it.
Not all creatures can regenerate.
If you cut a human hand it won't grow to a full human nor the human regrow a new hand
Some salamandras can regrow their tail if amputated but the tail itself won't becoma a salamndra
Planaria, Star fish, and plants can regenerate if the amputated organ has regenerative cells. The original organism will regrow the organ and the organ will grow a full organism.
Fungi, filamentous algae and protonema of mosses do not regenerate when fragmented in the sense that there is no real organ to regenerate. For example, the mycelia of Fungi is composed of many hyphea, creating new is independent of loosing them

Thanks for your contribution. You seem to address only the definition of regeneration, and not the difference it bears with fragmentation. Further, answers need to be backed up by sources, preferably references to papers from reputable journals, to allow others to background-read on your material.


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#Gateway Cloning How does gene of interest replace ccdB genes?
I knew that Gateway cloning used a site-specific recombination method, but I still cannot figure out how does gene of interest actually replace ccdB genes? Bacteriophage site-specific recombination
Does the paper explanation somehow clarify what I'm confused about?

Welcome to Biology SE! Thank you for showing your own attempt to answer this question. It would be helpful if you could state that this is a review paper on bacteriophage lambda site-specific recombination, and point to a specific section of the paper or quotation from the paper that you think might contain the answer to your question or that you are confused about.


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Strong activation of MAPK signaling pathway
I am reading a paper named "Mathematical models of protein kinase signal transduction". In that paper, I encountered a condition called "strongly activated pathways".
In that section, I need to calculate signal duration time for the strongly activated pathway. For strongly activated pathway, concentration of phosphorylated kinase at step $i$ is
$X_{i} = \frac{X_{i}^{max}R(t)}{K_{Mj}+R(t)}$,
where $K_{Mj}$ and $X_{i}^{max}$ are constants. $K_{Mj}$ is effective Michaelis constant of receptor, and $X_{i}^{max}$ is the maximum concentration. Here, $R(t)=Re^{-\lambda t}$
In the paper, it says signal duration $\sigma$ can be calculated as
$\sigma=\frac{1}{\lambda}\ln{\left(2+\frac{R}{K_{Mj}}\right)}$.
In the paper, $\sigma$ is defined as
$\sigma = \sqrt{\frac{Q}{I} - \tau^{2}}$,
where $I = \int_{0}^{\infty}X_{i}dt$, $\tau=T/I$, where $T=\int_{0}^{\infty}{tX_{i}dt}$,  and $Q = \int_{0}^{\infty}{t^{2}X_{i}dt}$.
I first calculated $I$ and I got
$I = \frac{x_{i}^{max}}{\lambda}\ln{\left(1+\frac{R}{K_{Mj}}\right)}$.
In addition, I proceed to calculate $T=\int_{0}^{\infty}{tX_{i}}dt$, but I cannot find solution. The same goes for $Q$. Thus, I couldn't get the result of $\sigma$ as shown in the paper.
Is my approach wrong? or Am I lost at some point?

You might have more luck over at Mathematics SE. Personally, I don't know how to solve those integrals, but the folks over there probably will.


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Clonal selection theory, how does antigen reach lymphocytes?
Clonal selection hypothesis often defined by four basic principles of which first two are

Each lymphocyte bears a single type of receptor with a unique specificity.

Interaction between a foreign molecule and a lymphocyte receptor capable of binding that molecule with a high affinity leads to lymphocyte activation.

If 1) is true and lymphocytes are differentiated to respond only to a specific antigen, the quanitity of lympocytes for a given antigen must be as low as total lympocytes / total antigen receptors. For 2) to happen, the very rare lymphocytes for an antigen must physically touch the antigen.
How is 2) achieved, assuming that 1) is true, and probability theory is a thing?
Edit: This question was heavily critiqued but once more, maybe the reason for that is the wrong reason. What Zhi said in 2019 perfectly reflects my own thoughts about the usual model of immunology, However, one B cell producing only one specific antibody would be unlikely to rapidly find its matching antigen. I do not mind the occassional random person I do not know projecting their prejudice on me, but, again, maybe done for wrong reason?
Shi, Z., Zhang, Q., Yan, H. et al. More than one antibody of individual B cells revealed by single-cell immune profiling. Cell Discov 5, 64 (2019). https://doi.org/10.1038/s41421-019-0137-3

Welcome to SE Biology. Please finish reading the [tour] and consult the help on asking questions. You will see that you need to give evidence that you have tried to answer this question yourself. What texts have you consulted? What you state about the theory (now fact) is incorrect. Each lymphocyte does not “only respond to one antigen”, it only responds to antigens that can bind to its receptor — hence polyclonal antibodies. And if you think something is statistically improbable, you need to present an argument that is at least partly numerical.

This is the role of antigen-presenting cells, which are in charge of carrying samples of antigens to the secondary lymphoid organs (lymph nodes, spleen) where lymphocytes live.
Once activated, B and T cells can activate each other through B-cell presentation and T-cell dependent activation.
It's also important that, for B-cells, the anti-body that they produce is still modified during clonal expansion through affinity maturation. This is essentially very fast mutation and selection that fine-tunes the antibody. So, there doesn't have to be an exact match to begin with, just a reasonably good one that will be improved during expansion.

Thanks. Exact information transmission in immune system is very fascinating. Similar to peer-to-peer networks in computer science, for how two nodes find one another, which is a very hard problem still being worked on. Jerne's original work called it "the immune network".

If antibodies as "packages" exist in 10^17 per milliliter serum, and they can magically connect antigen with lymphocyte through a sophisticated information relyaing mechanism, maybe similar approach can be used for P2P networks actually.

Actually major difference in p2p network is "antigen" wants to be known. So, query flooding requests are likely exactly analogous to antibodies in how they're already being used.


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Why are monocots more advanced than dicots. Shouldn't more complexity mean more evolved?
Features like pith, endodermis, pericycle, medullary rays and secondary growth are not present in monocots. How are monocots still more advanced?

”more advanced” seems subjective, here. Can you link a source for that claim or provide more explanation?

After seeing hutchinsons classification this question seems wrong , the categories of monocot and dicot are not correct to group 'types of angiosperms' and to conclude that one of the groups is more evolved or primitive . Sometimes it's the plants of monocot which happen to be more developed while it's dicots in some cases .

short answer no advanced is subjective, to a beetle having an exoskeleton might seem more "advanced"

Yeah , for a land animal  it is strength which helps it in fight  situation .while for a bird which has less land animal enemies due to its flight , having strength is not useful for some birds and hence some  are small making flight easier and have bright colours to attract mates . These two traits can't be compared since they are developed depending upon the different environment they live in


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What is the nature of seedless fruits?
Can seedless fruit be produced in nature without humans interfering with the fruit? And would that be considered a spontaneous mutation?

Is a mule "seedless fruit"? What might the difference be? Whether there's a spontaneous mutation or a hybrid that cannot reproduce doesn't matter, since the vast majority of these will not even be recognized by anyone (they can't propagate.) Furthermore, fruit can be seedless without genetic abnormalities, but based on growth conditions (granted this is very hit or miss.) Have you never found a seedless apple? (I have. I peel and cut up apples. Apples without seeds are not extremely rare.)

