text:
Traceability of a mature tree to its original seed via DNA
Is it possible to trace a specific seed to a fully mature tree?  For example, Can a seed be traced to the full-grown plant based on DNA?  Would it be possible for me to catalog a seed DNA and then years later be able to identify the full-grown plant to that seed that was cataloged?

I'd think it would be difficult to obtain the seed DNA without killing the seed.

Apart from the difficulty pointed out by @mgkrebbs, this is no different from the use of the DNA in forensic science... of course, if we are sure that the seed contains only one type of DNA.

@mgkrebbs — That really depends on the size of the seed — I worked in a maize lab and we regularly removed a small portion of the scutellum for genetic or other analyses (this can however impair seed viability). So, this could be done easily for trees with a large seed (e.g. nuts), but would be much more challenging for the many trees with tiny seeds. WesleyRios — you would need to determine viability over time after sampling to make this work.

As the embryo of a seed typically contains many cells, it should in theory be possible to obtain DNA from a seed without disrupting it (there may be pragmatic issues with protocol, depending on the particulars of the seed).
If you have the DNA and each seed has been produced by a separate fertilization event, then each seeds DNA would be unique and it should certainly be possible to identify an individual genetically, just like it is with animals.
Not all seeds are genetically distinct however. For example, many plants will also produce seeds asexually under appropriate conditions, a process known as apomixis. If the seeds are being produced asexually, then your only hope would be to identify different mutations in different seeds, which is a much fainter signal and likely to fail for your intended purpose.

Thanks for the response.  When you say "separate fertilization event", what do you exactly mean by it pragmatically speaking?   For example, if I have a tree that produces the seed during a specific time of the year, would that mean that the seeds for that season are part of the same fertilization event?  Hence, the DNA for all the seeds would be the same?    I appreciate the education.  Thanks again

Plant reproduce sexually by combining gametes, just like we do. In the case of a plant, the male gamete is pollen and the female gamete is called the ovule, which is analogous to an egg. So during sexual reproduction, your typical tree gets "pregnant" with massive amounts of "fraternal twin" seeds, each produced by a different grain of pollen meeting a different ovule.

@jakebeal: It also seems possible (theoretically: I don't know whether it really happens) that one pollen+ovule fertilization could produce many seeds.  E.g. in many plants we see individual seed capsules containing many seeds in a regular pattern.  If each one required a separate pollen grain, you'd expect randomness, no?

@jamesqf Surprisingly, no! For plants with seeds in a regular pattern, the ovules generally develop in a regular pattern, each putting up its own receptor for pollen (though these are often bundled together also). Corn is a particularly good example: each thread of corn silk leads to a separate ovule, which will be separately pollinated and become a separate kernel. It's biology, so there are probably exceptions, but in general it seems that flowering plants pollinate their seeds separately.

@WesleyRios, the implications of the above is that most every tree seed will be genetically unique.  You cannot tell from the offspring-tree's DNA what time of year its seed was produced, nor what year.  With significant effort in advance, you might be able to determine which two trees were the parent trees if you collect the DNA of each of the potential parent trees (which usually would be large number) before they die.


text:
How to incerase the efficiency of co-immunoprecipitation?
immunoprecipitation recently. My main problem is i am getting very clean and my target protein only (as you see in the lane 3,4,5,6) but when i reduced the NP40 concentration to 0.05 percentage i could see enriched pattern in the IP pull down (lane 1 and 2). but the main problem is that i can same pattern in the control also. I am using my lysis buffer for the washing also (2 times washing with lysis buffer 10 mins at cold room followed by 2 times with 1X pbs). I am Using Mag Strep "type3" XT Beads (Incubation 4 hours in cold room with beads).

Lysis buffer:
20mM HEPES-KOH pH 8
15 -per glycerol
150mM KCL
0.2 per NP40 (I reduced to 0.05 per)
1 mM DTT
1X protease inhibitor cocktail

Can anyone help me with this. Should i change the washing buffer what about the stringency. What are the other factors that could increase the efficiency of the co-IPs. I am trying to optimize the protocol. This is human cells.

What are you doing your Western for - your IP target protein or a known binding partner? Please give identifiers for your different proteins (i.e., Protein X, Protein Y, etc.) and indicate what exactly the samples, IP antibodies, and WB antibodies are in each lane. Or is this an image of a stained gel? Please label molecular weights as well, it's possible you're just staining heavy and light chain.

The gel is silver stained. I know my protein (70kDa) but i am looking for the interaction partners (which i am interested). It is a streptavidin pull down. I have given only the experiments only. From the left to right first two lanes reduced NP40. 3rd to 6th lane reduced   0.2% NP40.

source: Stack Exchange

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

sort: votes


text:
Bumblebee (?) identification
These bumblebees live on my balcony, in ventilation holes in doors and windows. I'm trying to find the exact name of the species, but I can't find any that look exactly like this. Their top segment is completely black and the bottom one is completely orange. I'm not 100% sure that these are bumblebees, but they behave like bumblebees, I mean, they fly horizontally and like nectar.
The location is in the southern part of Germany (Bavaria). The insects are ~20mm long, similar to the size of a honey bee.

The closest match is probably Bombus lapidarius, but Bombus lapidarius only have orange "tails", most of their bottom half is black.
It looks very similar or even identical to Bombus alpinus, but the problem here is that Bombus alpinus usually live in the mountains (and I'm in 300km from the closest mountains) and they are considered to be almost extinct in Germany.
Do you have any idea what they are called?

Welcome to Biology.SE! When you wrote "south of Germany" I'm guessing you mean in the southern part of Germany (what you wrote means somewhere to the south of Germany — i.e. could be Austria, Switzerland, Litchenstein, Italy ..). On this assumption I've made a minor edit to your post. Please also [edit] in the size of these insects since that can be essential to their identification. ——— Thanks!

@tyersome Yes, I meant the southern part of Germany (Bavaria). Thank you for the edit!

The animal in the photos is actually a female of Osmia cornuta. The horns are quite visible, which makes us exclude Osmia bicolor, and the thorax is entirely covered with black hair, which makes us exclude Osmia bicornis.

You are right, I mentioned this options in the comments to the other answer, but wasn't 100% sure. I spent some time observing those bees in the past few days and their behavior completely matches the behavior of Osmia cornuta. Fascinating creatures, never thought bees could be so big and hairy

Your pictures are quite blurry, but I think this is an Osmia, ie a Mason bee (and not a bumble bee). I think you can see a tendency of the “horns” that female Osmia bicornis (red mason bee) have on their heads on your pictures, so this is my guess. Females are much larger and generally darker than males on the thorax and head, and often quite black there while overall red on the abdomen.
Another option is O. bicolour, where females lack the “horns”of bicornis.
See eg this picture:

Head picture of female O. bicornis, to see the “horns” clearly (if it is indeed this species):

(Pictures from artportalen.se)
Another possible species in the same genus is Osmia bicolor (two-coloured mason-bee), which is more clearly divided in black-orange, see e.g.:

This species has an interesting biology, in that it is specialized on using snail shells for egglaying and preparing larval cells stored with food.

It looks similar on these two pictures, but completely different on other pictures of Osmia bicornis that I found. I'll take a closer look tomorrow and try to take better pictures to compare them.

They can differ quite a bit, but I find the pictures on e.g the wiki-page to be relatively unrepresentative. Look for the female “horns” in large, dark individuals, since this is diagnostic.

Pictures here are also ok (with good info): https://www.bumblebeeconservation.org/redmasonbee/  Also note that this is an yearly spring species, common in the first-flowering plants, so it fits your late-March observations.

No, definitely not this bee, the hair on their top half is yellow, while bees on my balcony have only black hair on the top half and are more hairy and thick in general.

Check Osmia bicolor as well (which is more clearly black-orange), but similar in overall body (e.g. https://www.artportalen.se/MediaLibrary/2019/5/9b1c2e64-6895-41ae-abfb-033f209cc68f_image.jpg). The reason I went for O. bicornis was the possible hints of the horns in your picture. However, sharper images would probably clear up the issue.

I updated pictures in the post, looks very similar to Osmia bicolor

@lawful_neutral I agree.O. bicolor is very likely. There might be closely related species in southern Germany that I don't know about, but this is a good bet.

https://www.botmuc.de/en/bees/ shows Osmia cornuta which is even more similar, so I'm not sure which one it is, but you are 100% right that it's a bee and not a bumblebee

Yes, I agree, and then the horns that I felt were visible also makes sense. O. cornuta isn’t common here (Sweden), so didn’t think about that species.

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


text:
Is there a term for the entire system of moving oxygen around?

The respiratory system brings oxygen to the blood, and also can include stuff like nicotine from smoking.
The circulatory system brings oxygenated blood (and all its little friends) to wherever they're needed.

Both the respiratory system and circulatory system are extremely important in keeping hypoxia from happening, but I'd like to focus specifically on the system of oxygenation.  I don't want to include the systems of smoking, or moving around nutrients.
Is there are term for the "oxygenation" "stop hypoxia from happening" system?  Basically just the parts of the respiratory and circulatory systems that move oxygen?

