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What is the proper anatomical name of the "band of Richer" that wraps around the quadriceps femoris?
There's this fascial band called the band of Richer that wraps around the quadriceps femoris muscle above the knee (in this illustration, look for it near the left knee). It seems to stem from the iliotibial tract. I could only find the term "band of Richer"/"Richer's band" from artistic anatomy sources, and it sounds like this particular fascial band is named after Paul Richer. Even though it seems to be noted in some sources meant for artists, surprisingly lots of them completely miss this very visible surface feature. In the photo next to the illustration you can clearly see parts of the vastus medialis above the knee bulges out because something is tying it tightly above.
So what is its proper name, if there's such thing? Is it simply "band of Richer"? What about its Latin name?

Suprapatellar tract (Kollmann). Yes, it does exist, but it isn't a ligament, as some illustrations in art anatomy books are trying to indicate.
The name Richer's band, is a term that emerged in art schools. Early 20th century books on Artistic Anatomy have this term imprinted as convention. You'll find it in Arthur Thompson, U. Parkes, Eugene Wolff, Faringdon Moses, and others, where the name of Richer's band is used (published before 1930). Only some of these authors have described it anatomically, but in all cases only partially. Up to the point of the appearance of Joseph Sheppard's Artistic Anatomy, this Richer's band had steadily grown into a thick and firm tendon. For the sake of art students, it has always been important to inform about this "band", since it has an effect on the exterior surface form of the thigh, which can be observed in the live model, as well as be admired in Greek sculpture of the classical period. Richer's band merely served as an explanation for this surface phenomenon in the art studio, and the term has never been used in medical books on anatomy. However, it has beed discribed in one way or another in anatomy books. Sobatta illustrated it, Julius Kollmann described it in his book, Plastische Anatomie, and so on. Kollmann calls it the suprapatellar tract. (Plastische Anatomie des menschlichen Körpers, third edition).

The reason why this thickening in the fascia of the thigh became known as "Richer's band" is because Dr. Paul Richer, collaborator and friend of the Anatomist Dr. Paul Poirier, made a clinical description of it in the last decade of the 19th century, Paris, to explain once and for all what causes the indentation in the skin covering the vastus medialis a few fingerbreadths above the kneecap.
Dr. Poirier, in the multi-volume edition of "Traité d'anatomie humaine, publié sous la direction de Paul Poirier (et A. Charpy)", in the volume on myology, illustrated mainly by Paul Richer, makes brief mention of this thickening band of the aponeurosis of the thigh, adding that he would be going back to this matter soon. In the anatomical illustrations of the lower extremity in this volume, done by Richer, this band had been meticulously added, but no further mention had been made to it in the text.
Poirier writes on page 286,
"je reviendrai plus loin sur les détails que présente cette partie antérieure de l'aponévrose fémorale, renforcée en bas par une band. arciforme (V. fig. 152)"
Translated, "I will come back later to the details of this anterior part of the femoral aponeurosis, reinforced below by an arciform band (see fig. 152)".
Poirier, who was a close friend of Richer's, it seems, had left it to Richer to coin it in his own words.
So we find in Richer's Anatomie Artistique, 1892, the following sentence,
"Il existe à trois ou quatre travers de doigt de la rotule une condensation des fibres transversales de l’aponévrose, formant un véritable faisceau ou ruban aponévrotique, que je  propose de désigner sous le nom de fibres arciformes inférieures de l’aponévrose fémorale.  (PL. 68, 70 et 71.)"
Translated, "Three or four fingerbreadths from the patella, there is a condensation of the transverse fibres of the aponeurosis, forming a real aponeurotic bundle or ribbon, which I propose to call the inferior arciform fibres of the femoral aponeurosis.  (PL. 68, 70 and 71.) "
But in Richer later book, published as an advanced course at the l'Ecole de Beaux-Arts, Nouvelle anatomie artistique du corps humain. Cours pratique et élémentaire, 1906, a more detailed description is given, which may serve as filling the gap left in Poirier's previous text.
On page 71 Richer writes,
"L'aponévrose d'enveloppe du quadriceps présente une disposition spéciale qui joue un grand rôle dans les formes extérieures de la région. (PL 24, 25, 26 et 27.)  Il existe, à trois ou quatre travers de doigt au-dessus de la rotule, une condensation des fibres transversales de l'aponévrose fémorale, formant un véritable faisceau ou ruban aponévrotique qui mérite de prendre le nom de ruban des vastes. En effet, ce ruban aponévrotique obliquement dirigé embrasse dans sa courbure l'extrémité inférieure des deux vastes, le vaste interne et le vaste externe. L'extrémité externe, épanouie en éventail, se confond avec le fascia lata, pendant que l'extrémité interne, formée de fibres plus condensées, croise le vaste interne suivant une direction perpendiculaire à celle de ses fibres charnues, à deux travers de doigt de son extrémité inférieure, passe ensuite sur la tubérosité fémorale interne et descend au-devant du couturier, avec le tendon duquel ses fibres s'entre-croisent à angle aigu.  Aux points où ce faisceau rencontre les cloisons aponévrotiques intermusculaires interne et externe, des fibres se détachent de sa face profonde qui descendent le long de ces cloisons pour aller s'insérer avec elles aux divisions inférieures de la ligne âpre. De sorte qu\in véritable anneau ostéôfibreux se trouve ainsi constitué, anneau disposé dans un plan transversal et incliné de haut en bas et de dehors en dedans, et enserrant étroitement toute la partie inférieure du muscle triceps."
Translated, "The envelope aponeurosis of the quadriceps has a special arrangement which plays a major role in the external shape of the region. (PL 24, 25, 26 and 27.) Three or four fingerbreadths above the patella, there is a condensation of the transverse fibres of the femoral aponeurosis, forming a veritable bundle or aponeurotic ribbon which deserves to be called the ribbon of the vastus. In fact, this obliquely directed aponeurotic ribbon embraces in its curvature the lower extremity of the two vastus medialis and the vastus lateralis. The outer end, spread out like a fan, merges with the fascia lata, while the inner end, formed of more condensed fibres, crosses the vastus medialis in a direction perpendicular to that of its fleshy fibres, two fingerbreadths from its lower end, then passes over the medial femoral tuberosity and descends in front of the sartorius, with the tendon of which its fibres cross at an acute angle.  At the points where this bundle meets the internal and external intermuscular aponeurotic partitions, fibres detach from its deep surface and descend along these partitions to be inserted with them in the lower divisions of the linea aspera. In this way, a veritable osteofibrous ring is formed, arranged in a transverse plane and inclined from top to bottom and from outside to inside, tightly enclosing the entire lower part of the triceps muscle."
Thus was born, the band of Richer.

I woud like to add on a personal note, that I chatted with a retired surgeon from Germany regarding the suprapattelar tract. I said that I was glad to see it being mentioned by Kollmann, although it is a rarity that presents more interest to painters and sculptors that to the medical profession. He reassured me however, that since the knee joint is a particularly difficult joint in surgery the suprapattelar region mentioned by Kollmann is well known by medical professionals since special attention is required in this region during operations. I therefore refute the previous answer given by kmm

There is no such ligamentous or connective tissue structure as depicted in the linked image. This is a visual artifact created by the border of the vastus medialis or just a fanciful artistic interpretation. Based on 25 years of teaching human anatomy, I suspect the latter, because the artist's image shows this band much more proximal than the distal extent of the vastus muscles.

Here is a link to a photo of a dissection of this region that shows no structure there.
Indeed, Gray's Anatomy's list of eponymous structures does not list it:

There is actually quite a lot wrong with that drawing. The rectus abdominis extends too far superiorly, which really shortens the thorax.

So what do you think is causing the vastus medialis to bulge out? I know this is a very old source, but I learned about this Richer's band from a very modern anatomy course, with very modern photographic evidence. This band behaves very similarly to the extra tendon from the biceps brachii that wraps around the hand flexors, causing them to bulge out. And this is not the only source either, in Paul Richer's Artistic Anatomy (Anatomie Artistique), it's also mentioned in diagram in passing, strangely enough, as "Richer's band".

Also I'm not quite sure what you mean by "the rectus abdominis extends too far superiorly, which really shortens the thorax". I think if you overlay the diagram onto the photo it's not even that far off, the measurement seems to line up well. Doesn't the rectus abdominis extend all the way to the fifth or even fourth pair of ribs, right above the bottom of the gladiolus, as the diagram depicts?

It's just the distal extent of the muscle as it grades into the quadriceps tendon. The muscle can hypertrophy with exercise, but the tendon won't, so it gives the appearance of a band. I have dissected easily 400 lower limbs and have never seen anything like this. There is no retinaculum-like structure (which is what think you are describing) at that position in the lower limb.


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Do bacteria produce proteins other than ribosomal proteins when grown in wrong culture media?
Someone I know has done an experiment using pure culture and given it to me for rna-seq analysis.
But there are a few problems

the bacteria she gave me as reference was initially a Staphylococcus sp. but it turned out to be Bacillus sp. Upon my analysis.
upon analysis I could only find ribosomal RNAs for Bacillus sp.

