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Where in the biological realm is vitamin B5 chiefly produced?
Can yeast produce pantothenic acid (vitamin B5)?
Do bacteria efficiently produce it?
Or does it only come from plants?
The Wikipedia page for pantothenic acid doesn’t seem to answer the question (other than mentioning that small amounts are found in, i.e. used by, every organism, and hinting at the facts that animals concentrate it and yeasts are, at the very least, inefficient at producing it).

I see that you reverted the title of this question. I suggest that you Google “biological realm” to find the context in which this strange (at least to me) expression is used.

realm /rɛlm/ LITERARY 1. a kingdom. "the defence of the realm"  2. a sphere, domain 3...

The title is an improved version of the initial title. The one you gave changed the meaning of the question. I think it becomes problematic when we change peoples' questions to better fit our answer (it quickly becomes a very lonely world / a monologue). I don't think you had any bad intent but I'm sharing the thought that occured to me when bringing it back to its original meaning with an small edit to the original question better encompassing part of your answer.

— Whenever I am obliged to translate a phrase into German, French or Italian I not only check with a dictionary, but do a Google search to check the phrase is actually used in the language, and with the same sense. That is what I did, and suggested you do, with “biological realm”. If you think my alteration changed your meaning explain. But invented expressions will not do.

Google has ceased to be of any value as a reference a long time ago. It is merely now a tool to dumb down people, increase dependence (consumerism) and serve brainwashing (propaganda). As for most people my personal experience is that most people have a poor mastery of their own language, and that is most true in the case of the English language. This is by design as a systemic effort to limit people's language is needed to limit their conceptualization of reality (reality is made of many nuances and subtilities, the more you restrain the language, the mote you limit people's grasp of reality)

*the more you...

Oh Dear — As people will tell you, I do the bad cop, good cop on this site. With your question I was doing the good cop: not only giving an answer, but explaining how I found the information; commenting to explain how to minimize mistranslation problems between scientific disciplines the way I do for languages. Now you can use whatever search engine you like, or none, or Wikipedia (set to the language of interest) or PubMed or... But the point is if the searched phrase does NOT appear in the context expected, you should SUSPECT it MIGHT not be commonly used in that context.

…and a title is, well, a title. Its function is to communicate to people the flavour of your question. It is not a platform for extending people's grasp of reality. If you use terms that appear strange to biologists, and use outdated terminology to refer to compounds, the chemical nature of which has been known for years, you will certainly communicate something, but not what I suspect you want, and not in a way that will solicit the specialist answer required. To me, at least, such a title signals that you are not a serious biologist and this is probably a naïve question about "vitamins".

I understand you good intent, but I'll happily be considered a non-serious biologists by anyone who mainly only can judge based on my vocabulary (or by anyone at all for that matter).

General Considerations
Pantothenic acid is a precursor for the synthesis of Coenzyme A which is essential for most, if not all, living organisms. As bacteria appeared on earth before plants, and can currently live in environments where there are no plants, it is difficult to envisage their being unable to synthesize pantothenic acid. The situation with yeasts is less obvious, but as independent free-living single-cell organisms, the expectation would be that they had retained this synthetic ability of their evolutionary precursors.
Pantothenic acid synthesis in different organisms
Pantothenic acid is produced by a wide range of bacteria, with the structure of the enzymes of the pathway of its synthesis, e.g. the final enzyme, pantothenate synthetase, available from many different species, as can be seen from a search of the Protein Data Bank.
Indeed far more detail is known about the process than in higher plants, because of the greater ease of conducting molecular genetics on the former.
One way to check for the existence of a pathway in a particular organism is using KEGG, and this approach shows the pathway for the synthesis of pantothenic acid is present in Saccharomyces cerevisiae.
Efficiency
The poster refers repeatedly to the efficiency of production of pantothenic acid but appears to be misusing the word, and it is not clear in this context what he means. In science efficiency expresses the percentage of input energy or material that is converted to an intended output. For example in biochemical thermodynamics, inefficiency might be the loss of chemical energy as heat (in processes where the aim is not to produce heat). In a general sense such efficiency exerts selective pressure on organisms, and this will be greatest in rapidly-growing organisms such as bacteria which are subject to competition for resources. All organisms have regulatory mechanisms to ensure that there is sufficient of the product of a pathway when it is required, but that energy and precursors are not wasted by producing it when it is not required. Such regulatory mechanisms tend to respond more rapidly to changes in bacteria than in eukaryotes (such as plants), with their longer division times, but there is no reason to believe that any organism that synthesizes pantothenic acid does so inefficiently.
It is possible that the poster is interested in which organisms might present the most abundant sources of pantothenic acid for those organisms such as mammals that cannot synthesize it themselves. This may relate to the size of the ‘pool’ of this metabolite in the cell. However that is a completely distinct question from synthesis and efficiency thereof. I doubt whether there is much literature on this as it appears that human deficiency of pantothenic acid is very rare, so that this has not been a particular dietary concern.

For the term "efficiently", let's define it like this: The more efficiently an organism produces pantothenate, the less its growth and replication would correlate, in an environment replete with all other nutrients, with the amount of exogenous pantothenate present in / added to that environment (despite disposing of pantothenate internalization/transport mechanisms/ability).

There might be a better term, and if you find one please tell me and I'll edit the question/text accordingly.

@Hans — I'm sorry but you are not defining anything. You are stating a consequence of this mysterious thing which seems as mysterious as the thing itself. Correlation of growth and replication? Why? And why should pantothenate be in or added to the environment? You seem to have some basic concern or agenda that you are not spelling out. What are you after?

I'm trying to understand which organisms are most pantothenate-"independent" in their growth and replication. As you wrote, it's possible that all life on earth requires it metabolically, if you factor out growth/division metabolic load, there is some logic in assuming that those whose growth/division is most independent of exogenously-sourced pantothenate most efficiently produce it themselves. If you have a better term or a better way to put it, as I wrote, please state it.

@Hans I think the issue is that assuming there is a correlation between growth and any one molecule, you'll only see it if that molecule is a limiting factor. Every organism that has a sufficient amount will see no relationship with growth, whether or not they produce it endogenously or how efficient or whatever.

@Hans — I also wonder if you possibly are thinking that because pantothenic acid is a vitamin for humans, it somehow is a limiting nutrient for all organisms. This would be a misconception. Essential amino acids are not considered vitamins but we require them in our diet, whereas bacteria (and even many lower eukaryotes that have retained the pathways make them quite happily). Of course there may be situations of this sort, where products needed for survival in an extreme environment are chemically difficult to synthesize for some reason, and some organisms have adapted better than others.


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Are there any organisms that do not respire?
I am not talking about not needing oxygen. I understand that there are organisms that do not need oxygen. I am asking if there are any organisms that do not respire. (Eg, only ferment) I would like to ask if there are any such organisms?
Edit:
Google searches show two contradicting points of view, as shown here and here

Homework questions are expected to show some prior research.

This is a genuine question, I am not doing any homework. I have done Google searches but nothing quite gives me the answer I am looking for (all answers relating to anaerobic respiration)

"homework" is not about the legitimacy of the question but the simplicity, simple questions are expected to show prior research to prevent mass asking of simple questions like homework questions. just edit your question to show some prior research and it will be fine. what and how did you research and what did you find and why is it not enough.

I see. Thanks for your suggestion! I have edited the post. Hopefully this is better!

Please state in (bio)chemical terms what you mean by “respire” and what you mean by “ferment”. Then everyone will be clear what you are asking. It may even enable you to find the answer yourself.

One example of a nonrespiring organism would be lactic acid bacteria
They're (nonrespiring) obligate anaerobes.
They don't respire, since they can't use an external compund (oxygen, nitrate, sulfur, iron, etc.) as a terminal electron acceptor. They instead use an internal terminal electron acceptor (e.g. Pyruvate). That requires constant regeneration of NAD. Lactic Acid Bacteria regenerate NAD by oxidizing Pyruvate to lactic acid. See this

If you are talking about organism that ferment, then you have LABs (described in markur's answer).
I am interpreting your question as you are asking an organism that is aerotolerant anaerobe (organism that cannot use oxygen but tolerate its presence). In that case, Cutibacterium acnes is an example.
Also, scientist recently discovered a multicellular animal that doesn't breath at all. A parasite named Henneguya salminicola having less than 10 cells hides in the muscles of salmon and does not breath oxygen. It is the only animal with no mitochondrial genome (a crucial portion of DNA stored in mitochondria that includes genes responsible for respiration). More about it in this article.

source: Stack Exchange

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

sort: votes


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What is the physiological difference between looking at small things vs far away things?
If you look at an item that is far away, vs a smaller version of the same item up close, such that both objects take up the exact same degrees of arc in your field of view, what do your eyes do differently to focus on that item? I know that your brain may interpret the information differently, but do your eyes themselves actually do anything different?
Edit:
What I've looked at so far:
I have already learned about the basics of how the eye uses ciliary muscles to bend the lens to look at up close objects, and then relaxes in order to look at far away objects.
What I do not understand is how, or even whether, the eye behaves differently when dealing with size. For example, what is the difference between reducing the font size on your computer monitor vs simply moving your computer monitor further away? You can reduce the seconds of arc taken up by the text by either method, and decrease the angle of the light hitting your retina by the same amount.
I have read many articles and watched videos about how the eye works, but all of these materials have focused on distance of viewed objects from the observer, without regard to size. My question here has to do with how or whether changes in size of an observed object elicts a different physiological response than moving that object closer and further away.

Welcome to the site. What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Our goal is not simply to be an answer site, but rather a site that promotes self-learning with some expert help along the way.