Short answer
"Oxygen homeostasis" is the best I can think of.
Longer answer
Don't forget the other half of the oxygen equation: carbon dioxide is an important waste gas and failing to remove carbon dioxide is just as much a problem as failing to deliver enough oxygen.
You could refer to "oxygen homeostasis" if you wanted to just refer to keeping enough oxygen in distal tissues; as you describe, both respiratory and circulatory systems are relevant for oxygen homeostasis. However, it's hard to separate from the rest of the gas exchange system. Carbon dioxide is very important in determining the rate of respiration, for example, as well as the release of oxygen in peripheral capillaries. Therefore, even if you want to focus on just oxygen, carbon dioxide is going to come up no matter what! As is the function of the vasculature, heart, and lungs: even if these organs have roles outside of delivering oxygen, their functions apply to all gasses exchanged and everything that is transported in the circulatory system. Very little happens in these systems that will only affect oxygen delivery without affecting anything else.
The efficiency of oxygen delivery also depends on what exactly you're inhaling; I find it a bit bizarre to include "smoking" as seemingly part of ordinary biological function, but if you want to go there it's reasonable to consider the role of carbon monoxide and anything else that may interfere with oxygen binding to hemoglobin.

I'm writing a paper in which I'm trying to split the understanding of oxygens role into two distinct phases as systems, one which explains getting the oxygen and where it goes, and another that explains the CO2 release.  While they do use almost entirely the same systems, I still want to treat them as separate functionalities for the sake of the writing being more like a story.


text:
What does z in lac z, y in lac y and a in lac a gene stand for?
In lac operon the 3 structural genes lacz, lacy and laca must have some reason behind their names. While lac refers to lactose but what does z, y and a refer to?

I’m voting to close this question because it is a question about the history of biology rather than a mechanism or process.

I think you'll have great difficulty finding the answer to this question, unless you can find interviews with or historical accounts by Jacob and Monod (probably in French) in which they mention this essentially trivial point.

@Tyersome, I believe we can only discover new things if we better understand the history of something. You can't name any gene randomly, selecting any of the 26 alphabets. There must be some reason behind their names. We ought to find that.

@Tyersome, I approached this site with the hope that my questions though not so interesting and just out of mere curiosity would be answered in the most appropriate way. Anyway, I definitely will take your advice, and hope to get it done soon.

The Jacob and Monod article on regulation is paywalled, but there do seem to be some PDFs floating around.
In this article, the terminology of z and y is introduced as designators for mutants (z+ and z-, y+ and y-).

The z appears to be linked to a term from a kinetic equation.
The y is not justified, implying that it is an arbitrarily chosen variable, and such choices are often by convention adjacent to the justified variable (e.g., the index variable i is often followed by additional indices j and then k).

The a component is not present in the original article, but its name seems likely to come as an abbreviation of its function as an acetyltransferase

The paper you cite is the original one describing the regulation of the structural lac genes, but it is not the original one describing these genes. You would have to go further back to find that. I am most sceptical that a geneticist would name a gene from a kinetic equation. What evidence do you have to support this? I would imagine y and z are just convenient letters of the alphabet, with a (for acetyltransferase) added later because they had got to the end of the alphabet. But I don't know.

@David In the paper, z is introduced early on as a term for enzyme activity, then later the presence of galactosidase is given as the z+ phenotype, which then links to the lacZ gene.  In the section for the phenotypic terminology is introduced, I don't see any citation for the terminology, leading me to conclude that the terminology is being introduced in this paper.

I used to know geneticists that would know the answer. I may try to trawl back through the literature but it can be difficult. All those old French journals will have been absorbed into something else and probably not digitized.

@David If you find anything better, please do share!


text:
Can we dilute PureExpress Cell Free Mix to increase number of reactions?
Since the PureExpress Cell Free mix is so expensive, I was wondering if it might be possible to just dilute the mix to increase the number of reactions we need to use.
From this image I found:

It seems like by just adding more 3PGA, amino acids we should be able to get more reactions out of a diluted solution. From my understanding, this would mean that 3PGA and the amino acids are the only consumables here. Would diluting just change the amount time it takes for the reaction to occur or is there something else that I'm missing here.

Really interesting question, but your image seems to show a crude cell free system and not a pure cell free system, unless I’m misunderstanding something!

Yeah, this was the best picture I could find to represent my understanding.

Try using this equivalent thing you can make in lab yourself for way cheaper. The protocol is a pain in the a** -- I've done it myself several times and it takes 2 people working in tandem for a long week -- but it does work. (The first author of this paper has gone on to create a successful company based on this exact cell-free system, Sutro BioPharma) https://www.jove.com/t/50762/protocols-for-implementing-an-escherichia-coli-based-tx-tl-cell-free
If you're at an academic institution and interested in trying this, I can walk you through it, some modifications that make it more efficient, and which parts have some "wiggle" room.
I would not recommend diluting PURExpress... Every component in cell-free reactions is essential and carefully calibrated. Modifying any of them can result in dramatically decreased efficiency. For example, would you be able to adjust all the ion concentrations as you dilute the mixture?
I recommend using minimum 5 µL volumes in a 384-well plate.
also good luck buying 3pga... there was a massive shortage for at least a year when i was doing this stuff... maybe it's better now.

Nice answer! It sounds like you have some good synbio experience. Would you like to join the SynBio SE site proposal?

The PURExpress system from NEB is incredibly expensive, for this reason I have avoided it all costs during my experiments with cell-free systems.
This is the paper I've used to create my own cheaper cell-free systems while also discussing reasons why using the NEB PURExpress system is not recommended:
https://pubs.acs.org/doi/10.1021/acssynbio.8b00427

"Although NEB provides a few different formulations of
the PURE system, the commercial system can’t be customized or optimized by the user, and the precise formulation of the commercial PURE system is not publicly available."

This might answer your question as to why I would not dilute the PURExpress system since the precise formulation is not publicly known. Thus, we can hypothesize what would work at various concentrations, but at the end of the day it is unknown what they specifically use in this reaction and how one could optimize it for their own purposes. It would take some trial and error if you really wanted to dilute/change the formulation.

"Our method co-cultures and induces all 36 protein producing E. coli clones in a single flask followed by a single Ni-NTA purification."

This is the method I personally use and it can be time intensive, however the payoff is the cost and ability to optimize your system for your specific experiment.

"The PURE system consists of several different components [7], that can be separated into three main categories: proteins (transcription, translation, and energy regeneration),ribosomes, and small molecule components (salts, buffers, NTPs, creatine phospate, and folinic acid)

If you were to go down the dilution route, I would suggest reaching out to NEB before hand to receive consultation for the purposes of your experiment and any consumables you may need to also purchase. This quote from the paper shows how your system has many considerations for consumables you may need to further research to maximize the expression of certain proteins. As for how this affects the reaction time, dilution shouldn't affect time, it will however affect the amount of product you get out of your reaction.

I guess in a macroscale, it wouldn't really affect the reaction time but in the scenario that there are reusable components then shouldn't it affect the reaction rate? (Thinking back to high-school physical chemistry)


text:
Do some animals have a tolerance to the negative effects of inbreeding?
Are some animals more or less tolerant to inbreeding? By tolerant I mean do they have a genetic mechanism that allows them to inbreed and corrects for issues introduced through this? When I started searching for this I quickly ran into theories on how inbreeding is avoided but did not find information on whether some animals have genetic mechanisms that make them less likely to get negative effects from inbreeding.

Can you expand on what you mean by genetic mechanism? Do lethal recessives that prevent development and thus prevent offspring count?

@kmm I hadn't considered that, I was thinking of more of a self-correcting technique that would prevent to many occurrences of the same genetic markers from being chosen or just a level of fault tolerance where the critical mass of bad combinations is higher than most other vertebrates.

@kmm I'm not very well versed in biology but I was looking for something similar to how TP53 works in humans and elephants to prevent bad DNA copies. I was curious if such a mechanism existed in some animals at conception to prevent the negative mutations of inbreeding. I'm not sure if such a parallel mechanism exist but I figured if they can correct for bad copies that it would be possible to correct for too many pairs being duplicates or rather not enough entropy. Again sorry a lot of my terminology is a mix of computer science and what I remember from high school biology.


text:
What is meant by 'topologically continuous' in the context of cell compartmentalisation?
I am reading the textbook 'Molecular Biology of the Cell', and I am reading the chapter about the compartmentalisation of cells. I have come across the following statement:

The nucleus and the cytosol, which communicate with each other through
nuclear pore complexes and are topologically continuous (although
functionally distinct).

With regards to the above statement, what is meant by 'topologically continuous'? Any insights are appreciated.

Note that I think this type of question would be better for a language forum. ——— As far as I can see this sentence would mean the same thing with "topologically" removed and thus appears to represent an author adding unneeded words because it sounds more impressive.

The word is needed to distinguish from functional continuity. Imagine how ridiculous the sentence would be without those 2 words: "The nucleus and the cytosol, are (topologically) continuous, although (functionally) not continuous.

What "topologically continuous" appears to mean in this context is that materials can flow between them.
So far as I am aware, this is not a well-defined mathematical term, which is part of what makes this confusing. In topology, some spaces are continuous and others are not, but the meaning of "continuous" in topology is rather more general than the authors usage here.


text:
Geometric Interpretations of the DNA Double Helix
In mathematics, a helix is a shape which has constant curvature and constant torque (see Wikipedia here. What are the biological implications of the DNA double helix having constant curvature and torque, or is there none?