Questions here are expected to demonstrate prior research, like things you've read that motivate your question or show where you've gotten in trying to find an answer. It's also expected to look at existing questions here, for example searching https://biology.stackexchange.com/search?q=seedless

Some examples: https://biology.stackexchange.com/questions/19093/confusion-regarding-seedless-grape-and-the-normal-process-of-germination https://biology.stackexchange.com/questions/16754/how-are-oranges-in-the-us-or-anywhere-made-seedless https://biology.stackexchange.com/questions/80153/how-can-seedless-fruits-not-be-gmo - do any of these answer your question? If not, why not?

Seedless fruits are the result of a biological process called parthenocarpy – the development of a fruit without prior fertilization. Seedless plants are not common, but they do exist naturally or can be manipulated by plant breeders without using genetic engineering techniques.
Spontaneous mutations are naturally occurring alterations in the DNA due to slippage in natural processes. Also, as said before, The seedless plants are rare but can occur naturally ,i.e., without any human interference. So, yes it can be considered as spontaneous mutation.
If you cross a horse and a donkey, you get a mule. Mules can't reproduce — they are, in essence, "seedless".
Source: Seedless fruit is not something new


text:
CO$_2$ in photorespiration
"Photorespiration is wasteful to plants as it reduces the amount of CO$_2$ available for fixation" my textbook says.
But we also know that photorespiration takes place when the concentration of CO$_2$ falls within the leaves. But CO$_2$ is also released in photorespiration. Why can't the CO$_2$ released here be fixed by RuBisCO?

Could you please give a complete citation from your text book and identify it by name, title, and publication date. That way we can cross-check it. You will be aware that posters on this site need to demonstrate that they have tried to answer this question themselves, but haven't done so. Have you searched this site for other questions on "photorespiration"? If not do so, and in any case tell us why what you found does not answer your question.


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Do all Physocyclus globosus have pedipalps?
While browsing photos of Physocyclus globosus (short-bodied cellar spider) on iNaturalist, I noticed that some have pedipalps while others does not, they are not Physocyclus globosus or not all Physocyclus globosus have pedipalps?
(If you didn't know, here's a picture of a (presumed) Physocyclus globosus, see pedipalps?)

(photographed by me, CC0 waiver)

Welcome Stkimension. I'm not clear what you're referring to when you say "eye humps". Could you be referring to the pedipalps or chelicerae? Perhaps something else?

I mean pedipalps

Just readed the Wikipedia article, seems like only male one have pedipalpsEdit: wait some female have too

The type reference doesn't say anything about differences between male and female in the species. The 1893 revision into Physocyclus might say something

All arachnids have pedipalps (males, females, spiders, harvestmen, scorpions, pseudoscorpions, tarantulas, ticks, solifuges, etc). Pedipalps are part of their basic anatomy. In scorpions and pseudoscorpions the pedipals are the pincers/claws.
As mentioned in the other response, the male pedipals of spiders typically have enlarged ends for holding sperm, and so they are more noticeable. And the pedipalp size is often used to separate the sex of mature spiders for many species.
Further, the shape of the sexual organs (palps for males and the female epigynum) are observed with microscopic examination for species identification in most spider species.

In general, female spiders have small pedipalps with no enlargement on the ends, whereas males have larger ends tufted with hair for carrying sperm during mating, and sometimes, for display.  Maybe you aren't seeing the ones on the females because they are very small?  Not an expert here, but pretty good with invert zoo in general. Anyone else?

Original research: So turn out the one with bigger eyes thing have moulted more times (not just older but also they have to catch  enough preys as i seen a Physocyclus Globosus daughter moulted much sooner than her mother, but after some months the mother catched a huge prey and moulted just a day after that)
Sorry i can't upload the photo i took because i don't want to be doxxed but i've collected some moulted skin and will took a photo of it soon
thanks everyone
edit 20241103
WAIT no the one with bigger "eyes", longer legs and smaller abdomen are male


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Why low noise / low light camera on microscope?
I see plenty of back illuminated CMOS cameras, low noise cameras, high sensitivity cameras for microscopes.
What's the point? Is there a use case for it or is it pure marketing?
We have a lot of light available for microscopy imaging.

I've used such cameras for fluorescence microscopy and had to deal with very low-light, high-noise conditions, especially when looking at transient signals like calcium imaging or flavoprotein autofluorescence.
In many of these applications additional light would cause photobleaching, and for live-cell imaging additionally cause phototoxicity/death of the imaged cells.

so it's very specialized. and for fluo it should be CCD, right ? not a CMOS ? or cmos works too ?

@ker2x I'm not an expert in sensor engineering/physics, but I believe CMOS is more sensitive and can get you single-photon detection which is then amplified immediately, which is necessary to overcome the noise added in digitization.

@ker2x I wouldn't call fluorescence microscopy "very specialized". It's used in numerous fields, and in some areas of cell biology it's used quite extensively.

possibly confocal as well ? i don't know the intensity of the lasers

Confocal cuts light by a ton, yes. Effectively you get two attenuations of the light: going through the confocal first cuts it into a tiny window, then going back through it again cuts the emission light into a tiny window.

@MattDMo I suspect that ker2x was meaning specialized application for the camera, rather than the technique.

Nearly all modern image sensors are CMOS, and most reasonable-sized sensors are also back illuminated.  Even if you don't need the sensitivity, you're probably still going to use one because that is what you can buy.


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Can instincts disappear after a long period of non-usefulness?
I recently dived into the topic of instincts and now I have a question, where I haven't found anything about.
There's this thesis (I think mentioned here amongst others) that, through epigenetics, learned instincts can be passed along in genes and can over time be permanently integrated into the genome.
But...
Why is there no mentioning about how instincts can disappear over time, if they're simply not useful anymore? Or is it just not possible?

If its like any other genetic trait, there needs to be selective pressure for it to be counter-productive to be weeded out. Merely not being useful is not necessarily sufficient. though I suppose over extremely long periods of time it may get diluted out by mutation if it presents no beneficial or ill consequences.

@DKNguyen - That would make a good answer.

OP: The Russian fox farm experiment would give you a lot of information on the loss of instinctive behavior through selective pressure.

@anongoodnurse That's super interesting. I had no idea there was an experiment being run like that and with such definitive results showing themselves so quickly.

@DKNguyen - A solid example of your very on-point  answer. The back story of the experiment is also very interesting. :)

so basically how does the evolution of behavior work. simple question do you know  how tissues or organs are lost in evolution

@John what does that have to do with behavior?

Because behaviors are lost in the same way, it can take a long time to lose a an organ or tissue if it has no direct detriment. it is lost through drift.

oh, thanks. very interesting. I guess, I'll read into that somewhere soon

If it is like any other genetic trait, it will only be weeded out if there exists selective pressure that makes it counter-productive. Merely not being useful is not necessarily sufficient. Though I suppose over extremely long periods of time, it may get diluted out by mutation and propagation of those mutations if it persists in having no beneficial or detrimental effects.