Please read about the lens of the human eye.

@anongoodnurse I've read a lot about the mechanisms by which the eye works including but not limited to the functioning of the lens and the muscles/tendons surrounding it. Now, I've only gone as deep as learning about ciliary muscles / zonular tension, but so far I've found nothing that moves in the direction of answering this question, which is why I'm here. What specifically regarding the lens are you referring to? Thanks. Again, I'm asking specifically about situations where the same percentage of your field of view is taken up by these different-sized versions of the same object.

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


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Where, online (preferably free) can learn medical topics in depth, specifically gastroenterology?
Where, online (preferably free) can learn medical topics in depth, specifically gastroenterology?
I'll try to be concise and to the point:

I have an Associate of Science degree where I actually specialized in Biology
I am asking for online classes, texts, videos, or other resources
My specific interest is in gastroenterology
My need is to understand the subject in depth I imagine several months of research will be required for me to find the answers I need.
Free or nearly free / very cheap sources are the only sources that interest me as I'm rather poor.

This is the end of the concise part The next part is to provide context and is skippable if you understand the question already really.

I'm sorry to hear that your health is failing. In short, you can't become an expert just like that, it takes several years of full-time training to become expert. However, there is much publically available information for many topics on the NCBI if you search. The latest research is published in journal articles, but these require specialist knowledge to interpret.

@MattDMo Thank you I am aware that asking for personal medical advice is considered off-topic. I am asking for education advice on the topic of biology. The context section was simply provided to help people understand what context I'm asking from, as to be as complete as I can in my query.

@bob1 Thank you for the link to the NCBI, I regularly read research (not just research articles) I figure I have about 2-10 to acquire enough knowledge. Simply reading the latest research, while fun, will not help me much as the research when it leads to treatments nearly always leads to treatments for people with significant money or charity cases, and I just don't make a compelling charity case.
I am seeking to spend the time and effort (not money) that is required to learn the topic of gastroenterology.

Check out https://clinicaltrials.gov for information on ongoing and upcoming... you guessed it! Clinical trials! You don't have to be independently wealthy or a charity case to join a trial, you just need to be (relatively) close to a participating hospital. Many patients are often eligible for trials, and don't participate simply through lack of knowledge of their existence, either their own or their doctor's. If you live near a research hospital, they often have many trials ongoing.

Also, upon rereading your question, I've decided to retract my close vote. I suggest editing out the "context" part at the bottom. We have to be very careful treading around questions like these, because askers can potentially take the first reference off the list of 10 someone provides, skim it and decide that's their answer, then treat themselves accordingly without involving a medical professional or understanding that a single datum of research does not necessarily indicate the way things truly are.

@MattDMo - I wouldn't do that. There's a lot going on here.

Although I voted to close this question, my advice is too long for a comment.
The short answer is, you can't. You can't read enough to learn "gastroenterology". You can go to med school (my oldest classmate was 44), or PA school (much less time). You need to know most of the basics of medicine/biology to understand one organ system, because they are interconnected. Gastroenterologists (off the top of my head) must also understand immunology, endocrinology, neurology, and anatomy (not to mention more basic basics like molecular biology and biochemistry.) Yet, there you are, without an answer. What can you do?
You can pore over the literature, but you won't understand it. You won't know relevant search terms, and whether what you read is reliable. But it doesn't hurt to try. Use Google Scholar instead of Google.
You can write in to various publications (free) where difficult cases are discussed and ask for physicians to help solve the problem or that print difficult cases that were eventually solved to see if they've seen a case like yours or can help you with your problem (The Washington Post and the New York Times are two of the many publications that highlight difficult cases.)
You can "hire" a good patient advocate (not all patient advocates are created equal.) Some people, even physicians, do this work pro bono. A good, empathetic physician who does patient advocacy work would be best. They will review all your medical records with a fresh eye, accompany you on your doctor visits, ask the doctor any questions you might not know to ask, and explain to you what your doctor said (patients don't "hear"/retain about 75% of what doctors tell them, and why they are recommending x, y, or z.) They will also give you an opinion (you need to see someone else/this doctor is competent and trustworthy/other).
Sometimes doctors don't know the answers, but since they can't find anything abnormal, they can tell you whatever is going on isn't going to end your life. Sometimes doctors think they know the answers when what they think is incorrect. The problem is that you don't trust your doctors so far, so the only option is to keep seeing specialists until the issue is diagnosed or resolved. It's expensive, and optimally, get an appointment at a medical center especially well known for excellence, and where cases are reviewed by a board comprised of various specialists.
But what you cannot do is "learn gastroenterology".
I know this doesn't answer the question as asked. But the answer to the question as asked is "nowhere".

Thank you so very, very much for your well-written and informative response! I genuinely do appreciate the thought, the effort, and the insight you have shared with me. You have provided me with some new avenues I had not understood existed! I am very tempted to mark this as the answer to my question, and after an additional month of continuing my search, I will!

I would like to ask, though, who is being helped by "closing" the question? And what can I do to prevent said closing?

Closing a question is a site-specific cultural thing, and it doesn't really "hurt" anyone. It does help to keep off-topic questions off the site. I only answered because I'm a physician who did pro bono patient advocacy work, and because I understand all too well from personal experience what it's like to know something isn't right, yet be unable to find a physician who is capable of making the correct diagnosis. In one case, the ninth doctor I saw immediately diagnosed me correctly, and I had the needed palliative surgery and medications. ...

...I also know how helpless non-medical people can feel in navigating the system. I cared about all my patients, but had a particular soft spot for all patients with difficult diagnoses. That's the reason I provided the answer even though it's off topic.


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If tinnitus is, in many cases, caused by damaged ear hair cells, couldn't it be solved by a mini cochlear implant that sends a constant signal?
If my understanding is correct, tinnitus is in most cases caused by damage to the inner ear hair cells, especially on the basal parts of the cochlea, which correspond to high frequencies. So, for example, you lose a few hair cells on the high frequency range (such as 14,000 Hz). This causes your brain to over-compensate the lost signal by essentially down-regulating the activation threshold of that range so much that it ends up assuming the cell is always on, rather than always off.
If that is correct, wouldn't a simple cochlear implant that replaced the lost cells by a dummy electrode that sent a "silent" signal 24/7 solve tinnitus? That electrode would emulate the signal that the lost hair cell would send when silent. That way, as soon as the brain receives that "silent" signal, it would up-regulate the activation threshold, and the ringing would stop.
There are ongoing trials that involve injecting stem cells, or small molecules such as FX-322, in order to re-grow lost ear hair cells, and these trials have shown some success against tinnitus, so, there is some evidence that restoring the absent signals lets the brain renormalize. The catch is, we shouldn't need fully functional hair cells to cure tinnitus. Replacing these cells with a dummy "always silent" cell would do the same job. Of course, the patient wouldn't be able to hear on these ranges, but I don't think most tinnitus sufferers want the ability to hear snapping shrimps, they just want to shut up the ringing.
Is my logic or understanding flawed?

How would you attach the electrodes without occluding the opening of the cochlea or otherwise interfering with the rest of the hearing range? It's  also highly invasive and expensive as the demands of asepsis and precision required are enormous. Apart from those concerns, do you have evidence that an approach like "sending a silent signal" might work? (Perhaps tested on other less-invasive parts).

@JiminyCricket. aren't cochlear implants a common procedure? Except these need to cover the entire hearing spectrum, and be connected to an outside device that sends precise signals, and decode these into the right impulses to emulate cells. So, we have these relatively complex devices as a common procedure already! A dummy electrode that just sends a 24/7 "silent" signal looks trivial in comparison. I could be (and probably am) wrong, but I'd love to learn why/how!

Short answer
You are right, with a few caveats.
Background
Most tinnitus cases are caused by sensorineural hearing loss, as you rightfully indicate, namely due to a loss of hair cells in the cochlea. The deafferentation of the auditory cortex and subsequent chronic inactivity of this region in the brain ultimately leads to the generation of intrinsic brain activity in the auditory cortex, which is perceived as a 'ringing in the ears' (PloS Med, 2005).
Cochlear implantation has been shown in a multitude of studies to ameliorate the symptoms of tinnitus; for a review see Linhares de Freitas Borges et al., (2021). CIs basically mask the tinnitus sounds by swamping it with electrically evoked activity in the auditory system.
A CI is a medical device for treating severe-to-profound hearing loss. It bypasses the damaged hair cells in the cochlea, and restores activity in the auditory nerve by direct electrical stimulation of auditory nerve fibers (Fig. 1). CI is, however, not a first-line treatment for tinnitus and remains in the experimental phase for that purpose, at least as far as I know. Tinnitus has been mainly addressed as a secondary outcome to hearing performance after CI for treating deafness, although prospective randomized controlled trials with tinnitus relief being the primary outcome are underway (Assouly et al., 2021).
However, your idea of a single-electrode 'dummy implant' isn't very feasible, because it is difficult to insert a cochlear implant such that one or more electrodes are in direct electrical contact with the cochlear region corresponding to the frequency (or frequencies) of the tinnitus (Fu & Shannon, 2002). The cochlear regions with hair cell damage differs between patients and depends on the type of hearing loss. Therefore, a regular CI with a multi-electrode array is inserted that covers the better part of the cochlea (barred the low frequencies).
Furthermore, a 'silent' (i.e., below threshold) electrical stimulus would make not much sense, as you wouldn't know when sufficient electrical activity was generated. Rather, these folks are treated with a CI and fitted with a with a clinical program to restore hearing function in that ear.
Another note of importance is the fact that CI results in substantial loss of the residual hearing in the implanted ear due to insertion trauma, and scarring later on. That's why treating an ear with tinnitus due to localized trauma (e.g., noise-induced hearing loss, for instance due to occupation or in professional musicians) may not be a good idea, because a CI doesn't restore acoustic hearing, it allows for the restoration of some hearing function, but it will never be anything like a normal ear. That's why, in general, only ears with severe-to-profound hearing loss should be treated with a CI, including for tinnitus patients (Punte et al., 2011. In the end, it will be a cost-benefit consideration between physician and patient to determine whether the loss of residual hearing weighs up against the chance and extent of treating the tinnitus.