Note that the helix has local variability due to local concentrations of ions which have small effects on the curvature, which is therefore not mathematically constant. The DNA can vary from completely curved to completely straight... Using a statistical-mechanical model of DNA bending and protein-DNA looping, recent revised estimates for curvature variations are 1.6-fold and 3-fold, respectively (Zhang et al., 2006a).https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4190679/

The standard text-book answer to this question is illustrated by the cover illustration of one edition of, well, the standard text book which I reproduce alongside an image taken from a teaching site of my own in which you can view several different aspects of the double-helix in 3D.

[Views of DNA looking ‘down’ the axis of the helix. On the book cover the bases are black filled shapes of purine and pyrimidine structures, in the image on the right the purines and pyrimidines are red and blue outlines, respectively, with the sugar–phosphate backbone shown in white.]
The regularity of the helix (constant curvature and torque) maximizes base stacking, which involves the π–π interactions of the purine and pyrimidine rings. This is important for maintaining the structure of the double-helix and hence facilitating its function. Base stacking is discussed in another question on Stack Exchange Biology, in that standard text, Berg et al. , and in a chemical article in Wikipedia.
Although concerning a single-stranded RNA rather than a double-stranded DNA, I take this opportunity to illustrate the biological significance of base stacking by considering the anti-codon loop of transfer-RNA. As is well-known (see e.g. this StackExchange Biology answer), there is frequently ‘wobble’ at the 5′ position of the anticodon loop, allowing certain non-standard base-pairs at the third (3′) position of the mRNA codon. As the image below shows, this can be partly attributed to the poorer base-stacking at this position in the anti-codon loop (G-34 in the illustration) compared to the other two positions, allowing greater flexibility.

[Anticodon loop of yeast phe-tRNA, created by the author from 1ehz.pdb]

One is tempted to answer that the helicity confirms a higher stabilty in respect to possible forces trying to separate the two strands. However, the logic of teh question (and such answer) is faulty, as it implies that there is a non-helical alternative to double helix, and that the helical form was evolutionarily selected. I doubt that this is the case (let me know that I am wrong).
So more correct way to see this is to say that DNA just happens to have torque. (Note that it is not exactly constant, as the DNA istelf is not straight, but folded, wrapped around the histones, etc.) One could even say that all linear polymers have torque, except that for some of them the torwue is zero.
Remark
One could compare double helix with the allophorms of carbon, which can adopt forms continuous in all three dimensions (diamond, graphite), two-dimensional (graphene), one-dimensional/helical (carbon nanotubes), and zero-dimensional (fullerenes/buckyballs). Are there any similar candidates for storing genetic information?


text:
Compatibility between spytag/spycatcher versions
Background
SpyTag and SpyCatcher are peptides which can associate via a spontaneous amide bond. Because of this, they can be fused to proteins of interest as tags to cause the proteins to bind. There are (currently) three versions of the spytag-spycatcher system, where each system contains a different version of spytag and catcher (i.e. system 1 contains spytag1 and spycatcher1, system2 contains spytag2 and spycatcher2, and system3 contains spytag3 and spycatcher3).
Question
My question is, how compatible are the spytag and spycatchers between different versions? So, for example, would spytag1 bind with spycatcher2?
Prior Research
I found the following statement from this paper:

The new variants showed backwards compatibility, reacting efficiently with parental versions (SpyTag002 with SpyCatcher: 1.0±0.06×104  m−1 s−1; SpyTag with SpyCatcher002: 5.5±0.03×103  m −1 s−1;..

But these numbers don't mean a lot to me. Would you expect to see near complete binding as with spytag2-spycatcher2?

I have worked with the coupling of SpyCatchers and SpyTags of different iterations and can confirm that they are all backward compatible. While SpyCatcher003 and SpyTag003 pairs have the quickest reaction rate, reactions of all pairs (including SpyCatcher and SpyTag version 1) should go to completion under the right conditions.
The SpyCatcher002-SpyTag1 is no exception. As you quoted in the Angewandte Chemie paper, the rate of reaction is 5.5x103 M−1 s−1. Rate = k[A][B]. This means that 10 μM of SpyCatcher002 and 10 μM SpyTag will react with a t1/2 (50% coupling) of 18 seconds at pH = 7.0. However, 10 μM of SpyCatcher002 and 10 μM SpyTag2 will t1/2 of 5 seconds (rate constant is 2x104 M−1 s−1). If you are reacting 0.1 μM of each, their respective t1/2s are about 8 and 33 minutes, respectively.
To get the reaction to go to completion (>90% coupling), you'll need to wait ~12 times as long as the t1/2 (since every subsequent t1/2 doubles in a second-order reaction). This will, of course, depend on your concentrations. However, when using low concentrations (0.1 μM), complete coupling of SpyCatcher002 to SpyTag002 will take 1.5 hours, whereas SpyCatcher002 to SpyTag will take 7 hours at 25C. SpyCatcher002 to SpyTag1 will take 3x as long to go to completion; therefore, I'd recommend using at least 1-2 μM of what you want completely coupled with an equal or 2-4x excess amount of either Tag or Catcher and run the reaction overnight. Higher concentrations (>=10 μM of both Tag and Catcher) should go to completion in 30min-1hr. When performing coupling reactions for more than a few hours, I'd recommend you perform them at 4C. Loading 10 μL of 1-2 μM of your protein should allow you to see the band shift on an SDS-PAGE gel with Coomassie stain.
In my experience, temperature and pH are important factors when performing coupling. pH > 8.0 tends to reduce the rate of reaction significantly, as does pushing the temperature upwards of 37C (the protein prefers 25C and pH = 6.0). Most of the reactions I perform in the lab are at 4C overnight at pH = 7.4 between SpyCatcher003 and SpyTag1, and coupling is nearly complete. However, others in our lab have worked extensively with SpyCatcher002 and SpyTag1 reactions, which also tend to go to completion under the right conditions. Moreover, sometimes the protein that the SpyTag is fused to will alter the kinetics of the reaction, and short linkers to SpyTag may reduce your coupling efficiency.
While others are certainly more qualified to answer this question, hopefully this gives you enough information to work with!

Very nice answer! Want to help support the proposal for a SynBio StackExchange site?

I am currently working with these tags, so going off experience here. The binding efficiency is not 100% even when the correct versions are mixed e.g. version 2 spytag and version 2 spycatcher. I believe this is the original paper (https://pubs.acs.org/doi/pdf/10.1021/ja910795a) it reported 60 % binding efficiency after an hour (I presume for version 1) and this paper (https://www.pnas.org/content/pnas/109/12/E690.full.pdf) revealed 40 % binding efficiency in the first minute (unclear whether version 1 or 2 but I presume 1).  In terms of between versions I can only speak to a mistake I made once by accidentally mixing version 1 spycatcher with version 2 spytag. There was visible binding that could been seen by SDS-PAGE however, it was very faint and required significant amounts of protein to view (~10 mg/ml). I never did any sort of quantitative measurements on binding efficiency as it was a mistake. But from subsequent correctly run experiments, I could see it was significantly lower so I would always use version 2 with 2 and version 3 with 3 etc as they were designed to have maximum binding efficiencies.


text:
What is the relationship between the oxygen affinity of hemoglobin and the maximal oxygen uptake (VO₂ max) of the human body?
I was curious about whether any of the numerous documented human hemoglobin variants conferred a quantifiable athletic advantage but the only thing I've found of any relevance is the relative oxygen affinity of each hemoglobin variant. From the bit of research I've done it seems to be the case that a higher oxygen affinity causes the hemoglobin to hold onto oxygen more tightly and not release it into the plasma at the same rate as normal hemoglobin, leading to the body overproducing red blood cells to compensate for this (erythrocytosis). On the other hand, lower oxygen affinity causes the hemoglobin to release oxygen more readily, leading to the underproduction of red blood cells (anemia).
Assuming the quantity of blood cells were normalized between the two (so the consequent erythrocytosis/anemia is mitigated) would the lower oxygen affinity confer an increase in maximal oxygen uptake? How about higher oxygen affinity?


text:
When transmembrane proteins destined for the plasma membrane are in the ER membrane are they in their final folded form?
I am studying how transmembrane proteins are made and I have read that proteins that are destined for the plasma membrane are initially in the ER membrane and do not get translocated into the ER lumen unlike other proteins.
I was wondering when a transmembrane protein destined for the cell membrane is in the ER membrane, is in its native form (e.g. final, folded form?). I am asking this because I read that the ribosomes are on the ER membrane, and that protein translocation through the ER membrane occurs co-translationally, meaning that it's occurring as the mRNA is being translated. Would the protein get folded as it's moving through the ER membrane?
Any insights are appreciated.

This topic isn't fully understood, but proteins seem to be considered to become folded within the ER membrane, and the transmembrane integration system is compared to chaperone functionality. I found a nice review-paper to this topic. Check its sources for further reading to specific interests. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2814870/

The speed of folding/refolding is much faster than translation speed. So I expect much folding to happen during translation. Of course, proteins that become exposed to the different extracellular environment may refold then.


text:
What if target DNA doesn’t have restriction sites
All the examples on DNA cloning I have encountered have assumed that the target gene and vector both have compatible restriction sites at just the right locations (probably for ease of explanation). Instead suppose I have a vector that has restriction sites for multiple restriction enzymes, but my target DNA sequence doesn’t have a restriction site for any of them, how would I go about creating a recombinant DNA from these?