So my question is does a bacteria that is grown on a wrong culture media produce any proteins even in small amounts?
Will it have a lot of rRNA transcripts? Because I see all the sequencing reads map to ribosomal region. Are those not dependent on growth conditions? Or is it that Bacillus can survive on different media in a vegetative state and thus have a large number of ribosomal RNA?

From my experience, bacterial RNA-seq libraries derived from exponentially growing cells that have not been prepared using an rRNA depletion kit will result in >80% of reads mapping to 16S and 23S rRNA genes.
Ask your colleague if they used a bacterial rRNA depletion kit prior to RNA library preparation.
It is also my understanding that rRNA tends to be more stable than mRNA when exposed to ribonucleases given its structure and sequestration in ribosomal proteins. If your colleague performed rRNA depletion, my next hypothesis would be that the non-rRNA species were degraded due to poor technique during library preparation (samples too warm, contaminating RNase).

I will ask them and let you know the exact thing done. Thank you @acvill for your help.

If the cells are growing at all, then they are actively expressing a whole bunch of different proteins.
Ribosomal RNA, however, makes up the vast majority of all RNA in a typical cell, however.  There are also far fewer different rRNAs than there are mRNAs, so the relative concentration per rRNA is even greater.
As such, unless rRNA is excluded (e.g., using methods like those described in the linked paper), the mRNA reads will typically be swamped by rRNA reads.

I am getting very few reads for other proteins. Like you said they maybe getting swamped by rRNA reads. Thank you @jakebeal for your answer.

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Kansas Insect (Black Bee/Wasp?) Identification
I live in Kansas (Pottawatomie County), and I found a bee-like insect in my bedroom. The creature looked like this:

The insect about 5 cm long in size (as you can compare it with the window blind), and it appeared once in the morning (9 AM) and once in the evening (8 PM). It seems to be dark in body color, with some yellowish color on its legs and wings.
Could you please tell me what is the name of this bee-like species? And is this thing toxic / dangerous to human?
In addition, what would be the best way to kill it? Do spiders prey on it? Does ultraviolet (UV-A) light attract this insect so that I can kill it with a bug zapper? Or should I call the pest control for help? Edit: Or do I have to kill it at all?
Thank you so much for your help!

@anongoodnurse Thank you so much for the help! So would it be safe to say that these wasps' sting is unlikely to cause life-threatening symptoms?

@anongoodnurse Hello, thanks for helping the OP. Do you think you could make your comment an answer? As you know, it's not ideal to have answers in comments.

@BryanKrause - Sure, sorry!

It's a paper wasp; it looks like maybe a Northern Paper Wasp (better photo needed.)

Northern Paper Wasps are most commonly found in the Midwest states. They are likely to build nests near humans as that is where a lot of wood can be found (homes, barns, sheds, fences, firewood, landscaping, etc.). The wasps use wood to create their nest.

They are 15mm to 21mm (0.59" to 0.82") long, which fits your photograph. They are considered beneficial to keeping caterpillars under check:

Northern Paper Wasps are so effective at this pest control that they are almost welcome in organic gardens since their presence negates the need for chemical pesticides.

...is this thing toxic / dangerous to human?

It stings, the sting can be painful and may cause localized swelling, but they aren't likely to sting unless you irritate it (e.g. try to kill it and miss, etc.) If you're allergic to hymenoptera stings, leave it alone and get someone else take care of it! If there are children in the house, it is probably better to kill it than to risk their getting stung.
If it appears daily, there is probably a nest somewhere in your house (a wall or attic) with a small space where the wasp can access your interior. The larger the nest, the more easily wasps get irritated, so if you ever see two wasps in your house at the same time, call an exterminator with experience in wasp nest destruction. If it were a bee, you would call a nest extractor, who could relocate the hive.

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How much Kanamycin is too much for selection in dh5α E. coli?
I'm using Kanamycin for selection after electroporation of my plasmid containing a kanamycin-resistance gene at a concentration of 50mg/L prepared in 1000x stock that is usually kept in frozen aliquots.
When preparing LB plates for selection, I usually prepare a 300ul dilution of the 1000x stock (30ul kan + 250ul h20) and spread that onto my plates evenly. This usually works fine.
However, on some occasions, if I let the plates sit for a week or so, I'll go ahead and reapply more antibiotic just in case.
Is there an amount of kanamycin that is toxic to the E. coli, even if they've been successfully transformed? Are there any side effects I should be aware?

Can't answer for what is too much, but kanamycin is a highly stable antibiotic. No need to replenish after only two weeks:
https://bitesizebio.com/10252/ye-olde-antibiotic-plates/
https://bitesizebio.com/9655/antibiotic-stability-keep-your-gunpowder-dry/


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Are living cells electrically neutral?
I found random scientific table which had a comment attached:

the cells must be electrically neutral.

Per my knowledge whole intracellular solution contains more electrons than protons (definition of negative charge) when cell rests and extracellular space is more or less electrically neutral, means it contains same number of protons and electrons at any time.
Could someone tell me whether my understanding is wrong or this comment below this scientific table I shared?

There are two ways to think about the "charge" of a cell. One way is by looking at all the chemical species inside the cell and calculating their sum charge. If you do this, you're going to get a neutral solution up to many decimal points of rounding error. Therefore, we don't really care or bother to do this. You'll get the same for the extracellular space, and really anywhere else you measure outside of a physics experiment. Electrical forces are incredibly strong, and when you get even modest charge separation the result is lightning.
In a table like is presented at your link, you can sum up some of the "major" anions and cations but you won't get anywhere near neutral; the comment is just making sure you don't think that based on the table there are no other charges there, we just don't care about them that much for membrane potential, they're boring and static. The reason we don't care about all the other ions so much when we calculate membrane potential is easy to see from the equations that actually tell us about membrane potential. Take the Goldman equation:

In this equation, you'll see we don't sum all charges inside and outside the membrane. Instead, we look at the ratio of concentrations of ions multiplied by their permeabilities through the membrane; anything that isn't permeable gets multiplied by zero and we ignore it entirely. The reason for this is that the potential across a membrane we measure isn't because there are measurably more or fewer positive or negative charges on either side, but that there is an imbalance in permeability of ions relative to their charge and concentration. Without any electrical forces involved, ions will tend to diffuse until their concentrations are equal on both sides of a membrane. However, if there is charge involved, the net diffusion is influenced by electrical forces such that for each ion there is some voltage at which the net movement of that ion is zero even though the concentration is not equal: that's the reversal potential for that ion calculated by the Nernst equation. The Goldman equation gives the weighted sum of all of those ions that can transit the membrane to give the overall equilibrium potential when there is zero net flow of charged ions.
I'll recapitulate the reference I quoted from Alberts et al here:

For a typical cell, 1 microcoulomb of charge (6 × 10^12 monovalent ions) per square centimeter of membrane, transferred from one side of the membrane to the other, changes the membrane potential by roughly 1 V. This means, for example, that in a spherical cell of diameter 10 μm, the number of K+ ions that have to flow out to alter the membrane potential by 100 mV is only about 1/100,000 of the total number of K+ ions in the cytosol.

Extrapolating from that, if we really only had the ion species in Table 11-1, what would that mean? Intracellularly, that table shows about 140.5 mM of net positive charge inside the membrane. 10 um sphere * 140.5 mM * 6 * 10^23 ions/mol = about 3.5 x 10^11 positive ions to move over 1.3 x 10^-5 square cm of membrane. 3.5 x 10^11 / (1.3 x 10^-5) / (6 x 10^12) = about 4500 volts to get to neutral - there aren't any biological voltages anywhere near that range.
Back to the title question:

Are living cells electrically neutral?

Yes, if we think about the summed charges inside the solution of a cell. However, if you look across the plasma membrane of a cell, you will find there is a miniscule charge separation at rest, principally because membranes are permeable to potassium ions and there are more positively charged potassium ions inside cells than outside of them (for most cells and solutions). Because a few more potassium ions flow out of the cell than flow in, there would be a little more positive charge flowing out than in if the voltage were zero; this creates a voltage across the membrane until there is a balance between charge and concentration gradients, and we say that most cells are electrically negative (in a typical range of -50 to -100 mV for mammalian cells). However, this is just charge sitting across the membrane that acts like a capacitor, you'll find positive charges sitting against the outside of the membrane as they get pulled toward the negativity inside the cell.
Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K., & Walter, P. (2002). Ion channels and the electrical properties of membranes.

Thank you for clearing out these misconceptions. Now I've understood that resting potential (~-70mV) what is commonly suggested by many sources, is potential difference across membrane (so charge difference in regions near membrane), which does not mean that whole cell is negatively charged.
But, Could you elaborate more around why cell (let say at rest) is thought to be neutral at default? Why even small charge could not it have? Would it actually be similar to lighting phenomenon?

