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How can animals defecate or urinate in fear if the nervous system seems to opposes it?
How do animals defecate and/or urinate in fear even though their 'flight or fight' response seems to oppose it? I have seen many cats and dogs urinate and defecate when they experience extreme fear. It also happens with most other animals in shock or fear including humans.
The 'why' is probably to deter predators which has been made excessively clear by my research but this is what is puzzles me despite my attempts.
From a book(made by doctors and teachers for medical exams ): Another website for medical exams
It is clear that sympathetic nervous system inhibits both these functions.
My teachers said that adrenaline is complementary to the sympathetic nervous system and has the same effects on the body.
But the real life observations seem to contradict.
Also this question:
Fear induced defecation does not clear my question regrading the aforementioned contradiction.

Not sure where you're getting these materials exactly, but I don't think anyone has called norepinephrine "sympathetin" for 75 years.

@Bryan Krause Probably because this is in context of sympathetic nervous system. In the chemical coordination chapter of the same book, it says "epinephrine/adrenaline and norepinephrine/noradrenaline" when talking about adrenal hormones

Even so, the only places I see the word used are (often sketchy) test prep websites. There are only 12 results on Google Scholar and many of those are duplicates/not actual papers. It's not as if the word is suddenly used when you start talking about the sympathetic nervous system, it seems like it's just used by some pathetic test prep materials that probably all copied each other.

It's overly simplistic to think of the sympathetic (SNS) and parasympathetic (PNS) as purely inversely activated; it's possible to activate both at once or suppress both at once. It's also overly simplistic to think of them as unitary responses; it's possible to activate parts of the SNS and not others, or parts of the PNS and not others.
Freezing, urination, and defecation in stressful situations are associated with corticotropin releasing factor (CRF, also known as CRH) in rodents. CRF is part of the response to stress and influences both parts of the autonomic nervous system. The effects of CRF are different in different parts of the digestive system (Taché & Bonaz, 2007; bold emphasis added by me):

In contrast to the inhibitory effects of CRF and urocortin 1 injected into the CSF on gastric and small-intestinal motor function, these peptides stimulate colonic transit and defecation and induce diarrhea through increased sacral parasympathetic outflow to the large intestine in female and male rats, mice, and gerbils

In humans, parasympathetic activation is also associated with some peoples' responses to trauma and PTSD, specifically the feeling of immobility or inability to act (Corrigan et al 2011).

Corrigan, F. M., Fisher, J. J., & Nutt, D. J. (2011). Autonomic dysregulation and the window of tolerance model of the effects of complex emotional trauma. Journal of psychopharmacology, 25(1), 17-25.
Taché, Y., & Bonaz, B. (2007). Corticotropin-releasing factor receptors and stress-related alterations of gut motor function. The Journal of clinical investigation, 117(1), 33-40.


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How are probes in capture sequencing synthesized?
In capture sequencing it is common practice to use a panel containing ~10,000 probes. How are these DNA molecules synthesized? I imagine that there is a way to do this in parallel, but I haven't been able to find a reference to this.

Yes, the oligos are synthesized in parallel on a microchip (or microarray). This is commonly based on phosphoramidite chemistry. Various methods can be used to control which areas of the chip are open to attachment of a new nucleotide, including "light control, electochemical, and inkjet printing methods."

source: Stack Exchange

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

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Allowed Deviations in fixed bond length and bond angles in peptides from the typical values
I am using frag builder python module to generate peptide structures to compute the interaction energy for ensemble of peptides of a given sequence for a fixed bond lengths and bong angles. However, the fixed bond angles are slightly deviating from the typcial values seen in the literature. For instance, the bond angle of $C_{\alpha}--N--C$ is less than the typical value of 121 degrees and the bond angle of $C_{\alpha}--N--C$  as produced by frag builder is 111.7 degrees. Hence peptide plane is still planar. Yet the distance between the two successive $C_{\alpha}--C_{\alpha}$ is 3.721 A. Is it quite wrong to deviate by 10 degrees?

I don't know "frag builder" protocol; can you please provide a citation? Building a conformer is relatively simple compared to subsequently energy minimizing it. Can you also hint at the size of the peptide, and what it's interacting with? The planarity of the peptide plane depends on how its moieties are H-bonding to other groups.

@Ryan Fragbuilder article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3961104/ . Size of the peptide I am working on various sizes of peptides such as 6, 10, 18, and 34. The planarity of the peptide bond is unaffected. as it is still planar.

@Ryan Also, it is just interacting with itself in a vacuum. I am minimizing only van der Waal interactions and electrostatic interactions.  I will extend this minimization with the solvation effect later.

Single-conformation descriptions of the native-state ensemble, under ambient conditions, are expected to have close to ideal geometries. This is a result from Statistical Mechanics; the probability of non-ideal geometries (say a given conformer $i$ with internal energy $E_i$ compared to a native/ground-state energy $E_0$) scales with their Boltzmann factors, $e^{-\beta (E_i - E_0)}$. But many backbone dihedral angles are isoenergetic, especially outside of tertiary structural constraints.
FragBuilder has fairly extensive treatment allowing for rotamer sampling and conformer regularizing. I expect you used its built-in energy minimization with the MMFF94 force fields, as in (code quoted from 1):
pep = Peptide(sequence)
pep.regularize()
print pep.get_energy()

So the question can be rephrased, can the dihedral angles $\phi$ and $\psi$ be more than ten degrees from their ideal values? And the simple answer is yes. That's well within the variation of conformations within a given rotameric energetic minimum.
Here's one study looking at these dihedral angle fluctuations in solution. It cites the Dunbrack library. In that paper, they study the dependence of side chain dihedral angles on main chain ones, and they sample angles $\phi$ and $\psi$ in 10 degree bins showing that a large variation in these angles is possible, especially outside the context of regular secondary structures.
I wanted to cite a current paper from a good theoretician, so I found this from DJ Wales. Here they use a state of the art sampling approach to generate a tripeptide library, whose statistics are compared to experimental structures. You can read their procedure, but I'll quote the relevant part here:

For each tripeptide, the low-energy conformations contain many $\phi$,
$\psi$ combinations, and the observed rotamers of the central amino
acid are averaged over these backbone configurations, resulting in a
backbone-independent library...Using tripeptide structures allows
local spatial effects on rotamers to be probed without interference
from stabilization in protein folds.

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Ecological regime shifts and natural resource variability
I am thinking of the interaction of two different uncertainties; ecological regime shift uncertainty and natural resource variability.
For example, for fishes, we know that the fish stock is exposed to an abrupt decrease in risk (regime shift). Also, there is always natural resource variability, which represents another source of uncertainty.
Are there any scientific evidence that natural resource variability increases/decreases after the occurrence of a regime shift?
I gave an example for fishes but it can be any sort of common pool resources.


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What is the Latin term for animals which dust bathe?
I have lost track of this term. I am sure that I encountered a Latin word (not a taxonomic word) which applies to all animals which dust bathe.
I fact, I am not even sure how to describe a word like this, cutting across species.

There are some words like pulverulent (adj.), Pulveratores (n.), pulveratrix (n.) (based on Latin  pulver- , pulvis meaning dust, sand, pulver) but OED gives them as obsolete and rare. They are ornithology terms to define birds that use dust bathing as a means of feather maintenance.

Thanks, that must have been the word I saw, I think.


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Are there any genetically modified GMO squash with a vine growth habit which grow back from the root?
When I cut Scottish thistles with scissors, the thistle grows back from the tap root.
When I accidentally step on squash vines, the squash vine dies.
I was wondering if genetics research has produced more robust foliage which withstands being stepped on. It seems like some cultivars of squash have healthier stronger stems and leaves, than other cultivars.

Hi and welcome. We ask for evidence of an attempt to answer this yourself when posting. Have you searched the internet for any such genetic modifications of squash? Do you understand the physical make-up of a thistle taproot and why it's able to regenerate top growth when severed off at the base? Neither the taproot nor the squash vine are foliage. Foliage is dispensable to a degree; plant vasculature is not.


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What is meant by the steady-state activation of a receptor?
I am reading a journal paper about the insulin-like growth factor 1 receptor. In this paper, there is the following statement:

Finally, we show that the IGF-IR and the PI3K subunit p85 and Akt are
detected in cholesterol-rich membrane domains under conditions of
steady-state IGF-IR activation and that phosphorylated Akt and IGF-IR
are detected in CEMs with IGF-I stimulation.

I am not sure what is meant by the "steady-state activation" of the IGF-IR receptor. I have searched the definition of steady-state with regards to proteins and I have read the following:

The ‘steady state’ is defined by a zero net change of a parameter in a
system. For example, the abundance of a protein might not vary during
the time of observation because rates of translation and degradation
are balanced. The cell is said to be at the steady state with respect
to the concentration of this protein.

However, in the context of this paper, I don't this is what steady-state refers to since they are talking about the activation not levels of the receptor.
Does anyone know what is meant by the steady-state activation of a receptor? I think it refers to the activation that occurs without any exogenous stimulation (e.g. addition of insulin/IGF-1 to cells). Any advice is appreciated.

Did you read the Methods section of the paper? That's where you'd find this information. It's possible they mean what you guess, but I'd expect that to be called baseline or constitutive activity or something like that instead; still, the best source is the methods section.

As mentioned above, it is best to check with Method or a reference paper.
One method might be to introduce mutations in the kinase domain of IGF-1R, thereby constantly increasing kinase activity.
Other possible methods include overexpression of the IGF-1R gene to increase the number of IGF-1R receptors in the cell and enhance signaling, deletion of genes for inhibitor proteins that regulate IGF-1R or genes that negatively regulate signaling.


text:
What really is an allele?
My textbook says:

genes which code for a pair of contrasting traits are known as alleles.