You could use a guide RNA and CRISPR/CAS for any sequence. However, the accepted answer is cheaper and more straightforward if you don't mind a slightly altered sequence (typically, a silent mutation or a change outside of the region of interest).

If you're synthesizing the insert then you just design it with restriction sites that are compatible to the vector. Otherwise, you can design PCR primers that have restriction sites in them. That way when you amplify your insert you'll attach the restriction sites to it. EMBL, Addgene, and NEB all offer somewhat more detailed explanations of this on their sites.


text:
What is the actual mechanism by which ApoA-1 Milano exhibits its phenotype?
ApoA-1Milano is a variant of the apolipoprotein A-I protein that was discovered by the University of Milan when sequencing the genome of those native to the village Limone sul Garda. The mutation has been shown to dramatically reduce the occurrence of cardiovascular disease for those who carry it. There has been much research invested into developing a means of delivering a synthetic version of this protein to the tissues of people already suffering from cardiovascular disease.
Typically with protein variants as high profile as this one there'd be some consensus or theory as to why the variant performs in the way that it does. For instance, the G171V mutation in the LRP5 gene results in a variant LRP5 protein receptor that reduces the ability of the DKK1 inhibitor to bind to it, resulting in greater LRP5-induced canonical Wnt signaling, which augments load-induced bone formation, which increases bone mass/density.
So a known mutation with a known protein variant as a consequence, the exact structural difference of which is known, and the exact intermolecular consequence of this difference is known, and finally the resulting phenotype is also known.
But in the case of ApoA-1Milano I can't find any literature regarding what the specific intermolecular consequence of this variant is that confers the reduced risk of cardiovascular disease phenotype. Big pharma has gone so far as to inject the variant protein into living human beings since the beneficial nature of it is so definitive but there doesn't seem to be any consensus as to how this variant is beneficial?


text:
Would the amino acid profile of lab-grown human meat perfectly match the dietary nutritional amino acid requirements for humans?
Whey protein is the food which has the most ideal (yet not perfect) amino acid profile for humans, whereas gelatin for example has a very poor and incomplete amino acid profile for humans. Would human meat grown in a lab such as they are working on with the meat alternatives match our amino acid requirements perfectly since it is actually human tissue?
UPDATE: I was not aware of any hazards that could be involved with consuming human tissues, so I am expanding the question to involve if there is any way to produce human meat safely in a laboratory setting.

I like the thinking behind this question, obviously human cell lines would not be viable for the numerous safety concerns but I guess it may be theoretically possible to engineer a synthetic tissue from another lineage that matches our exact nutritional requirements?

@JEJS What would the safety concerns be against consuming lab grown human tissues?

@wdbwdb1 disease vectors for a start, cooking does not destroy all infectious agents, by definition anything that spreads in humans vat grown cells can infect human cells thus posing a risk to the consumer. this is also why eating great apes is a very big risk.

@wdbwdb1 In addition to John's comments. Cannibalism is also a source for prion disease such as Bovine Spongiform Encephalopathy (BSE) a.k.a Mad Cow Disease and Creutzfeldt-Jakob Disease (CJD) among humans. An interesting case study is Kuru among the native population of Papua New Guinea from funerary cannibalism - https://en.wikipedia.org/wiki/Kuru_(disease)

I was not aware of any hazards that could be involved with consuming human tissues, so I am expanding the question to involve if there is any way to produce human meat safely in a laboratory setting.

I'm not an expert in nutrition, but I wouldn't necessarily expect human meat alone to exactly match human dietary amino acid requirements, at least not in the exact same abundances in which they are required. Many amino acids (including essential ones) are heavily involved in metabolic activities that have little to do with muscle tissue, like synthesis of hormones or neurotransmitters, so you wouldn't necessarily expect the concentration in muscle to match the dietary needs of a human perfectly.


text:
Why is haemophilia unviable in later stages of life?
A sentence in my textbook is:

The possibility of female being haemophilic is extremely rare because mother of such a female has to be at least carrier and the father should be haemophilic (unviable in the later stage of life)

I know that haemophilia is an X-linked recessive disorder. Hence mother should be carrier and father must be affected for daughter to get affected. But I'm unable to understand what "unviable in the later stage of life" means.

I suggest that this question is more suited to SE Medical Sciences.

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. ——— I mention this because if you had done the expected research you would have realized the premise of your question is incorrect. Note that under researched questions may be subject to down-voting and closure. Thanks!

I suggest the exposition does not usefully touch on the Question title but still - and based solely on the actual wording - if "unviable in the later stage of life" came into it that would be down to aging weakening every system it came across.

Mortality.
The reason the most common examples of haemophilia in history occur among nobles is not because the nobles were a particularly sickly bunch of people. It is because they lived sufficiently pampered lives to actually become adults, and reproduce their haemophilia.
In the same era, a commoner or even a rich merchant family would not be very likely to keep a full haemophiliac  male alive until marriageable age.
In our modern world, the almost-heroic level of medical care that is needed for a haemophiliac to live a normal life is much more common, and thus both carriers and active haemophiliacs tend to survive more often.

I think what they mean is that those affected with haemophilia rarely survive to the adult life. This is less of a constraint for women, since a woman carrying only one recessive gene will not be affected by this disorder.

It must be a really old book though, as my dad's a haemophiliac and I'm 50 years old. He spent a lot of time in hospital as a kid and was told he's the oldest one with his level of factor to survive being born.

@PeteKirkham impressive! It is probably also a genetics book - if it were on epidemiology, changing duration of survival with a condition would be something to discuss seriously !


text:
Are there any sustained efforts to model existing ecosystems?
Are there any ongoing, sustained efforts to obtain enough data about an ecosystem or part of one to build a viable computer simulation of it? All I can find (e.g. in Brazil or by google) appear to be sandboxes for demonstration or experimental purposes.
What I envision is a true model that can predict the future development of an existing system, and of course run simulations to predict the impact of certain external changes: Deforestation, temperature and precipitation patterns, introduction of non-native species etc.
Such a model would require a fairly detailed and complete biological inventory as well as detailed knowledge of the species' interactions, and a detailed map of the physical and chemical makeup of the location or region (water, ground, atmosphere, radiation). This would obviously be a vast undertaking, but with the potential of tremendous insights. Last not least, such a model would be a tremendous planning tool.
Are there any projects attempting this?

https://madingley.github.io/about/

The two hyperlinks both point to the same page. Is this a mistake?

@acvill Thanks for the observation. Fixed. (The google program, which is freely available at github, looks like a lot of fun.)

Such a model would require a fairly detailed and complete biological inventory as well as detailed knowledge of the species' interactions, and a detailed map of the physical and chemical makeup of the location or region...

I suggest reading about the The Simons Collaboration on Computational Biogeochemical Modeling of Marine Ecosystems (CBIOMES).1 This collaboration has produced ample research concerning the modeling of marine microbial communities in terms of spatial composition, metabolic interactions, nutrient flow, and seasonal variation.
Here are the research efforts highlighted on their website:

Developing New Computational Modeling Frameworks

Developing a New Trait-based Understanding of Microbial Communities Based on Metabolic and Elemental and Macromolecular Constraints (led by Zoe Finkel/Dal)
Constraint-based Modeling of Marine Microbial Community Metabolism and Physiology (led by John Casey/MIT)
Statistical Modeling of Microbial Communities: Niches, Traits, and Interactions (led by Andrew Irwin/Dal)
Thermodynamically Constrained Metabolic Networks for Ocean Modeling (led by Joe Vallino/MBL)
Models of Marine Microbial Biogeography and Biogeochemistry (led by Mick Follows and Stephanie Dutkiewicz/MIT)

Collecting and Compiling Relevant Datasets

Ocean Color and Biogeochemistry (led by Shubha Sathyendranath/PML)
Data and Tools to Define the Biogeography of Marine Microbes (led by Ginger Armbrust/UW)
Microbial Growth, Interactions and Biogeographies from ‘Omics’ Data (led by Jed Fuhrman/USC)

Bringing Together Models with Data

Advanced Statistical Analysis of Marine Microbial Systems (led by Christian Müller/Flatiron Institute)
Unifying Data and Models through Biogeography (led by Chris Follett/MIT)
Data Assimilative Modeling of Marine Ecosystems (led by Chris Edwards/UCSC)
Statistical Network Inference and Time Series Analysis (led by Jacob Bien/USC)

Concerning specific geographic sites, one of the best understood marine ecosystems is the San Pedro Channel off the coast of Los Angeles, which has been studied since 1998 as part of the SPOT project.2 Sampling efforts from this site include sensors that capture continuous in situ measurements of dissolved oxygen, fluorescence, temperature, salinity, and pressure, as well as monthly charters that collect seawater to measure nutrients (nitrate, nitrite, phosphate, silicate) and chlorophyll at 12 discrete water column depths. Peruse the publications section of the SPOT website to better understand the ecological and geochemical research that the SPOT project has enabled.
If you are further interested in the global effort to characterize and model the dynamics of marine microbial communities, I recommend a 2015 review by Fuhrman, Cram, and Needham3, which discusses methods to analyze microbial networks through space and time.

References

https://cbiomes.org/
https://dornsife.usc.edu/spot/
Fuhrman JA, Cram JA, Needham DM. Marine microbial community dynamics and their ecological interpretation. Nat Rev Microbiol. 2015 Mar;13(3):133-46.

