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Using punnett squares to express sex/gene linkage and recombination frequency
I have been using punnett squares to visualize mating experiments. I am looking at a pairing which is known to have a crossover event occur. I know from empirically collected data the recombination frequency is ~3%. Can punnett squares be used to express the results bearing the recombination frequency in mind or should I consider a different visualisation technique?
The end result of what I want to achieve is the expected genotypic/phenotypic outcomes taking recombination into account.
In addition the pairing has a sex-linked mutation which further complicates things e.g. aB/Ab x Ab/Y
Here is an example punnett square:
 a-B/A-b x A-b/Y
 -------------------------
 | x   | A-b     | Y     |
 -------------------------
 | a-B | A-b/a-B | a-B/Y |
 -------------------------
 | A-b | A-b/A-b | A-b/Y |
 -------------------------

If a want to represent a recombination event in the punnett square (e.g. to produce a-b/A-b and a-b/Y does this mean I would  need to add a-b as an additional trait to the punnett square like so?
a-B/A-b/a-b x A-b/Y
 -------------------------
 | x   | A-b     | Y     |
 -------------------------
 | a-B | A-b/a-B | a-B/Y |
 -------------------------
 | A-b | A-b/A-b | A-b/Y |
 -------------------------
 | a-b | A-b/a-b | a-b/Y |
 -------------------------

If that is the case, that would give me a frequency of 16.666666% for each.

Although generally Punnet square is used to show the expected progeny in case of validity of Mendel's laws of segregation and/or of independent assortment, you definitely can represent the outcome of any cross using Punnet square. It would be useful if you drew the square of your results and posted it here sharing your doubts with the community.

Thanks @FabioMarroni, I have modified my original question with example punnetts.

Punnett squares show the possible gametes from each parent.  I suppose you could write out all the possible recombined gametes with their frequency in the same format, explicitly stating the percentage of each (usually 50% or 25% is assumed but not written).  So if you have the female at the top of the table (sorry, I tried some html tags but they're not taking; I should RTFM)
........ AB - Ab - aB - ab
....... 48.5 1.5 1.5 48.5 %
ab 50%:  24.25 0.75 0.75 24.25 %
Y 50%:   24.25 0.75 0.75 24.25 %
Per your last sentence, the male can only pass on its X genotype, which I've assumed as ab for a backcross, or Y - no crossover - so this would be a 4x2 Punnett square.  The odds of each box in the square (not considering lethality) are still found by multiplying the odds of each allele as ratios, then converting to percentage.  You have to add up all the percentages that match a phenotype as you score it to find phenotypic ratios.
This page explains this idea with better formatting, but not for a sex-linked trait.

The Punnett squares are a general way to visualize the product of any two polynomials; for example, you know that the result of (a + b)(c + d) is the sum of the four terms ab, ac, bc, bd. You may put it this way:
  | a   b
----------
c | ac  bc
d | ad  bd

Suppose that the female sex gametes are of two types, X1 and X2, which are transmitted with probabilities 0.9 and 0.1; suppose that males form three types of gametes, X1, X2, and Y, with probabilities 0.45, 0.05 and 0.5. Then, you may visualize the outcome of a general population mating this way:
    |Fem   X1   X2
    |      .9  .1
--------------------
Male|
X1  |     X1X1  X1X2
.45 |     .405  .045
    |
X2  |     X1X2  X2X2
.05 |     .045  .005
    |
Y   |     X1 Y  X2 Y
.5  |     .45   .05

(You may note that this situation roughly depicts the population genetics of color blindness)


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Basic clarification on definition of "unicellular"
Biology noob here, trying to expand his basic scientific knowledge.
https://en.wikipedia.org/wiki/Unicellular_organism

A unicellular organism, also known as a single-celled organism, is an
organism that consists of a single cell, unlike a multicellular organism that consists of multiple cells.

But to me, this is ambiguous. Is a unicellular organism one that contains one cell and one cell only? Or is a unicellular organism one that contains one kind of cell, but lots of copies of that cell? So for example, are plants not unicellular because they contains groups of different types of cell, or are plants not unicellular simply because plants contain more than one cell?

Why the downvote?

The definition in the question seems to clearly (to me) refer to unicellular as a single cell only. The second half of the definition states "unlike a multicellular organism that consists of multiple cells", which seems to exclude any organism composed of two or more cells (regardless of what "type" the cells are)

Ok, so a unicellular organism is a single cell that can survive on it's own (under the right conditions). Is this what the definition means?

A unicellular organism is an organism that is one cell.

I don't have any particular issues with this but answer, but it would help a bit to have citations, references, etc. It also doesn't really add much on top of existing answers.

Concise answers that fully answer the question are better than verbose ones that add nothing extra.

a unicellular organism is a single-celled organism that can conduct all the functions needed to survive on its own, in one cell. whereas multicellular organisms have different kinds of cells for different functions.
in the plant example, the plant is multicellular because it has different cells performing different functions, for example palisade cells are mainly responsible for photosynthesis while spongy cells are mainly for gas exchange.
keeping that in mind, there can always be exceptions in multicellular organisms where some are able to survive as single-celled organisms
hope this cleared stuff up.

A unicellular organism is one where a single individual can survive all by itself under the right conditions. Some unicellular organisms live in colonies with many others of the same type or other types, and survive better in cooperation with the others (e.g. in biofilms)  but each individual there has the potential to be independent.
Multicellular organisms need more cells to survive (how many I don't know, likley organism specific).

Another way to think about it is if you take one cell, is that a recognizable organism, or is it just a part of an organism? Just to confuse things, there are certain organisms that seem to be a bit of both, like the slime molds. From wiki, "Slime mold or slime mould is an informal name given to several kinds of unrelated eukaryotic organisms that can live freely as single cells, but can aggregate together to form multicellular reproductive structures."

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Why are heterologous expression systems such as mammalian cell lines commonly used for studying interactions between neuronal proteins?
I am reading papers about heterologous expression systems and I have seen that they are used a lot in neuroscience to studying interactions between proteins that are normally expressed in the brain.
I have seen that in research papers, CHO cells are used as a model cell line to study the interactions between neuronal proteins. This is done through overexpressing a protein of interest that is natively expressed in neurons in CHO cells and investigating interactions of that protein with another protein (that is endogenously expressed in CHO cells but also found in neurons).
However, I was wondering, what are the advantages of using CHO cells instead to study interactions between neuronal proteins instead of a cell culture of neurons? Wouldn't it be more accurate to study interactions between neuronal proteins using cultured neurons instead? Any insights are appreciated.

Should depend on the interaction being studied. If the interaction happens within a single cell a cell line should suffice.

@ceno980 I do not know why your question is being downvoted. I feel this is a genuine question researchers come across when they getting into new arena.

One of the advantages you already stated that depending on protein of interest if it's already expressed in CHO cell line, researchers use that.
Apart from that, this question is more of a general type. I will try my best to logically put down the things.
You are right, it's more appropriate to study proteins using cultured neurons. But, there are many practical factors that may compel us to avoid cultured neurons.

Ease of Culturing cells
Its way easier to culture cell lines such as CHO/HEK293/HeLa compared to neurons. Neurons are very sensitive and culturing them needs serious expertise and still, things can get wrong. There are many labs across the world that have dedicated technicians to avoid individual differences between cultures which can topple up experimental results. In contrast, culturing common cell lines doesn't need that level of expertise (relative comparison). Furthermore, for neuronal culture, several serious ethical guidelines need to be followed and require a good amount of funding to set up the facility. In addition, to have neurons develop processes and ready for study generally 10-12 days are required which prolongs the length of study. With common cell lines, you can perform an unlimited number of experiments and get results in a relatively short amount of time.

Ease of expression
Sometimes, the endogenous level of expression is not sufficient enough to visualize the interactions. More importantly, you do not have a tool to visualize these endogenously expressed proteins in cultured neurons. At that point Transfection and overexpression comes in handy. Transfection and overexpression in cultured neurons are way more difficult compared to common cell lines such as CHO, HEK, HeLa, etc. The efficiency is very low. It needs serious optimization and still, everything may go in vain. If endogenous expression levels are sufficient enough, knock-in expression is an option. Still, it requires several months to have such knocked-in mice and the success of knock-in is very low with larger proteins such as fluorescent proteins. Indeed new techniques are getting developed such as viral methods etc. Still, they are not well established across the globe.
In the case of common cell lines, it's relatively easy to transfect/optimize the conditions to obtain abundant protein of interest for the study.

Thus weighing time, money, expertise, and whether or not cultured neurons absolutely necessary to draw meaningful conclusions generally determine which cells to choose.

Thank you for your reply. Regarding your statement: "More importantly, you do not have a tool to visualize these endogenously expressed proteins in cultured neurons." I was wondering, is it not possible permeabilise the cell membranes of the neurons and then use indirect immunofluorescence to detect proteins that are endogenously expressed (even if they are expressed at a very low level)?

(1/2) Good question.There are some reasons for this.Let me clarify one thing first. Endogenous doesn’t necessarily refer to proteins present inside the cell rather it means ‘natively expressed’.Not always you want to permealize and visualize intracellular proteins. For example 70% of the FDA approved drugs target membrane proteins. Coming back to your exact question,currently we don’t have antibodies for many of the proteins of interest.Cross reactivity,low affinity etc are the common issues with available antibodies.