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What is the approx. diameter of a completely "folded up" human DNA molecule, in inches?
The human DNA molecule would be about 6ft if stretched out to a straight line.
I'm curious what the diameter of the DNA molecule normally is when it is "all scrunched up" or "bundled" up, inside the nucleus of a human cell.
(I heard it was 30 billionths of an inch.)

Are you after the diameter of the double helix or the diameter of a chromosome? both are easily searchable.

We don't use inches in science. If you are a "student of biology" you need to get used to the metric system. If you need to convert to space shuttle disaster units, there are resources on the internet.

here measure it yourself, the scale bar is 1 um https://www.researchgate.net/figure/Metaphase-chromosome-plates-and-karyotypes-of-male-A-and-female-B-Phayres-flying_fig9_278095129

Can you cite some sources for your "6ft" fact and your "30 billionths of an inch" claim?

That's flying squirrels John.

As phrased the question is a bit confusing. In the most literal sense the diameter of a DNA molecule doesn't change much. Also, there isn't much bare DNA in the nucleus. It's largely wrapped around little spools made of protein called nucleosomes. The chains of nucleosomes are wrapped together to form chromatin fibers which make up the chromosomes. The chromosomes pull together into multiple 3-d blobs in the nucleus. Is it the diameter of those blobs that you are looking for?

Based on this picture, Chromosomes range from 2 to 12 micro-meters μm.
1μm is nearly 1/25400's of an inch
The 10-base system is more popular for science, and inches are not standard for science, but if they were, your answer would be 3/25400's to 1/2540 range.
For reference, standard writing paper and standard copy paper is about 100 μm, 0.1mm, 1/254's.


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What are the different factors involved in ageing?
This is a big edit of the previous question
Thanks to first comments and answers of the previous question, here is a more specific question:
An organism faces ageing. This ageing is linked with differentiated stem cells, who are not able to duplicate indefinitely. They reached an Hayflick limit. At some point, the lack of stem cells able to duplicate correctly enters the degradation of the organism.
Now, given this information, my documentation showed factors of ageing:

Loss of Telomere during replication: At each replication, the lack of telomeras enzyma in a differentiated stem cell triggers the loss of some of the telomere. At the moment all the telomere is lost (when the number of duplication reaches the Hayflick limit), the cell enters senescense.

What are other factors that involve in the ageing of an organism? I'm specifically interested in:

Factors linked to the organism behaviour

Not in:

Factors linked to agression (this part would be too important)

In Factors linked to the organisme behaviour, could be identified:

Skeleton degradation: do degradations of skeleton exist and how do the body take care of the skeleton?
Muscular degradation: musculare degradation does not seem to occur as long as minimal physical effort is done
Healing: this is not a complete repair-process, as healing often leaves marks: what is the reason of such partial achievement?

EDIT
One more question: Is the theory of gene-based ageing based on some specific genes, or only on the alteration of DNA by external causes (radiations, raidcals...)?

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

Please only ask one question at a time, and read the Help to find out what types of questions are acceptable here. Those regarding hypothetical situations are not, and medical rather than biological questions are more suited to SE Medical Sciences.

Sort of a "catch 22" ; anyone over 90 has some compromised health condition. And tradition is to put some cause on the death certificate other than "old".

@blacksmith37 But then why do anyone over 90 has compromised health condition?
David I understand the rule but I asked one question. The side question is only there for understanding of what I am asking

It's not really possible to answer this question the way you phrased it. Nothing on this earth is immune to physical wear and tear. A tractor can't get sick, yet it won't run forever if fuel is supplied. Much of the pathology in old age is simply the result of some kind of "wear and tear" (e.g. atherosclerosis.) If there was no wear and tear  of any kind (which is impossible), sure, anything could last forever.

@anongoodnurse But how does wear and tear come? Because a tractor is worn outby friction and temperature changes, but if you change the spare parts it will be functionnal forever. And our body produces by itself its spare parts (it produces new cells all the time)

No, you can't change out worn tractor parts, that's evading the issue. The body does not make "spare parts". You can't grow a new heart or new kidneys. There is friction in blood vessels from blood rushing by. You can't escape Physics, and I don't want to argue. Reading will serve you better than arguing.

@anongoodnurse Please calm down I am not arguing, I am trying to understand the concepts and physical laws behind ageing: is it some sort of entropy?

From the [help/dont-ask], If your motivation for asking the question is “I would like to participate in a discussion about ______”, then you should not be asking here. Please familiarize yourself with how this site works by taking the [tour] and then reading through the [help] pages starting with [ask].

@tyersome Please don't put your own appreciation on my question like that: I am asking a question, I got partial answers so I ask for details. This is not a discussion.

@tyersome About your comment and to people saying it's a stupid question, I would like to highlight that Calico Labs work on that since 2013. So this is at least a plausible subject, thus a question on that subject is not stupied

I see no comments saying this is a "stupid question" — it is however poorly written. Some examples: you ramble over multiple subjects, include irrelevant details, and use made up words (e.g. elderness — that is why it was underlined in red when you typed it in). You are also expected to demonstrate that you have done some background research before posting. If you want a positive response, I suggest reading through the [help], doing some research (document this with citations to reliable sources), and then rewriting (make sure your edits address the feedback you already got).

I’m voting to close this question because it has multiple problems (documented in comments from multiple users) including multiple questions, no evidence of prior research, and being likely to generate opinion/discussion. Despite community input poster has not attempted to make improvement.

@tyersome To be honest I have only got input as "question does not apply" and that's it

@totalMongot I think the biggest issue is that it seems to be mostly an invitation for discussion, rather than a specific, answerable question. That doesn't make it a bad or stupid question, it's just that its more of a discussion/philosophical question rather than a biological one. The philosophical part is about proximate/distal causes and which to emphasize. Any level of explanation is defensible; which level is "best" is an opinion.

I voted to close this question, so it is clear that I do not condone it. However I feel that one should show a little simple kindness to posters whose first language is not English and help improve their questions and their fluency, by correcting questions. Poster: Note 1. that in English we talk about "ageing" (the process) and "old age" (the condition) — "elderliness" exists only in dictionaries. 2. Your use of pathology is incorrect. I am not an expert on medical terms, but in general speech you do not suffer from a pathology, but a disease, a broken ankle etc. 3. Try to keep it simple.

@David THank you for th input, I edited the question also for the other issues (too broad, opinion based..)