Then that means T and t are alleles. Further, it says:

Mendel also proposed that in a true breeding, tall or dwarf pea variety the allelic pair of genes for height are identical or homozygous, TT and tt respectively.

This line confused me, it will be of great help if you can help me out.

It would be helpful if you mention the full name of the textbook rather than saying "my textbook".

@NilayGhosh i am sorry, here is the link of the pdf of the textbook: https://ncert.nic.in/ncerts/l/lebo105.pdf  see the page number 72 of the textbook, definition of allele is given there and allele is written is bold letters.

That's a poor definition of allele. Alleles don't need to have anything to do with traits - different alleles can code for the same or different traits.
Alleles are simply different versions of a genetic variant. The most simple way to think of what an allele is the base pair (A, C T or G) which exists at a particular place in the genome. You have 2 alleles at any place, which can be the same allele or different. In your case, the alleles are coded as T and t - if both are the same, e.g. TT, then it's called a homozygous genotype, if they are different then it's a heterozygous genotype.

Thank you sir, i really appreciate your knowledge, i didn't knew what exactly is allele, but your answer made everything clear, thank you again.

sir is it possible to have a gene which is exact copy of another gene  (same in everything, including bases) or only different versions of a gene are possible ?

I don't know if I'm understanding the question correctly, but gene duplication is a common process.  Immediately after duplication there would be two identical copies of a gene in the same genome, although those two copies would usually diverge quickly.

Basically allele is an alternative form of gene. For example let us consider a ball. A ball has a property called color. Color has some alternative forms like it can be red,blue,black,etc. So in this case gene is the element which define the ball's color that is the property defining element of our body and it can have many different variants of properties defined in different individuals like the colors red,blue,black,etc and these respective variants of a single property are called allele. Let us consider a gene defining our skin colour(the property) then it can define blackish or white skin color(variants) then the gene has 2 alleles. Homozygous gene means that it has 2 same alleles or alternative form of genes on the homologous chromosomes like having 2 same alleles on homologous chromosomes defining oval face.

Thanks a lot! I wish I could upvote, but I don't currently satisfy the requirements to upvote.


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Cell culture contamination
I've been culturing my cells over 2 weeks and just yesterday these things popped up in my flask , I'm not sure if they're contamination or not.uesterday they looked white and today I found one of them in black .Any ideas on what these things are?

we would need a picture to in any way ID what you are seeing.

What kind of cells are those? My immediate first reaction when I saw the image was mycoplasma. Bleach them immediately and clean the incubator thoroughly.


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Can one use DSSP (secondary structure assignment) for short peptides of size 6, 10 and 18?
I have large number of PDB files of peptides of size 6, 10 and 18. I wanted to cluster the peptide structure based on the secondary structure. I used DSSP in mdtraj module in python to assign DSSP code to backbone residues of each peptide sequence of various sizes of various pdb files. My question is whether it is reliable to use DSSP for peptides?

Surely visual inspection will tell you. The PDB provides a viewer.  Alpha-helix prediction would be low hanging fruit.

It predicts incorrectly for some of them. That is why I am doubtful

Well in a way you know the answer then. But as I remember, DSSP assigns a conformation description to individual residues based on dihedral angle. That is not quite the same as predicting secondary structure for an extended region of a chain. Have you checked the original paper, and can you add an example of incorrect assignment?

They use electrostatic interaction between backbone $C-O ---  H-N$ and compare whether the value is less than some cut off value. I guess this creates the problem

you certainly can run DSSP as you did but the algorithm is designed for full length proteins but it will work on these short structures too.

At the moment your answer is just an assertion, lacking detail or supporting citation. It could be made into something more valuable by explaining the algorithm and what aspects of it cause it to fail with short peptides.


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Free energy difference between change in protein structure and its reverse?
I have seen in many articles that a protein variation (A- > B) and its reverse (B- > A) must have the opposite value of the free energy difference (ΔΔGAB = − ΔΔGBA).
But i’ve alse heard that in experimental data this is not true!
So i am a little bit confused; can anyone explain it? Which is the case?

Welcome to Biology StackExchange! The Gibbs free energy $G$ is a state function, hence the free energy difference of the reversal process $\ce{B->A}$ has the opposite value of the forward process $\ce{A->B}$, $\Delta G_{\ce{B->A}} = -\Delta G_{\ce{A->B}}$. Please edit you question and include references (articles, books ...) where they state that this is not true. Otherwise, we cannot know what exactly they mean, and also cannot give you any meaningful answer.

I have modified your title to indicate the type of “variation” you seem to be referring to on the basis of one of your tags. But you should make this clear in your question, or if this is incorrect say precisely what you mean. “Protein Variation” could mean many things, and protein folding would not be on my list.


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Is it possible that East Asians are a hybrid between modern and achaic humans?
As I understand it, all populations outside Africa have at least 2% Neanderthal ancestry. In eastern Asia and I think Papua New Guinea in particular that percentage could be more than 4%.
Now you also have the Denisovans from which a full genome sequence from a small bone fragment have been found in Denisova cave in central Asia. The latest research suggests that some Asian groups have about the same Neanderthal ancestry as other non-African populations but more Denisovan ancestry.
Question: If we theorize that East Asians (Chinese, Koreans, Japanese) with their characteristic features are not the result of recent evolution as per the "recent out of Africa Theory" but are instead the result of hybridization between modern humans and some form of archaic human (just like the Neanderthals and Denisovans) that have yet to be found.
To what degree could this theory be proven or disproven from genetic studies?

East Asians do not have "characteristic features". in other words, there is no specific feature or set of features unique to the East Asian nationalities you list that is not present elsewhere in the world. Your premise is faulty.

@natb All peoples have "characteristic features" to some degree. I was mostly thinking of things like skull morphology.

@Agerhell individuals certainly do. Groups of people such as "East Asian" do not. Skull morphology is not applicable here.

Firstly, as one of the comments said, there is nothing particularly unique about the set of 'features' that East Asians have, other than having fairly high levels of Denisovan ancestry. Any region in the world has some kind of unique phenotypic features if you look hard enough.
Genetics has fairly unambiguously shown that all non Africans originated from the out-of-Africa (OOA) event; Europeans, East Asians, Native Americans, Aboriginal Australians etc, are all from the same smallish source population that left Africa some time between 40-50kya. Of course there was plenty of migrations out of Africa that predated the out of Africa event, but there’s no strong evidence that they left any trace in existing populations. There’s been some hints by e.g. Pagani et al 2016, but this is very hard to prove convincingly, in part due to things like archaic admixture. If it did happen, it was likely a very small contribution.
Simply, you can fit models of human population history to allele frequency differences using something like Treemix and get graphs like this:

Which show that East Asians are nested exactly where you would exepct to see them following an OOA event (i.e. equally divergent from Africans as Europeans, Native Americans etc).
Humans and Archaics are very highly diverged in relative terms and if East Asians were some kind of mixture between modern humans and some unknown Archaic, they would stick out like a sore thumb on a model like this.
You could also look at something like cross-coalescent split times, which look at the divergence in genealogical trees across the genome between pairs of populations. Again, if East Asians were some uknown mixture, these trees would be hugely divergent from those you see in e.g. Europeans. They aren't:

This is really a separate question that I may ask in another thread. Can it be calculated somehow how much of the genetic difference/distance between african peoples and other peoples that are due to the +2% Neanderthal genes that non-africans have due to some crossbreeding with Neanderthals soon after leaving Africa?

Good question - make another thread and I will have a go at answering it

There is evidence that Europeans and Africans have admixture from other hominin groups, so it is not just Asian populations that have such admixture. We are all such hybrids, if anyone is.
The reference you may be looking at shows that in east Asia there may have been more than one period of interbreeding with Denisovans.
There is new evidence that there may have been several groups in Africa that merged to become what is now the human race even.
It’s pretty settled that we all have strong connections to Africa and Neanderthals and other brethren hominids.
The examination of DNA has assembled complicated migration histories - leaving and coming back into Africa - migration across and back to Europe.
I think take-home in general here is that we were not really separate species and our ancestors didn't really see each other as being so different that we would not mate.  All these subspecies coexisted for thousands of years and we probably interbred as often as we were in the same place. There were very few of us at the time... we just didn't meet each other so often.
I wouldn't jump to the conclusion that the Denisovan inheritance is unique to Asians somehow. The racial genetics of old have also been long debunked in terms of differentiating races into distinct subspecies. In short: the oft-referenced racial groups have all interbred with each other and with archaic hominins to a degree that makes their distinctions fuzzy.

Neanderthals and Denisovans are not human subspecies, but rather other hominin species (different from hominid). Otherwise this is pretty spot on.

perhaps some people say that ... all I can say is that different species cannot interbreed to produce fertile offspring... which clearly Neanderthals and Denisovans.  science is not 100% consistent and terminology requires some flexibility if you are going to deal with real systems. allow others to choose their words and you may find they have something to say..?

Others may choose their words as they like. I am merely reporting the current consensus in the field of paleoanthropology. The terms hominid and hominin are distinct and not interchangeable.


text:
Quantifying species detection probability using sign surveys as a function of distance in known occupied sites
I ran a pilot study to determine the probability of detecting a rare African small carnivore using scat (feces) detection dog surveys to assist with future population monitoring and occupancy surveys. A primary objective is to determine the search effort (in kms traveled with sniffer dog) needed to have a 95% probability of detection. I trained two dogs over two seasons and tested the method on a telemetry monitoring site and all surveys were within known home-ranges from four collared animals (true site occupancy is known). Rectangular walking transects ranged from 1.6 to 3.2 kms in length. We recorded distance from start of transect to each scat found. We found 112 scats ranging from 0-5 per transect. Species ID was confirmed through DNA barcoding, I intended on doing individual ID, but could not get lab funding, thus only have species detections. I am a field biologist and it has been quite a few years since my MSc. I am struggling to find examples that are similar to my data structure and aims for guidance. Resources for direction or suggestions for data structure and programs/packages would be useful.