@ceno980 (2/2)(continued) Therefore you see studies genetically attaching fluorescent proteins/epitope tags to the protein of interest to study/visualize them.Still they are not perfect. That’s a different topic for discussion.

Thank you, for your reply it really helped

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Does 1kg of lettuce have more energy than 1kg of beef?
Given that each trophic level of the food chain has a decrease of 90% of available energy, would it be fair to say that 1kg of lettuce has more energy than 1kg of beef? If it's not true, can you explain the reason?

Re: "each level of the food chain has a decrease of 10% of available energy", could you clarify, ideally with a reference? Also, I'm guessing you mean available calories from digestion rather than e.g. fusion energy :)

Here is a source from NatGeo:  "only about 10 percent of energy stored as biomass in a trophic level is passed from one level to the next." https://www.nationalgeographic.org/encyclopedia/energy-transfer-ecosystems/

Thanks for the ref; assuming it's roughly correct, you should probably correct your question to be "a decrease of 90% of available energy", as passing on 10% reflects a loss of 90%.

Reductio-ad-absurdum - is there more energy in a kilogram of Uranium than in a kilogram of water?

Each level of the food chain has stored less energy than the stuff it eats, so I see where you're coming from - but it takes a lot more than 1kg of lettuce to make 1kg of beef.

This situation will only improve once we genetically engineer solar powered cows.

@criggie that's actually a bad analogy. There is more energy in 1 kg of water than in 1kg of Uranium. Fusion releases more energy per mass than fission, don't you know.

@PcMan Actually, E=mc^2, so they both contain the same energy, ultimately (in the same inertial frame, at least).  How much of it you can practically release in various circumstances is a different question.

Talkin about how much energy one can use in various circumstances... a human body will use more energy digesting lettuce than will get from burning whatever it can burn from the lettuce constituents. Whatever nutritional value the particular vegetable has, it is not energy.

@J... it depends which one is higher from the ground… or moving faster!

@Tim That's what the "same inertial frame" was about.  Different depths in a gravity well are different non-inertial (accelerating) frames.  Objects moving at different constant velocities are in different inertial frames.

What about a pound of sugar cane vs. a pound of lettuce?

1kg of beef has more energy than 1kg of lettuce but it isn't directly related to the trophic level energy loss.

Given that each level of the food chain has a decrease of 10% of available energy

You're all mixed up here. What the rule is saying is that if you start out with n units of solar energy, you lose 90% of it for every trophic level it passes through; Only 10% passes through as stuff that "stays around" materially (i.e. used to build the structure of the organism rather than being burned away as fuel to keep it alive). That means that it takes about 10x more energy to produce the same amount of edible calories in beef than it does in vegetables and grains, if they are separated by one trophic level.
It's not talking strictly talking about the energy density in food, but instead about how wasteful it is to produce the food containing those edible calories from the point of view of the total solar energy invested. For the same solar energy, you can feed a lot more people calorie-wise with vegetables and grains than beef.
It's kind of like thinking how many vegetables a rabbit eats over the couple years of its life from birth to when the rabbit becomes food for you. How long could you feed yourself on those same vegetables? Weeks maybe? How long could you feed yourself, if you ate the rabbit? A few days at most. You can imagine all those vegetables weigh more than the rabbit, but supply more energy than the rabbit meat, while the same mass of rabbit flesh has more calories than the same mass of vegetable. The rule isn't talking about calorie density of food.
Obviously, there are complicating factors, such as the actual composition of the food, since that determines calories and nutrition (which isn't related to solar energy).
The reason the same mass of beef has more energy is that 10% that sticks around keeps on accumulating. This is also the reason toxins accumulate in animals higher up the food chain. A little plankton might have a tiny bit of mercury in it, but a small fish might eat a billions of plankton. And, then a large fish might eat a thousand small fish. And, you might eat one large fish. If that mercury stuck around in everything that ate it, all that accumulated mercury ends up in you.

+1 for the rabbit example. Though I do wonder why you didn't use chicken or for that matter cows.

@slebetman I did not use cows because humans can't eat the same food as cows. I used rabbits instead of chickens because I was thinking of vegetables and grains only came to mind afterwards, plus I was watching Non Non Biyori and they were feeding rabbits the same thing that people eat.

Also this is how charcoal has a higher energy density than wood, despite being made by burning wood. Yes, during that burning process some of the energy (carbon content) is lost, but you get rid of so much water and other useless components, that the end product has a higher energy density than the raw materials.

Another complicating factor is that you have to eat 13 kg of lettuce every day.

The technical term of relevance here is "embodied energy", and is just as useful when considering the energy efficiency of EVs and other systems. 1 kg of beef embodies far more energy than 1 kg of lettuce.

The so-called '10% law' is a common, albeit very rudimentary, rule-of-thumb in foodweb analysis. It's commonly attributed to Raymond Lindeman, though he cited a wide range of ratios in natural systems. The point it's trying to make relates to the transfer of energy between trophic levels, not about the energy density of plants or animals in each trophic level.
The '10% law' would generally be parsed as 'it takes 10 kilojoules of energy stored in grass to make one kilojoule of energy stored in a herbivore, and 10 kilojoules of herbivore to make one kilojoule of a carnivore'.
Energy density of various foods is routinely measured. The US Department of Agriculture estimates the energy density of beef (15% fat, broiled) at 10470 kilojoules per kilogram, and the energy density of lettuce (Romaine) at 720 kilojoules per kilogram. One kilogram of lettuce clearly provides less food energy than one kilogram of beef.

The key here is that a "natural" cow - that is, one that grazes in meadows, rather than being confined to a feedlot - uses 90% of the energy in the grass &c that it eats to do things like walk around collecting that grass, avoiding predators, and making baby cows.  Only 10% (or less - I'm just using the "10% law") of the energy extracted from the food it eats gets turned into beef.  But OTOH, humans can't get much energy from eating grass, so would almost certainly use more energy to collect the grass than they'd get from it.

@user253751 other things, like cows

@jamesqf A significant proportion of the energy in grass is also needed for digesting grass, at least for ruminants.

@jamesqf that's an answer in its own right.

Plus, humans don't eat the entire cow, but only part of it, so there is an additional loss there that may not be included with the 10% law.

@user253751: In case you haven't noticed, they do :-)  But unlike most of those things, grass (and other forage) grows naturally in many places, with minimal if any human effort.  Cows (and other herbivores) collect the energy in their forage, again with little effort by the humans (or other carnivores) who'll ultimately consume the meat.  What matters is not the trophic energy levels, but the energy profit (gain/expenditure) of the consumer.

The (food) energy in 1kg of lettuce or 1kg of beef depends on each's composition, not on its trophic level. Normally we can digest fats, protein and carbohydrates, but other organisms like certain bacteria and fungi can even digest components like fiber and cellulose than we can't. Water doesn't provide any energy, but is still part of an item's weight, so food scientists normally calculate available energy for people based on the dry weight of fat, protein and carbohydrates, using average calories per g for each of the 3 classes of components.
The trophic levels/food chain 90/10 rule refers to how much biomass is produced in an ecosystem, not the energy content of a certain piece of that biomass.

Dry weight is important to the question, too.  If you've ever made your own dried food, you may have noticed that there's a lot more "food" left after drying meat vs vegetables.  A quick search says about 25% of the mass of beef is non-water, but only about 4% of lettuce.

Note that the decrease in food energy from one trophic level to the next is 90%, not 10%, if only 10% of the energy is actually passed on to the next level.
To compare 1 kg of lettuce with 1 kg of beef is not a very fair comparison for several reasons.

Most cows don't "beef up" on lettuce; they are usually either grain-fed or grass-fed.

Cows don't get their calories directly from the foods they eat to begin with--they eat to feed the bacteria in their stomachs, from which they derive their own sustenance.  (This not being a direct transfer may have some complications in terms of whether one should consider this to be one trophic level or two.)

Because of the energy transfer ratios, the cow will eat many kilograms of food to put on one kilogram of weight.  But in the process, the food is also changed in its form from being mostly simple carbohydrates to having considerably more fat and protein which are higher caloric-density foods.

Clearly, 1 kg. of beef will have more food calories than 1 kg. of lettuce.

I believe your point 2 is intended to cover digestion in the rumen and is indeed a major source of energy for the animal. However, cows do also digest some protein and fats on their own; this source https://extension.umn.edu/dairy-nutrition/ruminant-digestive-system#fat-digestion-1001418 indicates the rumen fermentation provides about 50-70% of the cow's energy. Fats are indeed more energy dense than carbohydrates, but proteins are similar to carbohydrates. It's having more fat and less zero-calorie water that boosts meat calorie density.

@Armand Yes, I'm aware of some of that which is why I used the term "complications".  Yes, fat is about 9 Calories/gram, protein is 4, and carbohydrates initially produce 2 but another pass through the citric acid cycle produces another 2.

The points about feedlots and cow digestion are really distractions, I think.  So consider instead a wild deer that you hunt for meat.  You've obtained a lot of food energy for little effort.