Fig. 1. Cochlear implant system. Source: Mayo Clinic
References
- Assouly et al., BMJ Open (2021); 11: e043288
- Fu Shannon, Ear Hear (2002); 23(4): 339-48
- Linhares de Freitas Borges et al., Brazilian J Otorhinolaryngol (2021); 87(3): 353-65
- PLoS Med (2005); 2(6): e194
- Punte et al., Cochlear Implants Int. (2011); S1: S26-9

Thanks for taking your time to provide this extremely information-rich, well-researched answer. Just a small clarification, if I may: as we know, cochlear implants are designed to restore hearing, not to treat tinnitus. If treating tinnitus requires a simpler mechanism (i.e., constant stimulus, and covering just the outer part of the cochlea), it is still possible that there are simpler interventions that don't require drilling the cochlea, right? Or would anything in that space absolutely need to be internal?

@MaiaVictor thanks, happy to write about this stuff! I happen to work in the field :) I have clarified the answer (CIs are indeed designed to treat hearing loss, no more, no less). I however am afraid I don't understand what you mean with 'the outer part of the cochlea'. The cochlea is a bony structure and the auditory nerve cannot be accessed electrically easily through this bony capsule because of resistance issues. The reason that it is inserted in the cochlea is to maintain tonotopic (frequency specific) stimulation...

...this way functional hearing can be more easily restored. Because often tinnitus is caused in deafened ears, treating deafness and collaterally tinnitus is an interesting option. In case tinnitus is caused by causes other than profound hearing loss, a simpler solution may work, yet you have to mask the tinnitus by providing perceivable sounds. Therefore you could generate electrical white noise, but that would impair normal hearing, effectively making you hard of hearing. Inserting a CI at least provides you with meaningful stimuli. I have added the 'masking' effect in the answer, thanks!

I was thinking of stimulating the auditory nerve as it comes out from the cochlea, but now I see why that would be impossible. Thanks again for your answer. This disease is debilitating, and the fact it doesn't have a non-psychological treatment is depressing. I hope this will change soon.


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Cancer: computing the proliferation of DNA mutations in cancer cells
I have a question about cancer. How is it, that in a cancerogenous cell, once a specific gene changes, subsequent DNAs in cells end up exponentially acquiring more and more mutations?
Can, these mutations, for instance starting from a given, be computed?
Is there key genes, responsible for subsequent sequences of mutations in subsequent cell divisions, that are the subjects of what is targeted with drugs (to, fix, in this way, at a manageable level, the problem (and it's it possible to develop drugs that discover and target the responsible genes, ...?

This doesn't seem to be related to bioinformatics, it's more of a general biology question. You might want to ask on [biology.se] instead. One key thing you might want to consider is that in many cases, the mutation that causes cancer does so by affecting the DNA error correcting mechanisms of the cell. A classic culprit is P53.

Please edit the question to limit it to a specific problem with enough detail to identify an adequate answer.

The preliminary answer to approach your question are 'driver mutations' and its a specialist area of oncology. You need both the correct tissue, control tissue and funky bioinformatics regarding extracting minority alleles amongst the 'contaminants' in context to identify the mutations 'driving' the cancer. The Broad Institute have worked on this problem for a long time.
Your main question appears to be that given a 'driver mutation' what happens next. The question appears to be about biology of oncogenesis and its a different forum (Biology SE) in my opinion but is way outside my area.

Your assumptions are correct. There are genes that amplify mutation rate, once they get mutated/dysregulated.
Mutations in cancer are classified into different types. Each type has its own signature, which can be tracked back to its origin, since the sequence pattern is characteristic for e.g. specific enzymes or failed DNA repair.
One such mutation type is caused by e.g. APOBEC3. This enzyme usually mutates viral DNA. But cancer found a way to have APOBEC3 mutate its own genome. This increases the genetic variability of cancerous tissues and might allow them to gain new survival benefits. Jakobsdottir et al. 2022
Another enzyme that cancer is using to mutate itself is AID.
I don‘t think that drugs are used against APOBEC or AID. However, their relevance as a potential target for therapy is actively discussed (Olson 2018).


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How exactly does the human penis grow during puberty?
I learned that testosterone triggers the growing process, but I was unable to find anything else about this process. What exactly happens inside the penis during this period that causes it to grow? How does its structure change when it grows?

Welcome. Can you add your own research efforts? The question is broad and there should be a lot of info out there on the internet

Sorry if I don't know how to ask correctly yet. Does Googling the questions I asked and paraphrased it many times without getting anything beyond basic knowledge count as research?

Most of the results say "it just does that during puberty", or some are a little more detailed and say "testosterone causes that". I think the answer may lie in some specialized textbooks, but I didn't study biology at higher education level so I don't know what kind of books to begin reading in. Should I change the question to "Which book can I find this information in?"

https://pmj.bmj.com/content/postgradmedj/51/594/200.full.pdf. It would help to know what level of detail you're looking at. Do you want to know about the histology of the penis, the gross structure (shape/size), endocrine interactions, etc? Each of these is its own rather large field.

@MaximilianPress I see, so this is a more complicated question than I thought. If I wanted to know about how the cells and tissues structure changes, that would be histology, right?

@PennPaper yes that is my understanding. I would update your question with information about what you're specifically interested in, which appears to be how shape and composition of tissues changes over time. You might also consider migrating the question to SE Medical Sciences.


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Auxin-what happens to the auxin chemicals if the Sun is just above the plant?
The Auxins goes to the shady side for the elongation of the cell. This moves depending on the direction of sunlight. But, what happens to the auxin chemicals if the Sun is just above the plant?

Have you attempted to answer this question yourself by scouring the internet? Basically this question is a 1-liner and we encourage a bit more background and leads in a question.

Nope, There is no answer to the question. I always search it in the Net before i ask it here!

What did you find?


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Identify bone found on beach in Scotland
Found on a beach in Scotland, it's about 10cm long, any ideas what it is?

You should add the size too. it's a piece of skull. what's on the other side?

I cannot seem to add another picture but is is the same but 2 reccess on both sides. Is around 4 inches

It’s been suggested that it is A seal skull?

without scale this impossible to answer.

@karen you can upload 2-3 images, perhaps try a screenshot of thw image if the phone camera is too many mp for the site.


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Understanding the general dynamics of protein diffusion in cell plasma membrane
Background
I am doing an undergraduate research project on the modelling and analysis of protein diffusion in plasma membranes. I am a physics and computer science student so naturally, I have many knowledge gaps in cell biology.
My understanding so far
I have been reading so many papers, but I still can't have a comprehensive general picture of protein diffusion in the membrane and what precisely that entails. From my understanding, the widely accepted model is the one with the underlying cytoskeleton actin mesh-like filaments which compartmentalize the plasma membrane. In this model then, are only transmembrane proteins affected in their diffusion by the mesh-like structure, which they sometimes touch (because the filaments are close to the inner side of the plasma membrane)? Moreover, peripheral proteins or other types of proteins, because they do not touch the actin filaments, do they just diffuse freely in a Brownian motion?
I understand that generally, proteins undergo diffusion either

freely (Brownian motion)
in a compartmentalized hop-diffusion way
or through irregular diffusion given lipid rafts (which generate concentration gradients).

Questions
But which proteins are we talking about, is it peripheral, transmembrane or else? Where are these proteins in the bilipid layer? And which direction are they diffusing, is it lateral diffusion or diffusion within the bilipid layer? Are all these 3 diffusion models going on at the same time but each affecting different categories of proteins? I can't have a clear picture of this ecosystem and would appreciate some insights on these questions so that I could begin my research with the simulations.

You might want to go to the library and have a look at Alberts „Molecular Biology of the Cell“, an older edition of which is also available on the NCBI Bookshelf. Publication-grade knowledge might be too detailed at your point of education and might not fill in the „big picture“. We know a lot more about directed processes on the cell, so read about: endocytosis, glycocalyx, secretory pathway, receptor internalization/sequestration, clathrin coated pits, etc… I mean „Brownian motion“ is nice and all, but we‘re talking about living things here ;)
For your questions:
Which proteins? Transmembrane proteins, receptors, pumps, pores, actin associated proteins, motor proteins (Myosin) etc.
Which direction? You’re looking at lateral diffusion (like lipid rafts). The bilipid layer is too thin to support anything else but lateral diffusion, since as far as I know, membrane proteins are pretty much „stuck“ at the membrane, unless they react to a signal pathway. If we‘re talking about selective pores/pumps, then movement through the membrane might be interesting to you. Also: flippase can flip lipid molecules from one lipid sheet up to the other.
Note that temperature has a big effect on cell membrane fluidity. Cells regulate the fluidity by embedding cholesterol into the lipid layer. One can measure the fluidity using FRAP (fluorescence recovery after photobleaching). That method might help you understand how diffusion in membranes works.
And yes, all the different diffusion models are going on at the same time. And so do tons of other processes. Welcome to molecular biology.