Edit added to the question to focus on the different parts of the body that suffers from degradation

Another rephrasing of the question could be :
"are humans potentially immortal?"
which we (as eukaryotes) are not, because of the end replication problem in DNA polymerase activity- due to the unidirectional nature of DNA synthesis. During semiconservative replication the end of the lagging strand  (3'-end) of the DNA is not possible to synthesise by polimerase δ (POLD1, POLD2, POLD3, POLD4), which  discontinuously synthesizes approximately 150 to 200 base pairs long okazaki fragments in 5'-3' direction (DNA-POL δ always moves in 3'-5'over the template, but the template for the lagging strand is 5'-3' itself). This causes periodic breaks in polymerisation, and the reattachment needs RNA-primers to be present.
The last RNA primer at the 3' end of the DNA sits at a distance of about 70-100 bp to the very 3' end of the DNA, therefore about 50- 100 bp of DNA length is lost every cell division. (see http://genesdev.cshlp.org/content/26/11/1167)
To not loose coding (Exons) nor regulatory (Introns,etc) DNA sequences, telomere are present at the end of the DNA. They are repeat sequences of TTAGGG in vertebrates that loop to protect the terminal regions of chromosomal DNA from progressive degradation and other false altercation.
However since these telomere get shorter in somatic cells every division cycle , you could argue humans have a natural "due date". Luckily the germline is potentially immortal due to the activity of a reverse transcriptase-enzyme Telomerase, that elongates telomere; badly its also active in most cancer cells.
Telomere where discovered by Barbara McClintock who was who was awarded the 1983 Nobel Prize in Physiology.

I think it's a mistake to overly associate telomeres with aging of organisms rather than aging of cells.

Thanks for the answer but I don't really understand : in the beginning you say "we are not immortal as eucaryote" (which means? sorry I 'm not good at biology ^^) and in the end you say that we are potentially immortal thanks to telomere?
@BryanKrause Interesting, are elderness diseases linked to organism aging or cells aging?

@totalMongot Well, by the contrast I'm making by definition elderness diseases are a part of organism aging. It's just that this answer conflates that with telomeres which have some role in limiting how many times cells divide, it's just overly simplistic to think that's the specific process behind aging of an organism.

So if I understand correctly, the problem in the process you described is cancer?

I found in some article  (I doubt of them BTW) that telomere shortening might also affect stem cells: is it true?
https://novoslabs.com/causes-of-aging-stem-cell-exhaustion/

Hello, could you please gives more hindsight about the specificity of eucaryote that makes us vulnerable to the end replication problem in DNA, compared to others? Is it because non-eucaryot organisms do not have DNA (because no nucleus in cell)?

Of course the have DNA!


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What diseases affect small arteries similar to atherosclerosis in aorta?
I have read about artherosclerosis and I understand that it is a phenomenon caused by external lipidic cells coming into the body and creating a plaque that, when it breaks, will obstruct the artery.
The fact that it only affects "big arteries" is my understanding from wikipedia:

Most of the time, patients realize that they have the disease only when they experience other cardiovascular disorders such as stroke or heart attack

Actually I might be wrong because it also mentions:

These symptoms, however, still vary depending on which artery or organ is affected

My question is: Why do artherosclerosis affects only big arteries like aorta or cerebral arteries, and not the entire bloodstream grid of the body?
PS: I also read articles from INSERM but they do not mention where artherosclerosis happens.

Where did you read that it only affects large vessels? Can you please provide a quote and a link?

@anongoodnurse Thanks for your comment, I might have misunderstood. I quoted some elements that led me to think that, and other elements I've just noted

I don't understand what is making you think that from anything you quoted, nothing at all says "only large vessels". Strokes and heart attacks mostly involve fairly small vessels.

You are not reading enough to understand atherosclerosis even fairly superficially. You can get an answer by reading the first hit on Googling peripheral vascular disease.

@anongoodnurse Thanks, indeed by googling it I found that these diseases are in any sort of vessels and the main cause is atherosclerosis
Would you like to answer the question by stating that every part of bloodstream grid could be affected?

I think this question, which is purely about diseases, with no clear biological aspect, would be better asked on S.E. Medical Sciences.

@David - "...with no clear biological aspect..." Are you actually stating that medicine does not fall under the class, "Biological Sciences"? Can you please provide a source for that opinion? I must have missed that tidbit as an undergrad Biology major, a gras student in Molecular Biology, and medical school. I am sooooo inattentive!

@totalMongot - I'd be happy to, thanks!

@anongoodnurse Thanks to you as well
I guess David suggest that "where and when" a disease happens interests specifically medicine of the human body, while biology is a much larger domain. But I agree that m question is included in Medicine that is (nearly entirely) included in Biological sciences

Atherosclerosis can affect everything from the largest vessel, like the aorta, to small arteries with a diameter of <2.5 mm (this is labelled small vessel disease.)
Large vessels develop atherosclerosis early in life (in early childhood, in fact) and progresses rather slowly, but can be catastrophic (e.g. ruptured aortic aneurysms), whereas small vessel disease tends to occur in older individuals, and can progress more rapidly. Atherosclerosis of large vessels is often associated with smoking and hyperlipidemia, whereas small vessel disease (often called Peripheral Vascular Disease or Peripheral Artery Disease) is more often associated with diabetes, hypertension and is higher in races other than Caucasian.
There is a truly vast amount of information in the literature on atherosclerosis, but I have never seen a claim that it occurs only in the large vessels. However I have seen articles that can give that impression by focusing only on large vessels, so I can see where that misunderstanding comes from.
Large and small vessels atherosclerosis: similarities and differences
Understanding Peripheral Vascular Disease
Small vessel coronary artery disease: How small can we go with myocardial revascularization?


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How many cuts are done during CRISPR-Cas9 in one cell?
In a CRISPR-Cas9 experiment, the protein cuts the site matching the cRNA part of the gRNA. My question is: How many cuts are possible if multiples sites matching the cRNA are found in the cell?
Especially, considering DNA is made of multiple chromosomes, if more than one chromosome have a site matching the cRNA, will they all be cut? Does it depend of the quantity of Cas9 protein brought in during the experiment (meaning is some Cas9 protein "consumpted" at each cut)?

The main limitation on guide RNA design is the availability of a PAM site (NGG for Cas9) proximal to the target sequence. Addgene has a great article on gRNA design that may address some of your questions.

@acvill Thank you I'll check the link. But I'm not sure that it adresses the question: the question is not about designing what sequence the gRNA should have, but what are the possibilities of sequence (everything - magic versus a pool of possibilities)

It seems like your question is less about gRNAs and more about oligonucleotide synthesis. Insomuch that gRNAs are just oligonucleotides, any gRNA sequence can be created by solid-phage chemical synthesis, either as a DNA construct to clone into an expression vector or as a ready-to-load RNA for use with purified Cas9.

@acvill thank you  the link you gave between oligonucleotide synthesis and gRNA does give me elements to search for. So every gRNA could be synthetized?