Just to complement @DKNguyen's excellent answer, think about this: if you were raising cows on lettuce, how many cows would you have and how much lettuce would you have? Obviously you could not have more cows than lettuce, because then you couldn't feed them. That's another rule of biology: "you'll eventually always have less predators than prey" (because when the number of prey falls below the number of predators, the predators will starve to death and reduce their numbers). So there you have it: the total amount of lettuce you would have would much more than compensate for the total amount of cows you were raising. The total amount of energy in lettuce would be far superior than the total amount of energy in beef.
But clearly, in the real world, we do not raise cows on lettuce. However, the same principle applies to whatever we use as cow feed.
Side note: I hope that makes you think about how very inefficient (and wasteful) it is to consume meat on such a large scale as we do.

Welcome to Biology.SE. Your post seems to be about the relative amount of energy in higher tropic levels, but that isn't what the OP asked. Please only post answers that directly address the question. This could be a comment, but is not appropriate as an answer. To critique or request clarification from an author, leave a comment below their post once you have sufficient reputation. Comments posted as answers are subject to removal, or you can delete this yourself. ...

... For details about how this site works, please take the [tour] and carefully read through the [help] including what is on-topic and what is not, and [answer] and [ask] good questions.

@tyersome: It IS what the OP asked for.  Specifically "If it's not true, can you explain the reason?"  This answer is a decent attempt at explaining the reason.  (And the base question can be answered with a simple search for the energy contents of beef & lettuce.)

@tyersome I understand how this site works. My answer addresses exactly what the OP asked for. Just like jamesqf said right above: I gave a perfectly reasonable and sufficient explanation for the second part of the question, "If it's not true, can you explain the reason?". If this is not an appropriate answer, nothing is.

@tyersome If this is because I said "to complement Nguyen's answer...", my answer stands alone on its own. In fact I find it simpler and more to the point. I only said I was complementing his answer because he gave a lot of information (not all of which is necessary to answering this) and it's the chosen most upvoted answer, so my answer is likely to be read after his being read.

@jamesqf & CoralBleaching — No the original question was "Does 1kg of lettuce have more energy than 1kg of beef?" — You are discussing what you infer that the question should have been, but I see no evidence that this is correct. This question is based on confusion between the total energy present in tropic levels and the energy density of those trophic levels, but that just makes it an insufficiently researched and poorly thought out question.

@tyersome I think I understand better what you're trying to say. You're telling me I should answer the question in the most literal sense possible. In this case, it would be appropriate only to break down the chemical compositions of lettuce and beef and demonstrate that he's wrong. I'm of a different opinion. I think we should address the context of where the question came from, whether it's ill-posed or not. As a user of this site, I know this saves everybody's time. And the accepted and most upvoted answer is the same as mine, but overcomplicated. You should complain there too.

only about 10 percent of energy stored as biomass in a trophic level is passed from one level to the next.

"biomass in a trophic level is passed from one level to the next" is a lot of words to say that the cow eats the lettuce.  This conversion from lettuce to beef is a lossy process.   Similarly, if you hypothetically continue to farm down the trophic pyramid, growing bears and feeding them your cows, it's likely to take about 10 kg - likely more - beef to produce 1 kg of bear meat.
A 300 kg cow will give about 180 kg of beef. But growing that animal for approximately two years is likely to require about 1,300 kg of grain and 7,200kg of silage/roughage. The "90%" number is a rough approximation; 180 kg is 13% of 1300, the silage or pasture gazing can count for something and bring it reasonably close to the 10% rule of thumb. Intentionally bred animals like some fish or poultry can be more efficient than beef.
The important thing to consider is that when you drive by unimaginably huge fields of grain being farmed 40 feet at a pass by massive combines and wonder how people could ever grow hungry, be aware that we're wasting a lot of those calories by turning them into beef.
As a side note, the cow will (generously) average about 40 liters (40 kg, 10 gallons) of water per day for those 2 years, for a total of (730 days * 40 kg water/day) / 180 kg beef) = 160 kg water actually drunk by the cow per kg beef produced. That's a lot, but that's not counting all the water used to grow that grain and roughage (and lettuce)...generous numbers for that growth is how you end up with insane quantities like 10,000 liters of water per kg beef.  If you assume that the water in the cow's urine is recycled to the water table and that the water that drains into the soil goes into the same aquifer or transpires from the grain goes back into the water cycle, the numbers are much more manageable - but it's still a lot of water. If you substitute for the veggie burger at dinner, feel free to leave the water running while you brush your teeth, you've saved more water than a week's brushing by not consuming that meat.
As a bonus side note: At a high level, both protein and carbohydrates have an energy density of 4 (kilo)calories per gram. Fat has an energy density of 9 calories per gram. However, 1kg of raw beef is not 1000 grams of metabolically available protein, it's actually a combination of water, collagen, elastin, about 200g protein, and about 50g (depending on the cut and cooking process) of fat. Similarly, 1 kg of lettuce is mostly water, quite a bit of indigestible cellulose, and about 30g of actual caloric carbohydrates. So your question could also be interpreted as "Does something containing 30g of carbohydrates have more energy than something containing 200g of protein", and the answer to that is a definitive "no", the former has 120 calories and the latter has 800 calories.


text:
Do the genes for external viral epitopes mutate faster than for viral machinery (e.g. Proteases)?
To fight SARS-COV-2 we use vaccines which train our immune system against viral epitopes like the external S(pike) protein. Since these structures change a lot, would it not have been a better idea to develop drugs which inhibit viral replications (such as protease inhibitors do with HIV)?
I know that vaccines make sense, but couldn`t it make sense to give such antivirals a shot?
Coronaviruses caused quite some trouble within the last years (SARS, MERS), to focus on more genetically stable structures would make sense. Who knows, perhaps there is going to be a new pandemic in the near future....
My question is, are these structures really genetically more stable? And If so, why are there no drugs yet? I know drug development takes normally quite long (over a decade). Why is it more difficult to develop antivirals than to develop vaccines?
Best wishes,
Mourinho_1

Yes, this is correct for (at least some) viruses. E.g., in HIV pol and gag genes are singificantly more conserved, while the genes responsible corresponding to proteins involved in viral attachment to cells. Some elements even explicitly have word variable in them, such as variable loops.

Thanks a lot for your answer. I have some issues finding a paper about this. Could you help me out? I would highly appreciate it.
Best wishes, Mourinho_1

As I have already mentioned in the comments, the mutation rates are indeed different, at least in some viruses. As an example we can take HIV, where pol, gag, and other genes essential for viral replication and interference with the cellular machinery are singificantly more conserved than the env gene, coding for the viral envelope.
Mutations vs. substitutions
To be more precise, one has to distinguish between the mutation rates and the substitution rates. The former are actually pretty much the same along the genome, since they are determined by the chemical processes. These are the rates that one observes in an in vitro experiment where virus is allowed to replicate for one generation, and thus the question of the viability of the new virions does not arise.
Substitution rate is what one measures in vivo, since mutations in the genes needed for replication, such as the polymerase gene, result in "dead" virions, which are present in the blood samples at negligeable concentrations. On the other hand, the substitutions in the envelope gene, which are responsible for the constant adaptation to the host, present much higehr variety.
As a consequence, when looking for the articles on the subject, it makes more sense to look for fitness rather than mutation rate data. Such as, e.g., right panel of figure 5 in this article:

Thats so cool! Thanks a lot!

My understanding is that if you look at the viral genome population and do a mutational analysis, generally there isn't a lack of mutations, substitutions etc in those conserved genes, it is purely that the viruses that are mutated at those essential sites aren't viable and don't produce an infection in subsequent hosts, hence the conservation.

@bob1 Not sure how this differs from the difference between the mutations and the substitutions as explained in my answer. Btw, I liked your answer - mine was intended just to give one example.

@RogerVadim there isn't much difference - it's the old quasi-species problem but I believe you can measure it outside of a single-cycle infection process. I like your answer too - it's a lovely example of a classic virology problem, that I hadn't considered in my answer.

The answer is that drugs and vaccines do different things.
Drugs treat the problem (sometimes before it starts - this is known as a prophylactic), whereas vaccines are intended to prevent the problem from starting in the first place, so vaccines are a form of prophylactic themselves.
One of the problem with drugs is that the vast majority of them have some side-effects, some serious, some not. In many cases, long-term taking of a drug will result in some damage to the taker. How serious this damage is depends strongly on the drug, how long it is being taken for, and how much is being administered.  Vaccines, on the other hand, are generally well tolerated usually being comprised of either proteins from the species of interest or weakened/inactive forms of the pathogen they are preventing. Vaccines encourage your body to prevent harm from an invading pathogen by giving it something to recognize before an actual infection happens.
Vaccines are generally developed against parts of the infecting organism that the body can see - in the case of enveloped viruses (like SARS-CoV-2 and Influenza), this is the bits that poke through the viral envelope, such as the S (spike) protein or HA/NA of influenza.
These sites do change a lot and the virus is under selective pressure to evade the antibodies that bind to these sites, leading to breakthrough infections. However, the same happens for drugs - the virus is again under selective pressure from the drug, so drug resistance happens. Indeed, we have seen this happen in real-time with influenza, where the first generation of anti-influenza drugs (called Amantadines) are no longer effective because of changes in the proteins they target.
As it so happens, there is one drug for SARS-CoV-2 called Remdesivir. This is a nucleoside analogue, that pretends to be one of the nucleobases that comprise the genomes of RNA viruses, and it is effective against a range of RNA viruses. However, check out the side effects part... Resistance to this drug has been observed in the lab for SARS-CoV-2 and other viruses. You might think that it would be pretty hard to develop resistance to something that behaves as part of your genome, because the proteins that process the genome are fairly stable - they can only tolerate a few changes before they are no longer functional, but we still see resistance developing because there is some wiggle-room.
Drugs are being developed to target stable parts of the genome or bits that can't be mutated for a range of viruses, but it is very difficult to do because it requires massive screening of compounds for effectiveness, then screening for toxicity/side effects etc in the host(s), then further development to make the drug deliverable in a form that the body can uptake and transport and finally clinical trials.