Welcome to the site. May I recommend that you take a [tour] and visit the [help] for more information on this site and about composing a good question/answer.

I'm assuming that you are looking to be able to detect unknown populations of this animal? If so, it seems to me that to get a 95% level you would need to test this on areas which are outside as well as inside known ranges, unless the animal has some very specific environmental requirements for habitat. Did you see this one? https://onlinelibrary.wiley.com/doi/pdf/10.2981/wlb.00393

This might be a better for fit for CrossValidated, or for the r-sig-ecology@r-project.org mailing list. Are you essentially trying to compute the expected effort required to detect at least one scat during a set of surveys?

I will check those lists thank you. I only surveyed in known HRs to control for Occupancy to evaluated detection probability (prob of detecting at least one scat) as a function of effort (in kms moved) and influence of co-variates (dog, weather etc). Thus as distance increases, detection probability should increase. I also want to do the same with spotlight distance sampling (visual observation). The goal is to provide survey recommendations for EIAs and presence/absence surveys to develop habitat suitability models.


text:
Does sleep schedule affect circadian rhythm?
During the circadian rhythm, the internal human body temperature supposedly peaks around 4-6 pm. Let us assume that the average person goes to bed around 11 pm and sleeps for 8 hours. In that case would someone whose sleep schedule is offset by +2 hours — i.e, goes to bed at 1 am but still sleeps for 8 hours — have an equally offset peak body temp, i.e. at 6-8 pm?


text:
request for insect identification
A number of these insects have appeared in a house we are staying in on Fire Island. I would be grateful for any identification. Its length is roughly the width of the distal segment of my finger. A top and bottom view of the insect is uploaded.

Thanks for the identification.


text:
What is the danger of biasing the sampling when using Monte carlo in protein/peptide structure prediction
I am reading this paper in the link.
In introduction, paragraph 3, the last few lines are as follows

In theory, MC methods can be as ac-
curate as MD methods, but MC may suffer from lower efﬁciency when
using ﬁne-grained representation of the system, especially with large
number of explicit solvent molecules. There is also a danger of biasing
the sampling when using MC.

What does it mean danger of biasing the sampling when using MC. Is MC not reliable in protein/peptide structure prediction?


text:
What are the factors affecting reaction time and/or reflex velocity?
So there was this video of a cat killing a snake: Cat reaction time
and another of a bobcat killing a rattlesnake Bobcat kills rattlesnake
And then this from wikipedia on sand cats:

In the Ténéré, a desert region in south central Sahara, sand cats were observed preying foremost on small rodents, and the young of cape hare (Lepus capensis), but also hunting greater hoopoe lark (Alaemon alaudipes), desert monitor (Varanus griseus), sandfish (Scincus scincus) and venomous Cerastes vipers.
This paper claims that vipers and rattlesnakes have fastest strike rateMongoose are known predators of cobra.

These mammals are able to hunt them because of their faster reaction time and/or relex velocity.
So how is it that these animals have faster reaction times given that the length of signal transmission is actually lesser in those reptiles?
From wikipedia:

 Myelin  is considered a defining characteristic of the jawed vertebrates (gnathostomes), though axons are ensheathed by a type of cell, called glial cells, in invertebrates.
A reflex arc is a neural pathway that controls a reflex. In vertebrates, most sensory neurons do not pass directly into the brain, but synapse in the spinal cord. This allows for faster reflex actions to occur by activating spinal motor neurons.

So those factors are eliminated. For the mentioned case, it might be that those reptiles don't have as good of a perception as their predators but again they have a higher ratio of electrical:chemical synapses. (In case of a fly it is probably the smaller body and electrical synapses)
So what are the general factors affecting the speed of a reflex/reaction time? If a specific system is of help, the visual reflex system of the feline will do just fine.
Why was the snake unable to escape being hit by the paw?(The snake has an extremely fast strike velocity and the most likely factors are eliminated. At such close ranges, stimulus perception should not differ much either)

PS Those links are mostly posted to show source and research but most of that is GK so don't read unless you wish to

Given the finishing sentence, are you asking for the structures and delays within a reflex arc including musculature? Any specific species and sensory system you are interested in? As you rightfully indicate in your post, species and size matter.

Yes I am asking for those kinds of factors other than the mentioned.  Also feline relexes are fast so that will do. As for sensory system, not so specific but in the above fight it was probably visual vs (visual+thermal)

Having said that - does this answer your Q? One of the As is pretty good

That is pretty good. Can  you also tell why a rattlesnake is unable to retract its head despite its high strike velocity to avoid the paws?

That might have to do with agonist being quicker than the antagonistic muscle's, like a croc's beak that crushes bones but cannot counteract two hands holding it shut.

I recommend specifying the Q to focus it on the snake's evasive maneuvers when your original post is answered by the linked post, otherwise your current Q might face closure, being a suspected dupe.

Strike velocity isn't a reflex arc, it's just the motor side; no sensation involved necessarily. Doesn't seem to make sense to compare it to stimulus-response.


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What is the difference between the books "Molecular Biology of the Gene" and "Molecular Biology of the Cell"?
I am a CS guy who is taking up studying biology in my free time. Both of these books have been recommended to me, but I am not sure of the differences. Can someone explain the differences, and perhaps offer a suggestion for me?
The books are:
Molecular Biology of the Cell - Bruce Alberts
Molecular Biology of the Gene - James D. Watson
Thanks!

Welcome to Biology StackExchange! You can find table of contents for both books online: Molecular Biology of the Cell and Molecular Biology of the Gene. Generally speaking, MB Gene focuses more on molecular genetics, while MB Cell covers a wider span of topics about cell biology. Since you say you are new to biology, I think MB Cell will be more useful as it will give you a broader overview.

This is a site for biologists about problems in biology. I think that your question is off topic for that reason. But in any case, it is badly framed. You do not say why you wish to read about biology in your spare time. Are you interested in the mating habits of the lesser spotted toad, for example? Neither of these books will fit. Or do you want to get into bioinformatics? In the latter case asking strangers who have a completely different background and in general have never been involved in teaching anyone, never mind CS students, is, in my opinion, an exercise in futility.

Full disclosure, I have not read both books. However, I think I can explain the difference between them just by looking at the table of contents.
Molecular Biology of the Cell has 5 parts: Introduction to the Cell, Basic Genetic Mechanisms, Methods, Internal Organization of the Cell, Cells in Their Social Context. Molecular Biology of the Gene is basically the second part expanded into an entire book.
Even if Molecular Biology of the Gene sounds more like what you are looking for, I would still recommend reading Part 2 of Molecular Biology of the Cell first. I think it would give a good overview of how the system works before looking at how particular parts function.

How do you know what the poster is looking for? And should you be answering questions about the content of books on a site dedicated to problems in biology? I think not.


text:
Identify this ladybug-like insect, with yellow eyes and cream spots
I have spotted this cream spotted ladybird like insect on my terrace. I live in Hyderabad, India and it's rare to see such an insect here. I have tried using image searches but haven't found any good matches. The underbelly is brown with some spots of yellow at the side. It is approximately 1-1.25cm in length. It's very hot around here generally but today is a cool day (30 deg C) and lightly sunny.

Excellent photo. That's a basil plant, no? Can you [edit] to add your approximate location in the world to aid in identification.

Thanks. That's a mint plant, commonly called pudina here. Location is Hyderabad, India.

Could it be Clinteria? https://indiabiodiversity.org/group/beetles_of_india/observation/show/17244829

I think (without any expertise in this area, so take with a grain of salt), that this is a beetle in the genus Clinteria. This is a genus of beetles found in Asia and are relatively common.
Specifically I think this is Clinteria klugi, which has large pale yellow to red spots on the elytra and broad similarly coloured bands of the edge of the pronatum.
Lots of good photos can be found on INaturalist.
Incidentally, I think you might be confusing the bands on the pronatum for its eyes. The pronatum is kind of like a shield for the thorax, and in the case of this beetle, the head too. The eyes will be dark (as is needed to absorb visible light) and on the head, which is tucked under the pronatum.

Solved. The pictures match exactly what I had seen. Also check https://sar.fld.czu.cz/cache/article-data/SaR/Published_volumes/2020-1/115-132_jakl_2.pdf for more details about the beetle.


text:
Why is the nitrate concentration in a root hair cell higher than the nitrate concentration in soil?
For the exchange of nitrates and other mineral ions to occur between the root hair cell and the soil, the root hair cell needs a higher concentration of mineral ions and nitrates than the soil so that active transport can happen from the soil to the root hair cell. Please can someone explain how and why the root hair initially has more nitrate ions than the soil and what the point of absorbing these minerals is if the root hair cell already has more?
Sorry if this questions is worded badly or some of the information is wrong.

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Database for commercially available restriction enzymes?
I need a database that contains a complete list of commercial restriction enzymes: name of the enzyme & recognition site.

You are probably talking about type II endonucleases, there are a few databases available from the companies which sell these enzymes like NEB or Thermo Fisher. Additionally tools like NEBcutter, where you can paste a sequence and get all recognition sites for restriction endonucleases in this sequence are useful.
I linked them below in the references.
Edit: Thanks to @Michael_A I have added the lonk to the Rebase Database. It is a database which tries to be a complete ressource on restriction enzymes.
References:

NEB Enzyme Finder
Anza Restriction Enzyme Finder Tool
NEBCutter
Rebase

I think you should add rebase to this list, it is is an overt attempt at a 'complete' and includes information about commercial availability.