@LashaBukhnikashvili I don't really know what to say besides what I've already written in this answer. It's not perfectly neutral, but it's so close you might as well consider it as such. There's just no process to create any substantial level of charge separation, biologically or otherwise.


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Why do people make "aaagh" noises when they make an effort (e.g. trying to hit a ball hard)?
I'm referring to, for instance, grunting in tennis. It refers to how many tennis players make loud "aaagh" noises when hitting a ball. In daily life, people often also do this when trying to lift something heavy, and etc. Recently, I noticed cats also make a similar noise (albeit smaller) when they are jumping onto a level that they can only barely reach.
Thus, the question: are there biological reasons why people cannot help but make such noises when trying to do something physically challenging? Does making noises help them achieve it for physiological reasons, or only for psychological reasons?
I searched online and wasn't able to find an answer.

There's smattering of research papers published on the topic of grunting and physical exertion, including at least one on tennis. The ones I've skimmed seemed to have small sample sizes and focused on testing physical performance with and without grunting, not on the physiology of the act. Next time you do any kind of brief physical exertion, pay attention to what your body does naturally. Most people will inhale in preparation, briefly hold their breath at the moment exertion, and exhale through the motion. A sequence that seems to prime the body to grunt.

@MikeyC do you mind sharing the references you found? Thanks!

@MikeyC that breathing motion is called the Valsalva manoeuvre

@bob1 - The question is why do people grunt [when doing the Valsalva maneuver], not "What is it called when people take a deep breath, close their glottis and exhale against the closed glottis?"

This is not an opinion-based question; there is an answer (or are answers). I VTC because of lack of any research.

Mainly because they are English speakers - this kind of utterances is specific to a phonetic system and culture. E.g., Russians are more likely to use "ehhh/uhhh" when mzking an effort and "aye/oye" when simething hurts them (rather than "auch").

Hilarious. Agree with MikeyC and RogerVadim. Clearly the answer is so obvious, I don't think it requires a "real research answer", that's just woeful pedantry. It's not biology, just a consequence of physics. The answer to the question "why noise" is because noise/vocalization/phonation comes about when the glottis is partially closed. After closing it (Valsalva maneuver), air remains unexhaled, so remaining pressurized air follows with a vocalization as the glottis goes to a full relaxation state. Partial Valsalva maneuvers are also vocalized. A slackening glottis is the entire explanation.

@SPr - That is absolutely not "the entire explanation." Muscles groups are strengthened or not depending on if there is a grunt or no grunt (according to studies). It is indeed physiology, and physiology is part of Biology. So it is an unconscious attempt to strengthen oneself against a task. Maybe you should question your assumptions before declaring something "the entire explanation."

@anongoodnurse - I am aware of that. It was a hint to the OP of something they could research.

Thank you all. Why don’t some of you write a formal answer though?

@JLi Answer to your Q is strictly two-fold in my view: (i) people hold breaths to maximize output from muscles and afford higher rigidity, which is handy when you need leverage and power, by essentially increasing the pressure inside the torso; and (ii) people make the grunting noise because of the physics of vocalization, due to the relaxing of the glottis which must occur between holding breath and releasing breath to continue respiration. I think the semantic pedants should provide more than complaints to demonstrate that other factors are at play. Sometimes you have to provoke an answer ;)

@SPr Thanks, makes sense!


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How many different DNA molecule classes does a person have?
Books always refer to human DNA as a unique molecule, and two different humans generally have different DNA molecules. But how many different types of DNA molecule does a person have?
In order to make this more understandable, let's give a physical/mathematical definition of molecule equivalence classes. Two molecules are in the same equivalence class if they have the same atoms in the same relative position to each other. And we say these two molecules are equivalent. In other word they are chemical clones of each other, like two $H_2O$ molecules are equivalent.
My question is this: how many equivalence classes of DNA does one human have (before being damaged or mutated)? 1, 23, 46, 92 or another number? Does a human have 46 or 92 different kinds of DNA molecules or just one that wraps differently to give different chromosomes? The same question could be given for a whole person or a single human cell.
Yes, I have looked on the internet and even asked a biologist. It seems the answers are always confusing to me because of the definition of the terms. What biologists seem to call "the DNA molecule" seems to be an ensemble of different equivalence classes of molecules, and I am finding this confusing.

It's worth doing some research before posting here. A fine start might be to look up "chromosome" or "human chromosomes".

Despite your interchange with @jakebeal perhaps persuading you that you are "right", you should try to appreciate why your question has been so badly received. We don't understand you. Not because we have no mathematics, but because you are talking in terms that do not relate to what we know and how we think about chromosomes. So even with your explanation, equivalence class means little to me. If we are talking about molecules of DNA, presumably one molecule is one chromosome. So, to us, your question becomes "how many chromosomes?" which you can find from the Internet. So what do you mean?

@David  one same molecule could wrap differently to produce the different chromosomes. I talked with biologists who believed this was the correct answer, admitting it was confusing. I don't believe it is the correct answer, it seems unrealistic. So far I believe the correct answer is that humans have 23 or 46 or 92 different DNA molecules. I don't care about being downvoted. I don't care about points. I just want an answer and help others if I can. Thank you

And I was trying to help you, not by telling you how to get points, but how to get an answer. And no, different chromosomes are not formed by different conformations of the same DNA. This has been known for ever because of their different sizes and appearances, but they have all been sequenced now. And if you are talking in multiples of 23, I assume you are entering the semantic wilderness of whether one strand or two strands of DNA constitutes a molecule. You can find that fruitless question has already been asked and the answer is yes.

It seems to me that you are becoming confused because you are thinking of DNA in the same way that one things about small molecules.
When molecules are enormous, however, they act more like a material than a simple molecule and have no single structure.  A good starting place for learning how to think about DNA as a large molecule is to learn about polymer chemistry.
Furthermore, a critical difference between these molecules and prototypical small molecules like water or glucose is that the small molecules are largely rigid in their structure. Biopolymers like DNA, RNA, and proteins (not to mention complex carbohydrates and lipid structures), on the other hand, are flexible. This means that the number of geometric configurations of such molecules is infinite.
This flexibility is critical for life, since it allows the molecules to retain their integrity even while interacting with other molecules to perform biological processes. That extends even to modification of the molecule itself, e.g., via epigenetic modification. In biology, we often talk about this as though the molecule is the same (again, treating it more like a material rather than a small molecule), even though technically its chemical species has indeed changed. With such an unbounded number of potential variant species, however, this sort of shorthand makes pragmatic sense for discussion, even if it does not match the definitions from Chemistry 101.

sorry to think of molecules as ... molecules. Thank you so much for your wisdom pointing out exactly my problem.

@ceillac It's an easy mistake to make, since early chemistry classes generally focus on either small molecules or crystalline ionic solids, both of which are far more well-behaved and easy to understand than the weirdness of enormous wibbly-wobbly biopolymers.

I was being ironic. This site has become a parody. I am out

@ceillac Would you care to point out what I am misunderstanding in your question? I'm happy to attempt to amend or clarify.


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How many MAOA alleles are there?
The question is about the human gene MAOA.
I've seen MAOA-H and MAOA-L mentioned in papers.
The page https://www.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000189221;r=X:43654907-43746824 does not describe the gene alleles as far as I can tell.
There is a base sequence of exons provided at https://www.ensembl.org/Homo_sapiens/Gene/Sequence?db=core;g=ENSG00000189221;r=X:43654907-43746824 however since all the nucleotides are already written in I don't understand which base pairs can vary and which are always the same.
So is there a reference that describes in detail all the known MAOA alleles and which base sequences they have?

I recommend searching a resource such as dbVar that is targeted towards human genomic variation, rather than serving up slices of the human reference genome.
The human reference genome is a single sequence that, as you say, does not try to represent genetic variation. It is merely a reasonably good representation of what a single haploid human genome copy might be expected to look like.
I searched MAOA on dbVar and found 426 different variants (alleles observed via DNA sequencing) that have been described. A minority of these have been annotated as either pathogenic or benign (see "Clinical Assertion" column), but for the most part we don't know what effect these alleles have, if any.
For richer information about specific disorders related to MAOA mutations (alleles), you might also consider looking at OMIM. However this will only include instances of alleles thought to affect phenotypes.


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Are all fibrous roots considered as adventitious roots?
I have just started studying about morphology of angiosperms.
I'm learning about roots right now and I came across the following.
In monocots, adventitious roots are a characteristic feature whereas in dicots true roots are a characteristic feature.
When I was younger, I had learnt that fibrous roots are a characteristic feature of monocots.
So I studied further to find that, in monocots, the fibrous roots develop from the base of the stem after the radicle goes absent. And since the roots here do not develop from the radicle but the base of the stem, they are called adventitious roots.
So with this information, I have the doubts:

Are all fibrous roots adventitious?
If all fibrous roots are adventitious, then are all adventitious roots always fibrous?
Are all monocots fibrous rooted?