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Identification of butterfly from caterpillar
i visited a butterfly house and they didn't know which butterfly will be the caterpillars in the picture, my first guess is 'papilio aegeus'. I think the eggs/ caterpillars were on a 'paulownia tomentosa' plant, but i'm not sure. (Identified with the app 'flora incognita)
My first guess would be papilio aegeus.
Thanks to all answering and helping me out.

I'm sure you meant to add the picture (it's surprising how often people forget). Please take our [tour] and refer to the [help] as and when. It'd be helpful if there's some idea of scale to the creature if possible.

Yes the pictures are missing, i deleted them on accident, but added them now. I'm sorry and thank you for telling me. For scale i just can say they are 2-5 mm.

Where and when were these pictures taken? What is the size of the critter?

Like i wrote the pictures are taken in a butterfly house and the caterpillar is 5mm. It was 4 days ago.
Butterfly houses mainly don't have food plants for the caterpillars, so the butterflies are laying eggs on not suitable plants.


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What's this housefly-like bug?

When it flies around it looks like a slightly lazy housefly.
About a centimeter long.
Has a pointy beak (slightly blurred here by the shadow).
Loves flying at people. Tickly when it sits on you. Hard to brush off - clings on hard. Very resilient - you can swat it a couple of times and nothing will happen.
Makes a crunch when properly squashed. Sighted in central Israel (Beit Shemesh).
What is it?

it is a louse fly https://en.wikipedia.org/wiki/Hippoboscidae they bite and the wound can take several months to heal completely.

Good to know. Thanks @trondhansen !

BTW Your reference points to another reference that says this particular type is a Pigeon fly and a further reference says that they will not normally bite humans unless they can't find their regular host (pigeons) around - and there are lots of those here! Also says that if desperate enough to bite humans, their bites are just "itchy".

i know too little about them to make an answer,one of the types we have here is the deer louse fly and they bite many types of mamals including humans,i live in norway but the deer louse fly is common in most areas where one can find deer-roe deer-moose.


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Can changes of transposable elements in Drosophila be detected using RNA-Seq?
Not sure if this is the right forum for such a question, but please refer me to the correct one, if possible.
Does anyone has experience in working and detecting transposable elements using High-throughput techniques?
We would like to  identify the sequence of our TE and were wondering if this is possible via such methods (bulk- or scRNASeq)?
any ideas of others methods to run reach this goal would be appreciated.
thanks

With RNA-seq you will capture only retrotransposons. If that's your goal, then I would suggest enriching isolated RNA somehow,  (e.g. using microbeads that have a library of complementary sequences). Keep in mind: Some RNAseq workflows require polyadenylated RNA.
Why not use whole genome sequencing? Blumenstiel 2014
Or why not do something like this (it's just a quick idea, please back check with professionals):

Design multiple primers against Long Terminal Repeats or Terminal Inverted Repeats
Amplify transposons from Genomic DNA from drosophila
Excise Band from gel, extract transposon sequences of preferred size
Fragment DNA
Ligate sequencing adapters. Amplify. Your high throughput sequencing library is now done
Apply to sequencer

Please know that switching from bulk to single cell might increase your cost by a factor 50. (One cell costs very roughly 100 dollars, so sequencing 100 cells costs 10 000). So you need a good reason to switch to single cell.

thanks for the answer and also the link to the paper. It looks interesting.
I didn't plan on doing scRNA, it was just to know if this might be a better option than bulk.
Just to understand it better, you mention I can only identify retrotransposons with RNA-Seq. Is this because of the polyadenylation necessity?

RNAseq sequences RNA. It doesn‘t need polyA, necesserily. It only measures Retrotransposons since retrotransposons are the only transposons that are RNA at some point in their lifetime.

@AssaYeroslaviz  - note that the most differences between RNAseq and other NGS techniques lies in library-generation (includes e.g. reverse transcription). The sequencer itself always sequences a 'similar' DNA-library in the end that was ligated to adapters, no matter if the isolated source is mRNA, gDNA, miRNA, PCR-products, etc.


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Why are there so many carbonic anhydrase structures in the Protein Data Bank?
I've been looking through PDB — the Protein Data Bank — and I noticed that the protein with the most structures is human carbonic anhydrase II (UniProt: P00918), with over a thousand X-ray structures.
This seems surprising to me, as carbonic anhydrase is a zinc-containing enzyme which catalyses a really simple reaction, and doesn’t seem to be part of any key signalling pathways.  In terms of relevance to disease or as a drug target, all I could find was on DrugBank was a few glaucoma drugs which have this as their target (diclofenamide, methazolamide, acetazolamide), and those are really old (60 years).
So, what is it about carbonic anhydrase that makes it so interesting?  Is it that more or better drugs are needed to target it? (For what disease?)  Is it that it’s a really interesting scientific model of a metalloenzyme?  Or something else?

Answering this question really needs some hard work, and we expect the poster to make a start looking through the PDB entries in terms of date/CA type/species/whether they have an associated paper/whether they relate to a complex with another molecule. Have you looked at some of the recent and older papers in which the work is reported to see how they justify their work and who funded it? Please do, and let us know what you find.

It certainly is related to disease! There are tons of inhibitors (as David mentioned in the comments Aslam & Gupta 2022 ). The reaction is simple but maintaining the pH of your blood is essential (keep a perfect equilibrium between $CO_2$ and $CO_3^{2-}$). It's essential because pH determines if hemoglobin binds/releases $O_2$.
It's so famous because every beginner biochemistry course will talk about carboanhydrase at some point. The enzyme is very stable and can be purified relatively simply from blood, which was possible even 60 years ago. It helped early biochemists understand enzyme kinetics. Carboanhydrase in particular was interesting, since it has a ridiculously fast turnover rate ($10^6$  molecules per second). That makes it perfect to describe enzyme kinetics ($K_m$ and $k_{cat}$) and also chemical equilibria in general.
Bob1 pointed out that some courses even require you to crystallize, make an x-ray structure of carboanhydrase and submit the result. So carboanhydrase is like the absolute tutorial enzyme of biochemistry, which explains the inflated structure count.

It certainly is related to disease. I had a look at the hits on PDB, and a huge number are of inhibitors of CA. I searched for "Carbonic Hydrase Inhibitors" and found a short piece on this topic on NCBI Bookshelf that starts: "Carbonic anhydrase inhibitors are a medication used to manage and treat glaucoma, idiopathic intracranial hypertension, altitude sickness, congestive heart failure, and epilepsy, among other diseases." Why else would you determine the structure of protein that has already been done, and who would fund you?

@David True, I found a few links to diseases too but the number of structures still seems like way more than the disease relevance would suggest.  Surely not enough to be the most studied enzyme - still somewhat puzzling

@AlexI I think you will find that as per the second part of Markur's answer, a number of courses for biochem will have "purify, grow crystals, X-ray diffract and submit structure" as part of the course requirements.

@AlexI — This was a comment/criticism of the first sentence of this answer. It was not an answer to your question. I do not answer questions in comments. When/if I have considered the matter I will give you a balanced answer.

Carbonic Anhydrase is heavily researched because of carbon dioxide capture.
It’s hoped to be used in getting $CO_2$ from combustion exhaust to hydrogen carbonate, and thence to other capture reactions in industrial settings.
Also for possible more efficient plant $CO_2$ capture, so plants can grow better with less water loss.

This is very interesting, but would mainly make sense if those were (eg) extreme thermostable or pH-stable versions; rcsb.org has 1000 structures of plain old human CA2, so I feel this can't be the whole answer


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Source for Squirrels Dislodging Nuts to Drive-Off Predators
I was reading a recent article by the Boston Globe on Harvard's Arnold Arboretum and it off-handily mentioned something very interesting:

‶I love the hickory collection,″ [Michael] Dosmann admits. ‶You have these tall trees that reach up to the heavens. You’re walking under a tall canopy of almost pure golden yellow.″ But be careful, Dosmann jokes. ‶Sometimes the squirrels intentionally try to dislodge the hickory nuts while you are directly underneath, just to frighten you out of their territory. You might get knocked in the head by a hickory nut, but it’s worth that gamble to experience the hickory collection in autumn.″

The idea of squirrels being able to drive away a predator like this is really amazing, but I am doubting if it is true. On one hand, Dr. Dosmann has a PhD in Ecology from Cornell University and is the the head curator for the arboretum, so I don't think he is exaggerating to impress a reporter. On the other hand, this behavior would require a lot of intelligence and I question how effective it would be on any human-sized predator.
I could not find any other sources that mentioned this behavior, but that could just be because I am not sure what key words I should be searching for. Searching 'squirrel antipredator behavior' on Google Scholar mostly returns articles about when squirrels flee from a predator, but I can't think of another phrase that would describe this behavior.
Has anyone heard of squirrels driving possible predators off by dislodging nuts at them? If not, are there any similar behaviors in other organisms?

I've both heard of the hypothesis and experienced it (although their aim isn't that good). They don't do it every time you walk under a nut-bearing tree with a squirrel in it, though. It may depend on how habituated they are to humans in their territory. I am also struggling to find references.

One of the reasons I want a formal source is it is easy to see how this belief could come about through a bias in data collection. If squirrels drop nuts by accident at a constant rate, completely independent of humans' presence, then squirrels will only be observed to drop nuts when humans are nearby (since when there are no humans nearby, no one will observe the drops). Without video cameras or other equipment to measure how often nuts are dropped when humans are not nearby, I do not see how you could rule out this possibility.

Your thinking is correct, and I'm pretty sure the same point has occurred to Dr. Dossman. Maybe he can provide you with a source? I'm serious here; it's not that hard to reach scientists these days. Or you just may be correct.