Since viruses typically hijack much of the cell's own machinery, and even viral-encoded proteins are often closely related to similar functional proteins of the cell, it's difficult to identify an anti-viral that doesn't also have a negative effect on the cell. With bacterial infections, bacteria have important components (like cell walls) that are missing in human cells and so can be targeted with more impunity. Many antibiotics target such bacterial-specific molecules.

@Armand Yes exactly. However, people are working on developing drugs for things like the influenza RdRP active site, which can't really mutate without losing functionality, but it's really really hard to do, and there's still evidence of resistance mutations.


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Validity of report of reverse-transcription of Covid-19 vaccine mRNA in cultured human liver tumor-derived cells
The following paper reports results suggesting that when Huh7 cells (severely karyotypically abnormal immortalized cells derived from a human liver tumor) were incubated with the Pfizer/BioNTech COVID-19 mRNA vaccine BNT162b2 the lipid nanoparticles were taken up. The paper argues that the vaccine mRNA was reverse-transcribed and suggests that the LINE 1-encoded reverse transcriptase activity might be involved.
Aldén et al. (2022) Curr.Issues Mol. Biol. 44, 1115–1126 “Intracellular Reverse Transcription of Pfizer BioNTech COVID-19 mRNA Vaccine BNT162b2 In Vitro in Human Liver Cell Line”
The clinical relevance of these results, if correct, relates to the possibility that the integration of viral cDNA may occur in human liver tissue following administration of the vaccine, that the integrated gene for the virus spike protein may be subsequently expressed and could therefore be responsible for some of the rare side-effects of the vaccine.
Question: Do the results really indicate reverse-transcription of viral mRNA and integration of the cDNA into the genome of this cell line? If so, to what extent is this relevant to side-effects of the vaccine administered in the clinic.
Footnote
The publisher of this journal, MDPI, has been classified as a borderline predatory publisher — hence my scepticism — although the subject is far from my field.

HuH-7 cells are an immortalized cell line derived from a hepatoma (liver cancer), and while they can be used as a surrogate for hepatic cells in some assays, they are different in many ways. Beware of papers that purport to show unexpected results using only one cell line.

I’ll note that there are many pairwise statistical comparisons (t-tests) in the paper, yet no mention of a multiple-test correction. Though that’s not a critique of the science, per se

See some... other kinds of evidence: https://pubmed.ncbi.nlm.nih.gov/34344759/, esp. relating to the integration into human genome, and note that there is an incredible conflict of interest in this paper's authors. They have a good reason to scare monger.

I do not wish to answer this question, which I felt was unclear and for which I do not have the expertise. However, because of the interest shown in it I have rewritten it. I have made the title meaningful, described what the paper reports and replaced the ambiguous "is this serious" by precise questions. I have deleted the reference to another publication quoted in that work because any questions on its validity belong to a separate question (assuming that the purpose of this list is to post-review papers). If the poster thinks I have changed the meaning, please explain rather than roll back.

"Is the claim for integration of spike protein mRNA into the DNA of this cell line valid?" - Explicitely, if hidden, the authors do not claim integration, they claim retro-transcription.
If so, to what extent is it relevant to side-effects of the vaccine administered in the clinic.

"Is the claim for integration of spike protein mRNA into the DNA of this cell line valid?" - Explicitely, if hidden, the authors do not claim integration, they claim retro-transcription only: “At this stage, we do not know if DNA reverse transcribed from BNT162b2 is integrated into the cell genome.”
"If so, to what extent is it relevant to side-effects of the vaccine administered in the clinic." I think that edit over-does the question as there is no restriction to "significance and validity" of that study (nor others, no study claims to have found causality for side-effects).

Further to my edit of the question. The original referenced one specific paper and asked only “Is this serious?”. Hence my reversion to this one paper. The purpose of this site is not to re-referee papers, so the interest in this one must indicate that people think it has biological importance in relation to the vaccine mentioned in the title. I tried to specify the results reported that might be important, and why. This is open to improvement.  An alternative general question might be about integration of vaccine mRNA copies into human DNA after inoculation, but I think that has been asked.

@PeterBernhard — The reason for invoking integration into the genome is that the preparation in which the reverse-transcribed virus DNA was detected was “purified genomic DNA”. This is certainly the implication, and the context in which the paper was written. However I now notice that they write "At this stage, we do not know if DNA reverse transcribed from BNT162b2 is integrated into the cell genome" so I will modify my edit accordingly.

Great answer, thanks for making me feel appreciated. The "foregoing study" Nogoodnurse linked to did a subsequent study using available "paper work", i.e. data. Now, that data seems reaped in looking for RNA, neither DNA nor RNA that might have been transcribed from retrotranscribed m-RNA. Can you dig? They used data not produced searching for "chimeric transcripts". What they were rebuked for, then, was a adapation work. - What is the reason why this study did not undertake what they say is needed in the future? (long DNA-, not RNA-,  sequencing)

Re: Intracellular Reverse Transcription of Pfizer BioNTech COVID-19 mRNA Vaccine BNT162b2 In Vitro in Human Liver Cell Line by Alden et al. (  Curr. Issues Mol. Biol. 2022, 44(3), 1115-1126; https://doi.org/10.3390/cimb44030073 )
Regarding the question: "Question: Do the results really indicate reverse-transcription of viral mRNA...?" They provide results suggesting this, but missing key additional data (see Figure 5 comments below).
Regarding the question: "Do the results really indicate ... integration of the cDNA into the genome of this cell line?" No, they provide no evidence of that (see Figure 5 comments below).
Regarding the question: " If so, to what extent is this relevant to side-effects of the vaccine administered in the clinic." As they fail to convincingly show the above points, and are working in a cell line system of questionable relevance to normal human cells in the body, this paper seems to have no real relevance to side-effects of the vaccine administered in the clinic. See below comments.
This paper is NOT reliable. A non-exhaustive list of problems in no particular order appears below, but first let's consider their Results:
Figure 2: Yes, they show that BNT162b2 vaccine mRNA enters the cultured cells. However, all their statistical comparisons except for those against the controls are invalid -- see pt. 2 below.
Figure 3: They fail to show that BNT162b2 affects LINE1 mRNA levels. First, the control plots are visually not different from those of the vaccine-treated samples. Second, essentially all their statistical comparisons seem to be invalid -- see pt. 2 below.
Figure 4: Fluorescence always makes pretty pictures, but this figure again seems to fail to show anything useful. First, the LINE1 protein antibody used binds to the LINE1 ORF1 protein, which does not have reverse transcriptase activity, rather than the ORF2 protein, which does contain reverse transcriptase activity. An anti-ORF2 Ab is available, but they did not use it. Also, from Fig. 3 we see no significant difference in LINE1 RNA levels, so LINE1 protein levels would be unlikely to vary. Finally, the statistical comparisons shown are likely to be invalid -- again, see pt. 2 below.
Figure 5: This section claims to detect reverse-transcribed BNT162b2 in DNA preps from buffer-washed cells previously exposed to BNT162b2. Maybe they have, but key controls are missing.
The one piece of evidence shown is successful PCR amplification of a segment of the vaccine sequence. They do show some useful controls, such as lanes for cells not treated with the vaccine, but miss other essential controls such as cells treated with a different mRNA vaccine not containing that amplicon, and DNA from relatively karyotypically and morphologically normal cultured cells treated with BNT162b2, another mRNA vaccine, or nothing. It's all too easy to have a few stray molecules of a DNA fragment present in the lab (like the BNT162b2 PCR amplicon) contaminate other samples and lead to false positives after lots of cycles of amplification. They also provide no evidence any reverse-transcribed BNT162b2 is integrated into the cells' genomic DNA.
As for the paper's significance to BNT162b2 influence on actual normal human cells, there really isn't any because of how abnormal this immortalized liver tumor-derived cell line is in terms of of genomic stability and of gene expression. It's sort of like using Godzilla as a model organism for humans.
The promised non-exhaustive list of problems:

It's clear they don't understand some of the features they discuss, such as LINE1 elements, calling LINE1 "endogenous reverse transcriptase" when they are actually transposons. They also seem to think there is just one LINE1 gene, not understanding that they are present in thousands of copies throughout the genome (having "jumped" into many genes).

It's clear they don't understand how to do statistics properly. If you just do more and more comparisons between different experiments, eventually you will find a difference just by chance. To correct for this, you must reduce your significance threshold to take into account the number of comparisons you make. An easy way of doing this is called "Bonferroni correction" and there is no evidence they used it or any other such correction.  As far as I can tell, after the Bonferroni correction is applied, essentially none of their meaningful comparisons end up being statistically significant.

Their main "control" consists of no vaccine, rather than a dummy/different vaccine. Effects associated with vaccine presence could for example be due to the lipid nanoparticles or modified RNA -- that is, they could be non-specific responses.