On a single molecule level, Cas9 from Streptococcus pyogenes cuts but does not move to other targets for a few days (Raper et al. 2018). In contrast, Cas9 from Staphylococcus aureus cuts multiple targets, though also it takes hours for a single round (Yourik et al. 2019). However, inside a cell, even S. pyogenes Cas9 is rapidly dislodged either by RNA polymerase (Clarke et al. 2018) or FACT histone chaperone (Wang et al. 2020). So even if only one Cas9-sgRNA complex enters a cell, it will be able to cut multiple targets. There are several methods to measure the efficiency of Cas9 cleavage of multiple target and off-target sites that differ in accuracy and sensitivity. The PCR amplification-free method, RGEN-seq, is the latest innovation in this field (Kuzin et al. 2021).
References

Raper et al. (2018) Functional Insights Revealed by the Kinetic Mechanism of CRISPR/Cas9. JACS, 140(8), 2971–2984.
Yourik et al. (2019) Staphylococcus aureus Cas9 is a multiple-turnover enzyme. RNA, 25, 35-44.
Clarke et al. (2018) Enhanced Bacterial Immunity and Mammalian Genome Editing via RNA-Polymerase-Mediated Dislodging of Cas9 from Double-Strand DNA Breaks. Mol. Cell, 71(1), 42-55.e8.
Wang et al. (2020) The Histone Chaperone FACT Induces Cas9 Multi-turnover Behavior and Modifies Genome Manipulation in Human Cells. Mol. Cell, 79(2), 221-233.e5.
Kuzin et al. (2021) RGEN-seq for highly sensitive amplification-free screen of off-target sites of gene editors. Sci Rep, 11, 23600.

Thanks but I have a misunderstanding: are'nt "However, inside a cell, even S. pyogenes Cas9 is rapidly dislodged either by RNA polymeras" and "So even if only one Cas9-sgRNA complex enters a cell, it will be able to cut multiple targets" contradictory?
I might have misunderstood, could you please clarify?


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What cells are secreting Wnt pathways and under which conditions?
Former question: Where and how happen these operations in the Wnt signaling pathway?
I have read about the signaling pathway on wikipedia:

Wnt comprises a diverse family of secreted lipid-modified signaling glycoproteins that are 350–400 amino acids in length.[11] The lipid modification of all Wnts is palmitoleoylation of a single totally conserved serine residue.[12] Palmitoleoylation is necessary because it is required for Wnt to bind to its carrier protein Wntless (WLS) so it can be transported to the plasma membrane for secretion[13] and it allows the Wnt protein to bind its receptor Frizzled [14][15] Wnt proteins also undergo glycosylation, which attaches a carbohydrate in order to ensure proper secretion.[16] In Wnt signaling, these proteins act as ligands to activate the different Wnt pathways via paracrine and autocrine routes

Where happen these chemical reactions described in this quote ?
My understanding is that they happen outside of cells, before the arrival of the Wnt ligand on the receptor that is located at the surface of the cell. Am I correct?
If yes, were does this happen precisely in the body? Where the ligand comes from?

EDIT:
From comments: The Wnt ligand is secreted by other cells and transmitted from cell to cell, this is an autocrine process.
The question is: Under which conditions does this process start in one cell?

Comments have been moved to chat; please do not continue the discussion here. Before posting a comment below this one, please review the purposes of comments. Comments that do not request clarification or suggest improvements usually belong as an answer, on [meta], or in [chat]. Comments continuing discussion may be removed.


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What is this insect, is it a butterfly?
I am not sure if this is the good place: I am wondering what sort of insect is in this picture. It is approximately 10 millimeters long and 15 wide with the wings.

I have found one of them each day for one week, in my flat, near the coast of France. Tonight I found three of them at the same time. I am wondering if they are dangerous/damaging....
Thanks in advance for any help

Welcome to Biology.SE! Identifications questions should also include the species-identification tag (done for you by MattDMo) and an estimate of the size of the organism. Please [edit] your post to include this essential information. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Looks more like a moth than a butterfly to me


text:
QA/monitoring in recombinant vaccine manufacturing
On a16z[0] podcast on vaccines[1], an interesting tidbit came up: vaccine manufacturing in cell cultures is expected to hit a major challenge in terms of quality control due to unpredictable behaviour of cells.
The issue was mentioned only in passing during the podcast, specifically Rajeev Venkayya[2] said:

First of all, we need to see if these vaccines can be scaled up from a manufacturing standpoint very, very quickly. And not just be produced at scale but also produced with a reproducible high quality.
This is one of the biggest challenges that you run into when making biologics at large scale, particularly when we're talking about hundreds of millions or even billions of doses.

I'm wondering how monitoring and quality assurance looks for cell cultures in an industrial setting. What are practical examples of what can go wrong with a cell culture that affect the final output (e.g. a vaccine) and how does one detect these issues? Is cytometry involved for "cell interrogation" or some more specialized methods are used?
I tried researching this question on my own, but quick googling didn't yield much. I'm a software engineer with deep learning experience, I look at this issue from a computer vision point of view and wonder if anything my field could do to contribute to solving this issue.
[0] a VC firm with a science leaning
[1] which is very good! https://a16z.com/2020/08/14/vaccines-vaccinology-renaissance-covid-pandemic-beyond/
[2] board member of Coalition for Epidemic Preparedness Innovations

Can you clarify what you mean by "observability" for cell cultures? It would help if you expanded a bit on the relevant points raised by the podcast, as it's an hour long and questions on SE sites should be self-contained.

Thanks for the comment! Unfortunately, this specific issue has been mentioned in passing so not much more detail is available to me but let me try to clarify the question. Specifically the use of "observability".

@MattDMo expanded my question. let me know if that helps!


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Narwhal tusk evolution
I was reading about whales and wondered why did only narwhals, among all other species of whales, evolve to have tusks? Is there a specific environmental reason, for example something unique about the Arctic environment that requires them to have a tusk for easier survival?
I researched a bit and found many reasons why narwhals have tusks (e.g. weapons for fighting other male narwhals to compete for mates, sensing the environment, attracting female narwhals, echolocation, stunning prey for easier hunting) but couldn’t find a reason why other whales do not have tusks.
Sources:
https://www.google.com/amp/s/api.nationalgeographic.com/distribution/public/amp/news/2017/05/drone-footage-narwhal-tusk-mystery
https://www.google.com/amp/s/ocean.si.edu/ocean-life/marine-mammals/why-tusk-real-life-unicorns-sea-and-tusks-make-them-famous%3famp=
https://oceanconservancy.org/blog/2019/03/08/exactly-narwhal-tusk/
https://scholarblogs.emory.edu/evolutionshorts/2014/04/25/the-evolutionary-significance-of-the-narwhals-tusk/

Can you tell us more about what you found out? https://www.google.com/search?channel=fs&client=ubuntu&q=narwhal+tusk+evolution  "Why not others?" would have to do with differences in selective pressures (operational sex ratios, ecological context, etc.) between ancestors of narwhals and their closest relatives ...

@BenBolker Thanks for the answer! Edited accordingly, is this better?


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Weird Black Worm (Possibly Flatworm?)
I was out walking one night (In Florida) when I spotted this creature sliding around in the grass. I believe it may be a New Guinea Flatworm, but not quite sure. Could anyone please provide a definite ID? Thank you!


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Evolution of Heteromorph Ammonites
I was reading about fossils and thought of this question: what was the purpose of the shells of heteromorph ammonites (for example, ammonites of the genus Nipponites)?
Wouldn’t the odd shapes of these shells cause more drag? So why did their shells evolve to be that way?