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Methods to obtain the mass distribution of an ensemble of bacteria?
Are there any mainstream methods to obtain the mass distribution of a bacterial population?
What kind of assumptions to they make?
Could anyone point me to some references?

Well, careful centrifugation can separate cells based on size.

Short Answer:
Flow Cytometry or Dynamic Light Scattering (DLS) might be the most "mainstream" methods out there that might give you a size or volume distribution. Then you need to do some reading how to get bacterial mass from size or volume.
Image Cytometry:
Krößbacher et al. 1998 used electron microscopy (which is not mainstream)
Oldewurtel et al 2021 used Phase microscopy and complex image pipelines (also not mainstream, but definitely cheaper than electron microscopy). They also stress that "surface-to-mass ratio remains nearly constant", which is very nice, since that means that one does not need a weighing scale, but only know the size of bacterial particles.

Therefore, cellular dry-mass density varies systematically with cell shape, both during the cell cycle or after nutrient shifts, while the surface-to-mass ratio remains nearly constant on the generation time scale.

Flow Cytometry:
Knowing that one can determine bacterial mass from its size, one might just use flow cytometry to get the size distribution (see Felip et al. 2007) and then calculate the mass.
Dynamic Light Scattering
DLS can also determine size distributions of particles and was used with bacteria (Vargas et al. 2017).
(Field-Flow Fractionation)
Something fancy I found: Sharma et al 1993

Thanks, and how do people estimate the density of bacteria? (needed to go from a size distribution to a mass one)

@Gyromagnetic: Do you really need the exact mass distribution (as opposed to a relative mass distribution)? Either way, you can here use macroscopic measurements, looking at the average volume and mass of a bunch of cells.

In addition to Markur’s answer, Coulter counters suck the cells through a small capillary (in an electrolyte solution), which also serves as a conductor in an electrical circuit. They then estimate the cell volume by the change of conductivity of the capillary.
In my experience this method is more easy and robust than many others (e.g., flow cytometry) and as far as I can tell, the device is rather cheap and low maintenance – on account of being established and mass-produced technology.
Some relevant assumptions that go into it are:

If you care about relative volumes: All cells are equally affected by the electrolyte solution and have the same conductance properties. If you care about absolute volumes: The cells are not affected or in a known manner.

Cells do not stick to each other in a way that prevents disentangling double measurements, i.e., two cells entering the capillary at the same time. (If this happens by pure coincidence, you can statistically handle this.)


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What makes humans feel cold?
I have seen various sources talking about the effects of oestrogen on temperature: all of them agree that it makes you cold but they seem to explain the reason differently. One states that oestrogen dilates vessels and improves blood flow to extremities which lowers body temperature but another stated that it reduces flow to the extremities by thickening the blood and a different source states that the hormone reduces flow by restricting vessels.
This leaves me to wonder two things: which of these is correct and do we feel cold because the nerves in our skin are cold (and our internal temp near constant), perhaps because blood flow to them is restricted, or because the hypothalamus is cold?

Your „neurons in skin“ assumption is the right answer. There are receptors specialized on cold perception (McKemy 2013)
They can be activated by menthol (analogous to capsaicin from spicy food activating heat receptors), that‘s why mint chewing gum feels cold, it has menthol.
However, I don’t know how these receptors work biochemically, the mentioned paper talks about changed ion transport as a direct consequence of cold, causing receptor activation and calcium signaling.


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Why aren't complex-stabilizing proteins like transcription factors considered catalysts/enzymes?
I'm not asking the question on a superficial level. Obviously, (most) transcription factors are not acting directly on a substrate to produce a chemical change. I pose the above question as more of a philosophical inquiry.
First, a definition: A catalyst is a substance that increases the rate of a chemical reaction and is not consumed in the reaction. As every biochemistry class emphasizes, catalysts do not change the equilibrium constant of a reaction, only the rate.
So for example, if we take the following example of transcribing a gene of length $n$ ($G$) into a transcript of length $n$ ($M$).
$$
\ce{RNAP + G + nNTP <=>> RNAP + G + M} \mbox{    (Reaction I)}
$$
The hydrolysis of the NTP's bonds drives the reaction forward (source). The Gibbs free energy has decreased. Obviously, there is some probability that the NTPs in solution would spontaneously polymerize into the length-n transcript, this possibility is unfathomably infinitesimal though.
The RNA polymerase is acting as an enzyme here, since it's 1) increasing the rate of an otherwise slow reaction and 2) not being consumed in the reaction. Our nomenclature is consistent as we usually reserve "-ase" suffix reserved for enzymes.
Transcription factors bind elsewhere on the DNA and facilitate (or impede) the formation of RNA polymerase complex from its constituent subunits ($mS$). Assume we have an activating transcription factor $TF$. We can model this as:
$$\ce{TF + mS <=> TF + RNAP} \mbox{    (Reaction II)}$$
Putting these reactions $I$ and $II$ together, you might have:
$$\ce{TF + mS + nNTP <=> TF + RNAP + M}$$
From our understanding of activating transcription factors, we know that this will increase the rate of the transcription reaction. The TF is not being consumed in the reaction. So, what am I missing here? Why isn't this transcription factor considered a catalyst for helping to stabilize the initiation complex?

TFs are a big group and at least some are considered catalysts - e.g. histone deactylases/acetylases. Because they aren't part of the reaction; your supposition about the reactions II and III are incorrect. In chemistry the TF would go over the arrows!

If this is a question about philosophy you are on the wrong site. If you are using this as a platform to make an argument, you are misusing the site. If this is a question about historical linguistics, SE English Language and Usage might be more appropriate. And, paradoxically, your definition of an enzyme in naïve historical terms, although used in chemistry and taught to undergraduate biochemists, does not conform to what we know or think about enzymes. You must be aware that biochemists regard enzymes as macromolecules that participate in chemical reactions to increase their rate.

I think the rewording of this question is devious. It sets up a straw horse because of the weakness of his original question. Biochemical classes talk about the properties of enzymes, not catalysts, and we do not talk about "factors and catalysts". If you want to ask a question about catalysts, ask it on SE Chemistry. It also suggests he is not interested in knowing why biochemists describe proteins the way the do, but is indulging in what our Help terms a "rant". Using the site as a soap box for his jesuitical casuistry.

I’m voting to close this question because it is an attempt to start a discussion regarding a point of view rather than a question seeking an answer.

Because the TFs DO NOT PARTICIPATE in the catalyzing reaction themselves, and that reaction involves breaking of chemical bonds in the substance that's being catalyzed and forming temporary chemical bonds between it and the enzyme, which is not the case with the TFs.

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.

Do you mean TFs (transcription factors) instead of TTs? Please [edit] your post and clarify.


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Do cancer cells use as much NADH as normal cells?
Recent literature shows that cancer cells have a different electron transport chain mechanism from normal cells and both of cancer cells and normal cells use NADH as electron donors. So, is there a difference in the number of electron donors required between cancer cells and normal cells? What possible mechanisms could explain this difference?

Reference:
Huang, Huaiyi, Samya Banerjee, Kangqiang Qiu, Pingyu Zhang, Olivier Blacque, Thomas Malcomson, Martin J. Paterson et al. "Targeted photoredox catalysis in cancer cells." Nature Chemistry 11, no. 11 (2019): 1041-1048.
Kim, S. Y. (2018). Cancer energy metabolism: shutting power off cancer factory. Biomolecules & Therapeutics, 26(1), 39.

Could you please explain in your own words what is proposed. It is not apparent from the figure and “different ETC mechanism” conjures up some alternative form of the various complexes, which is highly improbable. I am not going to read the original paper to find out — questions here should be comprehensible in themselves.

Also see Warburg effect. http://en.wikipedia.org/wiki/Warburg_effect_(oncology)

"MAS" (according to one of the papers you quote) is the malate-aspartate shuttle. That is, electrons from cytosolic NADH cross the mitochondrial membrane, but the inner mitochondrial membrane is impermeable to NAD(H), a key point not very clear from your diagram/description

Short answer:
Yes, NADPH is definitely enriched in cancer cells, since cancer tends to rely more on glycolysis. That way, much less NADH is consumed into the electron chain. It was even proposed to treat cancer using NAD+ precursors to shift NAD/NADH balance: Santidrian et al. 2013

Tumor cells also generate high levels of reduced forms of NAD+, NADH, and NADPH as important cofactors and redox components (4, 5). These altered metabolic activities can be linked to mitochondrial dysfunction that inhibits OXPHOS, increases ROS, promotes uncontrolled growth, and causes DNA damage that further supports a metastatic phenotype

The energy metabolism in cancer might be one of the most skewed and dysregulated aspect of any cancer cell.
One reason is actively discussed: Hypoxia. Cancer grows. Fast. Faster than blood vessels can grow into the tumor to support it with oxygen. So the tumor is constantly suffocating. That's why cancer relies on oxygen independent metabolism (Glycolysis, aka the "Warburg effect"). In the later stages of cancer transformation however, it seems that a cancer cell can re-activate oxidative phosphorylation (OXPHOS, or mitochondrial electron chain with oxygen as terminal electron acceptor).
This review (Zheng 2012) name some very interesting reasons why that is the case:
Glycolysis yields more metabolic precursors for growth

i) Glycolysis is more suitable for cancer growth. Since proliferation of cancer tissues is faster than normal tissues, it not only needs energy, but also needs metabolic intermediates for the biosynthesis of macromolecules. Many intermediates from glycolysis and the truncated TCA cycle can be used to synthesize macromolecules, such as nucleic acids, lipids and proteins, which are required for cancer growth and proliferation (2,30).