Depending on how you define "model an ecosystem" the answer is somewhere on the spectrum from "yes, it's routine" to "no, that's impossible."
Let's start with the positive side. Ecosystem modeling based on inventories of species, information about their interactions, and spatial and environmental context are routinely used for analysis, prediction, and recommendation. For example, the Ecopath software tool, developed for modeling marine fisheries, appears to have been in pragmatic use for three decades by a wide community involving many different categories of stakeholders.
Now to the negative side. There is an inherent issue of scale and stochasticity in any question of ecosystems, not to mention their entanglement with scale-free and chaotic processes. Indeed, two of the prime examples of inherent unpredictability due to chaotic dynamics are population growth versus ecological limits and weather prediction. That doesn't mean we can't learn quite a lot about a system, though, as chaotic systems still operate within regions of the model space that can often be well-characterized and have high predictive value.
So, what to make of these apparently contradictory positions?
The takeaways that I would recommend are:

Ecosystems can be and are modeled effectively, but the models must be carefully formulated with respect to the questions that are being asked.
In modeling an ecosystem, more detail is not necessarily better, as the wrong type of detail can ruin the predictive power of a model.


text:
Can the spike protein created by the Covid mRNA vaccines be created independently of the human body, and is there a higher cost to that?
How different in principle is using the bodies own mRNA to create the coronavirus spike protein differ from other methods of using genes to manufacture other drugs or proteins and is there a cost benefit to it?
Take the scheme for instance that uses genetically modified genes in goats to manufacture spider silk, as shown in this link - The goats with spider genes and silk in their milk or Yeast cells genetically modified to create morphine-like pain killer
I understand that in the case of the Covid vaccines the human body's genes themselves are not modified, but it is the principle of using the body's own cells as a manufacturer of some desired protein that I'm inquiring about.
Even without any cost-cutting benefit does the way Covid mRNA vaccines work differ in principle from other gene based compound manufacture?

I’m voting to close this question because it is not about a biological mechanism or process.

It is about a biological process which in this case uses the human body as the system of manufacturing. Whether a cost benefit is a secondary issue, but it clearly has to be a factor given the huge scale on which it is being applied.
Is the scale the only reason why Covid has enabled mRNA vaccines managed to go mainstream or is just fortuitous timing?
The scale and the economics matter.

I don't think you're looking at this the right way and taking far too literally the meaning of "manufacturing" in this sense. You're comparing a vaccine to mass production of bulk materials. The mRNA- or viral-based covid vaccines produce very little protein in comparison.

@BryanKrause I'm not acquainted with the science here, as you can see that I have only asked one question here previously.
The question can be broken into 2 parts. 1. Whether  the spike protein can be manufactured independently of the human body, 2. If it can, why the human body is being used to produce it and whether is a cost benefit to it.
I assume for the layman there is the implied assumption that the human body is the only place the spike protein can be synthesized, but seeing that is not the first time gene manipulation have been used to create compounds is what prompts the question.

This site should find a way to enable discourse regarding the rapidly growing and extremely relevant field of bioengineering. Currently there is no "home" for it on Stack Exchange.

Bryans comment suggests he doesn't understand that the mRNA vaccine is also bulk manufactured. Bryan also says that the mRNA vaccine results in "very little protein" without citation, v questionable assertion.

(mRNA, protein) manufacture is an entire biology discipline relevant for medical and non medical industry. OPs question is a good one - is it easier to manufacture the mRNA than the protein, and is that part of why the vaccine is an mRNA vaccine.

If this isn't allowed, why don't the mods auto move it to medicine to help new users? Or even suggest moving it? Negative reinforcement only in the website rules? Way to crush discourse...

@Amanda — If you want to have a discussion about how the site works please use the [meta] site rather than antagonizing Bryan (who like all moderators is a volunteer). ——— However, I encourage you to first familiarize yourself with how this site is supposed to work by taking the [tour] and then carefully reading through the [help] starting with with [ask] and [answer] questions effectively. In particular, note that Not all questions can or should be answered here. Thanks!

@vfclists Come support the SynBio Stackexchange proposal? As soon as we hit 100 people with 200+ reputation, an interdisciplinary site will be launched where questions like these are clearly on-topic. https://area51.stackexchange.com/proposals/125068/synthetic-biology?referrer=MTFmYjRhNDUzOTZkYmY1NjU0ODE5ZjczMWY0Y2RiMDFlNTQyOWI1MWZkNzQyMzRhYjk2MWU0YzAyNjE3NjA0M930KtpvebSN1XkrLHnQGy7CghuJQAyr-Me9iSdHtWfZ0

What you describe, creating the spike protein independently and delivering it, is exactly what is done by subunit vaccines, such as the COVID-19 vaccine developed by Novavax.
As already noted in @Amanda's answer, mRNA is great at amplifying a delivery, so you need a lot less to be delivered.
The manufacturing process for the vaccine itself is a lot more modular as well, since you can address a new target simply by adjusting the contents of the mRNA. It's not necessarily simpler overall, though, since there are different challenges related to nanoparticle encapsulation and delivery.
The stability is also not necessarily better than for a subunit vaccine: proteins are sensitive and unstable, but so is mRNA.  The degree of sensitivity for mRNA, however, is more predictable than for protein, since the mRNA itself is a much simpler and more regularly structured molecule.

It is quite costly and difficult to manufacture and store proteins. It's very likely more efficient to have the human cells create as much protein as they can, from a relatively small amount of mRNA. Remember than one mRNA molecule can be translated into protein many many many times, so the manufacturers need to only make one mRNA molecule to get many protein molecules, whereas it would be more expensive to manufacture many protein molecules.
It's kind of a "give a man a fish, he eats for a day, teach a man to fish, he eats forever" situation. Better to give the body the instructions (mRNA) than the product, for cost effectiveness.


text:
Connectivity Relation between axon terminal synapses and dendrites
With regards to the synapses between axon terminals and dendrites, what is the relation between a given neuron's axon terminals and its neighbouring neurons' dendrites?

Does each axon synapse on only a single dendritic spine from another neuron, whereby all other connections that axon makes are with distinct neurons, or
Can multiple axon terminals from a given neuron end up connecting to a single neuron via multiple dendritic spines?

@BryanKrause am seeing you are both a neuroscientist, and programmer. Mind if we connect separately about neurons and AI? :-)

Cleaned up the comments and wrote a formal answer. I generally check the Biology.SE chat: https://chat.stackexchange.com/rooms/1997/the-biosphere every day or two, and will respond to pings there. I'm okay answering some questions there outside the StackExchange Q&A format, but won't necessarily commit to having any long conversations. If there are some specific things you'd like to ask about or you're looking for some direction I'm happy to help with what I can.

Synapses are pretty much one-to-one
Here's some EM pictures of synapses, from Wikimedia commons:

You should gather from these images that these are super organized structures. There's a dense, dense gathering of cellular machinery at the synapse that creates a dark electron-dense region shown by the arrows. There's no room for more than one cell to be directly involved in this area, it's one membrane closely coupled with another membrane. It's as if you put the palms of your two hands together.
Some neuromodulators (and sometimes traditional neurotransmitters) are not released synaptically, though, and are just dumped into the extracellular space from where they diffuse in to the cleft or bind outside the synaptic region.
There can be multiple connections between two given cells
Though a synapse is a one-to-one connection, axons make multiple synaptic contacts as do dendrites. Though this can mean that cells receive and send input to 1000s of different cells, it's also very common for there to be multiple individual synapses between two specific cells.
For some examples, Tamas et al 1997 looked at synapses made from inhibitory interneurons to excitatory cells in visual cortex:

All presynaptic cells established multiple synaptic junctions on their postsynaptic
target cells. A basket cell innervated a pyramidal cell via fifteen release sites; the numbers of synapses formed by three dendrite-targeting cells on pyramidal cells were seventeen and eight respectively, and three on a spiny stellate cell; the interaction between a double bouquet cell and a postsynaptic pyramidal cell was mediated by ten synaptic junctions.

Note in this paragraph they are literally talking about 5 specific pairs of cells, where they trace both cells in EM. This is an exhausting process. The presynaptic cells were one basket cell, three dendrite-targeting cells, and one double bouquet cell. The post-synaptic cells were all pyramidal cells except one was a spiny stellate cell. In the five pairs they found 15, 17, 8, 3, and 10 connections. Of course they could have missed some, too.

Tamas, G., Buhl, E. H., & Somogyi, P. (1997). Fast IPSPs elicited via multiple synaptic release sites by different types of GABAergic neurone in the cat visual cortex. The Journal of physiology, 500(3), 715-738.


text:
Is it true that oxygen levels in water limits fish size?
This answer says that breathing water is inefficient, and that may act as a limiter to the size of fish. I've heard this in a couple of other places as well, but cannot recall the sources. However, the Wikipedia page on allometry indicates that metabolic rate and oxygen consumption scale logarithmically with mass, which implies that the ratio of required oxygen to mass will be lower in larger animals than smaller ones. As such, I would think that the size of respiratory organs would shrink relative to the over-all size of the animal as it is scaled up. The answer linked above even says:

Gills grow in proportionate scales to body size, generally for every 100% increase in body size there is a 50-90% increase in gill size.