Are all fibrous roots adventitious?
-Yes. Take note that adventitious roots do NOT originate from a radicle (first root of a germinating seed). Adventitious roots grow primarily from the nodes of the stems and leaf of some documented plant species. In case of germinating monocot seeds, they do have radicle but the embryonic root dies as the monocot plant grows. The dying embryonic root will soon be replaced by new growing roots from the nodes of mature stems of the monocot plant. These thin and numerous roots are now the fibrous roots which are classified as adventitious roots since they now originate from a stem, not from a radicle.

If all fibrous roots are adventitious, then are all adventitious roots always fibrous?
-No. Example are the plant cuttings of dicot plants. Stem cuttings of a dicot plant will still produce roots that resemble the taproot system yet they NO longer originate from a radicle. Hence, they are now adventitious roots since their new origin is the stem. Therefore, dicot plant cuttings develop adventitious roots that are not fibrous.

Are all monocots fibrous rooted?
Yes.

I'm not sure that I get #3 in the question because of the odd phrasing. Anyhow, welcome to the site. Please take our [tour] and refer to the [help] for guidance. Enjoy Biology.

Adventitious roots are plant roots that form from any non-root tissue and are produced both during normal development and in response to stress conditions, such as flooding, nutrient deprivation, and wounding.[1]

Are all fibrous roots adventitious?

As per the definition, yes, the fibrous roots system consists of adventitious roots that arise from the base of the stem.

If all fibrous roots are adventitious, then are all adventitious roots always fibrous?

No.

Are all monocots fibrous rooted?

Yes, a fibrous root system is universal in monocotyledonous plants and ferns.

References:

Bianka Steffens, Amanda Rasmussen, The Physiology of Adventitious Roots, Plant Physiology, Volume 170, Issue 2, February 2016, Pages 603–617, https://doi.org/10.1104/pp.15.01360


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What exactly does my body do with oxygen? Why do I need it?
I know that my body and brain need oxygen in order to survive. If I stop breathing, my lungs (and blood) can't distribute oxygen to my body anymore, and I could get brain damage and die. What exactly is being done to the oxygen, and why do I need it?

it is expected that you atleast do some research before asking a question here,this is a starting point for research into this subject https://www.nursingtimes.net/clinical-archive/respiratory-clinical-archive/every-breath-you-take-the-process-of-breathing-explained-08-01-2018/

Oxygen is used to oxidize (burn) molecules and generate energy.
A fire combines oxygen with carbon containing molecules (like coal) and releases energy (heat) as well as carbon dioxide and water.  A fire needs oxygen or it will stop.
You need oxygen because inside your cells is an oxidation process much like a fire.  Oxygen is combined with carbon containing molecules like sugar.  When they combine, energy is released.  As opposed to a fire which releases the energy as heat, your body captures the energy in a chemical called ATP that can then be used in the body to do a little dance, and make a little love.
The oxidation reaction in your body also releases CO2 and H2O which you exhale.


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Identifying unknown biting insect
Pattaya (Thailand). Unknown insect (similar to a beetle) that bite: long 2 mm, large 1 mm. It has 2 front claws. Pictures attached.

Probably it lost some legs when killed (I felt the bite and I instinctively crushed it).

That looks like the head of an ant. Without better photographs and the rest of the body, it will likely be unidentifiable.

Hello, it is not the head, is the whole body. I will look for a better camera to take a proper picture and post it here.

@acvill you right, I took a proper picture... 90% is just the head of an ant!


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Identification of tree seed pods observed in Western Australia near the city of Perth in February
These where observed during a holiday in Western Australia near the city of Perth in February 2019. I assume they are tree seed pods. But from which tree?

I don't know the exact species, but this is likely to be a Hakea species. These are a widespread genus of plants in Australia, with a hard persistent woody seed that splits open after heating (usually fire) or plant death (as in your case) to release two seeds.
You can see some photos of seed pods at Project Noah, showing the classic bifurcate seed pod.

That looks plausible to me. Thank you very much!


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Identification of bird observed in Western Australia near the city of Perth in February
This bird was observed during a holiday in Western Australia near the city of Perth in February 2019. Maybe somebody can help me figure out the species.

I think the bird's name is Willie Wagtail and It's scientific name is Rhipidura leucophrys..

That looks right! Brilliant! Thanks!

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

The white eyebrow  (“leucophrys”) confirms the ID.


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What's so special about nitrogen?
I understand why carbon is essential for life. It's able to form long chains and has four binding sites. But what about nitrogen? Proteins are the most important class of molecules for life (except maybe DNA), and they require nitrogen. Why can't we make enzymes and other structures without nitrogen? What's so special about nitrogen?

…or oxygen or hydrogen or carbon or sulphur or … You could ask this question on SE Chemistry, but I think they would expect you to study some chemistry first.

I think you need to distinguish between "why do OUR major functional macromolecules (proteins) require nitrogen?" and "would any similar life require nitrogen, or could alternative macromolecular chemistries be possible?".


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Deflated bag-like species on beach: Identification

I encountered this on a beach in Chandipur, along the Bay of Bengal in India. Quite a few of them were scattered in different locations. Identification of this controversial object is appreciated.

Out of curiosity - why "controversial"? Were you in disagreement in a group?

Sea cucumber.
There are over 1700 known species, all inhabiting the sea-bed, mostly in deep waters, but can be found on the continental shelf in many areas.
An echinoderm (alongside sea-urchins and starfish), belonging to the family Holothuroidea, they distinguish themselves from sea urchins by "lying on their sides". They're radially symmetrical with a weak lateral symmetry - they have a preferred "top side", having leathery skin and a lack of external appendages (legs, eyes etc.).
They come in quite a variety of colours, most with tube-feet on the surface. They have a mouth-end where can sometimes be observed everting their delicate tentacle-like mouthparts to feed. They are also fed upon as larvae by small fish, and as adults by humans in many parts of the world where they are dried and sold in markets.
The specimen in the photo is a smooth variety, and appears to have line or plastic thread wrapped around it's hind parts - perhaps from local fishing.


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Do symptoms indicate 'strength' of someone's immune system?
(I am a layman, forgive any misconceptions)
A friend recently got a cold; she had a sniffle, a sick feeling and it was barely more than an annoyance.
A week later I get - presumably - the same cold; I get temperature and lethargy, plus the usual cold features such as sore throat, and spend a few days in bed.
To illustrate the point further: most times I get a cold I feel terrible; have a fever, lethargy etc. I will spend various days in bed hoping for it to go away.
My friend on the other hand doesn't even understand what a fever feels like. For her, colds just make her 'sneeze more'.
Who is said to have the stronger immune system?
Is it that her immune system is 'strong' enough to fight off all viruses easily without breaking a sweat? Or does it imply her immune response is weaker, producing less symptoms than mine?
Or is saying that one of us has a 'stronger' immune system a gross oversimplification?

A person is said to have a weak immune system when he/she gets infected very frequently. Such individuals tend to get more tired than others, their wounds heal way slower than others.
You may want to read more about weak immune systems here.
Different symptoms or duration of infection don't decide the immunity status of any individual.
Every human body has its own way to deal with pathogens. A body that has previously encountered a certain pathogen will behave differently to the body that is encountering the same pathogen for the first time. This usually happens because the antibodies pool differs from person to person.
Another reason can be the type of pathogen variant. The seasonal cold which seems the same for two people might be actually different. This happens because pathogens (bacteria, viruses) mutate themselves over generations. The strain might vary between two individuals.
Another reason can be the lifestyle also. A person who workouts frequently may show different symptoms of any infection when compared to a person who has a sedentary lifestyle. The more you exercise the stronger your immune system gets.


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RNA sequencing and taxonomic analysis of gut microbiome
I've been searching for methods of RNA sequencing, and I always find that the step of rRNA removal is emphasized. However, in my research, I need to analyze both functional and taxonomic data from the RNA extracted from stool to study the gut microbiome.
Do I just to just synthesize cDNA and then use nextera xt for library preparation? or should I use another kit such as truseq stranded total rna / scriptseq v2?

It’s unclear what you are asking. You want to do RNA-seq of a microbiome, but you also want taxonomic data, and you are worried that rRNA depletion will prevent taxonomic identification? You’ll need to do metagenomic sequencing and assembly in order to have contigs against which to map your RNA-seq reads

https://www.nature.com/articles/srep26447 Actually i want to try this methods mentioned in this article .. by studying functional and taxonomic data using just RNA-sequencing. But I didn't found any other article to understand the approach. when I start searching for library preparation kit I always find that there is a rRNA removal step.

mOTUs does some taxonomic analysis... not sure whether this is what you need.