The fundamental flaw: as a stand-in for human cells, they use only a highly chromosomally abonormal cultered liver cancer cell line Huh-7. According to a description of the line, "The majority of Huh-7 cells show a chromosome number between 55 and 63 (mode 60) and are highly heterogeneous." (normal cell count is 46) In addition to "...containing many mutations and INDELS, it is worthy to note the Huh7 cells have a point mutation in the p53 gene."

The LINE1 protein they image likely appears in tumor cell lines (like the Huh-7 line they use), but not in normal cells. From "Methods Mol Biol. 2016; 1400: 261–280.
doi: 10.1007/978-1-4939-3372-3_17 ""Using immunohistochemistry, we found nearly half of human cancers stain positively for ORF1p, with immunoreactivity in some common cancers approaching 100% of cases. No staining was observed in the cognate normal tissues"

The Zhang et al. (PNAS May 25, 2021 118 (21) e2105968118; https://doi.org/10.1073/pnas.2105968118 ) paper mentioned in this paper is discussed in my answer to a Medical Sciences StackExchange question: MedicalSciencesQuestionAboutZhangPaper
The summary of my answer to "can the SARS-COV-2 RNA modify our DNA[based on this paper]" is "The short answer is maybe, but rarely, and the whole Covid virus has never been seen to integrate into the cell's DNA intact. Any integration requires "helper" molecules not found in the Covid virus, and only very rarely found in a normal cell."

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I've also commented this on your Medical Sciences SE question: Highly relevant to this question:  "Host-Virus Chimeric Events in SARS-CoV-2-Infected Cells Are Infrequent and Artifactual"

The paper may be reliable in its finding that
"BNT162b2 mRNA is reverse transcribed intracellularly into DNA in as fast as 6 h upon BNT162b2 exposure",
however, the authors   apparently refrained  from trying to find integration into the genome of the hepatitic cells. They do not claim to have found integration into the genome.  They say,
"(f)urther studies are needed to demonstrate the effect of BNT162b2 on genomic integrity, including whole genome sequencing of cells exposed to BNT162b2, as well as tissues from human subjects who received BNT162b2 vaccination."
In that context they do not  refer to a previous study which - before the question had been edited anew -  had been linked to: Zhang et al., Reverse-transcribed SARS-CoV-2 RNA can integrate into the genome of cultured human cells and can be expressed in patient-derived tissues. Interestingly, this study did not use tissues from human subjects who received vaccine (or had been infected), however in their setup used whole genome sequencing to detect recombinded virus-host-DNA. This study did not.
Isn't  whole genome sequencing easy to do these days? Was there a   lack of "tissues from human subjects"? In fact, mentioned previous study by Zhang et al. (on virally infected cells) recurred to existing RNA-analysis (existing data) when trying to find out about normal  cells, after they had examined artificially LINE1-upregulated cells in vitro.   That may hint  to what does not go without saying,  which neither the study challenged by question nor its  co-study mentioned above explains and elaborates on,  and  only to experts seems obvious and apparent:
The study  questioned did not undertake to prove whether retrotranscribed DNA - which was  undebatedly found  - is of host cell genome origin (post integration) or of viral origin  (post retro-transcription).
Both studies do not speak of "free viral cellular DNA". That  may be  some blunt way to describe the issue, however, first, the technique of recombinant DNA vaccine shows very cleary (and very unexpectedly)  that DNA in cells may exist without being integrated into the genome of the host cell. Adenovirus vector  technique is  based on viral DNA in cells  not being integrated into the genome (There is no  finding of vaccine recombinant DNA  being retro-transcibed into the genome (after transcription to m-RNA)).
Second, it is accepted knowledge that several virus species persist latently in host cells in so called episomal form. E.g. herpes virus DNA is known to persist episomally  in the nucleus without  integrating into the host cell's genome. The following quote refers to adeno associated virus (different from Adenovirus used in vaccine): "Although AAV vector genomes can persist within cells as episomes, vector integration has been observed in various experimental settings, either at non-homologous sites where DNA damage may have occurred or by homologous recombination." Deyle and Russell, Adeno-associated virus vector integration; see also, e.g., Chong et al.Transfection types (...): "Stable transfection refers to (...) integrating foreign DNA into the host nuclear genome or maintaining an episomal vector in the host nucleus as an extra-chromosomal element (...). The transgene may then be constitutively expressed even with the replication of cells (...). In contrast, transient transfection does not require integrating nucleic acids into the host cell genome (...)"
This shows that retrotranscription as a first step may very well be distinguished and proved independently from integration into the genome.
The study in question here proved retro-transcription of vaccine m-RNA. Different from Zhang et al. they did not do any "whole genome sequencing" to find out about integration. The authors do not give reasons.  In case of positive findings, we still wouldn't know if CoV-DNA integrates  in normal tissue.
Whereas the first study  searched for
"chimeric transcripts"
i.e. DNA sequences that comprise quote "partial (...) subgenomic RNA sequence that was flanked by a duplicated host cell DNA target sequence" to lay proof of integration into the genome, the study challenged here did not. You will not find the word "chimeric transcript" being mentioned in the description of the methods employed:
"Genomic DNA was extracted from cell pellets  ... PCR was then performed using primers targeting BNT162b2 (sequences are shown in Table 1) (Remark:no chimeric sequences among)  ... Bands corresponding to the amplicons of the expected size (444 bps) were cut out and DNA was extracted ... The sequence of the DNA amplicon  was verified by Sanger sequencing."
However, it seems unanimously accepted that chimeric transcripts are  valid proof of integration - if validly found. The latter had been questioned by peer review in respect of the study by Zhang et al.
To sum up: There is no reason given for not using "long sequencing" technique that might have found chimeric transcripts. Alternatively, the study might have given reasons why chimeric transcripts cannot be accepted as proof of integration. The study questioned here seems to self-restrict itself in significance and reach.
It may be some biased opinion to think of the previous study having been reviewed as technically not valid in respect of its findings of  chimeric transcripts as a reason why the study challenged here refrained from long sequence technique (Remark: mentioned previous study did not either in respect of tissue from patients, in its non in vitro follow up,  as it then used pre-existing data that resulted from RNA, not DNA search and sequencing which in my opinion might explain the artifacts they were blamed for).
Final remarks: Merits of this study may lie in the use of nano lipids in combination with cancer cells. It had been shown before that any cell can possibly uptake the nanolipids; however, in respect of the previous study by Zhang et al., this study results in some strong argument for LINE1-expression not being dependent either on artifically induced over-expression nor - as it used nano lipids - on viral infection  (host-virus membrane fusion or receptor mediated endocytosis). Natural infection may very well appear as a prerequisite for upregulation of LINE1.
Still, any study might be challenged for  not being "reliable" or "serious" (quote pre-edited version of this question), in my opinion, as long as  the mechanism of LINE1 activation, of inducing LINE1, remains unknown.
There are no known side-effects of LINE1 integrating DNA, and they have not been searched on by the study questioned nor are there any other studies up to date on effects of CoV-DNA integration. It is beyond the scope of this study to offer cues  that hint at chimeric transcripts (integration) coresponding (not to side-effects but) to severity of disease  (Zhang et al.: "...in some patients-derived tissues ... a large fraction of the viral transcripts could have been transcribed from SARS-CoV-2 sequences integrated into the host genome.")

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Red and White Flower or purely Pink? Phenotype of a Flower Species with a Co-dominant Trait
As I understand it, co-dominance is when both genes in an allelomorphic pair produce both their effects equally on the organism in question whilst incomplete dominance applies to an instance where a mix of the effects of two alleles are present — i.e. where one allele is not completely masked by the other.
However, I had this notion challenged by the following paragraph I obtained from a reputable online source:

Carnation plants show co-dominance for the anthocyanin gene. There are two alleles:
$F^A$ – allele for anthocyanin pigment (red flowers)
$F^N$ – allele for no anthocyanin pigment (white flowers)

[...] a carnation plant heterozygous for this gene would yield pink flowers [...]

Shouldn't the phenotype of the flower be red and white as opposed to being pink, as the alleles have been said to exhibit co-dominance? Anything I am probably missing out on?

EDIT
I have bountied this question because I think I have a major hole with my understanding on this topic somewhere; to give you some perspective, I am a High-School Sophomore currently on an introductory course in Mendelian Genetics/Inheritance.
I read through @swbarnes2's answer where they say:

In the case of flowers, if you have two different alleles for the same pigment gene, you will see a blending, because all the pigment-making cells will produce from both alleles.

In such a case (if this always happens), where do the ideas of codominance and incomplete dominance come in? According to my textbook, the following terms are defined as:

If both genes of an allelomorphic pair produce their effects in an individual (i.e neither allele is dominant to the other) the alleles are said to be co-dominant.

Incomplete dominance applies to a case where the effect of the recessive allele is not completely masked by the dominant allele (in this case, I assume, a blending would occur)

(I do get that this may not apply to carnation plants, but would it be safe to follow the phenotypes predicted by my textbook definitions for all other cases?)
Hope someone could clear my doubt; I am extremely confused to read (in the comments section) why co-dominance would not mean both colors/phenotypes are shown simultaneously — like being red and white (as opposed to them mixing into pink).

"from a reputable online source" -- I appreciate your direct quoting of the source, but could you also provide a link to it?