Which is entirely compatible with the (admittedly naive) application of allometric organ scaling. How, then, does access to oxygen limit fish growth?

water contains drastically less oxygen, it is not about gills vs lung anatomy. air contains about 21% free oxygen, while water contains about 1% dissolved oxygen.

I've heard this point made before, but I'm really struggling to understand it's relevance. If the issue is about the concentration of oxygen in the water, then I would think that should impede oxygen absorption rate only by a constant factor. This constant factor should already be accounted for by a constant factor increase to surface area for absorption. Then, when comparing larger fish to smaller fish, the difference should be in the logarithmic function of the mass increase. Is this incorrect?

this may help you understand, why is it harder to breath at high altitude, lower oxygen content due to lower air density. above a certain altitude the oxygen content is too low to survive on. If you are taking in less oxygen you are producing less metabolic energy.  the mass of the organism has no effect on the oxygen content of what they are breathing, and the efficiency of a breathing mechanism cannot compensate for such a large difference.

I'm afraid I still don't follow :s It's clear to me why breathing less dense air would prove problematic for animals in general, but it's not clear to me why that would put a cap on animal size. Surely, if there is enough oxygen at a given altitude for a small creature, then another animal with double the metabolic rate would simply need to breath twice as much air. I don't mean that they absorb oxygen more efficiently, perhaps their lungs are just twice as large, so twice as much oxygen can be inhaled, regardless of it's density.

you can only speed up breathing so much before it results in less oxygen uptake, gas exchange takes time. the other problem is water, bigger lungs means more water loss via breathing, soon you reach the point you can't replace the water as fast as you lose it, the same thing happens will gills in salt water.


text:
What is happening with this hummingbird and how can I help him?
Today I noticed a hummingbird next to my feeder (California) which looks very strange. From my observation it seems that something sticks from its head. This thing is rigid (does not look like a spider web) and bothers the bird (from time to time the bird tries to use a leg to get rid of it).
The bird can fly (slower than other hummingbirds) and it seems like it eats from the feeder (but puts its head deeper into the feeder than other hummingbirds).

What is this? And more importantly how can I help the bird?

Welcome to Biology.SE! You might have better luck at [Pets.SE], since this is essentially a veterinary question. If you do decide to try there (please check their help section for suitability), please either request migration or delete this post before reposting there (cross-posting is impolite). Good luck!

@tyersome thanks for the reply and sorry if this question is inappropriate here. I was looking at pets but thought that it might not be the right place as hummingbirds are unlikely to be pets (agree that this is more a veterinary question). If you think it is better to migrate it there, please migrate it.

No problem! I've seen a few wild-bird related posts at [Pets.se] , but I'm not active there so I can't guarantee this will work there. I'm not a moderator, so I can't migrate this. If you want to initiate migration, just flag your answer and select "in need of moderator intervention". Enter something like: Please migrate this to Pets.SE, I think it would fit better there because .... Alternatively, you can delete the post from this site and repost it on Pets.SE. ——— It also might be more effective to reach out to a local wild animal rescue organization for advice/help.


text:
Why did whales end up larger than most sauropods and what is a whale's limits?
I understand that due to the square-cube law (when something grows 2 times but its volume grows 4 times and it goes on) sauropods were massive but not enough when compared to whales because whales got around the square-cube law by using the buoyant force to balance their bodies in the water. In addition, being mammals allowed them to breathe, oxygen-rich air while fish were limited to oxygen-poor water, this thenceforth allowed whales to grow many times more than the largest fish. So my question is what is the limit to whale size and if there is one what is their true potential?
A question presented by the scientific community and given to the public.

Food is pretty important. I wonder if the air oxygen argument actually holds since they need to hold their breath whereas fish get a continuous supply.

this would probably be better received on the biology stack since it is not about worldbuilding.

Probably better on biology.

@DKNguyen nearly all the plankton is in the top 100m of the ocean, and a blue whale takes about 1-minute to each that depth because they can swim at 10 m/s and they only have to inhale every 30 / 90 minutes.

Re size, note that the whale shark (a fish) at up to 18.8 m in length is as large as some of the whales.  Some estimates put the extinct Megalodon shark even larger.

Basic error: "when something grows 2 times but its volume grows 4 times and it goes on" should be "when something grows 2 times but its volume grows EIGHT times and it goes on". Linear dimension cubed.

As best we can tell food availability is the relevant limits in whales.  its true that the bigger an animal gets the more energy efficient it is, it needs less food proportionally but still needs more total amounts of food. There is a limit to how much food you can find and eat, especially in the lean parts of the year. This is actually why we see dwarfism on islands lower food availability favors smaller size (less overall food needs). Finding food and even feeding itself takes energy and it reaches a point where the energy you expend is equal to or less than the energy you can extract from your food.
There are other limits like blood pressure, internal surface area, digestion time, heat buildup, but whales have not reached any of these.
https://science.sciencemag.org/content/366/6471/1367

So the depending factor here is mainly food like take for example the kiwi is a flightless bird that is in the same family as the ostrich and evolved to be smaller over time due to the lack of potential predators.

@ParinChitrada food is the limiting factor that determines maximum size. Food is NOT the only thing that determines size it is however what determines the limit on size.  there is a big difference between determining factor and limiting factor. there are plenty of small ratites. there are 40+ species of  tinamous for instance.


text:
How long to regrow hair?
This is one of the questions I wasn't exactly sure where to post. Basically, I want to make an X-Men parody, and for the part of Professor X I need to shave off my hair. Now I have a simple french crop, not really long or anything, but I was wondering if there's an estimate for how long it would take me to regrow my hair. Again, sorry if this is the wrong site, but I just thought "human body", so I guess it fits.

According to https://en.wikipedia.org/wiki/Human_hair_growth:

Scalp hair is known to grow between 0.6cm and 3.36cm per month. The growth rate of scalp hair somewhat depends on age (hair tends to grow more slowly with age), sex, and ethnicity. It was previously thought that Caucasian hair grew more quickly than Asian hair and that the growth rate of women's hair was faster than that of men.
However, more recent research has shown that the growth rate of hair in men and women does not significantly differ and that the hair of Chinese people grew more quickly than the hair of French Caucasians and West and Central Africans.

Depending on your age, follicle-condition, nutrition or possible inhibiting factors it can vary how long it will take until your hair has grown back to the previous length.

With that in mind, I should be back to full lenght in 1-2 months. That's doable, thank you.

@MatNX Pleasure (gern geschehen), if you take the average (1.98 cm/month) and estimate a french crop with about 4 cm, it should take about two month ;)


text:
Differentiating between hormones triggered on specific types of happiness?
Achievement:- Dopamine
Applause:- Seratonin
Discovering something new:-?
Remembering something after a long time/struggle:-?
Nostalgia:-?
Lust ;-Testosterone/Estrogen
Romantic Love:- Dopamine?
Attachment:- Oxytocin or Vasopressin?
Cuddling pets/babies:- Oxytocin or Vasopressin?
Motherhood:- Oxytocin & Vasopressin?
Also, is happiness in all cases equal? I mean that is happiness just differing in magnitude rather than type when comparing different activities? For eg, happiness on discovering something new is the same exact as happiness on kissing your crush, just differing magnitude and triggered by a different hormone?
Like in video games, we have damage versus status effect (losing hitpoints versus getting paralyzed or stunned), is that a better analogy to the various kinds of happiness or is it more like fire damage versus ice damage,

My apologies, but I'm having a bit of difficulty understanding your question. Can you try to edit it to focus more precisely on a specific aspect of what you are interested in?

which hormone is triggered when

How about Noradrenalin,  Melatonin, Tyramin & Tryptamin ? Not to forget the countermechanic, enzymatic groups that catalyze the oxidation of monoamines via monoamine-oxidases..

I think you need to narrow your question a bit, as right now it could be answered with several full textbooks. That said, a simple answer is that there is no such thing as a "happiness hormone" (despite some pop sci articles attributing this to one hormone or another), and all that you've listed are associated with far more than the pairings you've written here. You can give someone heroin and they experience happiness, but we don't call heroin a happiness drug.


text:
What is the difference between effective and efficient selection?
I always thought of the efficiency of natural selection in the context of molecular evolution. I.e. that linked selection and smaller population size cause less efficient selection. It took me a while before I even noticed that people also say the efficacy of selection.
When researching the answer myself, I found that older papers talk more often about efficacy (like this one). I also found that besides the natural-selection context, it seems efficiency of selection is also used in the context of breeding (like here). However, you can certainly find cases when used in the context of natural selection. Finally, there are about 4x more papers that contain the words "efficiency" and "natural selection" compared to "efficacy" and "natural selection".
So, is effective and efficient natural selection the same thing? Is "efficacy of selection" and "efficiency of selection" be used interchangeably?
-- EDIT --
I am interested in the use of these two words in the context of natural selection only. Unlike in other contexts, in natural selection dictionary definitions of the two words do not make much sense.

I think it is a case of Humpty Dumpty in Alice in Wonderland. The words meant exactly what the authors chose them to mean, which unfortunately we cannot tell, because there is no authority that gives these English words precise definitions in biology. As I keep saying, biology is not physics.

I think that in this case, they are used synonymously, even though they do indeed have a subtle difference in definition. This is a common synonymy in biology, many researchers are not native speakers and there exist many native speakers who do not appreciate the difference between the two enough to use it with precision. For instance, here you see it used more or less interchangeably. Effectiveness, efficacy, efficiency...