Glycolysis generates Energy Quicker (despite being inefficient)

ii) Too efficient products of ATP may not a good thing for cancer cells. If cancer cells use high-efficiency glucose, ADP is converted to ATP. The high concentration of ATP will inhibit phosphofructokinase 1 (PFK1), the rate-limiting enzyme in glycolysis and pyruvate kinase 1 (PK1), and glycolysis will be inhibited. Inhibited glycolysis is unfavorable for cancer cell growth. Although glycolysis yields less ATP than OXPHOS, the speed of ATP generation in the former is quicker than in the latter, which is suited to the energy demands of rapid proliferation tissues such as cancer and embryonic tissues (11). Generally speaking, rapid proliferation tissues rely more on glycolysis for ATP production whereas differentiation tissues rely primarily on OXPHOS for energy production (13,31). If using glycolysis inhibitor 3-bromopyruvate (3-BP) treats tumors, it is more efficient for rapid growth of tumors than slow growth of tumors.

Glycolysis enhances Invasion

iii) Hypoxia is often observed in cancer tissues, and glycolysis offers growth advantage of cancers under this hypoxic environment (4). Glycolysis produces lactate which is released into the extracellular space. An acidic microenvironment provides a growth advantage to cancer tissues over normal tissues and enhances the invasion and metastasis of cancer cells (32,33). In addition, lactic acidosis inhibits glycolysis and favors aerobic respiration as a means of energy generation (14).

Glycolysis is less Cytotoxic

iv) Due to the decrease of mitochondrial OXPHOS, less reactive oxygen species (ROS) are generated, which are cytotoxic to cancer cells (34,35).


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Why’s brush bordered columnar epithelium found in intestine and not brush bordered cuboidal when I’ve been explained that they have the same function?
I searched for differences between their functions which would result in their positioning but none of it satisfied the answer to my above question.

Would "It is what it is, and it appears to work perfectly fine that way" be a sufficient explanation? Or does it need to be teleological, like "the gut lumen is plenty wide enough for a collumnar epithelial lining, whereas the tubules of the kidney aren't" kind of thing? Otherwise I don't understand the question. Btw, on this site, you are expected to show evidence of your search, not just state that you did one. Thanks.

I guess teleological was the word to be used I’d like to know why the columnar epithelium is the one chosen to be in the intestine. And for the research part I tried searching it in multiple ways on the Internet, how should I prove that? By attaching files of my searches? Or was that not the correct method of research. Thanks for replying

Actually a link to any of the sites you looked at (1, better 2) would have sufficed. E.g. "Wikipedia (link) says nothing about the difference between columnar and cuboidal...)" nor does Y (link). It's not any more difficult than that. We're not lunatics. We're here to help. I tried, I hope I succeeded. In evolution, teleological often doesn't really explain things.  Birds don't have wings so they could fly. Birds are able to fly because their ancestors evolved wings, among other modifications.

"...I’d like to know why the columnar epithelium is the one chosen to be in the intestine." This is a teleological statement. Nothing chose columnar epithelium for the gut. It developed because it works best. Maybe many more functions are required of it, so it must be a larger cell (I really don't know.) To guess why is only that: a guess. It's the function of the cell + evolution/selection that determines the outcome.


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why do spirogyra turn brown after formation of zygospore?
in the sexual reproduction of spirogyra, the reproductive parts of the 2 spirogyras come together to form a structure called zygospore. after this formation spirogyra turns brown. why is it so? i want to know the reason of colour change only

Can you provide a reference for this happening? Are you sure this is actually something that happens naturally versus an experimental manipulation (e.g., staining)?

my professor asked me this. He said this happens and that no one has been able to answer this. i was thinking the reason is death

"I said so" might be good enough for your professor, but it's not sufficient for this site. We expect questions to demonstrate prior research, which includes evidence that a thing happens before asking "why".

i am sorry for the inconvenience but he is not a very good teacher


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Explanation for the results of Topoisomerase I treatment of ERCs - Gel Electrophoresis
This part of a 1997 paper published in The Cell (David A. Sinclair & Leonard Guarente, 1997) discusses the presence of extrachromosomal rDNA circles (ERCs) in greater numbers in old mutant yeast cells when compared to young ones. All the lanes to the right of the "old untreated" lane are treatments carried out to the old yeast cells.
There are two scales on the figure, the left hand side has a scale for the length of linear DNA, while the right has one for circular DNA (I think?) which appears to move faster through the gel than linear DNA of an equivalent size.
Excluding the Kpn1 lanes and the young yeast cell lane, there are two clusters of bands around 19.3kb ccc and just above 40.4kb ccc. Would I be right in thinking that the writers are saying these clusters are due to the presence of concatenated ERCs (near the 40.4kb ccc marker) and non-concatenated ERCs (near the 19.3kb ccc marker)?
I don't understand the results of the topoisomerase I treatment, it doesn't look to change the gel much when compared to the old untreated yeast lane. The description states that the topoisomerase I treated rDNA migrates more slowly through the gel, though this doesn't seem evident from the figure. There is a "linear genomic [rDNA]" label on the LHS above the 40kb ccc on the RHS, though I am unsure what it is referring to. Presumably it is the size of fragments of the genomic rDNA after it has been treated with another restriction enzyme? But there is no prior restriction enzyme treatment mentioned. This is the part I am least sure about.
Excerpt from the paper relating to the figure in question is below, and the full paper is linked here.

Several experiments were performed to investigate whether the circular rDNA molecules were oligomers of the 9.1 kb rDNA repeat. The
rDNA molecules had a faster mobility relative to linear DNA size
standards in the absence of ethidium bromide, a known property of
circular DNA (Figure 3, between the 19.3 and 40.4 kb size markers).
Digestion of old genomic DNA with KpnI (which cleaves once within the
rDNA repeat unit) prior to electrophoresis reduced the ladder of bands
to a single 9.1 kb species, demonstrating that the circular rDNA
molecules consist of directly repeated multiples of the rDNA unit
(Figure 3). Further, cleavage with BamHI had no effect on the banding
pattern since rDNA is refractory to this enzyme. A partial KpnI digest
reduced the abundance of the large circular species, while increasing
the abundance of smaller ones. This implies that the large species are
comprised of interlocked smaller circles (i.e., concatamers) that are
released during digestion. Finally, treatment of the DNA with
topoisomerase I, an enzyme known to relax supercoiled DNA, caused the
mobility of these DNA species to migrate more slowly, coincident with
the linear genomic rDNA (Figure 3). By quantitating the levels of
total linear and extrachromosomal DNA from old wild-type cells (see
Experimental Procedures), we estimate that the amount of ERC DNA in
old cells can reach levels equal to the total linear yeast genome.

Thank you for your help.

I’m voting to close this question because this site exists to answer specific problems in biology that are likely to be of general interest. It is not a journal club to discuss the details of particular published papers.

I think it's okay to ask about particular papers, but some problems about this post are that the title is not a question or suggestive of a question, and the apparent question asked here is buried deep in the body of the post.

Thanks for your help! have changed the title and the length of the post. Just wanted to provide some context without people having to comb through the paper.


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Koshi and Goldstein substitution matrix
In their article (Context-dependent optimal substitution matrices for exposed residues (Koshi-Goldstein, 1995)), more precisely in the substitution matrix displayed in Figure 2, one one hand, the legend says:
"Graphical representation of the probability of a mutation from the amino acid in a given row to that in a given column during an evolutionary time of 40 point-accepted mutations per 100 residues"
And on the other hand, I've noticed it is a lot more likely for an amino acid to be deleted than to be inserted (cf. screenshot, blue is low probability, orange/red is high probability).

Taken from: context-dependent optimal substitution matrices for exposed residues (Koshi-Goldstein, 1995)
How could one explain that? If that was true, all proteins sequence would slowly become smaller and smaller, right? Is it because it doesn't consider when proteins sequences merge? (I'm no biology expert, I'm sorry if the vocabulary I'm using is not exact. You are encouraged to correct me).

You should always provide a complete citation; "Koshi and Goldstein" can be one of a number of papers, and you shouldn't leave it to your reader to guess, nor should you reproduce figures without a proper reference to where it came from.

I have made the necessary adjustments in my question. Thank you for your insightful feedback.

Year is helpful but still not a complete citation. You'll want the title, journal, page numbers; these days a DOI is a nice add. And "Koshi-Goldstein" makes it appear like you are talking about one person with a hyphenated surname, not two.

It seems that there IS a deletional bias across genomes Kuo & Ochman 2009:

Based on over 5,000 indel events in noncoding regions, we found that deletional events outnumbered insertions in all groups examined.

That would be one mechanism of genome shortening. However, there are mechanisms that also increase the size of the genome:

DNA polymerase tends to do "replication slippage". That's when DNA polymerase detaches from the DNA during replication and re-associates upstream. That way, whole genes can get duplicated (which is also a driver of evolution, since there‘s a second copy to mess around with)
Transposable elements (ancient viral sequences) keep replicating and re-inserting into the DNA.
Overall, natural selection keeps genes at full length and functional

So although small edits tend to be on the deleterious side, big edits are the opposite, causing an overall expansion of the genome.

Worth considering selection, too. Populations need not follow mutational biases if selection favors something different.


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Additional to SNP (variant) calling, what is genotype calling in human genome?
Variant calling in human genome aims to determine in which positions there is polymorphic site or in which positions at least one of the dna bases differs from a human reference genome. Then beside variant calling, what is genotype calling in human genome?
Maybe I am not familiar with human genome SNP calling;  I would like to know the reason behind that the process of genotype calling is typically only done for positions in which a SNP has already been called.