What color does red and white make?

Mix them together & I'd expect pink. But that's purely for incomplete dominance, isn't it? Should be white & red (individually) when it's co-dominant

@BryanKrause I understand Shane's concern. Incomplete dominance is typically taught as as a blending of phenotypes (red + white = pink), whereas co-dominance is taught as the simultaneous expression of two phenotypes (red and white banding). This may be outside the scope of the question, but is seems like the genetics of anthocyanin pigmentation in carnations are in reality more complicated than presented in Shane's question.

@acvill I mean really, all the notions about dominance are outdated in modern molecular biology; they're good tools for understanding Mendelian genetics where one has access only to lineage information and not any molecular biology, but once you know more they are rarely actually meaningful distinctions. I think that's what's happening here; there's a blending between the understanding of the phenotypes as colors, and the understanding of the phenotypes as enzymatic reactions. I guess that's probably what an answer should explain, I do think I have a better idea now of where OP is coming from.

@BryanKrause I agree, though someone new to genetics doesn't have that insight, and your first comment came across as dismissive. Maybe this question concerning the molecular basis of incomplete dominance is relevant.

@acvill Thank you for the link; I took a look at it, but there wasn't much in there I could really understand, being a high school student!

Re: "why co-dominance would not mean both colors/phenotypes are shown simultaneously" Not mentioned here is the scope of the phenotype. Is it one flower? One cell in a flower? The whole plant? As Bryan mentioned, often "the notions about dominance are outdated in modern molecular biology". The red and white patches in your flower photo seem to me to be an example of "variegation" rather than co-dominance.

As I think other commenters have implied, I think that you are applying the definitions from the textbook more strictly than the writers of the textbook. In practice the dividing line between these things is not always so clear. A cleaner example of codominance might be one allele which affects color (red) and the other allele affecting something else, like pattern of expression- e.g. pigment only at the tips. In this case you can enumerate the combinations (all red, red tips, all white). Mechanistically I think this situation is rarer (?) but it's clearer for the definition.

Unfortunately, that nomenclature is kind of old-fashioned; it predates our understanding of what's going on at a molecular level.  Don't get hung up on the language.  Lots and lots of genes and alleles just don't fit into the paradigm of dominant and recessive, and trying to force them to fit doesn't really work.
In the case of flowers, if you have two different alleles for the same pigment gene, you will see a blending, because all the pigment-making cells will produce from both alleles.  There really is no such thing as "white" pigment; either it's causing a color outside the visual spectrum, or it's a broken version of a gene in the pathway that should be making a color-absorbing molecule.  We would usually more properly refer to this as "haploinsufficiency".
If you had blue and red alleles, it would likely make a purple flower, not one that was blue in some patches, red in others.
For something like blood type, AB blood cells make both A and B molecules on their surface (O is broken), but AB is just as good as A in terms of causing an immune reaction; there is no alteration in phenotype due to the lower dose of each allele.

This is not co-dominance, it is the result of either a transposon or a viral infection, similar to the tulip-breaking virus.
https://en.wikipedia.org/wiki/Tulip_breaking_virus

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Friend..you got the meaning of co dominance and incomplete dominance correct... but let me make co dominance easy... its just like mixing colors on a color plate...think it just like that.... otherwise in real sense both colors are indivisually expressed but being expressed in equal amount and with uniformity they appear as pink... other example could be ABO Blood group in humans....as for refrence https://www.genome.gov/genetics-glossary/Codominance hope it helps..

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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.


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Can a strand not be synthesised in 5' -> 3' direction?
I've been solving some biology questions, and according to one of them ( I have the responses too) the following phrase is false:
"Both strands are always synthesised in the 5' to 3' direction."
How can this be? From what I know DNA is always read from 3' to 5', and synthesised from 5' to 3'.
When is DNA not synthesized from 5' to 3'?

What do you mean “how can that be?”?  That’s the way it is. Deoxy-ribose is not symmetrical. Enzymes have substrate specificity. And plasmids have no bearing on the matter. Search for Berg on NCBI Bookshelf, and read the section on DNA synthesis. Pay careful attention to the chemistry.

I have looked trough the book you have recommended me, and it still did not give me the response I needed.  According to this book "At a replication fork, both strands are synthesized in a 5′ → 3′ direction.". Which I agree with, my question was why according to my book, it says that it is false that strands are always synthesized like that. Unless, it was referring to the direction of growth, in which case the lagging strand grows in the 3' to 5' direction, but it doesn't because my book uses the word "synthesized" not "grow". This is where my confusion comes from.

Am I right in thinking your concern is as follows? All known DNA polymerases add NTPs to the 3'-OH of the deoxy-ribose so that the direction of synthesis is 5′ → 3. In most organisms the two strands grow in both directions by a complex mechanism at the replication fork involving RNA primers and Okazaki fragments etc. However small circular genomes use a different mechanism — the rolling circle mechanism (described in Wikipedia etc.) — in which growth is just in a single direction. If so, and you still have a question about this, could you clarify what your question is.

It sounds like your guess was right and the exception is the lagging strand. The statement is phrased poorly, but it seems like they were going for the lagging strand. Either they meant for you to think that
-the lagging strand is growing 3' to 5'
or, more likely,
-the polymerase is only synthesizing on one (leading) strand at a time
While technically the book was correct, it was a trick question and phrased unfairly.
You are completely right that DNA is synthesized from 5' to 3'. I don't know of any exceptions to this, but hesitate to say anything overly definitive because there are so many rare exceptions in science. I can say with some confidence that DNA polymerase cannot ever synthesize in the 3' -> 5' direction. If you haven't already, I highly recommend checking out the Khan Academy article, Molecular mechanism of DNA replication! Nature Education also has a pretty good article on the topic, Major Molecular Events of DNA Replication.

I don’t even think the book was technically correct. It’s odd to say that DNA synthesis occurs 3’ to 5’ even if you are referring to lagging strand growth.

I agree completely, I was trying to cover all the bases since it's so unclear what the book was going for. I edited my answer so hopefully it's a little more clear though!

text books are rarely written by relevant scientists, the person who wrote the question probably did not understand it.


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:
How do honeybees requeen themselves?
It is said that beehives once queenless try to rear a new one by themselves. Beekeeping resources, books, websites, youtube videos, etc. have a very pragmatic human-centered view to the issue: what should the beekeeper do and don't. Some say, that the beehive can potentially rear a new queen on their own. I've also heard from beekeepers that they can be helped by introducing an extra brood comb from another hive.
I am interested in knowing the details on how this re-queening process takes place without human intervention.
Queens, like workers are female, hence they must come from diploid eggs. Hence only a mated queen can provide the egg needed to produce a new queen. Also it is known that queens are reared inside special queen cells which lie in vertical position in the comb.
It is known and it can be easily observed, that if the queen dies unexpectedly, the hive prepares for a substitute by building queen cups (will be queen cells).
But I wonder how do they actually get a queen from those cells.
The workers must either

carry an egg, previously laid by the former queen, from a worker cell into the cup,
or build the queen cup around a cell that already has an egg, or a young larva.

I can't imagine any other possible way.
So, how does exactly the requeening processes takes place?
Update. To be more specific about the details of the process of requeening I would like also to add the following questions:

Do they start breeding a queen from an egg or a young larva?
Do they choose this egg/larva at random?
Do we know a probability distribution for queen hatching dates? ie. the probability of a queen emerging (starting from a 0-day egg) after 15 days, 16 days, 17 days, etc.
What's the attitude of worker bees with respect to queen cells? Can a queen cell be destroyed by worker bees under certain circumstances?

Hi @Lagrange.el.Ciencia - very interesting question indeed! Unfortunately, I'm afraid though that you can easily find a satisfactory answer with a search engine. Could you please show us an attempt at trying to understand this, perhaps we could help you with understanding the parts you don't understand?

@SPr I couldn't find the answer anywhere on the internet, that's why I posted the question here. Can you post a link here to prove your point?

Does this or this not answer your questions? They would at least help focus your questions, I would advise to do that to increase the odds of getting a nice answer. Good luck!