@SPr Thanks, that's already a nearly complete answer. Would you mind also elaborating a bit about the subtle difference in this context? (also if you post it as an answer, I would be happy to accept it)

As a reader, when I read effective selection, it means it works, and is successful to a high degree. For example, 70% ethanol is effective at sterilizing your work bench (negative selection). It does the job well when you wipe several times with it. Conversely, when I read efficient selection, I read it as selection that is accomplished with the least amount of wasted time or effort. Paraformaldehyde or gamma ray radiation are more more efficient at sterilization (they work more stringently and the performance is better), but they are obviously not as practicable. Unsafe and costly.

You have a word problem here, not really biology.
Efficacy means "power to produce the desired result/effect"
Effective means "producing the desired result", stressing the ability to produce that result
Efficiency means "degree of being efficient"
Efficient in turn means "ability to produce desired result with little waste"
Efficacy and efficiency are not interchangeable as they have different meanings, albeit a subtle difference. You could on the other hand us efficacy and effective as synonyms, though properly the synonym of efficacy is effectivness.

Appreciate the effort but I did google the definitions of the words before I asked. The problem I have is that there is no "desire" in evolution and it's hard to guess what "little waste" would mean in this context. So I think the question "What is the difference in efficacy of natural selection and efficiency of natural selection?" remains unanswered.

The distinction made by @bob1 makes perfect sense:

Effective selection applies to the situation where selection may or may not work: e.g., in a small population subject to the random drift, the selection may be ineffective in the sense that deleterious alleles may fix with nearly the same probability as beneficial ones, the outcome thus nearly independent on the selection. On the other hand, in a sufficiently large population the outcome is largely determined by selection, i.e., the selection is efficient, as suggested in the first reference given in the OP:

Deleterious alleles can reach high frequency in small populations because of random fluctuations in allele frequency. This may lead, over time, to reduced average fitness. In this sense, selection is more “effective” in larger populations.

Efficient selection refers to the cost of the selection, as suggested by the second OP reference:

A new index of selection efficiency, i.e. the ratio of the probability of achieving the desired genetic gain in a target population to the cost expended for that gain, is introduced to define the optimum selection procedures that give the most opportunities for producing new commercial varieties.

The cost here may mean very different things - the actual financial cost to the breeder, the energy expenditure by organisms, the number of generations necessary for achieving the desired outcome. Thus, selection may be effective in the sense that we do arrive at the desired resultat, but inefficient in the sense, e.g., that it takes very long time to arrive at this resultat.
Brief googling for efficient selection confirms that this is often the sense in which the term is used.
Nevertheless, the third reference in the OP essentially speaks of efficiency in the same sense as effectiveness/efficacy, which is probably just poor English usage (I myself was not quite clear about the difference before reading @bob1's answer).

Thanks, so actually it will be mostly breeding vs nat. selection (the cost of time is very meta to me). Also, I would love to see Eyre-Walker's response to this answer ^^.


text:
SARS-COV-2 replication speed
What is the speed of replication of SC2? Any information, including in vitro data would be appreciated.
I would be interested to know the length of SC2 eclipse period, latent period and something like burst size.
Alternatively, per day CT values of qtPCR of COVID+ subjects would be also helpful.

According to Amy Rosenfeld, it is about 8 hours eclipse and 18-24 hours until "its done". Not sure if it means until burst or until the latent period is over. These times are in vitro and are cell line dependent. In vivo might be different. Burst size also cell depndent. Source: https://youtu.be/NP56XjzyPfQ?t=1301
In this video https://youtu.be/4S3DXXtRZZg?t=152, it is said, that each cell can produce up to 600k viral particles of SC2, but I'm not sure, what is exactly meant by the number. Later in that video: https://youtu.be/4S3DXXtRZZg?t=187 it is said, that the virus seems not to kill cells for about 5-6 days.


text:
Could an organism evolve to adaptively evolve?
Besides chance mutations sticking around because of their utility towards survival and procreation, could an organism evolve the ability to aid this process by mutating more frequently in beneficial directions in response to the environment (e.g. based on some form of past higher order evolutionary experience)?

cephalopods have some funky DNA editing mechanic that you should look into

Also look into humans! :) https://en.wikipedia.org/wiki/Somatic_hypermutation

You mean environmentally-responsive pre-programmed mutations, based on higher order experience? Like an animal in cold weather will tend to have more hairy babies than an animal in warm weather? AFAIK evolution conforms to higher order architectures which are only slightly tweaked in ways which are probably useful, like symmetrical limb lengths vary a lot more than non symmetrical chance mutations.

IMHO, the whole genome replication/recombination/mutation process and arrangement has evolved to increase the likelihood that changes will be beneficial or at least neutral.  In chromosome recombination, for example, new chromosome combinations are constructed from old, tested, gene sequences, while making sure that the new pieces are homologous to corresponding pieces in the parents' and grandparents' chromosomes.


text:
Do phagocytes need antibodies to be able to engulf pathogens (to function)?
I recently saw a question about monoclonal antibodies, that are specific to a certain virus, being split (into their constant and variable regions via an enzyme), and the question asked whether some statements were false or true.
One of the statements said that the virus could be engulfed by phagocytes if any were present. The statement turned out to be false and I'm not completely sure why. Is it because phagocytes need fully intact antibodies to function so that they can attach to them via receptors specific to the constant region of the antibodies consequently becoming attached to the virus and so being able to engulf it?
I thought that phagocytes could work on their own and that antibodies just made their job easier. Is that assumption correct?

Phagocytes don't necessarily need antibodies to recognize intruders, i.e. by presence of non-self sugars. Additionally, phagocytes can aid amplification of effective anti-bodies by presenting degraded pathogens to the adaptive immune-system. I found this concise summary of the innate immune system, that I would strongly recommend to read!
Now to your more specific question: Detection of viruses. You have to consider, that viruses are highly optimized to evade the innate immune system:
Viruses can happily replicate and mutate without proof-reading without negative consequences and with relatively low conceptual constraints, as they are so simple, compared to cells. This is why the innate immune-system is prone to miss viruses (at least those, that are optimized for a certain species). Imagine how big of a genome you would need to cover all possible viral substances by at least 1 innate gene! Read about hyper-mutation to understand the role of antibodies to detect even these highly evasive viruses.


text:
Why aren't there any competing biologies on Earth?
Why aren't there any competing biologies on Earth? I read sci-books about life based on silicon and I've read an article that said that other structures than DNA can encode genetic information.
So does physics allow for many competing biologies? What makes DNA-based biology the dominant biology on earth according to known laws of physics?

Silicon-based biochemistry is pretty unlikely, at least at the temperatures and pressures present at the surface of the Earth. While carbon-hydrogen compounds of any length are effectively stable and can include complex branching and cyclization, silicon-hydrogen compounds don't get much longer than trisilane or cyclopentasilane without falling apart. Also, Si-Si double bonds are rare, while there are a wide variety of relatively stable alkenes (C-C double bonds), alkynes (C-C triple bonds), and aromatics. We haven't even included oxygen and nitrogen yet! There is no replacement for carbon.

CO2 is an easy waste product to get rid of.  SiO2... less so.  Imagine having to excrete a kilo of quartz every day.

Chemistry is a bigger factor here than physics (though I guess chemistry is just applied physics at it’s core...). As a simple example, the oxidizing environment that (most) life on earth lives in strongly selects for certain biochemistries because it makes certain types of reactions much easier than others (and, in fact, you can find some really ‘exotic’ metabolic processes in things found in strongly reducing environments like geothermal vents in the oceanic benthic zones).

Actually, DNA could be the dominant life-form in the milky way galaxy, if it formed 9 billion years ago on the first habitable planets and unicellular extremophiles live in all our ice comets.

Optimization can result in lack of diversity. Look at how many body plans there were for aircraft in the beginning vs now.

Silicon is a 7 times less abundant than carbon and it explodes almost instantly when it's joined with the most common element, Hydrogen, (SiH4, methane equivalent), and it joins to oxygen (3rd most common element) so tightly that qaurtz SiO2 is one of the hardest rocks of all. So silicon mostly makes brittle rocky substances, whereas carbon makes billions of organic lego shapes which are fluid from syrup to mineral oil.

There are indeed almost certainly other potential alternatives to DNA-based biology and the RNA-based biology that may have predated it, which could be used to form viable organisms.
Many of them likely have some energetic disadvantage relative to DNA and RNA (e.g., requiring a higher bond formation energy, having a less flexible backbone) and those would naturally be expected to be outcompeted. But some probably aren't so different from DNA and could indeed have formed a viable alternative---if nothing else, the opposite chirality molecules are certainly candidates. Why aren't alternatives still around?
Surprisingly, it turns out that when time scales are long enough, we should expect a natural loss in the number of different independent lineages. Another more recent example of this is the fact that all modern humans are descended from Mitochondrial Eve and Y-chromosome Adam, despite the fact that these two individuals were members of thriving human populations at entirely unrelated times. Biodiversity is constantly being gained through divergence of existing lines and lost through lines that fail to reproduce. Over many generations of reproduction, this produces a random walk pattern that converges toward elimination of all but a single lineage in a given population even if all lineages are equally fit.
Now back to the origin of DNA-based life.  If abiogenesis is a rare and difficult event, then we would expect only one or a small number of life models to have emerged billions of years ago. Random fluctuations over all that time will tend to drive all but one toward extinction. With evolution at play as well, any lineage that randomly gains an advantage will be even more likely to outcompete the others.
And once there is life of any sort around? Well, potential alternatives to DNA are still nutrients, and therefore will simply be eaten by existing life forms before they have the chance to evolve into something new and interesting.