The article that you link to clarifies in the methods section that there are two different extraction protocols employed, one for 16S information (probably DNA extraction) and one for total RNA. In fact, the 16S data comes from a previous publication. I would suggest following the recommendations in these methods sections with regard to kits, sample treatment, etc., if you are intending to use their methods.
Alternatively, you can do total RNA sequencing, which will strongly bias towards rRNA, which makes up 80% of the total RNA pool. For trying to choose between total RNA sequencing vs. the two independent preps, you can look at this tech note and at the methods sections of any papers whose protocols you want to follow. The reason that rRNA depletion is so common is that if you are not interested in rRNA, it is kind of wasteful to lose 80% of your reads to it. Also, informative rRNA regions such as the hypervariable regions contain most of the taxonomic information, and these are specifically targeted by e.g. 16S amplicon primers, such that very little of the rRNA sequence from total RNA sequencing is useful anyways. Moreover, it is probably preferable to use DNA sequencing to determine taxonomy anyways, as it will probably track actual genome abundance a lot better than rRNA, which is after all probably imperfectly correlated with genome quantity.
If you do two separate preparations, I would strongly recommend not doing the two preparations at two different points, but doing them side by side from the same sample subdivided. It is not at all clear that this was done properly in the linked article. Minor differences in sample preparation are notorious for their effects on microbiome taxonomic/functional composition due to e.g. differences in toughness of gram positive vs. gram negative organisms.

You could also do 16s amplicon sequencing on DNA rather than RNA. Without having looked into it specifically, my gut tells me that DNA would be more accurate than RNA for looking at community composition. There are also commercial kits for extracting both DNA and RNA from the same sample.

@MikeyC this is accurate, I think it is preferable to use DNA. I will update to reflect this.


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Doubts about what is growing in my bacteriological cultivation
Foreword: I don't belong to the field at all, I am a high school student with a passion for science so I apologise in advance if I formulate the question incorrectly or make some mistakes.
Out of personal curiosity, I tried growing a colony of bacteria.
I was amazed today when I opened the culture and found a kind of white spider's web with a few black dots hanging from it. Can anyone tell me what this is? I assume it is mould, but I am not sure.

Welcome to Biology.SE. Please tell us what sort of media you are using — that may be of some help in narrowing down an identification. However, note that fungi are notoriously difficult to identify based on appearance. That being said, the white threads with black spots does resemble common bread mold (Rhizopus stolonifer).

If black dots seem to be swimming then it might be a yeast infection.

Almost certainly a mold (the black dots being some sort of fruiting structure with spores). As far as which mold, it's difficult to say. The typical way to ID a mold is to look at spore morphology under phase-contrast microscopy, but even then it can be difficult (sometimes impossible) to distinguish between common genera by microscopy alone.


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Can we cure cancer with CRISPR dead Cas?
Here's a silly idea I had this morning:

Sequence a bunch of normal patient cells.
Sequence a bunch of tumor cells from a biopsy.
Find a DNA sequence that we're reasonably certain exists in the cancer cells but doesn't exist in normal cells.
Create a guide DNA that matches the sequence identified in (3).
Send in a nuclease dead cas9 which stops cell replication through an AAV to all the cells anywhere in the vicinity of the tumour. It specifically binds only to the DNA in the cancer cells, and therefore disables DNA replication only for those cells. Then, target the now-stagnant tumour using conventional chemotherapy.
Alternatively, send in a CRISPR dead cas that induces apoptosis upon binding to the target strand, though this seems harder to pull off.

Would something like this work? If so, has this been attempted? If not, what specific step is impossible?

Related: https://www.frontiersin.org/articles/10.3389/fonc.2020.604948/full

“Fools rush in where angels fear to tread” Pope. And this is a question and answer site about problems in biology.

@David, I'm sure I don't know what you mean by that. If one of these steps is impossible, you can just tell me in an answer instead of quoting aphorisms.

The negative response you have received is probably because this is an opinion-based question since it is asking about a hypothetical situation. From the [help/dont-ask], avoid asking subjective questions where … you are asking an open-ended, hypothetical question: “What if ______ happened?” We expect answers to be based on verifiable facts and references, along with subject-related expertise. This also seems under researched (demonstration of prior research is expected). Please see the [tour] and consult the [help] starting with [ask] for details on what is appropriate for this site.

why would the crispr dead cas inhibit DNA replication? is there some work demonstrating that cas does this rather alarming thing, as opposed to being kicked off by the highly efficient replication machinery?

There are a lot of assumptions implicit in the system you describe, all of which need to be addressed prior to any serious discussion of your method's feasibility.

Sequence a bunch of normal patient cells.
Sequence a bunch of tumor cells from a biopsy.
Find a DNA sequence that we're reasonably certain exists in the cancer cells but doesn't exist in normal cells.

Depending on the tumor stage, its constituent cells may have a great amount of genomic heterogeneity.1,2 How do you know your biopsy will capture all the distinguishing variation?

Create a guide DNA that matches the sequence identified in (3).
Send in a nuclease dead cas9 which stops cell replication through an AAV to all the cells anywhere in the vicinity of the tumour. It specifically binds only to the DNA in the cancer cells, and therefore disables DNA replication only for those cells. Then, target the now-stagnant tumour using conventional chemotherapy.

What proportion of distinguishing mutations do you expect to have a structure that can be differentially targeted by a dCas9 effector? Are SNPs easily distinguished without off-target effects in healthy cells? Is the purpose of using dCas9 to mitigate off-target effects, as opposed to Cas9, for which off-target effects would be more severe (binding vs. cutting)? Can you provide a citation describing the process by which dCas9 binding prevents replication? Is it trivial to design and deliver a pool of AAV vectors that express a guide for each of your targets? Considering the cost (time and money) of your proposed treatment, can you provide a citation asserting that tumor growth stagnation prior to chemotherapy has an added benefit over chemotherapy alone?

Alternatively, send in a CRISPR dead cas that induces apoptosis upon binding to the target strand, though this seems harder to pull off.

Again, please provide a citation describing the mechanism by which dCas9 association induces apoptosis.

References

Turajlic S, Sottoriva A, Graham T, Swanton C. Resolving genetic heterogeneity in cancer. Nat Rev Genet. 2019 Jul;20(7):404-416.
Navin N, Krasnitz A, Rodgers L, Cook K, Meth J, Kendall J, Riggs M, Eberling Y, Troge J, Grubor V, Levy D, Lundin P, Månér S, Zetterberg A, Hicks J, Wigler M. Inferring tumor progression from genomic heterogeneity. Genome Res. 2010 Jan;20(1):68-80.


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Can blood vessels be weakend
Lets say everyday you fall off your bike and your leg starts bleeding at the same spot everytime. Do the bloodvessels at this spot get weakend and if yes, does less blood reach your foot because the bloodvessels are weakend?

So blood vessels in the human transport (circulatory) system are of three types: capillaries, arteries and veins.
Capillaries: Even if you get a slight cut or scratch, capillaries will get affected.
Veins: If you get a moderate (intensity) cut or scratch on a place on the skin where veins are close, veins will get affected and you will need immediate first aid eg bandage, etc.
Arteries: If the cut is deep enough to reach arteries, then arteries will be affected and this is a pretty risky situation as high pressure blood flows through the arteries which gushes out upon rupture.
As the intensities of cuts increase, and depending on the type(s) of blood vessels affected, healing times will differ.
I don't know what you mean by 'weakened'. If this refers to permanent damage, then yes it is possible. However, in most cases, given urgent medical treatment, the affected blood vessels eventually heal.
Hope it helps.


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Does baking soda interfere with digestion when cooked into food?
Baking soda is useful for tenderizing meats and leavening baked goods. In the case of meats, it allegedly breaks down proteins/amino acids.
However, does this usage pose a risk to digestion? Could the baking soda continue to neutralize the stomach acids? Or does its effect "wear off" after some time marinating? Or does it "decompose" sufficiently by the cooking?

The relationship between acid and bicarbonate is that 1 H+ neutralizes 1 bicarbonate (HCO3) molecule as represented in the following equation:
HCl + NaHCO3 --> NaCl + H2CO3
So assuming that the stomach has a pH of 3 and a volume of 100 ml (see table 1, HS = Health Subject, mean vol = 133 ml). A pH of 3 means a concentration of H+ ions of 0.001 mol/l (conc = negative log10 of the pH...10-3 mol/l). Now, assuming all the bicarbonate added makes it to the stomach, we can work out empirically how much bicarbonate it would IN THEORY take to neutralize all the acid in the stomach
The above means that for 100 ml (0.1 l) of stomach acid there is enough hydrogen ions to neutralize 0.0001 mol (n = C * V; 0.001 mol/l * 0.1 l) of HCO3. NaHCO3 has a molar mass of 84.007 g/mol. Using our very best chemistry:
Mass = number of mole * molar mass
Mass = 0.0001 mol * 84.007 g/mol
Mass = 0.0084007 grams.
Now, there's a about 5 g of baking soda in 1 teaspoon. This is a massive amount more than you see in the equation above.
So what happens to the rest?
Well, in real life, some reacts with the food during preparation, some (a lot) is lost to decomposition from heat, some isn't consumed, and last, but certainly not least; the stomach adds more acid to maintain its pH, which is essential for function of the proteolytic enzymes in the stomach.