@Michael_A Thanks for the tip, I added the info.


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Basis of the taxonomic classification of viruses
The Wikipedia entry on Virus Classification contains the following statement:

“Viruses are classified by phenotypic characteristics, such as
morphology, nucleic acid type, mode of replication, host organisms,
and the type of disease they cause.”

The use of such phenotypic characteristics for classification of plants, animals, and fungi ended with the discovery of DNA as the carrier of genetic information. At that time it began to be replaced by classification by genotype, so as to include evolutionary history.
Why would it appear that a similar approach has not been adopted towards viruses? Is it because there are no fossilized viruses?

Thanks for providing your suspicion David, feel free to google it

since some viruses do not have DNA that might be one reason.

Unless you are trolling, I think you will find that people such as @David (with nearly 24,000 reputation on here) will have a strong understanding of such basic concepts as phenotype and genotype.

Thank you for responding to my request for information. In order to attempt to rescue the question I have rewritten it in a less strident manner that reduces the (I am sure unintended) impression of superiority that it conveyed to me, at least. I have tried to improve the presentation of the quotation and made its attribution specific. I have also avoided the use of "we", which suggests a personalization which I, for one, find irritating. If you are willing to accept this modification I can proceed to address some of the points relating to classification of viruses.

I think you will find that you are entirely incorrect in your statement that we classify "higher" organisms by genotype. Yes, that may be a part of it, but until the advent of high-throughput genetic sequencing in the last 20 years or so, we couldn't do this much. Before the development of these technologies, genetic analysis was largely limited to fragments sequenced by Sanger sequencing and various PCR or similar based analyses.
Almost all of botany, zoology, and microbiology is phenotypic in nature. For instance, you might have heard of Eukaryotes and Prokaryotes, two of the highest divisions in nature - these are split on the presence or absence of a nucleus in the cell, not on genetic content. Flowering plants are split into the presence or one or two cotyledons in their seeds. Animals can be split based on the presence if a backbone or not The list goes on through almost all of systematics...
Likewise, we do similarly for viruses. For instance, the type of nuclear material is a major phenotypic feature that is easy to split them apart on; you won't find DNA viruses and RNA viruses in the same family of viruses, because they don't produce the same morphologies and have little genetic similarity.  So you can classify them by genetic sequencing and you would likely come up with similar phylogenies as the current system of phenotypic features. Indeed, so powerful are the higher groupings done by morphology, that we can now find small fragments of virus genome and identify which species they belong to or work out if they are novel through such things as metagenomic analysis

Is it not true that vertebrata, invertebrata, eukaryota and prokaryota are monophyletic, thus grouped by genotype? And for this reason monocotyledon/dicotyledon is no longer an official Plantae classification due to them not being monophyletic? Thanks for the info on viruses, I didn’t realize that

@imrobert No - eukaryota covers everything from plants to animals to fungi. Prokaryota covers bacteria and archaea.


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Is there a DNase that works at low temperature, and is it also commerically available?
In preparation for FACS, I need to keep mammalian neurons on ice (in PBS-- / BSA), but as they still die while waiting ~30 minutes, they release their DNA into the solution. This leads to cell clumps. Thus, I need to refilter cells on a 35 um sieve (Blue FACS tube caps) and I loose a lot of cells that get entangled in the clump (up to 2mm in diameter).
One way to avoid such clumps would be to keep the DNA chopped, so I would only lose the cells that die anyways, not the many additional ones that get entangled.
Therefore I would need a commercially available DNase that works at low temperature (~0˚), has no RNase activity, and ideally temperature sensitive (easy to deactivate).
I found the following leads, but none are a very good match, nor do I have any experience with any.

Heat-labile (Cryophile) DNase (Thermolabile).
Psychrophilic DNAse

Problem: it is a Non-specific nuclease, cutting RNA

Cryonase Cold-active Nuclease from Takara
Thermolabile and Double-Strand Specific DNase
Heat-Labile Double-Strand Specific DNase (HL-dsDNase)


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Do songbirds prefer clean water?
The other day, the water in our backyard birdbath (Eastern US) had become fairly murky. So my wife cleaned it out and replaced it with fresh. Seemingly immediately began an amazing run on the thing. Robins, sparrows, finches , wrens, and catbirds all took their turns splashing and fluttering. At times they even queued up for their shot at a bath.
This got me wondering, are birds affirmatively more attracted to apparently clean water than to more dingy stuff? An easy evolutionary explanation would be that clearer water might be less likely to contain dangerous organisms.
Our experience here hardly counts as a controlled experiment, not least because the water was changed shortly after I had restocked our feeders, so the increase in bathers may simply have resulted from the larger number of birds drawn by the newly available food. But I have never before noticed such bath mania after I have filled the feeders. On the other other hand, it hasn’t rained here in maybe two weeks, so that could be another confounding factor.
But we have had birdbaths in our yard for decades (including the one in question, and in the same location) and we don’t recall ever observing a similar rate of use. Thus my question, which I paraphrase here: does water’s clarity affect its attractiveness to songbirds?
(I’ve done some Googling but turned up nothing.)

clear water might be a factor in this too,i have a garden pond and a little stream where birds can take a bath but they only do so if the water is clear.

Water is used for cement, so murky water won't make the feathers last longer and mantain their static electrical balance.


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Compute a melting temperature in viennaRNA?
Posting here to get views, but may be more appropriate for bioinformatics or chemistry SE.
There are a variety of utilities such as biopython or primer3 that compute melting temperatures.
However, tools for performing thermodynamic calculations on oligonucleotides should in theory be able to do this. ViennaRNA is one such popular tool, which although it has famously difficult documentation, I can't find anything there about melting temps.
Frankly, I would trust Vienna more than some of the other tools, and I'd like to compute all my oligo stuff in one place.
It seems like I should be able to back-calculate a melting temperature from a delta G along with a series of parameters about concentrations etc. I found some equations that solve for Tm in terms of enthalpy and entropy, but I'm not sure how to get those values from Vienna either, which prefers to just give you the overall deltaG.
Can anyone clarify how to compute from ViennaRNA:

Enthalpy of folding
Entropy of folding
Tm

For context, I am mostly interested in using ViennaRNA's RNAlib via the Python API.

Have you seen this table of programs in ViennaRNA? I don't know exactly which one should be used, but there seems to be several that calculate interaction energy between two RNAs. For melting temperature, you can use $T_\mathrm{M} = \Delta H^\circ/(\Delta S^\circ + R \ln C_T)$. However, I am slightly worried if that is the best approach as you cannot change the sodium concentration in ViennaRNA, which

significantly affects the melting temperature.

thanks @Domen, I clarified in the ticket now that I am using the RNAlib API rather than vienna programs. I would accept using one of those binaries if needed (though it's clunkier than I'd like), but I'll return again to the fact that I'm not sure how to compute either $\Delta H$ (enthalpy) or $\Delta S$ (entropy). None of those programs seem to do that, and searching the API docs or the viennarna docs leaves me empty-handed.

Just FYI, biopython is now at version 1.81. The docs you linked to were from 1.76 (I'm not sure if this API has changed since 2019 or not). You can always find the latest version of that page here, and it'll show you the specific version in the lower left.


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What insect/bug species do these belong to?
I randomly saw what I thought was dust on the counter in my bathroom (NYC Apartment - higher apartment, >10 floors up) this afternoon (June 1st) ... but when I got closer observed that they were little bugs! They were stuck to the counter likely because I had spilled some oil on there and they were unable to get out of there and died on the surface (thankfully). I haven't seen these anywhere else in the apartment or bathroom.
What are these? Are these dangerous or a cause to be concerned? Are there likely more of these elsewhere? Any recommendations for their removal?
[1


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What is the precise definition of "cytokine"?
For example, both bone morphogenetic protein 4 and nerve growth factor are paracrine signaling proteins which promote growth of their respective tissues, and both are known to have some effect on the immune system - but BMP4 is considered a cytokine whereas NGF generally isn't. I'm having trouble understanding the criteria by which some nonhormonal signaling proteins are classified as cytokines and some aren't.

Welcome to Stack Exchange Biology. Please read the Help on Asking Questions. You will see that you are expected to show the research you have done to answer a question yourself and why what you have found doesn't answer your question. What have you found in searching for the term? The Wikipedia article refers to it as a "loose term", which is often the case for biological terminology, so rather than a "precise" term the best you can expect might be "common or accepted usage". There are few standards bodies in biology.

@David clearly I've done some degree of research on the topic as I gave very specific examples as well as compared their pertinent characteristics and detailed what about them I found unclear. As I stated, I'm asking a question about what's "generally considered" a cytokine i.e. "common or accepted usage." I was simply assuming there was some line of reasoning in regard to the common classification that I had missed - if you're telling me there is actually no consistency in how it's generally used, that's rather unsatisfying but I'll accept it.

You seem to have a general concept of cytokine that you assume we all share. No. State this and relate it to your examples: It is my understanding that a cytokine is “a molecule that [does such and such]”, to quote [authoritative source]. Consistent with this, X, which [does A] is generally referred to as a cytokine. On this basis I would expect that  Y, which [does B], would also be regarded as a cytokine, but it seems never to be described as such. Why is this? Is there some feature of cytokines that B lacks that is generally assumed but not explicitly stated in the definition above?


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I don't know what this is?
I went into my shed today and found this bloody spot with something I'm not sure what it was. Have any idea???