There are two potential circumstances where a bee colony loses its queen.
Scenario 1
The queen is old.  She is not laying eggs well anymore, which means that many, most, or virtually all of her eggs are left unfertilized, resulting in drones (males) instead of worker bees.  This scenario requires urgent attention, because the hive will not survive without a steady brood production, and once all of the queen's fertile eggs are gone, there can be no possibility of replacing her.
Worker bees are able to lay eggs--though few are aware of this, and it seldom occurs in the wild.  A worker bee's eggs would all be drone (male) bees from infertile eggs because the worker is not sufficiently developed to have even the possibility of mating with a drone.
Queen bees mate once, and lay hundreds of thousands of eggs over the next as many as six or seven years before reaching the end of their productivity.  They store the sperm in their body and are able to choose whether to lay a fertilized or unfertilized egg--at least, up until those stores are gone.
So when it becomes apparent within the hive that the queen is at the end of her useful life, it is urgent that she be replaced.  The workers will take some of her last remaining fertile eggs and place them in the special queen cells, fed by extra royal jelly (all bees get some, but queens just get a bigger dose of it, and the hormones in the royal jelly help the queen to mature).  Whether before or after the workers have done this I am not certain, but the worker bees themselves will turn traitor and, for the good of the hive, kill the aged queen to make way for a new queen.
Scenario 2
The queen is lost to some unforeseen misfortune.  If this occurs during the winter hibernation period, the colony will perish, having no possible recourse.  But during the breeding season, worker bees can take emergency measures to produce a queen from the last eggs laid.  If there are existing downward-hanging queen cells on standby, they will likely relocate those eggs to them.  If not, I have seen a few queen cells positioned horizontally like all of the rest of the brood, but made larger to accommodate a queen's size.  This may be what the Wikipedia article references.
Beekeepers do not usually appreciate the sight of queen cells, and tend to destroy them whenever they are discovered, for several reasons: 1) They do not wish to have rival queens develop that might fight with and kill their special hybrid queen (queens can be purchased from various breeds, including Carniolan, Italian, etc.) by which the beekeeper has sought to balance the temperament of the hive with the environmental conditions at the site; 2) beekeepers know that bees naturally will split, with a large part of the colony following a new queen to start a hive in a new location, if new queens emerge.  This will set back the production of the original hive as many worker bees are lost to the emigration; and 3) queens which fight well (there can only be one queen in a hive, so queens will battle it out to the death) are not necessarily the best egg layers--therefore, if a queen must be replaced, the beekeeper would prefer to take charge of this.
Additional Answers
Regarding the specific questions under the main one--and, again, these are answered according to my understanding:
Worker bees will move an egg that is not more than about three days old.  Beyond this it might be impractical to move it.  This is why action must be swift if there is a loss of the queen.  As eggs progress through the larval stages, they increase in size within the cell.  They are fed, cleaned, and generally pampered (climate controlled, etc.) throughout the process.  But a large larva could not be easily moved.
I've never heard of a drone emerging from a queen cell, and believe the worker bees must be able to distinguish fertilized eggs from unfertilized eggs.  That is the only point of significance to egg selection.  Any fertilized egg could become a queen.
In order to become queens, the larvae must consume adequate quantities of royal jelly.  A larva that had been fed on the worker-bee fare for a week or two already could hardly play catch up to join the royal ranks so late in the game.  Queens must be fed more of this royal jelly from the early stages onward.
I have never observed worker bees taking any interest or initiative in destroying queen cells.  Worker bees would be happy to use those cells, as needed, or leave them empty when not needed.  I have often seen empty queen cells.  The existence of the cell does not mean it must always be in use.  If any member of the hive would have a wish to destroy them, it might be the queen, who does not desire competition.  But queens do not do manual labor of any kind beyond their task of egg laying.  The worker bees actually control or greatly influence even the egg laying--by how much they feed and pamper the queen.
[NOTE: I used to do beekeeping as a hobby, and before that I worked for a beekeeper--moving bees, splitting hives, requeening/adding new queens to hives, installing queen excluders to keep the honeycomb brood-free, extracting honey, etc. This knowledge of bees comes in large part from actual observation of them and from anecdotal evidences, rather than from scientific papers. If papers (second-hand science) are preferred here above actual observation (first-hand anecdotal evidence), then perhaps this answer may come up short of the site requirements.  I am new here, and uncertain as to how rigid the rules might be; nevertheless, I am more familiar with the bees themselves than with papers written about them.]

thanks for the answer. I like to hear from first hand experience as well. I'm a hobbyist beekeeper with just one year experience. And in the recent spring I discovered that one of my colonies had lost the queen, in fact there was no brood in any form: larvae, capped cells, etc; except for a couple of queen cells. Based on the reasoning that the queens emerge after 16 days, hence before workers and drones, I concluded that those cells could not possibly contain a queen. Therefore I came up with the hypothesis that they could be rearing (out of desperation) a drone there, maybe laid by a worker.

This is an informative answer, and firsthand experience is often very useful. I don't particularly mind posting an answer largely based on your experience, but (as it seems you understand) I think it is still worth trying to track down a couple of related citations that at least roughly corroborate your answer. I don't know that you need technical literature, e.g. wikipedia or similar resources is fine.

Thanks to @S-Pr I found the answer on wikipedia. On the Supersedure section of the article it is written the following:
If a queen suddenly dies, the workers will attempt to create an "emergency queen" by selecting several brood cells where a larva has just emerged which are then flooded with royal jelly. The worker bees then build larger queen cells over the normal-sized worker cells which protrude vertically from the face of the brood comb. Emergency queens are usually smaller and less prolific than normal queens.
Although, There is no reference to a source. Maybe one of the citations at the end of the page has the answer.

This is interesting, but it doesn't answer all questions. First of all, how does a replacement queen get mated?


text:
What exactly makes red meat (probably) unhealthy?
It seems generally agreed that (even fresh, unprocessed) red meat is at least somewhat bad for human health.  But why exactly is this the case?  It's difficult to find any attempt at an explanation, especially for anyone not too familiar with diving deep into the medical literature.
Is it because the myoglobin in red meat is carcinogenic or otherwise harmful? That would seem to be the most direct explanation, and there are a few studies on this, but they don't seem to be widely cited in discussions on health effects of red meat.  If that is true, would it mean that one should avoid dark, myoglobin-rich fish and poultry such as tuna and ostrich just as much as mammal meat?
Is it only because red meat tends to be more fatty?  In that case, would leaner cuts of red meat have the same health effects as white meat?
Or is it possible that there is some deep genetic reason why the flesh of mammals is more harmful than the flesh of birds and fish for human consumption?  (I had wrongly assumed this was a strange idea, but acvill's answer gives a plausible explanation.)

The gut microbiome is partly to blame, at least for the associations of red meat consumption with heart disease.  Red meat has a high concentration of L-carnitine, which is metabolized by bacteria in the gut to produce trimethylamine, which is further metabolized by FMO3 in the liver to produce trimethylamine-N-oxide (TMAO). High blood levels of TMAO are associated with higher risk for both cardiovascular disease and early death from any cause.
Sources on the relationship between the gut microbiome, L-carnitine, and heart health:
New study links L-carnitine in red meat to heart disease
Red meat, TMAO, and your heart

Or is it possible that there is some deep genetic reason why the flesh of mammals is more harmful than the flesh of birds and fish for human consumption?

The NIH gives the following values for the carnitine content of different foods:

Food
Milligrams (mg)

Beef steak, cooked, 4 ounces
56–162

Ground beef, cooked, 4 ounces
87–99

Milk, whole, 1 cup
8

Codfish, cooked, 4 ounces
4–7

Chicken breast, cooked, 4 ounces
3–5

Ice cream, ½ cup
3

Cheese, cheddar, 2 ounces
2

Whole–wheat bread, 2 slices
0.2

Asparagus, cooked, ½ cup
0.1


text:
Does the mRNA of the covid19 spike protein contain any nuclear localization signals
Does the covid19 spike protein amino acid sequence, as used in the covid19 vaccines, contain a nuclear localization signal. Because if they do, isn't there a chance that the RNA can find its way to the cell's nucleus?
In the case of the AZ and J&J vaccines, which use adenovirus vector DNA to encode for the spike protein. Is there a chance that the DNA of the vaccine could get incorporated into the genome, as described here https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570152/ ?
There is a further discussion of this potential problem here
https://cassandravoices.com/science-environment/science/healthy-people-do-not-require-genetic-vaccination/

And what should happen there?

Avoid degradation, change the genome? HIV does this and has sequence motif similarity with covid.

You would need a reverse transcriptase, which is not present in the nucleus.

My understanding is that all of the sequence similarity with HIV is purely coincidental nonsense, and that the similarity is no stronger than similarity with completely separate genomes. It's like wondering if the mailman is your real father because you noticed he has a nose and by golly you have a nose too.

Well, there is the LiNE-1 RT which is localised in the nucleus.

Bryan, Whether you believe in coincidences or not is neither here nor there.

I kind of expected the question would be downvoted, but is no one really interested in the answer, have we all gone political now?

@ejectamenta I don't think this is a question of politics, but the fact that your question makes it appear that you have a significant lack of understanding about the underlying biology here. Perhaps you could try to explain the context of your question in more detail, illustrating what you know about the processes that leads to to be concerned about this in the first place.

"significant lack of understanding about the underlying biology here" I really don't see the need to cast aspersions or patronise. I also don't think this is the place to present a thesis. If back ground knowledge is required there is always Wikipedia. eg. https://en.wikipedia.org/wiki/Nuclear_localization_sequence I also don't see that my question is particularly out of place given the other questions being asked on stack biology.

I think OP's question is valid and the reasons people are suggesting to close the question are complete bogus. OP might come off as abrasive but that is no reason to vote close. The quality of the question is okay. I tried an attempt to answer it, but I still think that the largest obstacle here is that @ejectamenta may not appreciate the difference between DNA (human genome), the viral RNA genome, the viral proteome, and the spike proteins specifically, which are just a few specific proteins. And also that integrating into the genome and localizing to it are two completely different things!

The term nuclear localization signal is not to be found in your reference. How come you refer to protein, not to DNA/RNA?
Quote from your reference: "Some (...) requirements for targeted integration have been elucidated. The AAV components that are required have been identified. These include the ITRs (in cis), Rep78 or Rep68 (in trans), and a 138-bp sequence termed the integration efficiency element (IEE), located within the P5 promoter in cis..."
What you refer to is "integration efficiency element" or the like, it is not "nuclear localization element?

Does the mRNA of the covid19 spike protein contain any nuclear
localization signals?