Wow that's awesome. I never got to take a chemistry class, so this is super enlightening. Thanks!

Sodium bicarbonate is alkaline in nature and it breaks down in presence of an acid.
When you eat it it gets neutralized by the acid in your stomach,this will increase the PH a bit but it will normally not interfere with your digestion.
When sodium bicarbonate breaks down it splits into CO2,water and sodium,so it will add sodium to your body and it might have a negative effect on your blood pressure and kidneys.

So it depends on quantity and time, assuming the baking soda begins breaking down as it comes in contact with the raw meat (acidic)

sodium bicarbonate does not break down in contact with meat or it breaks down very slowly,it increases the alcalinity of the meat and act as a salt.you can read about  sodium bicarbonate here https://en.wikipedia.org/wiki/Sodium_bicarbonate

@trondhansen Can confirm. A glass full of baking soda water tastes a lot like a glass full of salt water.

it had been dangerous if it had a massive reaction in contact with meat or the human body.


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Is there any evidence or example of "trade" or "money" in single cell organisms?
Single cells (like bacteria or eukaryotes) are extremely complex "machines" which can take input and produce output, and generally just live life. The question is, is there any example of "trade" (as in, "commerce") between cells, or within a cell at the molecular level (trading one protein for another, or a generalized "currency" where you could trade a general thing like money for anything else? I imagine there are, but not sure if people have put cells into this mental framework before.
Receptors on a cell seem to be somewhat a form of exchange/trade, "give me a molecule and I will start this chain reaction for you". There's probably many other forms of trade in this light. But what about money/currency?
This is, generally, an open-ended question. To make it closed. Provide one complete example of trade and money, and/or link to relevant research.

Another example might be Rhizobium in root nodules (see here). It takes about 16 ATP to 'fix' one molecule of N2 into (2 NH3). The bacteria supply the plant with 'fixed' nitrogen, and the plant supplies the bacteria with nutrients and energy (possibly being the direct source  ATP?). 'Free' Rhizobium cannot 'fix' N2.

Look into biofilms for bacterial mutualistic relationships.

Trade or currency implies a value placed on it - as in one cell could hold out for 2 ATP vs 1 for another, which requires thought ...so no. There is exchange, but it isn't trade or currency.

Cross-feeding is a common type of symbiotic interaction in which one organism can utilize a substance produced but not utilized by another organism. It's very common in bacterial communities, and often mutualistic (though not always). But there's no perfect analog for currency in this context. More like bartering goods and services.

Lichens might be such an example. Algae living with fungi in a mutualistic relationship.

These are multicellular organisms, right? I am looking for single celled organisms or within single celled organisms.

@Lance Plenty of unicellular fungi combine with unicellular photosynthetic green algae or cyanobacteria to form lichens. Check out the article in my link.


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Are restriction sites added on to the ends of a DNA fragment or are they just conveniently there?
For a DNA fragment to be inserted, it must have two restriction sites on either end. My textbook makes it seem that this is naturally occurring but it seems a little too convenient, are they added in instead? And also, are promoter and terminator regions already present in the fragment or is the restriction site separated and reattached in order to insert them?

Depends on what you're trying to do, what materials you have to work with. What are you trying to do? What textbook are you using? What websites have you looked at?

I’m an A level student, using an aqa textbook. I’ve tried looking it up but the answers are over my head. I’m just trying to understand whether the restriction sites on the DNA fragments are added in sometimes rather than always naturally occurring.

Welcome to the site. Please visit the [help] and take a [tour]. In particular pay attention to the homework page. For these we require evidence that you have put some effort into working out the answer yourself.

I suggest you look up plasmids and have a play with the maps and sequence. Try Addgene for this.

That depends a bit on the method you are using, but mainly you are right, it is rather unlikely that a piece of DNA contains the right restriction site on both ends, let alone even two different ones for site directed cloning.
A common technique used to insert the restriction sites of choice is to amplify your DNA with PCR and special primers. These primers contain your wanted restriction sites next to the recognition sites and produce an overhang (at least in the beginning of the amplification reaction) which contains the restriction site. See the image (from here) on how this technology works.

Regarding promoter and terminator regions, I assume that you clone something into a DNA expression vector. Then these sequences are typically part of the vector and optimized for the cells to work with (bacterial or eukariotic).

thank you! that makes sense


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Is there such a science in which the knowledge of biological processes (e.g., evolution) would be mathematically axiomatized and inferred (deduced)?
There is the following Mathematical Challenge Twenty-three
Mathematical Challenge Twenty-three: What are the Fundamental Laws of Biology?
* This question will remain front and center for the next 100 years. DARPA places this challenge last as finding these laws will undoubtedly require the mathematics developed in answering several of the questions listed above.
And I'm just wondering if there's such a mathematical field in which we can formalize and prove biological theorems.

Given that evolution selects for anything that works, I'm not sure what kind of non-trivial Fundamental Laws of Biology might exist or what "biological theorems" might be.

@Armand I agree with your "evolution selects for anything that works" which in turns implies that biological events are fundamentally contingent and any possible mathematical formal theories must necessarily be of the nature of incompleteness.

However, I'm still holding out some hope that knowledge of biological processes could still be had by examining the proof life-cycle of a suspected biological theorem-statement B throughout an ordered sequence of formal theories:

Inception: When B is undecidable.
Conception: When B is provable (thus decidable)
Extinction: When ~B is provable (both B and ~B are decidable).

However, all this is purely just a thought (a hope).

I think the question is too open to give a definitive answer, but several directiosn can be pointed out right away.
Laws of biology are not rigorous
Due to the inherent complexity of biological systems, the laws of biology are less susceptible to mathematical analysis than those in physics or chemistry. Firstly, this is because many of these laws are statistical in nature. Secondly, because there are too many parameters influencing a biological system to study the influence of each of them in a controlled way.
As an example one could give the Central dogma of molecular biology, which holds true for many organisms and serves as an important guiding principle, but doe snot obey in 100% of cases - e.g., it is violated by RNA viruses.
On the other hand, Mendel laws could be formulated in very rigorous mathematical terms, but quickly get obscured when we are dealing simultaneously with many genes and traits, and have to resort to statistical reasoning, see quantitative genetics.
Population genetics
Population genetics puts evolutionary study on a rigorous mathematical basis, and much of the developments are based on simple but powerful mathematical models. Here it si worth looking at Crow&Kimura's An Introduction to Population Genetics Theory,a nd also on the texts on the coalescent theory Gene Genealogies, Variation And Evolution: A Primer in Coalescent Theory and Coalescent theory: an introduction.
Physics of biological systems
Biophysics is a well-developed field, although it studies only specific aspects of biological systems. Good mathematically solid reference here is
Keener and Sneyd, Mathematical Physiology: I Cellular physiology. See also this post for more discussion.
Finally, a more fundamental, but also more obscure view on the evolution and function of biological systems is from the point of view of spontaneous symmetry breaking and non-equilibrium thermodynamics, associated with the names of Phil Anderson, Ilya Prigogine and Erwin Schrödinger - you may find the list of references in this post.

Thanks for the answer and helpful information within.

Prelude

Fwiw, I think the situation for the thread question and for the Mathematical Challenge Twenty-three is very bleak, hopeless: It's not possible even in theory (no pun intended) to formally theorize life processes in general — natural biological life on any planets, or ALIFE (Artificial Life, e.g. John Conway's Game of Life).
First of all, there's uncertainty of physical facts. For natural biological life, that's manifested by Heisenberg's Uncertainty Principle which would govern not only sub-atomic particle reactions but also macro biological life's evolution.
Take a particular asteroid for example. Its birth, formation, interstellar trajectory are all but a Karma-Fourier summation/superimposition (so to speak) of physical uncertainties — from the uneven distribution of energy and matter after the Big Bang, to the random matter expansion after the super nova of the first generation star, to the chaotic swirling birth of the second generation star system, all the way to "What did the dinosaurs see before the chicxulub impact ?".
Secondly, although mathematics doesn't have Heisenberg's Uncertainty Principle, it has the counterpart: Axiom of Choice. If two choice functions f1 and f2 exist in which Choice is necessary, it logically entails an uncertainty, non-determinateness on whether or not f1=f2, and truth non-determinateness is also alluded to in the following passage:
"We prove that the satisfaction relation of first-order logic is not absolute between models of set theory having the structure  and the formulas  all in common. Two models of set theory can have the same natural numbers, for example, and the same standard model of arithmetic, yet disagree on their theories of arithmetic truth".