These are the intestines (greenish bits), kidneys (pale bean shapes) and probably liver (dark red) of an animal that has been eaten by a predator.
Exactly which animal they come from is almost impossible to determine without more of a sense of scale, however, from the size of fly in the front, I would guess probably mouse to small rat sized.
Which predator left these is also hard to say, though domestic cats often leave the innards.

Thank you! We do have feral cats around and thought that might be what it was. Well it was one of a few guesses lol

@MelissaE Yeah, cats are everywhere. Even your most domesticated if cats is capable if doing this, and almost certainly does if they are have free access to the outside at night. If you think this is the right answer, please mark as accepted by clicking the green tick mark.


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Is “random arousal” in humans still caused by/connected to “background” sex drive?
I’m not sure if the title is the best way to word the concept but I don’t know how else to put it briefly; though honestly this question itself might be a bit hard for me to communicate concisely in text so if any more clarification on my thoughts or question is needed, then just ask.
So what I’m curious about is the origin of spontaneous erections (e.g. those not caused by conscious sexual stimulation of any kind be it visual, mental, or physical; for example “morning wood”, or other “random” erections that can occur during the day unprompted) and how libido plays into those, since a drop or loss of libido is typically reportedly accompanied by a lack of these spontaneous erections including the “morning wood”. Even though this behavior of the body isn’t directly and consciously caused by active sexual stimulation (but seems to generally still link to overall reproductive activity and function?), is it still tied to general sex drive and libido levels, as its absence correlating to low libido—and its seemingly higher quantities/strengths occurring with particularly high libido—suggests?
For a particular example, asexual people are a diverse group with varying properties regarding their individual sex health or habits, but there are many who report having a naturally low libido for most of their life (without distress). A level as low as, or lower than, the level at which a typical person experiencing a sudden drop in libido—and a lack of spontaneous erections as a result—would “fall” to. Would these asexual people with naturally, consistently low libido (so not a sudden change, as in the context of the people with typical libidos experiencing a new and temporary drop, but instead a default and non-distressing state) just as a result of that low libido naturally experience these spontaneous erections less—less often, weaker, both?

I think that libido and spontaneous erections could possibly have a correlation as you say, since usually the explanation for spontaneous erections is a surge of estrogen, progesterone, and testosterone which could cause a high sex drive. Low amounts of those hormones could possibly cause low libido and thus cause low spontaneous erections, although if your interested in primarily testosterone and their effects on men, their are different forms with their potentially varying effects on libido. I think these studies could help you get a better look at this topic:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5649360/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2586969/


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Genetic differences between Africans and non-Africans due to cross-breeding with Neanderthals?
It is estimated that soon after the "out of Africa event" there was some interbreeding between Homo sapiens sapiens and Homo neanderthalensis. All non-African peoples are thought to have around $2\%$ of their DNA from Neanderthals due to this cross-breeding event.
Can it be estimated how much of the genetic difference/distance between Africans and non-Africans is due to this mixing event?

@bob1 If you take two populations identical in allele frequency and crossbreed one of those with Neanderthals you would initially expect close to 100% of the difference to be due to the crossbreeding event.

Yes, indeed. However, how many generations since the cross-over event between us and Neanderthal, and what is the genetic difference now?

Multiple cross-over events are thought to have occurred, (possibly more in some populations than others, not sure).

@JiminyCricket for Neanderthals? I think only a single admixture (not cross-over, that’s recombination) event occurred. You may be thinking of multiple admixture events with Denisovans.

1 to 2 percent according to a different source :  https://www.nytimes.com/2020/01/31/science/neanderthal-dna-africa.html#:~:text=From%20DNA%20recovered%20from%20the,percent%20to%202%20percent%20Neanderthal.

Admixture, the genetic merging of parental populations resulting in mixed ancestry  :  https://academic.oup.com/gbe/article/15/5/evad066/7145698

1-4% of the genome of present-day people outside Africa are inherited from Neanderthal ancestors. ( another source:  https://pubmed.ncbi.nlm.nih.gov/36167050/

Why don't you compose an answer @envs_h_gang_5, you seem to have the basis of one there.


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Can someone identify this insect?
I photographed this wasp like insect on a buttercup in my wildlife garden.  It can be no longer than 10-15mm.  The bands appear green rather than yellow but I suspect that might be due to the lighting.

Where are you located? Thanks.

Lincolnshire UK

I can't answer because I can't identify it positively, but I think it's a small paper wasp (there are 200 species worldwide.) Some of them are slender and very small with long wings like yours. A side view would be necessary for proper ID, by me at least!

Thanks for giving me a steer, I'll look at that group

Having looked through Steven Falk's amazing collection of photos, I'm now thinking its one of the Stem Boring Sawflies, most likely Cephus spinipes, a Grass Stem Borer, which Steven Falk calls the Timothy Stem Borer.
To quote his site "C. spinipes is one of our commonest cephids and is recorded widely as far north as Yorkshire in a variety of grassy habitats. The rather maggot-like, whitish larvae develop in the stems of grasses such as Timothy. Adults fly from May to July and can be numerous on buttercup flowers."
https://flic.kr/s/aHsmsWKR4q


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What does 'bend angle' of DNA mean?
Literally, what does the 'bend angle' of DNA mean?
I did some googling but I couldn't understand it.
How is it defined?

Welcome to S.E. Biology. Please 1. Give us a link to a publication in the which you encountered the term (so we can see its use in context) and 2. Quote to us what you found by googling, telling us what part of the explanation you did not understand. That will help us provide an appropriate answer.


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Are there any good demonstrations of phosphorylation cascades?
So I'm working on this 2D signal transduction pathway computer simulation, and I'm struggling to grasp this process of protein kinases phosphorylating each other over and over again during the "transduction" part of a signal transduction pathway.
Are there any good sources that demonstrate and explain this process in-depth? I'm looking for videos/charts/textbooks/blog posts etc. anything would work.

Just use Google Scholar and search for a review of your signaling pathway of choice. A good one is ERK/MAPK. It's been studied very closely for years and is well-characterized, as well as being involved in a number of key cellular processes.


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Is Eugene Koonin's probabilistic argument for the necessity of a multiverse to explain the origin of life sound?
About Eugene Koonin

Eugene Koonin, Ph.D.
NIH Distinguished Investigator
Evolutionary Genomics Research Group
NLM/NCBI
Dr. Koonin graduated from Moscow State University, Moscow, Russia and received his Ph.D. in Molecular Biology from the same University in 1983. He has been working in the fields of Computational Biology and Evolutionary Genomics since 1984. Dr. Koonin moved to the US in 1991, first, as a Visiting Scientist, and then, since 1996, as a Senior Investigator at the National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD. Dr. Koonin's group performs research in many areas of evolutionary genomics.
Sources:

https://irp.nih.gov/pi/eugene-koonin
https://www.ncbi.nlm.nih.gov/research/groups/koonin/

The paper
On May 31, 2007, Eugene Kooning published the paper The cosmological model of eternal inflation and the transition from chance to biological evolution in the history of life (https://link.springer.com/article/10.1186/1745-6150-2-15) in the journal Biology Direct.
The Background section of the paper says:

Recent developments in cosmology radically change the conception of the universe as well as the very notions of "probable" and "possible". The model of eternal inflation implies that all macroscopic histories permitted by laws of physics are repeated an infinite number of times in the infinite multiverse. In contrast to the traditional cosmological models of a single, finite universe, this worldview provides for the origin of an infinite number of complex systems by chance, even as the probability of complexity emerging in any given region of the multiverse is extremely low. This change in perspective has profound implications for the history of any phenomenon, and life on earth cannot be an exception.

Eugene also includes an appendix entitled Probabilities of the emergence, by chance, of different versions of the breakthrough system in an O-region: a toy calculation of the upper bounds. I will quote an excerpt, so please refer to the paper to read the full appendix:

A ribozyme replicase consisting of ~100 nucleotides is conceivable,
so, in principle, spontaneous origin of such an entity in a finite
universe consisting of a single O-region cannot be ruled out in this
toy model (again, the rate of RNA synthesis considered here is a
deliberate, gross over-estimate).
The requirements for the emergence of a primitive, coupled
replication-translation system, which is considered a candidate for
the breakthrough stage in this paper, are much greater. At a minimum,
spontaneous formation of:

two rRNAs with a total size of at least 1000 nucleotides

~10 primitive adaptors of ~30 nucleotides each, in total, ~300 nucleotides

at least one RNA encoding a replicase, ~500 nucleotides (low bound)is required. In the above notation, n = 1800, resulting in E
<10-1018.

In other words, even in this toy model that assumes a deliberately
inflated rate of RNA production, the probability that a coupled
translation-replication emerges by chance in a single O-region is P <
10-1018. Obviously, this version of the breakthrough stage can be
considered only in the context of a universe with an infinite (or, in
the very least, extremely vast) number of O-regions.

In brief, Eugene appears to be saying that abiogenesis, even when conceding very generous assumptions, is virtually impossible from a probabilistic standpoint, unless we have a multiverse with an infinite (or at least a hugely vast) amount of O-regions.
Did I understand Eugene's point correctly, and if so, are his math and argument sound?

Yes, I believe you understand his argument, but please keep in mind that there's no scientific evidence of the existence of an infinite multiverse, and to accept this (theoretical) explanation for evolution is in practice no more of an answer than (and as much a leap of faith as) "God created the universe and everything in it, including life." And as you've presented this as an argumentum ad verecundiam , please note that Stephen Hawkings (with Thomas Hertog) refuted the idea of a multiverse and an infinite universe in his last published paper.

@anongoodnurse This would be an objection against the multiverse hypothesis, but you haven't said anything about the probability calculation. Are you saying that the math is right but the inference to a multiverse is wrong?