Some jellyfish travel with currents and tides, so the nipponites can travel further with more drag if the use currents. Crioceratites have an open spiral which makes sense, if they turn sideways they can travel faster than an typical ammonite with the currents, and if they turn edgewise they are about the same. Cool question it's a very complex biophysics and geometry topic.

I'm not an expert in functional paleontology, but it has been suggested that the specific shape of heteromorph ammonites could be related to hooking on to macrophytes or branched animals:

Examination of ribbing pattern and its resolution in various parts of
the living chamber in 11 species revealed that the ribs were less
developed and had some traces of wear on the inner surface of the
hooked chamber, being well developed both on the lateral and outer
lower parts. This could indicate that the adult animals were
semi-loosely hooked (Ancyloceras, Macroscaphites) or permanently
clipped (Scaphites, Hoploscaphites) onto either horizontal or upwardly
angled stipes of non-calcified algal macrophytes or branched animals.
Comparison of the adult mode of life with those of modern cephalopods
suggested that ammonites of the suborder Ancyloceratina had developed
a stationary brooding phase that could have several ecological
advantages over free-swimming monomorph ammonites.


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Winogradsky column and hydrogen sulfide
For a science experiment for school, I have set up 15 Winogradsky columns, and will be looking at the microbial growth inside the columns over a period of 25 days.
I have read that, due to gas produced by the microbes, it is good to leave the cap loosely closed to prevent an explosion from gas buildup. However, I have also read that sulfate-reducing bacteria that grow in the column can produce toxic hydrogen sulfide gas. Wouldn’t the hydrogen sulfide also escape in small amounts and pose a health risk? What would be the correct protocol to follow here?

Hydrogen sulfide can be toxic at high concentrations, however, the amount that your columns will make is likely very low, and will almost certainly degrade/oxidize into something safer before it hurts anyone (who isn't a small organism in the column!). It will noticeably smell bad at levels well below what is dangerous. So maybe just make sure that the columns are in a ventilated space.
Remember, what is happening in the column is basically just rotting organic matter, like leaving a bunch of food waste in a highly compacted, sealed environment. It is sort of intrinsically gross, but it isn't any more dangerous to your health than forgetting to take out the garbage for a month (actually, it's probably a lot less dangerous than that!).
For example, this guide says the following (after constructing columns with different inputs such as e.g. eggs):

You may have seen worms, snails, shrimp or other small organisms in the water, but probably not many (if any) in the bottle with the egg yolk, because hydrogen sulfide is toxic to most organisms!

So, depending on what you put in there, a very H2S-productive medium is likely to create enough H2S to kill tiny animals that are trapped inside the column. But apparently not enough to hurt large animals like you, as long as you don't huff the column.

You will smell H2S at well less than 1 ppm . Long term exposure problem threshold is about 10 ppm . I smell it when i stir up the bottom of my pond or aquariums. I have never heard of a toxicity problem with the levels of H2S produced in a natural environment .


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What is a metabolite?
I am a mathematician and work on metabolic networks as networks. But I could not find a proper definition for a metabolite? Are they organic molecules? can a gene or a protein also be a metabolite?

https://en.wikipedia.org/wiki/Metabolite

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, we expect you to demonstrate that you have done 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). At a minimum please tell us where you looked and what you learned. Thanks!

If you go by meaning that "organic"  means made in the organism by biological processes ,then in vitro metabolites are surely organic ,if the reactions are occurring in-vitro.https://en.wikipedia.org/wiki/Metabolism

Thank you, indeed I meant in general because in a paper I found it is an organic molecule, but from the below comment I found it depends on the context.

Why was this question closed? It seems to be relevant to biology and helpful to a general audience to investigate a solid definition of "metabolite".

yeah, I think many people who are not a biologist they might have these kinds of questions.

This definition of Metabolism is similar to most I've seen in biology textbooks.

Metabolism: the sum of the chemical reactions that take place within each cell of a living organism and that provide energy for vital processes and for synthesizing new organic material.

The broadest definition I would give for "metabolite" is any molecule that's part of or a product of a metabolic reaction. They are molecules, but not necessarily organic molecules (in the traditional sense). For example, any metabolically active cell is going to constantly generate inorganic phosphate as a metabolite of ATP hydrolysis.

can a gene or a protein also be a metabolite?

I suppose A protein could be considered a metabolite, but it would depend on the context. most people probably would not be talking about proteins when making reference to "metabolites" in general way. For example, an enzyme acting as a catalyst in a biochemical reaction would probably not be considered a metabolite of that specific reaction (since it's not chemically changed in the process). But in a metabolic model involving protein degradation, it would have to be included in some way. However, amino acids (the monomer building blocks of proteins), are often incorporated into metabolomic analyses, and could be considered important metabolites in many different cellular reactions.
A gene is not a metabolite by any reasonable definition. A gene is not a biological molecule, but a unit of hereditary information. One could argue that the nucleic acid molecules (DNA or RNA) encoding a gene sequence are metabolites, but as with proteins, it would really be context dependent. Also similar to proteins, the structural subunits of nucleic acid polymers (nucleosides and nucleotides) are often important metabolites involved in a great number of cellular functions.
Is all of that about as clear as mud?

Thank you MikeyC, now many things are more clear for me.


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Tree identification
I went to Araku few days ago and saw this tree in a garden .

Here are the leaves

I know the pic of fruits is a bit hazy and out of focus,but it's the best I have.

These trees were in a cluster ,behind a patch of Nerium shrubs beside the pavement of the garden.

Please provide as much detail as possible for the most accurate ID. If you have additional photos showing the leaves in detail, the bark, the general shape/size of the tree, etc. please include them. Please also comment on the relative sizes of the flowers/leaves/tree in your images and include any pertinent info about the ecology/environment of the tree (e.g., was it in a forested part of the garden, along a sidewalk, part of landscaping, etc. etc.) Thanks

Last picture is flower buds

This appears to be a flower of a tree in the Syzygium genus.
Because there are many species (1200+) -- many which are intentionally planted as ornamentals outside of their native range or have the propensity to become invasive -- I cannot confidently provide a more specific species given the garden location in which you found your specimen (and lack of further details).
I include, as an example, an image from the University of Connecticut of Syzygium jambos, which is not native to India, but is known to grow in nearby regions.

Notice the similar floral architecture to your specimen: dominant androecium (literally hundreds of stamens), whitish color, 4-lobed calyx, prominent hypanthium, etc. Multiple flowers also similarly cluster at the end of branches as in your photo.

Read more about S. jambos's floral description  here.

Sometimes-similar Eugenia cannot be totally ruled out based on your limited photos/details, of which 25 species occur in India. However, Syzygium still seems much more likely.
Overall, I can update my answer with more details once you've updated your post.