The answer

So then, it's submitted in this answer, in so far as mathematics is the language of sciences, biology included, mathematical fundamental laws of biology and corresponding proofs are a tall order to accomplish.
However, it's also submitted here, there is a way forward.
As long as we're not naïve thinking that we're entitled know all biological laws – in full details – the way the Creator (Mother Nature?) does, we're endowed to be able to meta-mathematically formalize some kind of a categorization — a tree — of various FOL biological formal theories, and explore subsequent available pathways (branches) toward understanding a variety of different possible life forms, evolutions.
The meta-mathematical formalization of this categorization will still make use of the canonical definitions of FOL formal systems, theorems, provability thereof, but it also includes meta-proofs of syntactical undecidability as occasions arise.
In some details, the meta-mathematical formalization centers around:

Relieving Plato/Tarski/Gödel semantical truths, interpretations of the duty of being valid in making mathematical inferences: There are no longer meaningful semantical truths — only facts of syntactical provability. Iow, the only truth of a formula (interpreted as "sentence" or not) is the fact of it being provable or not, syntactically decidable or not.
A syntactical proof should be investigated in a context of a collection of relevant sets of axioms — not just one single axiom-set. Iow, a proof is only one instance in the set of proof-varieties (or formal-system varieties).

General Definitions

It's not feasible to detail all relevant definitions and proofs in one post so this answer might be a live post. But we can start with some definitions in the following sections.
Def-1 - Formal theories
A formal theory T (of an axiomatic formal system F) is the set of syntactical theorems of F closed under deduction via FOL rules of inference.
Notes:

The language of T is denoted by L(T) which is L(F).
(T ⊢ f) ⇔ (F ⊢ f) [f being a formula written in L(T)].
In (T ⊢ f), if T is well-known or understood we can omit T and write (⊢ f).
proof(f) ⇔ (T ⊢ f), where T is understood.

It's trivial that given f is a formula, given any two T1, T2, and given the following set definitions

S1 = {f | (T1 ⊢ f) and (T2 ⊢ f)}
S2 = { f | undecide(T1 ⊢ f) and undecide(T2 ⊢ f) }

S1 and S2 exist, S1 is non-empty, while whether or not S2 is empty is contingent on the nature of both T1, T2.
Def-2a - Provability inheritance
If (For all proofs of B: proof(B) ⇒ proof(A)) then:

theorem A is an ancestor of theorem B: ancestor(A,B)
theorem B is a progeny of theorem A: progeny(A,B)
theorem B is genetically inherited from theorem A: inherit(A,B).

Def-2b - Provability base-pairing & nucleotides
Let _C1, _C2 be axioms in the following manner

_C1 ↔ C11 ⋁ C12 ... ⋁ C1m
_C2 ↔ C21 ⋁ C22 ... ⋁ C2n

where only one of C11, ..., C1m is provable, and only one of C21, ..., C2n is provable.
Without loss of generality, each of C11 and C1i is then undecidable, and so is each of C21 and C2j.
Consequently, the formula
(C1i ⋀ C2j)
is also undecidable, which we can use as a new axiom and in which case in turn the theorem (C1i ⋀ C2j) is called a provability base-paring where each of C1i, C2j is called complementary nucleotide of the other.
Def-3a - Formal theory addition — f.(T1 + T2)
Let T1, T2 be general, f be a particular formula.
f.(T1 + T2) = S1 union {f} — up to deductive closure, and f ∈ S2.
Def-3b - Formal theory multiplication — f.(T1 * T2)
Let T1, T2 be general, f be a particular formula.
f.(T1 * T2) = S1 union {f} — up to deductive closure, and where (undecide(T1 ⊢ f) xor undecide(T2 ⊢ f)).
Def-4 - Grothendieck-Multiverse (gM)
A Grothendieck-Multiverse, denoted by gM, is a non-empty collection of theories in each of which the provability of a formula f is evaluated:
gM = { x | (x is a theory) and ((x ⊢ f) xor neg(x ⊢ f)) }.
A gM is also called an underlying provability realm (field) of all formulas written in a language L.
Def-5 - Contingency
The formula f is defined to be contingent when the followings are all satisfied:

f is not a logical theorem
neg({f} ⊢ ~(x=x)).

Proof-to-Truth homology/shadowing
Def-6 - Mathematical truth & falsehood
A mathematical truth is a quadruple (S,T,f,gM) defined per the followings:

S and NEG(S) are meta statements — written in natural language — with NEG(S) being the negation of S
T stands for TRUE
f is a FOL formula of which the provability S asserts
Exists(x):

TRUE(x ∈ gM)
TRUE(neg(x ⊢ ~(n=n))) [i.e., x is syntactically consistent]
TRUE(x ⊢ f).

A mathematical falsehood is similarly defined as (NEG(S),T,~f,gM), where (S,T,f,gM) is a mathematical truth.
Note:

If S is a meta-statement and TRUE(S), then where convenient,

S ⇔TRUE(S).

Similarly, if S is a meta-statement and TRUE(S) is false,

FALSE(S) ⇔ NEG(S) ⇔ NEG(TRUE(S)).

Provability-varieties — Proof lifecycle & extinction
Let f be an underlying formula, gW a Grothendieck multiverse that can be partitioned into the following three equivalence classes C1(f,gW), C2(f,gW), C3(f,gW):

C1(f,gW) = { x | (x ∈ gW) and undecide(x ⊢ f) }
C2(f,gW) = { x | (x ∈ gW) and decide(x ⊢ f) and neg(x ⊢ ~f)}
C3(f,gW) = { x | (x ∈ gW) and decide(x ⊢ f) and neg(x ⊢ f)}.

Def-7a
The set
{C1(f,gW), C2(f,gW), C3(f,gW)}
is called a proof (provability) life cycle relation R of f in gW, and is denoted by f(R(gW)), or f.R.gW or fRgW when convenient.
Def-7b
A triple
(Ci(f,gW),Cj(f,gW),Ck(f,gW))
is called a life cycle of f in gW — i, j, k being pairwise distinct.
Def-7c
The triple
(C1(f,gW),C2(f,gW),C3(f,gW))
is called the natural life cycle of f in gW.
In this case,

C1(f,gW) is called the inception (of the proof of f) in the cycle
C2(f,gW) is called the conception (of the proof of f) in the cycle
C3(f,gW) is called the exception/extinction (of the proof of f) in the cycle
R is defined to be the underlying natural life cycle relation.

Def-7d
Given a natural life cycle relation fRgW that is unique in a gW, C3(f,gW) is defined to be a Chicxulub extinction, on (the provability of) f, and denoted by Chicxulub(C3(f,gW)), per the following:
Chicxulub(C3(f,gW)) ⇔ (Exists(C3(f,gW)) ⇒ (Choice is necessary)).

I think the problem is trying to reduce all of the biology to a simple set of axioms. Even in physics one does not do this. Moreover, in physics one often formulates the laws in axiomatic form, but describing real situations requires combining several laws, taking account for specific geometry, characteristic scales, etc. - none of which is axiomatic or predictable from the first principles.

I agree. Such problem of placing importance on the semantics of the individuals in the domain of discourse, imho, also occurs in FOL mathematics and the the remedies seem to be based on two techniques: axiom-schemas (e.g. PA's induction-schema axiom), and going to 2OL, HOL.
My suggested answer is based on extending these two techniques a bit further: by going to meta level and inspecting possible homology (in functions, and relations) among related formal theories.

This, I think, would be in line with Grothendieck's universe (https://en.wikipedia.org/wiki/Grothendieck_universe) which is in essence a meta universe comprising of many FOL smaller universes (domains of discourse).


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Why do fish and marine mammals need special low density adaptations for buoyancy?
When one reads about fish and marine mammals, it is always said that for example blubber of marine mammals helps them with buoyancy because it is so low density and similarly for example sharks have large low density liver (possibly up to 30% of their body mass) and mainly cartilage that is about half the density of a normal bone (and it is implied this is necessary for buoyancy).
However, many terrestrial mammals like humans are already positively buoyant when having lungs filled with air (most humans in their normal weight), so it is not obvious why any kind of adaptions for marine animals are necessary as their body density composition could a priori be essentially just that of humans. There thus has to be a factor which makes it beneficial for e.g. marine mammals to have more something denser in relation to humans (like bigger muscles in relation to lower density tissue) which then needs to be compensated with such things as blubber. I am looking for what that factor is exactly.

The answer is that air in the lungs of a diving mammal is compressed, meaning that it takes up less volume than air at the surface. This phenomenon is called "Thoracic squeeze". The deeper the dive, the smaller volume the lungs and air occupy.
Because the air takes up less volume, the buoyancy of the lungs is decreased once the diver reaches a certain depth below the surface. You can experience this for yourself in a diving pool - take a deep breath and pointing your toes to the bottom, submerge yourself to about 1-2 m (3-7 feet) below the surface and you will start to sink as the volume of your lungs has decreased to a point where their buoyancy is counteracted by your density.
Positive buoyancy in a diving animal is a plus - it means that they don't need to expend (as much, if any) energy to reach the surface, they can rely on their body to take them up, no matter what.
I have no idea why sharks and fish that don't rely on lungs need low density tissues, other than to make them neutral buoyancy so that they don't need to expend energy to maintain their place in the water column.