Genotype calling is the process of determining the genotype for each individual and is typically only done for positions in which a SNP or a ‘variant’ has already been called.

Welcome to the site, please take a [tour] and visit the [help] for more information about this site and what we do at Stack Exchange sites. Please note that one of the requirements for questions here is some evidence of research from you (the asker) in your attempt to answer the question. If you think carefully about the word "genotype" you should be able to answer this easily.

useful info:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3593722/

useful info: https://training.galaxyproject.org/training-material/topics/variant-analysis/tutorials/dip/tutorial.html

According to https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3593722/
Genotype and SNP calling:

The process of converting base calls and quality scores into a set of
genotypes for each individual in a sample is often divided into two
steps: genotype calling and SNP calling. SNP calling aims to
determine in which positions there are polymorphisms or in which
positions at least one of the bases differs from a reference sequence;
the latter is also sometimes referred to as ‘variant calling’.
Genotype calling is the process of determining the genotype for each
individual and is typically only done for positions in which a SNP or
a ‘variant’ has already been called. We use the word ‘calling’ here to
signify the estimation of one unique SNP or genotype. However, we note
that some analyses can proceed without determining the exact identity
of each genotype, but instead allow uncertainty regarding genotypes to
be incorporated directly into the analyses.
Genotype and SNP calling can proceed, as in early studies, by counting
alleles at each site and using simple cutoff rules for when to call a
SNP or genotype. More-recent methods incorporate uncertainty in a
probabilistic framework. In the probabilistic framework, it is also
possible to further incorporate additional information regarding
allele frequencies and/or patterns of LD. We review these different
approaches below, starting with the simple methods based on counting
alleles.
Early methods for calling genotypes
Early NGS studies based both SNP and genotype calling on separate
analyses of data from each individual sampled. Typically, analyses
would first involve a filtering step in which only high-confidence
bases would be kept. The most common cutoff used would be a Phred-type
quality score of Q20 (QPhred = 20). Genotype calling would then
proceed for each individual by counting the number of times each
allele is observed and using fixed cutoffs.
In early NGS papers, in which only a single genome was analysed, SNP calling and genotype calling were more or less identical, as an inferred heterozygous genotype or a homozygous non-reference genotype would imply the presence of a SNP. For larger data sets containing many individuals, a SNP would be called if any individual was heterozygous or homozygous for a non-reference allele. However, this might not be an optimal way of proceeding, because the expected false-positive rate will increase linearly with the sample size.

Welcome and thanks for your answer. Basically this is a link only answer. It is best to answer the Q in your own words and use citations to support your argument. Ad verbatim copy-and-pasting large swaths of text from the internet is not very useful.

The quote isn't a very helpful or accurate one, I'm not really sure where you got it but I can appreciate how it may be confusing.
For all intents and purposes genotype calling and variant calling are the same thing. I suppose genotype calling refers to the process of determining the genotype that an individual carries at a particular point in the genome (i.e. the number of copies of each particular allele that exist at that position). Variant calling is the process of identifying whether there exists any variation across individuals at a particular locus, which clearly you can only do once the genotypes have been called. So you can't call variants without knowing the genotypes and by calling genotypes you are kind of automatically looking for variants. So there's not really a particular distinction to be made, it's just slightly different terms that might be used in different contexts. You'd be more likely to talk about variant calling in the context of genotyping lots of individuals in a cohort and assessing whether any of them vary from each other or a reference sequence.
As for the quote

... typically only done for positions in which a SNP or a ‘variant’ has
already been called

This is more getting at the point that genotypes are usually called at positions in the genome which are known to already vary in human populations by previous studies. Genotyping costs money and for a lot of functions, genotyping every position in the genome isn't really necessary since most of those positions don't vary at all between humans and so aren't very useful. Therefore, people figured out which positions tend to vary a lot between humans groups/individuals and just genotyped those instead of the entire genome. So instead of genotyping all ~3bn base pairs, you might genotype 500,000 which you know are likely to be variable. Nowadays, people are moving towards sequencing all base pairs in the human genome since it's more affordable to do so.
Just to add some more confusion, 'genotyping' is often used synonymously with calling genotypes on such genotyping arrays (or SNP arrays or SNP-chips as they can also be known as), whereas 'sequencing' is when you call genotypes at every position in the genome, not just those on an array.
In general, genomics terminology can be confusing because different people use different terms for the same thing, and the same term for different things, so it's always good to try and understand what each term means fundamentally rather than relying on the terms themselves.

Thanks a lot,  too few community members understand the related information.


text:
How quickly could mice evolve to avoid mousetraps through artificial selection?
So, we have a mouse problem in our attic.  I set traps routinely to keep the population down.  We have taken pains to exclude them by sealing cracks and holes, etc., but they still manage to find their way in somehow.  Alas.
In any case, I find myself wondering this.  More and more frequently, I find the traps disturbed, the bait taken, evidence of mouse activity, but no dead mice.  Clearly some mice are able to take the food without getting snapped, or they have learned how to set off the traps and then take the food.  It seems to be happening more and more, which makes it seem like they are getting smarter.
I'm curious about this.  Could I make the case that the mice who successfully steal sunflower seeds and peanut butter from me are more likely to successfully mate, and this forms a process of artificial selection?  There are quite a few uncontrolled variables, of course.  Here are just 3:

Surviving in the woods all summer long until fall, when they come indoors is probably a greater effect.
There are other houses around, all bordering the same large woodland area, and so plenty of other and different opportunities to get food.
I am probably not setting the traps exactly the same way each time, nor are all the traps equally sensitive.

BUT if there were to be a controlled experiment with a specific population of mice, calibrated traps, etc., how many generations would it take for "mousetrap-aware" mice to evolve?
NB - I am not suggesting that anyone undertake this study, as I'm sure it would violate many ethical boundaries!
-

I think evolutionary pressure in urban environments is a truly fascinating area of research. Nonetheless I am afraid the current question is open for discussion and won't fit in too well on this site I reckon. Adding your own research efforts so far can help focus the question and shape it into a more answerable format.

I have not attempted any research on this, lacking both the scientific background and the ability to control the experiment

You need to distinguish between evolving and learning. The traits to evade traps would not be lost if there was a single generation of rats not exposed to traps, but any learning would be lost (unless mice did something like explicitly pass on knowledge like humans do). In the same way human did not evolve from being able to ride horses to being able to drive cars.

Have you considered the possibility that something else is removing the food? In addition to rodent pests, leaving food out in the open could be attracting insect pests, like ants. I've personally witnessed ants clean the peanut butter off mousetraps, and it doesn't take long once they've discovered it.


text:
Identification of a strange skull
My father is a fisherman in the Baltic sea, and he has found this very strange skull. I would like to know to which animal it belonged. Can someone help identify it?

Unfortunately I don't have more photos or anything to measure the scale. This picture is all I've got.

You've got a coarse black cloth with a weave in the back-ground. If you can find the cloth type, you can probably make an estimate of rough dimensions. I'd hazard a guess of about 30-40 cm across the widest part and similar top-to-bottom.

Thank you for your suggestion! I've manage to get rough estimate of the dimensions - around 30x25 cm.

@BassAstral if you edit that information into your question, more people will see the dimensions and you are more likely to get an answer.

I thought it might be a vertebral scute from a sea turtle, but apparently there are none in the baltic sea

@timeskull in Baltic you can't exclude anything because just recently there was walrus here who unfortunately died. Here has been several findings common monkfish, dolphins, whales and other usually not Baltic species who usually get lost their way or are brought by ships (smaller). Same way many years there was grey seal living in Black sea who was probably taken from Baltic sea as pup by some sailor and released there when it wasn't so cute anymore and started biting.

Looks like this is a neurocranium of a tuna or a similar species (dorsal view on this site).
I've also found a very similar picture of Atlantic blue tuna from USA, which seems to support that this is indeed a neurocranium.(source of the picture).

Thank you all for your help!

Can you add an inline image and supporting information of your ID? As of now it's more of a comment than an answer. Additional supportive evidence can consist of checking whether size measures and habitat correspond to your specimen, and whether the area of distribution of your ID matches where the specimen was found etc.

Thanks @AliceD! I've added an image and some more information, although I don't know how to specify all of the required information. My skills and knowledge in that regard are rather limited.

Great answer! You cannot know how happy I am that you posted an answer. I thought I was crazy for thinking it was a skull (based on the atlas bone and the sutures). Wish I could upvote this 10 times.

Just upvoted this 15 more times. :) Rarely is such a definitive answer provided so quickly to a mysterious object, much less from the OP themself. Very well done.


text:
Graph of new species discovered per year
I'm looking for historical data on the number of new species described each year.
I found the RetroSOS report (page 3), which provides a time series for 2000–2009:
Year    Total number of new species described
------- -------------------------------------
2000    17,045
2001    17,003
2002    16,990
2003    17,357
2004    17,381
2005    16,424
2006    17,659
2007    18,689
2008    18,225
2009    19,232

This table suggests that the rate at which new species are described might be accelerating. To get a better sense of this, I'm looking for data going further back than 2000, and beyond 2009.