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Reason for partially double-stranded DNA of Hepatitis B virus
According to my school biology textbook and also Wikipedia, hepatitis B is the only Hepatitis virus to possess partially double-stranded DNA.
I found an image from here
What is the reason for the partially double-stranded DNA?
(It seems that it can be triple-stranded as well.)
I found this information in this research about duck hepatitis B virus

Similar to classical retroviruses, viral assembly begins with the formation of intracellular nucleocapsid particles that specifically package the pgRNA. However, all hepadnaviruses undergo a maturation phase during their morphogenesis that is characterized by the reverse transcription of the pgRNA prior to membrane envelopment and secretion as extracellular virions, rather than subsequent to entry into new target cells, as is the case for classical retroviruses (for a review, see reference 20). Thus, secreted hepadnaviral virions contain only the “mature” ds DNA, whereas intracellular pools of nucleocapsids contain nucleic acid species from all the intermediate stages of reverse transcription ranging from only pgRNA to single (minus)-stranded (ss) DNA as well as ds DNA, a fundamental observation made by Summers and Mason 2 decades ago (22)

What is the special advantage of having such a genome?

are there any other organisms with partially double stranded DNA or partially double stranded RNA as well?

I've edited your question slightly. "Reason for" is the way to express your question. ("What's the use of" is a vernacular expression implying that something has no function.)

I would recommend removing the second question. Hepatitis viruses with different genome structures are not closely related so there is no reason to expect that they would have similar structures.


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1% water solution of deoxycholic acid. How is it prepared?
According to Sigma, the solubility of deoxycholic acid is:

0.24 g/L in water at 15C

According to the FDA, Kybella (trademark) is a 1% water solution of deoxycholic acid.
How did they do this?

Which wikipedia site are you referring to?

[link]https://en.wikipedia.org/wiki/Deoxycholic_acid

Not sure this is really a biology question.

According to the sigma document you referenced (emphasis added by me):

"The free acid is soluble at 0.24 g/L in water at 15ºC, while the sodium salt is soluble at >333 g/L in water at 15ºC. Therefore, pH control is very important to the use of this product. Aqueous solutions precipitate as the pH is lowered to 5."

According to the FDA document (emphasis added by me):

"Each 2 mL vial of KYBELLA® (deoxycholic acid) injection contains 20 mg synthetic deoxycholic acid as the active ingredient and the following inactive ingredients: benzyl alcohol(18 mg), dibasic sodium phosphate (2.84 mg), sodium chloride (8.76 mg), sodium hydroxide(2.86 mg) in water for injection, USP. Hydrochloric acid and additional sodium hydroxide are added as necessary to adjust the formulation to pH 8.3."

The solubility of 0.24 g/L in water at 15ºC is determined by dissolution of the free acid in pure water. As you dissolve an acid in pure water, the pH will get progressively lower, and since this compound is less soluble at lower pH, it limits it's own solubility in pure water.
The sodium hydroxide in the KYBELLA is a strong base, which raises the pH and, when mixed with the deoxycholic acid, forms an aqueous sodium salt and water via an acid-base reaction. The conjugate base of deoxycholic acid in aqueous solution is deoxycholate. This portion of the compound remains unchanged, regardless if it is part of a free acid or a sodium salt. The sodium phosphate is a buffering compound which helps stabilize the pH and allows for finer adjustment to control the final pH to ensure it remains soluble.


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Is once per day the optimal sleep pattern for all mammals?
If a typical human body clock is 8 hours sleep, 16 hours awake, interested to know if any mammals have:

a 12 hour body clock (4 hours sleep, 8 hours awake)
a 6 hour body clock (2 hours sleep, 4 hours awake)

And very interested to know if any mammals' sleep patterns are on an "as-needed" basis - i.e. simply sleeping whenever tired, without ever establishing any particular pattern over the days/weeks

"typical human body clock is 8 hours sleep" - I recommend you to google "first sleep and second sleep" and how people used to sleep before 1800.

Dogs and cats regularly sleep for short periods during the day.  (And so do I, on occasion :-)) Then there are dolphins, which have only half of their brain sleeping at a time.

Thanks @BagiM very interesting. I did some googling as you recommend. Fascinating to read that the French used to sleep for some hours, wake around midnight for a few hours of housework or recreation, then go back to sleep for a few more hours. I'm not too sure how to verify any of these claims though. I wonder if there are scientific studies or 'go to' texts/resources that provide more rigorous evidence of sleeping patterns of humans and animals? Canonical papers preferably (but simple enough for a non-biologist to consume).

@stevec To find scientific studies on this topic search "segmented sleep" in scholar.google.com . There seem to be both studies of historical texts from various periods and antropological studies of contemporary preindustrial societies.

@stevec: Anecdotally, I do just that quite often - more in winter than summer.  I will sleep for a while, wake up and do stuff for a couple of hours, then go back to sleep.  I don't think it's at all unusual.  (I also work from home, so I don't have set working hours to force me into a perhaps unnatural pattern.)

Theres also a 4 hour cycle in humans, thats why we have meals every 4 hrs, and siesta make you live longer, i.e italy.

@aliential: Who is the "we" having meals every 4 hours?  Perhaps the British, with their afternoon tea, but it's hardly an American pattern.  More usual seems 5-6 hours between breakfast and lunch, anywhere from 5-8 between lunch and dinner, and 12 or so between dinner and breakfast.

@jamesqf "I will sleep for a while, wake up and do stuff for a couple of hours, then go back to sleep.". Would you do that for any sustained period though? As in weeks/months? I am very interested to learn of cycles that are not 24 hour cycles with one big clump of sleep (in either humans or other mammals). You could consider putting your ideas in an answer

@jamesqf i'm quoting a research publication from about 3 years ago on the subject of the discovery of a secondary body clock that accounts for meal regularity quoted as " scientists find new 4 hour body clock" thats what it sais, im french and the research made sense to me about humans having a regular rhythm every 4 hours.

@aliential: Yes, I do that biphasic sleep at least half the year.  Between roughly the fall & spring equinoxes, it is almost every night.  In the summer, with longer days, it might be about 1 night in 3 or so, and the waking period tends to be shorter.  As to making it an answer, this is just my own experience.  For an answer, I'd have to look up citations and so on.

@jamesqf a lot of references say: The circadian rhythm dips and rises at different times of the day, so adults’ strongest sleep drive generally occurs between 2:00-4:00 am and in the afternoon between 1:00-3:00 pm. Its very documented.