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

One mistake: Y chromosome Adam wasn't necessarily (and probably wasn't) human. Some estimates for his age predate modern humans by a long time. I can't remember off the top of my head if the same is true for MT Eve but it probably is.

@KonradRudolph From what I have read, the current estimates are consistent with species emergence estimates. The science is still unsettled, though.

"Random fluctuations over all that time will tend to drive all but one toward extinction." isn't this an extremely strong claim to make?

@Dunois It perhaps a surprising conclusion, but consider the fact that nearly every species that has ever existed is extinct, including entire massive and long-lasting taxa such as trilobites, and mass extinctions are frequent events on geological time scales. I think a stronger claim would be to assert that there would not be large-scale mass extinctions in the billions of years of difficult to observe microbial prehistory.

@jakebeal thank you for taking the time to respond to me. But I am confused: the statement I had quoted had been made by you in the context of the occurrence of abiogenesis in (our) universe. The supporting evidence you've provided here in your comment is specific to carbon-based life on Earth. I do not dispute your reasoning but isn't the extrapolation a bit tenuous here?

@Dunois The question is focused on life on Earth, and so is my answer and my comment.

@jakebeal my apologies, I had incorrectly assumed you had made that statement about the universe in general. Thank you for clarifying this!!

@Dunois If we go with the assumption that randomness is volatile enough to destroy all life, eventually, it follows that: random fluctuations over time will drive all but one to extinction, first, then drive the final one to extiction.

@Robino You seem to be fundamentally misunderstanding the result. It does not show that randomness destroys life, it shows that randomness is sufficient to allow some life to displace other life.

@KonradRudolph: Non-Homo sapiens sapiens ≠ non-human.  Even with the earliest estimates, both Y-A and Mt-E would still indisputably have belonged to the genus Homo.

@jakebeal In my defence, the question has been changed.

Jack Szostak's research group has looked at alternatives for RNA as replicators, see e.g. here, and they found that RNA is a far better replicator than the alternatives. So, it seems that RNA-World was preceded by a prebiotic world where RNA won the competition from rival nucleic acids. Then during the RNA-world period, the RNA-world evolved ever more complex ribozymes. More complex proteins were being made by primitive ribosomes, which in turn led to the evolution of DNA as a stable storage platform for information.
But this does not fully address the problem, because as @uhoh has commented on another answer, the mirror image of RNA would, of course, have the same performance. Life arose quite fast after the conditions on Earth were suitable for life, which is inconsistent with the idea that abiogenesis is a very rare event. The relevant processes that would lead to life appearing somewhere on Earth are very localized in nature. We're talking molecules interacting with each other in some tiny confined space rich certain energy-rich environment. The precursors RNA molecules cannot get diluted to much.
So, this process being a very localized processes on micron to millimeter-scales cannot possibly have led to a world-wide competition where alternative, equally good molecular systems such as the mirror image of RNA would have lost out. Given that life appeared very fast somewhere on Earth, it would have had to appear fast on many places on Earth with at least random chiralities and perhaps also implemented by totally different biochemical systems.
It's then hard to see why the different chiral versions of life would en up wiping each other out much later when they would come into contact with each other. Living organisms tend to not wipe each other out due to competition if they are not closely related, and the mirror version of life would not interact strongly with ordinary life. As pointed out here, a photosynthesizing mirror organism would cause problems for us precisely because it would convert CO2 into inedible compounds:

After doing some rough calculations on the effects of a mirror cyanobacteria invasion, Kasting isn't sure which would kill us first: the global famine or the ice age. "It would quickly consume all available nutrients," he says. "This would leave fewer or perhaps no nutrients for normal organisms." It would wipe out the global ocean ecology and starve a significant portion of the human population. As the CO2 in the ocean was incorporated into inedible mirror cells, they'd "draw down" CO2 from the atmosphere, Kasting says. For a decade or two, you'd have a cure for global warming.

But Kasting predicts that in about 300 years, the bugs would suck down half of Earth's atmospheric CO2. Photosynthesis of most land plants would fail. "All agricultural crops, other than corn and sugar cane, would die," he says (they do photosynthesis a little differently). "People might be able to subsist for a few hundred years, but things would get pretty grim much more quickly than that." After 600 years, we'd be in the midst of a global ice age.

The plot of the chirality disaster depends on the assumption that the wrong-chirality organics will be inedible. This is plain wrong, at least for sugars and there is a lot of xxx-racemase enzymes for other things.

While the discussion of heterochirality was squelched I think it deserves to be addressed explicitly, because unlike most "competing biologies" that one might imagine complementary chiral biologies have zero competitive advantage over each other.
The abstract of Emergence of homochirality in large molecular systems (Laurent, Lacoste and Gaspard (2021) PNAS January 19, 2021 118 (3) e2012741118) sums it up nicely, albeit based on a complex mathematical model based on cheminformatics and random matrix theory:

The selection of a single molecular handedness, or homochirality across all living matter, is a mystery in the origin of life. Frank’s seminal model showed in the ’50s how chiral symmetry breaking can occur in nonequilibrium chemical networks. However, an important shortcoming in this classic model is that it considers a small number of species, while there is no reason for the prebiotic system, in which homochirality first appeared, to have had such a simple composition. Furthermore, this model does not provide information on what could have been the size of the molecules involved in this homochiral prebiotic system. Here, we show that large molecular systems are likely to undergo a phase transition toward a homochiral state, as a consequence of the fact that they contain a large number of chiral species. Using chemoinformatics tools, we quantify how abundant chiral species are in the chemical universe of all possible molecules of a given length. Then, we propose that Frank’s model should be extended to include a large number of species, in order to possess the transition toward homochirality, as confirmed by numerical simulations. Finally, using random matrix theory, we prove that large nonequilibrium reaction networks possess a generic and robust phase transition toward a homochiral state.

It's a stretch from cheminformatics and random matrix theory to what may have actually happened, but it is helpful to know that nature provides a way for one member of a chiral biology pair to completely annihilate the other despite any specific competitive advantage.
This is important because today we see exclusively one chirality on Earth, and use it as a way to differentiate between processes involving life and those that don't.
That's discussed nicely, and at length in D. G. Blackmond (2010) The Origin of Biological Homochirality (Cold Spring Harb Perspect Biol. 2010 May; 2(5): a002147.)
And exobiologists may be tempted to apply this beyond Earth as well which means they need to consider non-life-based chiral selectivity carefully!

+1 Some things in evolution are just historical accidents and don't correspond to optimization against any selection pressure. Chirality is an obvious one, since it so clearly could have gone either way. But what else is just a historical accident?

Carbon
jakebeal's answer is very good, but the Wikipedia article on DNA alternatives is also very thorough.  In particular, when astrobiologists debate whether alien life is likely to be carbon based, the answer is often "yes", because no other element has the chemical flexibility of carbon.  While silicon is in the same group and can form long-chain molecules, it simply lacks the diversity of total molecular options, and the chains it can produce are much shorter on average than carbon (because it's a much larger atom and makes weaker double-bonds).  Note that any carbon replacement suffers the same problem as silicon: much larger and less chemically flexible.
Note that your article simply assumes a carbon-based backbone, and asks what other molecules could replace the common nucleic acids.
Crystals
Some folks talk about the possibility of radically different life forms, such as crystals.  Unfortunately, crystals are good at growing, but not good at adapting.  It is hard to imagine any kind of metabolism in a crystal-based system.
Energy
Way out in the woo-woo space, non-scientific folks like to play with the idea of "energy-based life forms".  While I fully confess to a failure of imagination here, I would just like to point out that all the life we know about works hard to maintain homeostasis, which gets increasingly difficult in high-energy environments.  This is because it takes energy to maintain the low-entropy configurations of living bodies, and all systems must emit heat to do work.  Of course, dumping heat gets increasingly difficult the hotter one's environment.
The most literal way to describe an "energy-based being" is one that has no normal matter as part of its body.  A being made entirely of photons doesn't make any sense at all.  That's because most photons simply don't interact with each other, so it would be like having a body in which none of the cells could communicate.  Planck-scale photons could use pair production to "interact" with each other, in some kind of ephemeral body, but it is hard to imagine how this could remain coherent over any kind of timescale.  Also, the electron/positron pairs would push the definition of "no normal matter".
Of course, we could just be talking about beings whose base metabolic rate is so high that they emit blackbody radiation in the visible spectrum (so that we see them as natural sources of light).  They would be made of ordinary matter, but such beings would consume pretty significant quantities of energy relative to terrestrial life.  We have a good example of a blackbody that emits strongly in the visible spectrum: the sun.  It has a blackbody temperature of about 6000k, and requires a massive scale of thermonuclear fusion to maintain that temp.  Needless to say, any beings operating in that energy regime would either be much, much larger than human-sized, or would require physics that is well beyond our current understanding (perhaps they are powered by hearts of micro-black holes?).
Obviously, such a biology would not naturally arise on earth. ;)