Here is an answer; as I'll explain, it's not getting the same numbers you quoted above (that could be a deep methodological rabbit hole), but it gives a reasonable answer.
I started from the data at ChecklistBank, specifically downloading this file (warning: 45 MB) and unzipping it.
The data file contained looks like this:
Biota [unranked]
  Animalia [kingdom]
    Acanthocephala Rudolphi, 1802 [phylum]
      Archiacanthocephala Meyer, 1931 [class]
        Apororhynchida Thapar, 1927 [order]
          Apororhynchidae Shipley, 1899 [family]
            Apororhynchus Shipley, 1899 [genus]
              *Arhynchus Shipley, 1896 [genus]
              *Neorhynchus de Marval, 1905 [genus]
              Apororhynchus aculeatus Meyer, 1931 [species]

So: we extract every line with the string "[species]"; pick out the 4-digit string following a comma; and sort and count these lines. This gives us a file with a count for each 4-digit string, which should be the year the species was described (there's of course more complication than that, but that gets us most of the way there).  Then we can filter out obvious mistakes and count the number of described species per year in what's left.

I drew blue rectangles for the Napoleonic wars, and World Wars I & II. I started to play with breaking out species described by Linnaeus but didn't finish troubleshooting ...
I posted the results here.
The numbers for 2000-2009 don't match the ones you posted above, but I assume that's because there are a million different ways you could count new species ... however, I think my method is at least reasonable/defensible ...
| count | year |
|-------|------|
| 9845  | 2000 |
| 9670  | 2001 |
| 11102 | 2002 |
| 10482 | 2003 |
| 10601 | 2004 |
| 9809  | 2005 |
| 10871 | 2006 |
| 11632 | 2007 |
| 10649 | 2008 |
| 9939  | 2009 |

system("grep \\\\[species\\\\] dataset-9837.txt | \
   grep -Pv '^[[:space:]]+\\*' | \
   grep -Po '(?<=, )[0-9]{4}(?= ?\\)?\\[)' | \
  sort | uniq -c > yrs.txt")
## 1. select lines with [species]
## 2. unselect lines starting with whitespace + * (deprecated synonyms)
##  -P = perl, v = complement
## 3. grab 4-digit string after ", " and before space/paren/square bracke
##    -o = extract only matched pattern
## 4. sort and count

## attempt to get Linnaean species
system("grep 'Linnaeus, 17.*\\[species\\]' dataset-9837.txt | \
   grep -Po '(?<=, )[0-9]{4}' | sort | uniq -c > linn.txt")

library(tidyverse)
dd <- (read_table("yrs.txt", col_names = FALSE)
    |> setNames(c("count", "year"))
    |> filter(year > 1750, year <= 2022)
)

linn <- (read_table("linn.txt", col_names = FALSE)
    |> setNames(c("count", "year"))
)

theme_set(theme_bw())
ggplot(dd, aes(year, count)) + geom_point() +
    geom_smooth(method = "gam",
                method.args = list(family = quasipoisson)) +
    scale_y_log10() +
    ## wars
    annotate(geom = "rect",
             ymin = rep(1, 3),
             ymax = rep(100000, 3),
             xmin = c(1803, 1914, 1939),
             xmax = c(1815,1919, 1946),
             alpha = 0.2,
             fill = "blue") +
    labs(y = "new species described")
ggsave("species.png")

Nice work. One larger problem is that plant names do not contain the year of publication, so you miss about 400k species and many more names. Synonyms would also need special attention as subsequent recombinations should not count as newly described species.

I do exclude lines starting with *, which I think (?) takes care of synonyms. Any idea where to get plant species checklists with year of description ... ?

https://powo.science.kew.org/ shows year of description, but I don't know if it can be ingested as easily as the COL data ...

For plants IPNI provides statistics per year of newly described names: https://www.ipni.org/statistics
For Fungi and Plant the annual rate of new species has been around 2000-2500 species/year each in the past decade according to https://nph.onlinelibrary.wiley.com/doi/10.1002/ppp3.10148


text:
ID Large, broad flat bone found in Gulf of Mexico
`1
Is this a tooth? A rib? Or a fish?
I found this in about 4’ of water in the Gulf of Mexico/Galveston.
It is slightly curved and the side edges have numerous pointy parts. On one side at the bottom it has what looks like the root or something that attached to something else. It is sitting on my thigh. I am a 5’9” male. Any help would be greatly appreciated.

Excellent picture, bizarre and intriguing object, I'll be following this one closely. Welcome to the site.

Well it seems like there was a similar bone found in Missouri and identified here. Turtle. This great site. Very detailed explanation of that question. I am satisfied that what I found was part of the back of a sea turtle.


text:
Are gene conversions and expansion/contraction of repetitive (satellite) DNA examples of directional, non-random mutations?
Are gene conversions and expansion/contraction of repetitive (satellite) DNA examples of directional, non-random mutations? For some context, it was brought to mind as a result of reading the following;
"Within the broad category of gene mutations we should consider not only the classical, purportedly random changes, but also the internally directed changes that are called gene conversion and duplicative transposition (collectively constituting molecular drive) (see Dover et al., 1981)." (From 'A Botanical Critique of Cladism', pp 14-15)

Please include your question in the question. A title is a title. This will also make you explain more fully and clearly.

For Repetitive Sequences:
Duplications of repetitive DNA (as in replication-slippage) are not "as random" as radioactivity, but still, there is no genetic mechanism that intentionally triggers the duplication of a gene. Also, during replication slippage the site of DNA-pol re-association is random, causing duplications of different lengths. So I'd still call it a change that's both "random" (in terms of sequence) and "non directed" (as in "lacks a direct purpose").
Together, I'd prefer the term "duplication" over "mutation" for the expansion of repetitive/satellite DNA, (while "duplication" is a type of "mutation")
For Transposons:
Your reference cites 'duplicative transposition', and a lot of repetitive DNA originate from transposons (Belyayev 2020). For jumping genes, I would prefer the term „recombination“ instead of "mutation".
The appearance/exchange of specific large sequences is called Recombination.
From Harret & Sherrat 1997:

In bacteria, two categories of specialised recombination promote a variety of DNA rearrangements. Transposition is the process by which genetic elements move between different locations of the genome, whereas site-specific recombination is a reaction in which DNA strands are broken and exchanged at precise positions of two target DNA loci to achieve determined biological function. Both types of recombination are represented by diverse genetic systems which generally encode their own recombination enzymes. These enzymes, generically called transposases and site-specific recombinases […].

Furthermore, so it‘s incorrect to categorize transposons as „non-random“, since they insert mostly at random sites and can cause random DNA-damage next to the excision/insertion site Wicker et al. 2016.

Indeed, the 3,000 bp flanking the excised transposons can contain over 10 times more mutations than the genome-wide average. Since DNA transposons preferably insert near genes, this is correlated with increases in mutation rates in coding sequences and regulatory regions.

In my eyes, a better example of "directed"/"intended" (but random in sense of sequence) mutagenesis would be AID, an enzyme that increases antibody binding variability by intentionally introducing point mutations at very specific and isolated sites inside one gene.

I can see how AID increases genome-wide mutation rates, but the individual mutations are still 'random' in the sense that there's no bias towards a specific sequence appearing at any site in the genome. On the other hand, it would appear to me that slippage at repetitive sites, and gene conversions (transpositions too though I didn't mention them), bias the appearances of specific sequences in the genome.

AID does not act genome wide. It‘s directed towards the variable region of immunoglobulin genes where it introduces random mutations in an isolated section in a controlled manner. You are mistaken, Transposons are not specific. They can even insert inside genes an inactivate them, and if too many transposons are active, they will destabilize the genome  (see piRNAs and infertility). In general, when talking about mutation, geneticists don‘t immediatley think about transposons. A far better term for large sequences changing location would be „recombination“

Understood for immunoglobin genes although the same point applies, the 'gene-wide' mutation rate doesn't bias the appearance of specific sequences or nucleotides (or does it?). I was not saying transposon insertion sites is non-random: what's non-random is the appearance of sequences specifically corresponding to the transposon sequence.

Yes, but the appearance of specific large sequences is better described with the term „recombination“ than with „mutation“. Yes, the term mutation is associated with transposons, BUT the mutation from transposon is due to random errors that come with sloppy deletion/integration of the transposon and subsequent DNA-repair (and not due to appearance of large specific sequences) Wicker et al. 2016.

Yeah, it makes sense to better describe it as recombination. What about expansion/contraction of repetitive DNA and gene conversions? Do you agree that this is directional mutation when it comes to appearance of specific sequences or do you think this is still, technically, random?

I'd say gene conversion is more recombination than mutation. I don't know about the expansion/contraction of repetitive DNA, isn't repetitive DNA just tons of inactive Transposons?

Not really. When repetitive DNA is being replicated, the nature of the repetitive region results in the slippage of the replication machinery, which can wind it backwards (thus re-replicating the same repeats, resulting in more repeats) or forwards (thus shortening the number of repeats). The actual repetitive sequences make it more likely that this kind of slippage happens during replication, thus biasing the appearance of more of the same repetitive DNA.

I see. This mechanism is not recombination then, obviously. I’d call this simply „(Gene) duplication“, when talking about this mechanism. Using the term „mutation“ isn‘t really incorrect, but still much to general or abstract compared to „Duplication“

Well ... i dont know if it's 'gene' duplication if you're not duplicating a gene, although short short repetitive sequences can be duplicated. From ScienceDirect: 'In replication slippage, a long stretch of repeat sequences in the DNA folds back and pairs on itself, forming an internal hairpin or stem–loop structure, during replication.' This seems to me to be a simple replication error, and therefore can be called a mutation. Of course you can be more specific in describing any kind of mutation.

Exactly, "mutation" is just too broad. It's good practice to specify the type of mutation, if you know it. If one says "cancer mutates" that can mean anything from chromosome breaks (aneuploidy) to point mutations. However, if one says "gene mutates", most people think that of (functional or non functional) point mutation(s).

Let us continue this discussion in chat.