@aliential : Evidently none of those studies bothered to look at me :-)

So as we know that every mammal needs atleast some amount of sleep or a resting period to perform cognitive functions through out the their day, this however can vary drastically based on the mammal's habits, such as if they are herbivores or carnivores, their place in the food chain (if they are a predator or prey), their habitat, their body size etc.
Starting with humans (to set a point of reference), we ideally need 7-8 hours of sleep in a day. Getting less or more sleep than this ideal can have a lot of different consequences (ranging from feeling tired and foggy to heart conditions and even death). A study performed by a group of researchers to find out the ideal sleep duration in humans showed that just after 14 days the people getting 8 hrs of sleep showed average cognition and a healthy mind, those getting 6 hrs of sleep per day for 14 days showed a similar reaction time to a person with blood alcohol level of 0.1% (which is considered legally drunk in most places), and the group getting 4 hrs of sleep per day for 14 days were tending to fall asleep while performing basic cognitive tasks. This show exactly how important sleep actually is.
Now moving on to some other mammals.
A very commonly discussed example is that of giraffes. Giraffes generally exhibit a cycle of just 2 hrs of sleep per day, and some days they just tend to not sleep at all. A lot of factors contribute to their sleeping habits. Firstly since they are herbivores, and primarily feed on leaves, they need to eat a lot of leaves to get enough energy for their body, having a large body also contributes to this. So, they tend spend about 75% of their day just eating. Other than this since giraffes are prey and a good source of food for lions, they need to stay awake and alert at all times. Sometimes they will take little 10 min long powernaps (this is when they are the most vulnerable, so they don't do it often).
Carnivores however (like lions) sleep a lot more, due to their diets (just like us they feel sleepy after eating) and also since they are minimal risk of being attacked as they are on top of the food chain.
Next lets talk about some sea mammals, they have a hard time trying to snooze because of them being underwater.
Dolphins have very interesting sleep habits as they have to actively come to the surface to breath. Dolphins practice something called "unihemispheric slow-wave sleep", this basically means that they only rest one hemisphere(or side) of their brain at a time(so that they can be awake and asleep at the same time), this is what uni(one) hemispheric(side) means. Slow-wave sleep refers to the deepest phase of sleep, meaning when the one hemisphere is sleeping it is out like a lightbulb. This way dolphins tend to sleep a lot, they have sleep cycle of about 8 hours of sleep a day (resting each hemisphere for 2 hrs at a time). So the dolphins you saw at sea world last year could have been half asleep (literally).
Some birds also practice this uni hemispheric sleep.
I can't think of any animals that sleep "as needed" because activities like sleep and wake are rhythmic and control various hormones and metabolic reactions of the body, this is primarily why we have sleep patterns so that other activities in the body can be done in a habitual manner. This is maintained by our "biological clock", which is the term used to define the natural sleep-wake cycle in animals. The biological clock is regulated by a hormone known as  "melatonin".
So yeah, these were some examples I remembered off the top of my head. I have provided some links to why sleep is important, ideal sleep habits in humans and other mammals and some other stuff for further reading.
Hope this answer helped you understand sleep better.
Sleep: a good investment in health and safety - https://pubmed.ncbi.nlm.nih.gov/19042703/
The Transcriptional Repressor DEC2 Regulates Sleep Length in Mammals - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884988/
How Animals Sleep - https://www.sleepfoundation.org/animals-and-sleep#:~:text=Giraffes%20need%20less%20sleep%20than,of%2030%20minutes%20per%20day.
Melatonin: what you need to know - https://www.nccih.nih.gov/health/melatonin-what-you-need-to-know
This is an animated video series explaining sleep in different animals (highly recommend watching this):
Part 1 - https://www.youtube.com/watch?v=HA1EPRbMMQU
Part 2 - https://www.youtube.com/watch?v=EJzUKsJ-uhA
Part 3 - https://www.youtube.com/watch?v=S4uX2KeEifM
Rare Genetic Mutation Lets Some People Function with Less Sleep (this might also interest you) - https://www.scientificamerican.com/article/genetic-mutation-sleep-less/


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What's the most recent common ancestor of reptiles and humans?
In the Phylogeny of humans and reptiles, what is/are some of the most recent common ancestors?

related: https://biology.stackexchange.com/questions/82206/why-arent-mammals-and-reptiles-considered-amphibians?r=SearchResults&s=14|11.8981, https://biology.stackexchange.com/questions/47957/why-are-turtles-classified-as-reptiles-and-not-amphibians/47968?r=SearchResults&s=15|11.3526#47968

I think that you are looking for the amniote common ancestor.
Amniotes are the group of organisms that have an amnion, a specific membrane around the egg, among other features. This includes reptiles, mammals, etc. but excludes amphibians and fish as indicated in your tree.
Wikipedia says:

The first amniotes, referred to as "basal amniotes", resembled small lizards and evolved from the amphibian reptiliomorphs about 312 million years ago,[7] in the Carboniferous geologic period. Amniotes spread around Earth's land and became the dominant land vertebrates.[7] They soon diverged into synapsids and sauropsids, which persist today. The oldest known fossil synapsid is Protoclepsydrops from about 312 million years ago,[7] while the oldest known sauropsid is probably Paleothyris, in the order Captorhinida, from the Middle Pennsylvanian epoch (c. 306–312 million years ago).

That citation 7 points to this paper, which used paleontological data to assign time estimates to various diversification events inferred from molecular phylogenies; this allowed them to approximately estimate the time of emergence of amniotes from the amphibian clade.

Could you please add in the [7] citation?

@MattDMo thanks, done.


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Why is my spirulina biomass getting destroyed in my new photobioreactor?
I have a 500L flat plate photobioreactor in my backyard. Whenever I add my culture to the PBR, after 3-4 days of growth, the culture becomes transparent and my biomass is wasted.
I add the stock at a 1:10 ratio (50 litres). My culture medium is Baum. The temperature varies between 12 to 25 degrees Celsius in 24 hours, and the pH is between 9 to 10. Circulation is done by an air pump and a water pump (for circulation of the biomass across the system, from one flat plate to the next).
Maybe it is caused by shock or the sheer stress of the water pump? Or something (like brass valves) releasing some toxic substance into the culture? What should I do?

Are you only growing spirulina? sounds like an infection of some kind to me.

Things to try - can you grow the spirulina elsewhere (i.e. not in your reactor, but in a jar or something similar)? This tests whether it is something to do with the reactor. Can you sub-sample from the reactor on days 1 -4 and get growth from those samples outside the reactor (also check pH etc at same time)? This tests whether there is a problem like infection in the reactor. Is your ratio too high - given log growth a 1:10 will consume all the nutrients pretty quickly - do you need more light. Does the temp rise too high inside the reactor (not air temp)? How about O2 concentration?

please add a bit more details about your setup,do you aerate the water,how do you fertilize your algae,where do you get water from for your setup?

please enlighten me what is baum?

@MaximilianPress It seems under a microscope. Only spirulina, but their springs were straightened by self-shading. We also changed the stock and water several times.

@bob1 Thank you. I'll work on it. The ratio for the first time was 1:20. The light is perfect (flat plate in the backyard). The mentioned temperature was the temperature inside the biomass. Aeration is done by an air pump and circulation is done by a water pump.

@trondhansen Same as before. We grew spirulina under the same conditions (water from water refinery kiosks (they are common in my city, as our drinking water is full of arsenic). We add all the materials (Baum) needed by the biomass at the beginning and aerate the system every 20 minutes with an air pump.

@trondhansen Baum culture described in Heinsoo, D. (2014). Cultivation of Spirulina on Conventional and Urine Based Medium in a Household Scale System. I do not recommend it.

Cyanophage? https://link.springer.com/article/10.1007/s10811-012-9853-x

@acvill Thanks, but I don't think so, since the sample is growing in the lab.