The math can be immaculate, but if it's based on unproven (or even unprovable) assumptions, the argument may be sound but reach an incorrect conclusion. As I stated on the other version of your Q on Skeptics, there are plenty of people prepared to accept the possibility of life on non-Earth-like planets, but we've no evidence either way. We have a sample size of 1 to draw inferences from.

Cross-posted from Skeptics.SE: https://skeptics.stackexchange.com/q/55692

I'm sorry, I meant to say abiogenesis, not evolution. I've said nothing about the math because it doesn't prove anything; it could be right, it could be wrong, it doesn't matter. There are many who like the idea of a multiverse as an explanation for abiogenesis, but we have absolutely no evidence of another universe, so it becomes speculative, i.e. philosophy, not science. What we do know for sure is that life arose in this universe. What we'll probably never know is exactly how.

This site is for questions about problems in biology that can be answered objectively. It is not a journal club or a forum for discussion of hypotheses. Your question may be suitable for some other online vehicle, but imho not this one.

There are two main problems here:

The logic assumes that a complete, simplified ribosome is the simplest possible useful unit, so has to spring up by a series of random events. This is extremely unlikely. But, if we assume there to be benefits to some of the intermediate states, so that they become the dominant form of self replicating molecule, those odds go way down. Some educated guesses as to what the useful intermediate states might be:

A simple enzyme to bolt amino acid residues onto RNA. This would allow RNA enzymes to access extra chemistry, some of which might allow the formation of cell membranes, another necessary precursor. This could be non specific, assigning them randomly, in a very inefficient process

The proto transfer RNAs above could be functional, but could also possibly bind randomly to a RNA strand, initially, without needing the large machinery of the ribosome. It'd produce at least 2 non functional proteins for every functional one, but maybe that's fine, if no other organism can use these amino acids floating around. Or, the RNA molecule is simply using amino acids as an energy store, so forming and breaking random chains is useful in some way.

There might be a stabilising RNA for the proto TRNAs, which might, eventually, go on to be our first ribosome.

It assumes this is the only way a ribosome could have developed. The possible solution space for a molecule of some sort being able to synthesize proteins is pretty vast. There's no requirement for it to be a ribosome.

In support of the first point, this is commonly what we'd see if, say, we introduce a bacterium to a new substrate - the first forays into that new substrate are grossly inefficient, but the bacterium thrives because it is the only organism that can use the new substance. Then, we see major selection pressures to make more efficient use of the resource, and we get some incredibly efficient piece of molecular machinery. The first self replicating RNA to be able to use amino acids, as anything from an energy store to a way of getting through lipids, would have a really good chance of going on to replicate a lot more. From there, the machinery for protein synthesis starts.


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Can plants be pathogenic towards humans?
In googling this question you’ll only find articles about plant pathogens jumping over to humans eg candida auris and pseudomonas aeruginosa.
My question is, like fungi can be infectious to humans (aspergillus, candida, tinea corporis), could a plant infect us?

Yes: Protothecosis is infection of the bloodstream by a genus of non-green algae. There are also odd reports of infection by green algae, such as this one.


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Who demonstrated plasmodium life cycle? Grassi or Laveran
Plasmodium causes malaria which goes through mosquito female anapheles through some of its life stages. But I am not sure which scientist experimentally demonstrated the life cycle of plasmodium. In texts, I found following text which talks about the work of Grassi in 1898:

And following data supports the fact that Laveran also worked on the life cycle of plasmodium in 1880 which is even way before than Grassi's 1898 experiment.

By chance, but also thanks to his tenacity and patience, he had seen the exflagellation of a male gametocyte, a phase in the life cycle of malaria parasites which usually occurs in the stomach of the Anopheles mosquito.
https://www.cdc.gov/malaria/about/history/laveran.html


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How did cells survive before the first appearance of topoisomerases?
How did cells operate before the first appearance of topoisomerases to relax DNA supercoils during replication? I read a recent paper on the early phase of topoisomerase evolution, but it doesn’t discuss the actual origin of the topoisomerases, or how cells survived before the first appearance of topoisomerases. Here is the paper:
Villain, P. et al, “Expanded Dataset Reveals the Emergence and Evolution of DNA Gyrase in Archaea.” Mol. Biol. Evol. 39(8), https://doi.org/10.1093/molbev/msac155


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When did the term "non-avian dinosaur" come in common use?
When I first learned about the prehistoric (mega)fauna that we now commonly call non-avian dinosaurs they where just referred to as dinosaur. I am trying to figure out when we made the collective switch in articles and literature to the use of "non-avian dinosaur".
Merriam-Webster provides us with a definition and indicates that the first known use is in 1988. But that does not indicate it was in common use nor general knowledge that birds are a descendant of dinosaurs which means we need to distinguish between avian and non-avian dinosaurs.
So can someone help me find when the trend to the more specific non-avian dinosaurs got started?

Don’t you mean when did it become common knowledge that birds are NOT the descendants of dinosaurs? People used to think they were so, and this was the mistake that occasioned the invention of the term you reference. It depends when you started reading Robert Bakker's explorations of dinosaur endothermy starting in 1968. Most of the dinosaurs — both the avian ones and the non-avians ones — went extinct at the K-Pg boundary. Most dinobirds died then and only one tiny branch of them survived: the little, ground-not-tree-dwelling but flighted toothless ones with beaks for cracking open seeds.

Is this specific to academic texts in biology and/or paleontology? If so, you might be better asking biologists or paleontologists.

@tchrist ?? Of all the life that survived the KT event, only birds are descended from dinosaurs. Doubt they ate seeds, termites are more likely. It's believed that all mammals that survived were insectivores.

@PhilSweet Birds are a kind of dinosaur in the same way that humans are a kind of great ape. That's different from saying something like reptiles are descended from  amphibians.

The term non-avian dinosaur is usually taken to be a term used in chronological classification schemes. There are three systems of classification that share some terminology and supplement as needed with unique terms. You can base all branching on the known fossil record. Or you can base some of it on hypothetical lineages, Or you can look at timelines and dateable events and use terms that relate to specific chronology. Non-avian dinosaur basically belongs to the third system.

@tchrist birds did not become entirely toothless until well after the K-Pg extinction.

@John Thanks for the quite interesting correction.

Here is what Google Ngrams has:

This suggests that the mid-70's are the first recorded instance, but it wasn't until the 90's that it began to gain use. What defines "common use" is up to you.

The understanding that bird are dinosaurs was not a sudden realization but a slow accumulation of evidence and convincing scientists along with the rise of cladistics and phylogenetics making such clarification useful. so this is probably the best answer you can get.


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Minimum growing conditions of a given plant
Micro-algae are organisms that can grow in aquatic environments and use light and carbon dioxide (CO2) to create biomass. Researches showed that Micro-algae biomass can be used as bio-fertilizer.
My mission is : to find which plants in the world are best suited to arid climates and to arid soil that was treated using the Micro-algae biomass.
This is my approach on how to accomplish my mission:
I' m into collecting chemical characteristics data of the soil , chemical characteristics data of the micro-algae biomass and other environmental factors like the temperature, rainfall and humidity of this environment. I want to use this data to determine whether a given plant can survive (adapt) in this environment. So I want to compare this environment (arid + Micro-algae biomass applied) characteristics (N, P, K, Temps, humidity....) to the minimum growing conditions of the given plant .
My problem is : How to determine that minimum growing conditions of a given plant in terms of the needed nutrients (N, P, K) , Temperature, water etc...?
I'm open to any biology/math resources and any other inspirations or approaches.

Depends very much on the plant you are interested in. Better studied ones such as crop plants or things like Arabidopsis will be well characterized; others not so much. Don;t discount things like formation of mycorrhyzal networks.

OK, Currently, I'm targeting plants that are food for humans/animals. Is there any data source of plants that are well characterized (like potato, Onion...). BTW I'm not a biologist I'm a Data Scientist.@bob1

We see this sort of thing quite a lot. To actually answer this question you will need to learn a lot of biology.  Is there a database: probably not (AFAIK), you would have to dig the literature for yourself, and you will find it mostly comes in the form of "plant variety (not species, individual variety within species) grown under abnormal X, but "normal" conditions Y,Z,A,B,C... etc". You might find ranges for some variables in reviews or horticulture textbooks/manuals/gardening guides. Seed packets often have climate ranges for sowing, but you would need to dig climate conditions.

Ok I got this. I think I will just start reading papers and books instead of wasting my time looking for a database. thank you so much @bob1


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Preservation of citrus fruit
A decade ago [1] the possibility of using Cas9 systems to impart desirable properties to oranges seemed within reach [1]. Antifungals like Imazalil can increase shelf life of citrus but are known to disrupt hormones and are perhaps carcinogenic [2]. A more recent article suggests that Cas9 is in fact being used to overcome "biotic stresses"[3]. Problems like citrus greening, black spot, and penicillium cost growers a lot and GM seems preferable to the chemicals mentioned in [2].
Does anyone actually know how citrus is currently preserved in the U.S.? Are both fungicides or GM at work? Neither? Both?
[1] A Jia H, Wang N. Targeted Genome Editing of Sweet Orange Using Cas9/sgRNA. Prasad M, editor. PLoS ONE. 2014 [accessed 2023 Jun 6];9(4):e93806. https://dx.plos.org/10.1371/journal.pone.0093806. doi:10.1371/journal.pone.0093806
[2] Temkin et al., Hormone-disrupting fungicides found on most citrus fruit samples tested by EWG, found online in Shoppeer's Guide to Pesticides on Produce, March 2023, https://www.ewg.org/foodnews/citrus.php.
[3] Tanwir, S.E., Soares, J.M., Welker, S., Grosser, J.W., Dutt, M. (2021). Genetically Modified Citrus: Current Status, Prospects, and Future Challenges. In: Kavi Kishor, P.B., Rajam, M.V., Pullaiah, T. (eds) Genetically Modified Crops. Springer, Singapore. https://doi.org/10.1007/978-981-15-5932-7_7

For example, I put a ripe store-bought orange out in mild, humid weather 10 days ago. Untreated, this orange would be coated with aspergillus and/or penicillium. it is completely zombified--hopefully in a good way...