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How do plants know to grow towards the light?
Plants lack a central nervous system. How do they know to drop leaves in full shade and to curve stems towards the current light source?

Welcome to the site. Please visit the [help]and take a [tour]. In particular pay attention to the homework page.  You might want to investigate phototropism.

Plants are not sentient beings, and do not “know” anything. If you chose to post here please use scientific language.

The curving of stems towards light sources is called phototropism.
It is a hormonal phenomena that responds to light. Just like human beings, plants have hormones in them.
The hormone that makes plant respond to light is auxin. It is a type of growth hormone, causing growth in the parts where it accumulates, and it does so in regions away from light. So, when a plant faces the light, auxin accumulates and causes growth of the side which is not facing the light. Thus, excessive and uneven growth leads to the plant to bend towards the the light.


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Is it possible to fuse DNA from two sperms and can a baby be born from that?
If this is possible, then isn't there going to be a chance to have a YY child?

Welcome to Biology.SE. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site as are "homework" questions 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. Under researched questions may be subject to down-voting and closure. ——— Please take the [tour] and consult the [help] starting with [ask] for details.

The question was clear to me. Assuming this person is not a professionally trained molecular biologist, it's impressive enough they even realize that sex chromosomes are a known feature of human genetics. They sound genuinely curious about the implications of making babies using artificial genetic editing technology on cells which if ordinarily otherwise left naturally unaltered clearly it would not be possible. It's a very important consideration we must face this century.

@JohnCollins — Clarity is good, but not sufficient. In addition, to not demonstrating the expected prior research and containing two distinct questions, this is off-topic because it is a homework question. On the homework page the question "What is a homework question?" is answered with "A question that addresses a basic biology concept that may seem trivial to biology professionals". Knowing that at least one X chromosome is required for viability is something I would expect anyone with even high-school level biology to be aware of.

@tyersome So did you have at look at the OP's profile? They say they are only fourteen years old. I.e., only having just begun high school. This to me seemed like a genuine answer arisen from pure curiosity and from what I recall of my own HS education the level of biology getting into actual chromosomal details would only have "homework" in AP Bio, which was primarily a seniors course with some exceptional juniors. We should be promoting such curiosity as much as possible, in the youth especially, but even in any age demographic -- so unfortunately ignorant of modern molec bio are most.

genuine question*

I don't think it is possible. There is a lot happening to the DNA of the sperm and the egg after fertilization, and just mixing the DNA of two sperm or two eggs would not achieve that. Also, a YY embryo would not be viable because the X chromosome contain vital genes that Y does not. That's why there are people with 1X but no one with 1Y.

Sperms contain X and Y chromosomes, but only as haploid sets.

Well, it would be difficult from specifically sperm, but if you mean from two members of the same sex -- two men, then the answer is yes. Yes it is (or, rather, will be) possible. Already, it has been done in mice (new baby mice were born from both only mothers and also only fathers):
https://www.cell.com/cell-stem-cell/pdf/S1934-5909(18)30441-7.pdf
In theory it would never be possible for two women to truly fully independently create a son (a male offspring) from their own cells, because neither of them would have the material for a Y chromosome. So that would need to be donated (just the Y chromosome). Two males could make either sex offspring (XX or XY). This would be possible through what is called induced pluripotent stem cell technology, likely CRISPR genome editing for performing the required epigenetic modifications (described in paper), and a whole variety of other quite new extremely complex advances in biotechnology which have recently been made (such as next generation sequencing for assaying the most viable possible artificially-induced sperm and egg [which could simply be made from skin cells] and variations thereof like ATAC-seq, which measures genome-wide chromatin and epigenetic information, microfluidics and nano-droplet technologies and the rise of single-cell assay capabilities of many kinds, and truly, an overwhelming further number of huge advances which would take too long to list here and which most people probably remain totally unaware of [or could even comprehend, unfortunately]). We are living in a "Golden Age" of what will without a doubt be forever historic massive, rapid leaps forward in our ability to become the designers of life, rather than the passive victims of its "natural selection".
It is not possible today, all of the mice made in the 2018 study, though they did survive through to birth and then some, were quite unhealthy and all died prematurely from genetic abnormalities (does this not happen naturally, all the time, too? Not just in mice but men as well!). But there's no doubt the understanding and refinement of the ability to do such a thing will only rapidly improve - in every field of science this has been proven to be true in modern times, literally exponentially so. And probably no more amazing than in the scientific understanding and bioengineering of living things -- once the structure of DNA was chemically precisely determined and understood (in 1953; when it was revealed not only how DNA is chemically bonded and of precisely what atoms in what 3D orientations but also why such a structure, that specific double helix anti-parallel complementary form, would make sense functionally as a source of information-containing incredible power -- the relation of its structure to the function of evolution, and of literally the birth and aging process of every animal) is when things really started to proceed at a rocket-launch speed clip. Now, at this point, your average person really does not fathom just how much our world is about to change.
It's likely in this century this will be a safe, totally feasible, possible technological power at our disposal. Now will it be legal? That's much more uncertain. But that's irrelevant to the question of is it physically possible, to which the answer is an absolute yes.

No it is not possible,
sperm are missing most of the biochemical machinery need to produce a embryo, sperm have most most of their functional components to make them lower investment and faster. Sperm are lacking several important organelles, including the most important ribosomes. They are not fully functional cells.
https://www.ncbi.nlm.nih.gov/books/NBK26914/

Who's to say it wouldn't be possible to supply such organelles, say by inducing the sperm genome into a pluripotent state via introduction of transcription factors (and probably some yet to be known method for unpacking the extremely densely packed genome, yes -- totally feasible, as, that must happen during the formation of the zygote post sperm-egg fusion, no?). The genome -- the full DNA molecular sequence, with all its unique variants (BTW - a tiny percentage: ~0.1%), is all that is really required. It has been undeniably established that life is but heritable information, stored as DNA

In other words though sperm may lack said required machinery, what they do not lack is the instructions for building them. I'd be very wary of claiming almost anything we can imagine as far as biological artificial manipulation to be "never possible". 1) We simply cannot know that with definite certainty 2) All signs are increasingly suggesting that the possibilities for bioengineering will not only encompass all that we could currently imagine but far more, beyond what we can yet even have realized

Also - did you read your link? I just did. Absolutely fascinating. I didn't even know this at all. But sperm are up until the very final parts of their lives (i.e. very near prior to being expelled as semen) exist cytoplasmically connected to apparently thousands or perhaps more of other essentially clonal daughters cells, and thus, share one continuous open giant elongated cytoplasm called a synctium - and thus as they complete their differentiation, are not only diploid-sufficient, but tremendously polyploid -- they are well supplied with all the normal machinery required for transcription..

.. and translation. You are citing the 2002 edition of The Cell textbook. Much more is probably known now on the details. But presumably the residual bodies of the synctium may be retrievable in the semen, so, it's very plausible that from a mere single sample of one male's ejaculate, a bioengineering could be applied to create new viable zygotes. In theory possibly millions even.

@JohnCollins you seem to be interested ins something very different than the stated question. I suggest doing some research and then coming back with a specific question.


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Is there species of mushrooms that grow in the wild in Mediterranean environment?
I'm looking for species of mushrooms which can grow wild (or with minimal human intervention) in Mediterranean environment (which is characterized by dry summers and mild, wet winters.), specifically in north and south Israel (I guess there are different kinds that are adequate to each area) and can spread over significant areas (in a scale of tens of kilometers)
Are there any known species that answer those characteristics? where can I read more about them, their abundance, and how to grow them? I found a-lot of unreliable information, and I'm looking for material with stronger scientific foundation.
Thank you.

Mediterranean is rather big: it includes the southern coast of Europe, Levant, and North Africa. E.g., this link claims 400 species known in Israel.

double posted https://earthscience.stackexchange.com/questions/22951/are-there-species-of-mushrooms-that-grow-in-the-wild-in-mediterranean-environmen

By spread do you mean that the "single" fungus spreads its mycelia that far or that it is capable of spreading via sporulation?


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How to memorize Transcription and Translation?
I often get confused between transcription and translation. Is there any way to memorize them easily like a mnemonic??

I prefer a conceptual distinction rather than a mnemonic in this case.
I've always thought of a transcript as an exact copy of record - that's the meaning of the word in English, and an RNA transcript is effectively an exact copy of the DNA message. Sure, there are complications like the uracil in RNA, and that the strand that is actually copied from has the complementary bases, but you still have a molecule containing the same message and you could easily go backward to DNA if you wanted.
A translation, however, is moving to another "language". When you make a translation of a document, you're not making an exact copy, you're taking the meaning of a source document and representing it in another form. Similarly, translation of mRNA into protein is moving from the language of nucleic acids to the language of amino acids. Once you've translated, you can't go back to an exact copy of the original. You could get pretty close, but the redundancy of triplet codes means you can never get the exact RNA/DNA bases back from just the protein.