I had a look through some web pages and came across one on shipping of oranges that indicates the storage conditions and treatments that may be applied to oranges.
This isn't necessarily about oranges in the USA, but ones from California are mentioned. It seems that there are a number of methods of maintaining shelf-life and that oranges are usually washed to remove dirt and contaminating fungal spores and then sprayed with a wax to inhibit loss of water as washing removes the natural surface waxes. To quote the article (emphasis is mine):

Quality / Duration of storage
Experience has shown that it is the care taken with preparation of the fruit for shipping which very largely determines whether individual batches withstand the rigors of transport. Such preparation for shipping is carried out in packing houses. These include:

Post-ripening of green or unsatisfactorily colored fruit to achieve a salable peel color in ripening rooms.
Removal of dirt, sooty mold, spraying residues and scale insects in washers.
Finishing of oranges which do not develop the typical orange color, but instead remain pale gold, green or with green spots, in a dye bath at temperatures of 45 – 50°C. Fruit treated in this way must be marked accordingly with a stamp (color added).
Coating with a layer of wax and treatment with preservatives and marking accordingly.
Grading of the fruits by size (gaging), color and other external features.
Counting, weighing and packing. Marking each package with details of number of fruit, quality class, variety and origin.
Storage until shipment in cold stores.

Waxing to prevent loss of aroma and weight is required because the washing process removes the natural wax layer. The film of wax sprayed onto the peel only partially seals the pores so that the fruits are still able to respire.

I suspect that the wax also helps prevent fungal growth through physical inhibition of spores getting to the fruit. In addition, storage conditions play a big role here - if you don't have any other fruit around your single orange, then it might not mature further (no ethylene) and it will have adequate ventilation to prevent rotting from too much CO2:

Care of the cargo during the voyage must be aimed at controlling respiration processes (release of CO2, water vapor, ethylene and heat) in such a way that the cargo is at the desired stage of ripeness on reaching its destination. Inadequate ventilation may result in fermentation and rotting of the cargo as a result of increased CO2 levels and inadequate supply of atmospheric oxygen (see Ventilation).

Fungicides are used in parts of the world, and I would be very surprised if they weren't in use in the USA:

Fungicides are diphenyl, orthophenylphenol (OPP) and thiabendazole (TBZ). Diphenyl can be recognized from its naphthalene-like odor. The fungicides primarily prevent blue and green molds, but they do impair flavor and indication of their use is mandatory.

As far as processing for juice, Pectinases are used to extract more juice from the pulp. GM from Aspergillus niger or Penicillium spp.
For citrus fruit with any bitterness, naringinase is used to destroy naringin.
Technically the pectinases are:
pectin methyl esterases,
pectin lyases,
and polygalacturonases
Info from page 141, Industrial Microbiology - An Introduction.

This seems like it should be a comment. The question is about preserving oranges, not extracting juice.

Perhaps change “processed” to “preserved” in the question.

I will do so. Didn't realize it was unclear.


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I am trying to identify this bone I found on the beach at the Delaware Bay in Delaware. It is 2 1/2 inches wide and 1 1/2 tall

This bone was found at Big Stone beach on the Delaware bay, Delaware. It weighs only 19 grams

Trypophobia warning maybe?

It's a pharyngeal tooth from a large fish like a drum or a parrot fish.

The pharyngeal jaws are for grinding and also contain a pharyngeal mill, where larger and smaller teeth grind coarser and finer coral pieces. Fish like the Black Drum use similar teeth to grind bivalves and molluscs.

They are ideal for scraping and crushing the tough and calcified materials that make up the parrot fish's diet, coral skeletons and polyps, and algae-covered rocks.
The teeth are typically arranged in several rows, with each row containing multiple tooth plates. The outermost row consists of larger, stronger teeth, while the inner rows may contain smaller and more specialized teeth for further grinding and pulverizing food particles. This multi-row arrangement provides parrot fish with an efficient means of food processing. teeth of that kind are also found in other fish, and they are reinforced to handle high mechanical loads. https://www.sciencedirect.com/science/article/abs/pii/S1047847720301039

Thank you for this answer!  mystery solved.


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Help identifying an insect
I live in Milan, Italy in the city center. I live in this house since 5 years and I keep finding the insect pictured below.
I see it throughout the seasons (temperatures here range from -1°C to +35°C in average).
I find it mostly in my bathroom which is not well ventilated and it is the warmest room in the house (about 23°C in winter even with the radiators off and up to 35°C in summer during very hot days if I don't use air conditioning).
The size is about 7mm in length and 1mm in width (including only the main body, i.e., excluding legs and antennae).
I find it mostly during the night but maybe just because I use brighter lights and I can see it more clearly on my white walls.
What is its name so I can research more about it (i.e., does it pose any risk to my health or to my belongings in the house?)?

Looks like a species of silverfish.
https://en.wikipedia.org/wiki/Zygentoma

They eat paper, cloth and stored foods like cereal, even organic wall paste, so yes they can damage your stuff, but outside allergies they are harmless to a person.

Could it be also https://en.wikipedia.org/wiki/Firebrat ?

Zygentoma is the name of the group there are several species, look at your local pest identification.  silverfish is the common name.

@John ‘Silverfish’ is the common name for a number of species in the Zygentoma group, but not all. Firebrats are, in my experience, the primary exclusion from the term, since their defining feature is that they’re not silvery to look at, but brownish-grey. Sort of like how members of the Odonata family are mostly called dragonflies, except those that are called damselflies.

Silverfish is what immediately leaped to mind when I saw the picture.


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The direction of the flies(Housefly)
Why do flies move crosswise and polygonally? Does the length of the flight path and the angle they turn mean?

I assume this was observed in a small room and the turns were when they approached an obstacle. They use optic flow for obstacle avoidance which kind of explains the straight lines. The retracing might be just be a neural adaptation to not get stuck in a space while still largely still traveling in the intended direction. Was the opening in the curve the direction of the door that the fly entered the room through.

This was observed in a small room. All the doors were closed. I watched this for over an hour. Don't they get tired?

Air is much more viscous when you're the size of a fly than when you're larger which makes flight much less energetic. It's more like they're swimming than flying. If my understanding of Reynolds numbers are correct, a fly in air is swimming 5000 more than a human is in water (Reynolds number being the ratio of inertial to viscous force and it being around 1 million for a human and 200 for a fly).

Thank you, @DKNguyen


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Why are these ants emerging from underground?

Every spring through summer season, I see these ants emerge from beneath my driveway and form these thick swarms on the surface.  They typically do this once or twice per day, and after a few hours they go back underground.
After they are gone, there are often some dead ants laying around.
What is the best explanation for this behavior? Why do the ants come to the surface as a group and then seem to later disappear underground?

type of ants and or a location had been helpful.

Some hypotheses:

depending of the species, this could be because ants from another colony attack this colony from outside, then many ants inside go out to defend their colony. This could be coherent with the fact that you see dead ones after they quit the surface.
This can be supported if you see some of them which are fighting and if you see a line of ants coming from another place.

They are disturbed and think they are attacked, e.g. if you see this everyt ime after you can pass on it, or after you play basketball here, etc. Just try and check if they respond to it.

They are disturbed because of environmental reasons, e.g. after watering your garden, water could suddenly flood their nest.

Less likely:

They just choose the best time of the day (temperature, ...)  to clean their nest, including dead ants, but they look too numerous for this.

They may prepare the nuptial flights of the winged ants and group to protect them, but I can't see any on the photo, so probably not.


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Bug/larva identification
What do you think these could be?

The photo was taken today from the inside of a bin liner, which contained waste from fruit and vegetables (carrot skin, banana peel, salad leaves, etc.), and (normally) nothing of animal origin.
Size: about 3-4 mm (body length).
Location: Europe/Belgium.
Behaviour: did not seem to move at all, or only extremely slowly.
Any ideas?

Possibly juveniles of the Clausiliidae family, of which there are many, many varieties. I'm having trouble pinning down the exact one, as pics of adult snails dominate the web. Unless an expert comes along, perhaps you can look after some 'till they grow-up, then take another picture?

Thanks! So maybe they are not even insects... :D They did look like mini snails to me, when I saw the photo, but I did not mention that in the post, as I did not want to sound silly. That worked, didn't it(!). As for your suggestion to follow their development, hmm, I don't suppose they will get the chance to 'grow up', unfortunately :/, but I will ask.


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How lethal is high dose UV?
I watched a Neil DeGrasse Tyson video about teraforming Mars where he goes over the topic of UV radiation and how our ozone layer protects us. He makes a statement that the UV on earth is actually only a small percentage, about 3%, and furthermore only 5% of that being the more harmful UV-B which causes sunburn and skin cancer.
My question is, what would happen to a human if they were to receive the full dosage of UV-B radiation from the sun, let us assume 500 times higher than that on earth, with no protection? Would it be fatal? And if so how fast would it kill you?

The answer is easier than you think. Have you ever had a sunburn so bad that it causes blisters? (I have, as a teen falling asleep on the beach.) Those sunburns are called second degree sunburns. With that amount of exposure, the least that would happen is a 2° sunburn over most of your body (some parts don't suffer this), which would lead to hypovolemic shock. Without treatment (which includes fluid resuscitation), you would probably die within 24 hours. If, by chance you survived the first 24 hours, the blisters that break open (and they would) would get infected because your immune system would be compromised by the damaged capillaries of the skin (that's one cause of the blisters in the first place.) Your lifespan would be a few days if you didn't die within the first 24 hours.
This is the best case scenario.
This is why burn units exist. Second degree burns over a certain percentage of your body are lethal.

You wouldn't get something like radiation sickness but something can be so unhealthy that can then lead to increased mortality. Whether or not something kills you is the lowest bar that can be set for whether something is healthy or not.
I couldn't actually find high wavelength resolution graphs for the solar irradiance at sea level since the values are vanishingly small on normal graphs.
However, if you take the the UV irradiance at outside of the atmosphere at 250nm to be 0.25W/m^2/nm and use that as a baseline for the UVB range of 280-315nm, then the irradiance 8.75W/m^2. Five hundred times that is equivalent to a 4.375mW UV laser producing a 1mm x 1mm square pot. The first thing you would notice is that you would go blind.

https://www.e-education.psu.edu/meteo300/node/683

Not a bad answer. For actual conditions on Mars: Mars is about 1.5 AU, so by inverse squared law = 1/1.5^2 = 0.44 so irradiance is 0.44 of Earth.

It depends on the wavelength. This paper1 provides the numbers:

This study was conducted to determine the toxicological effects of different wavelengths (250, 270, 290, and 310 nm) and doses of UV radiation on cell viability, DNA structure, and DNA damage repair mechanisms in a PC12 cell system. For this, we evaluated cell viability and CPD formation. Cell survival rate was markedly decreased 24 h after UV irradiation in a dose-dependent manner at all wavelengths (except at 310 nm). Cell viability increased with increasing wavelength in the following order: 250 < 270 < 290 < 310 nm. UV radiation at 250 nm showed the highest cell killing ability, with a median lethal dose (LD50) of 120 mJ/cm2. The LD50 gradually increased with increase in wavelength. Among the 4 wavelengths tested, the highest LD50 (6000 mJ/cm2) was obtained for 310 nm. CPD formation decreased substantially with increasing wavelength. Among the 4 wavelengths, the proportion of CPD formation was highest at 250 nm and lowest at 310 nm. On the basis of LD50 values for each wavelength, PC12 cells irradiated with UV radiation of 290 nm showed maximum DNA repair ability, whereas those irradiated with the 310-nm radiation did not show any repair ability. Toxicity of UV radiation varied with wavelengths and exposure doses.

You can find more details on this topic in ref.2
References

Masuma R, Kashima S, Kurasaki M, Okuno T. Effects of UV wavelength on cell damages caused by UV irradiation in PC12 cells. J Photochem Photobiol B. 2013 Aug 5;125:202-8. doi: 10.1016/j.jphotobiol.2013.06.003
Lawrence, K.P., Douki, T., Sarkany, R.P.E. et al. The UV/Visible Radiation Boundary Region (385–405 nm) Damages Skin Cells and Induces “dark” Cyclobutane Pyrimidine Dimers in Human Skin in vivo. Sci Rep 8, 12722 (2018). DOI: 10.1038/s41598-018-30738-6

I'm not sure you're addressing the OP's question directly, which involves damage to and even death in humans exposed to UV B radiation (280–315 nm), not skin cells in vitro or in vivo.


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Does somebody knows this european bird that i saw close to a river in an open grasland?
I saw today afternoon (10. June) this bird and would like to know the species name. It was on a sunny day in the middle of the Netherlands (central Europe) in an wet meadow close to a big river. I took several picture from the same individual, but they were two birds of the same species passing quite fast close to the ground of the meadow.

I'm no expert or from europe , but I think common linnet, based on a very brief google image search for "finch europe". Maturing reddish head and breast, gray neck,brown wings with dark tips.

thanks for your input. I was also considering this the marks are not that clear. sure the quality of the picture is also not great. but anyway.

I think marks aren't clear because juvenile heading into adult, but as I said, no expertise on this at all, other than some search skills.


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Laser in mirror experiment
Apologies if this question is very simple I performed an experiment where I would shine my toy laser at the mirror and it would be reflected.
Now here is what I tried:
I could see my laser toy , I inferred that If I could see it then external Light source must come and hit it such that it falls on the mirror and mirror reflects it back to my eye. So If I shine the laser light on the mirror in the place where my actual laser toy is I could get the laser to be reflected towards my eye.
Hence when I had my two eyes to be open light from laser toy fell on my right eye which I felt was strange. I expected the light to be in the middle because we have both eyes and the light hitting both eyes I thought would average out.
Then I closed my left eye and I could see that It fell on my right eye If I pointed the light where my eyes could see the laser.
I closed my right eye and I could make the light fall on my left eye!
So I had some questions here:
Why is it so that the images we see are inferred from the right eye for me , If we can also get images from the left eye why is right eye's image is taken to be the overall image?
What is the use of left eye in this case ?

Obligatory - Don't shine lasers into your eyes, you only have one set and run the risk of permanent eye damage!
We have dominant eyes, just like we have dominant hands and feet. This means that with both eyes open, you naturally adjust your hand/eye coordination to compensate so that your dominant eye receives the majority of the input.
A conventional test for this is to get a longish straight tube, such as that found in paper towels or Aluminium foil (AKA tinfoil) or similar (rolled up paper tube works too). Hold this so that with both eyes open you see a clear circle. Now close one eye. Now close that eye and open the other and compare. If you close your dominant eye, you will see that you can no longer see clearly down the tube, but if you close your non-dominant eye, you can still see fully down the tube.


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Septa fibrous in liver histology
I'm scoring liver fibrosis using Laennec scoring system, but i'm so confuse to differentiate between septa fibrous and fibrosis without septa. Anyone can tell me about the characteristic or structure of septa fibrous? Thanks a lot


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Heat-treatment for protein expression
I want to express thermophilic protein in E. coli and the first step purification is to heat the crude protein. Since I don't know the optimum temperature to denature the contaminants, I plan to heat the protein in three different temperatures. I currently have 120 ml crude protein and I wonder, is it okay for me to divide the crude protein for each temperature? So, I will heat 40 ml crude protein for each temperature.

Yes.
In fact this is exactly what you would do if you wanted to perform the experiment to determine which condition is best. For these sorts of experiments you use one batch and split it amongst the experimental variables, so that you don't have to deal with inter-batch effects (e.g. different concentrations of protein).


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Is there a link between SASP and fibrosis?
1/ Fibrosis: Fibrosis is the formation of excessive fibrous connective tissue in an organ or tissue during a reparative process.
2/ SASP: SASP is the accumulation of molecules and senescent cells in tissue, that triggers "dead" parts in the body
Is there a link between these two phenomenon? I'm specially thinking about the fact that SASP in an organ would not be able to replicate and recreate parenchymal tissue, leaving the place to connective tissue to replicate: This would end in fibrosis?
Question: Is SASP one of the factors leading to fibrosis?


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Insect decline and CO2 concentration
In the UK, where I live, for several years we have had cold dry springs which seems to delay appearance of insects. So irratic weather could cause species to emerge out of sync with their food species and that is an example of how climate change could lead to decline. But insect decline is occurring globally and not all areas have the same factors that could contribute like use of pesticides, habitat destruction etc.
One factor that is more global is the increase of CO2. Could it be that because insects rely on diffusion through tracheae to respire they are more affected, at part of their life cycle, by increased CO2? you might not think that the concentration of atmospheric CO2 at 470ppm and a 47% increase since pre-industrial era would be enough to make a difference but has anyone done the experiments to check?

Interesting idea - what did your searches of the literature tell you?

First question: is there a way to dissociate this from pesticide use? second question: is there a way to dissociate this from temperature? e.g. recent studies consider both of these to be major contributors to recent declines https://beyondpesticides.org/dailynewsblog/2022/05/climate-change-and-industrial-agriculture-are-supercharging-the-insect-apocalypse/

@bob1 I dont have access to journals but I found no mention of it in general web seach

Looks from your reference that CO2 concentration might not be significant


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Are mutation rates normally distributed? If not, what are they?
On average, there are  64 mutations per generation in the human genome. Is this constant, or can we expect variation in the number of mutations?

You have posed a different question in your title and in the main text which is a bit confusing. As a short hint: Quantities that are bounded (i.e. mutation rate can only be a positive number) cannot be normally distributed. But they can be, for example, distributed by the log-normal distribution.

this depends a lot on the mutation, different types of mutations have different probabilities. Its all based on the laws of chemistry.

Mutations in this context are being treated as discrete count data (there either happen or they don't). So the number of mutations per person in a given generation should form a discrete probability distribution. Because they are a single count variable bounded at zero (can't have negative counts) and finite (genomes don't go on forever), a Poisson distribution(pwɑːsɒn/) is probably the expected best fit. A Poisson distribution can sometimes be approximated by a normal distribution when the Poisson count mean (λ) is large (some say λ>20, some say λ>100).

Note: there are 60ish substitutions per generation, on average. There are probably many times that number including all mutations (e.g. microsatellites, centromeric satellite repeats, etc). There is almost by definition a telomeric mutation on every chromosome end at every cell division, which alone is comparable to substitution number per generation.
Figure 1d of this paper suggests that the distribution of substitutions alone is log-normal in cancer, as suggested by the commenter.
I am not aware of a reference for distribution of other mutations.

What does log normal mean

@ShannonT The lognormal is a distribution that looks normal after a logarithmic transformation of the underlying data. For more info I'd suggest googling it.