I take it you are talking about the coronavirus SARS-CoV-2, and asking whether its RNA genome contains any nuclear localization signals that act post-translationally as signals to specifically import the spike proteins into the nucleus. I cannot find any reports where any of the spike proteins are nucleus-imported, i.e. the spike proteins do not have any (working) nuclear localization signal as far as we can tell.
Some of the proteins coded within its RNA genome are however imported into the nucleus. These are not the spike proteins though.
If you are interested in where the proteins localize within the infected cell, I suggest the following article as a very excellent starting place:
A systemic and molecular study of subcellular localization of SARS-CoV-2 proteins
As for the mRNA, I cannot find any evidence that it localizes to the nucleus. However, there have been reports that other coronavirus' mRNA can localize to the nucleus, that CoV-1 contains a nuclear export motif, and that other coronavirus RNA can localize at the nuclear pore complex to interfere with trafficking between cytoplasm and nucleus space (i.e. at the gateway into the nucleus, but not inside!). This has been shown at least once more. However, these are not the spike proteins, but rather proteins like Nsp1 (non-structural protein 1) that are not categorized as spike proteins.
There has also been an interesting pre-print floating around since 2020 about the possibility of SARS-CoV-2 integrating into the human genome if we were to ectopically add a reverse transcriptase (RNA -> DNA writing enzyme) to the equation. Please read it with a grain of salt, I don't know that the paper has been peer-reviewed and unfortunately I cannot comment right now on the veracity of the research. It is also an in vitro experiment performed under circumstances that do not exist in humans, so the conclusions do not apply to discussions on the COVID-19 pandemic; it is only a proof of concept of integration-ability of the virus, rather that a demonstration that that occurs in vivo.
Here comes the cognate question:
Will we ever find the spike protein-coding sequences integrated into our genome?
A protein being inside the nucleus cannot integrate into the DNA genome though. With RNA, you would also require a reverse transcriptase to integrate it into DNA, which humans do not have. Therefore the odds of finding a spike protein-coding sequence in the genome, especially in the germline, if you are concerned with cross-generational effects, is virtually and practically zero.
EDIT:
You additionally ask in your edit whether DNA in the AZ and J&J vaccines could get incorporated into the genome (integration events). This is a known concern as it leads to carcinogenesis. You specifically ask about adeno-associated virus vectors. Below I quote an excerpt from  Ura et al. (2014) Developments in Viral Vector-Based Vaccines from part 3.3. Adeno-Associated Virus Vectors:

Generally, recombinant AAV vectors are generated by deletion of the
Rep and Cap coding regions between the ITRs. These regions are used
for endogenous transgene expression. Owing to the deletion of these
regions, AAV vectors cannot integrate into the host genome, and their
DNA also persists in an episomal form. This preferable feature in the
AAV vectors boosts their safety profile, by preventing the onset of
tumorigenesis.

In other words, the virus is recombined and its ability to perform genome integration is taken away prior to any considerations of use as vector for the deliver of genes or immunogenic particles, such as the ones you would see in CoV-2 vaccines.

The first clinical trial of a therapeutic retroviral vector took place
in 1990. Subsequent clinical studies have raised serious concerns
regarding genotoxicity, mainly due to possible viral genome
integration. The AAV vector has the ability to express episomal genes
without integrating itself into the host genome, and has hence been
approved by the EMA for clinical use.

As you can see, this has been in top consideration for a couple decades now, it is of course not an issue likely to be overlooked by regulatory bodies nor researchers or vaccine-producing companies.

Thanks for the detailed answer. I just would like to comment that the LINE1 provides a RT pathway that could be used with RNA (mentioned in the pre-print) and that the AZ vaccine being based on DNA would not require RT and could just use the existing DNA replicating machinery to incorporate into the genome, that is, if it were to gain entry to the nucleus, which apparently Adenoviruses are able to do.

You are right, I later read up on LINE1, I was not aware of those mechanisms at play. I plead some ignorance on the topic. I'm hoping that a better answer crops up, as I'm not a virologist and I don't follow the newest news about CoV-2 very much. Hope the brief answer was of some use. And luckily for us, CoV-2 is no adenovirus nor retrovirus!

I am more concerned about the vaccines, covid is difficult to avoid now that it is out in the enviroment, the vaccines however are (pseudo) optional.
The following article mentions "For the latest trial, the components of the gene-editing system – encoded in the genome of a #virus — are injected directly into the eye" https://www.nature.com/articles/d41586-020-00655-8
IMO, AZ, J&J and other DNA vaccines are a risk for genome takeup. The mRNA vaccines less so, but we are playing with unknowns here. Please consider upvoting the question so that it doesn't get deleted.

I hope you can admit and reasonably plead some ignorance about some of this too, since I think you may be connecting unrelated dots. If you want to integrate a sequence into the genome, say with gene-therapies based on CRISPR/C9, you can use strategies originally discovered in retroviruses... But that is not what is going on in the vaccine. The vaccine comes in 2 main variants: mRNA that codes for the harmless spike protein, and the spike protein itself. Both raise an immune response. Neither can be integrated into our genomes as they are. So absolutely no need for concern.

You're quite right that was the wrong reference to give, because, as you point out, the paper itself used a different technique. But to talk again about the vaccines, the AZ is a viral vector vaccine containing its spike encoding in a chimpanzee adenoviral vector as DNA. Isn't there the possibility that this could end up in the nucleus and inadvertently perform 'gene therapy'. Here's a better reference to what I'm talking about. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570152/

See edit in response to your edit.


text:
What is the map unit between the genes?
While doing some biology I came across this question:
The following tables present results of plant crosses involving two linked genes: S is a seed-color gene, and L is a plant-height gene. Each gene has two alleles with one allele exhibiting complete dominance over the other allele. Dominant phenotypes are yellow seeds, and tall plants; recessive phenotypes are green, and short, respectively. Assume that crossing-over between two genes occurs once.

Calculate the map unit between gene L and gene S. (One map unit = distance of 1%
recombination)
This question confuses me because what I understand from the table is that from crossing over we get short flowers with green seeds(0.01) and tall ones with yellow seeds(that 0.01 from 0.51). So as a result from the fertilization we get a 0.02 frequency, that as I understand also equals the recombination rate. And so the map unit would need to be 0.02*100= 2%. But the response I have to get is 20%, which I do no understand how to get to.

Here's a hint: you're right about 0.01 being the recombinant (crossed-over) double homozygous recessive offspring. I think you're forgetting that each offspring contains 2 gamete haplotypes, and so predicting the percent of offspring with a given genotype involves multiplying the frequencies of the individual gametes that produce that offspring. To calculate the gamete frequencies (and thus the recombination frequency) you need to reverse that multiplication process.
Full answer:
I find it easiest to deal with uniform genotypes first. Of the 4 offspring phenotype categories, only the double homozygous recessive category (short/green) has uniform genotype - llss. If l and s were unlinked, 1/16 of the total offspring would be short/green=llss.
However, many fewer than 1/16 are short/green=llss, so linkage is confirmed and (as you note), ls must represent one of the crossed-over haplotypes. The other crossed-over haplotype is then LS. Thus, the parental (non-crossed-over) haplotypes must be lS and Ls.
Let's call r the recombination distance (in map units) between l and s. Each recombination between l and s produces 2 recombinant gametes: 1 ls and 1 LS.  Thus the fraction of ls gametes - f(ls) - will be (r/2)/100 and the fraction of LS gametes - f(LS) - will also be (r/2)/100.  Since each F1 offspring consists of 2 gametes, the fraction of offspring with an ls/ls genotype will be f(ls) x f(ls) = (r/2)/100 x (r/2)/100 = r^2/40000 = 0.01 (from F1 data).
Solving for r, r^2 = 0.01 x 40000 = 400, so sqrt(r^2) = r = sqrt(400) = 20.
r = 20 map units

From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here. In particular, the OP has asked many homework questions with little or no effort towards meeting the criteria for such questions on this site. Answering such questions encourages undesirable behavior and is actively harmful to students. In addition, please don't post multiple answers to the same question — you can and should edit your posts instead. Thanks.

Thanks for your suggestions!


text:
Genetics question on recombination frequency
A space probe discovers a planet inhabited by creatures that reproduce with
the same hereditary patterns seen in humans. The phenotypic characters are
height (T=tall, t=dwarf), head antennae (A-antennae, a=no antennae). For
heterozygotes with tall and antennae phenotype, the offspring are: tall-
antennae, 47; dwarf-antennae, 2; dwarf-no antennae, 40; tall-no antennae, 11.
What is the recombination frequency for the experiment?
A)13%
2)2%
3)87%
4)11%
The recombination frequency can be calculated by dividing the number of
offspring with a different combination of traits than their parents by the
total number of offspring and multiplying by 100 to express the result as a
percentage. In this case, there were 47+2=49 offspring with a different
combination of traits than their parents, and a total of 47+2+40+11=100
offspring. Dividing these values and multiplying by 100 gives us
49/100*100=49%, but how we get 13%

Welcome to the site. Please take a [tour] and visit the [help] for more information on the Biology Stack. In particular note the homework policy - askers here, particularly for questions that are obviously homework, are expected to show some attempt at answering their own question.

You don't seem to have the original phenotypes for the actual parental types (F0s), only their children the F1s (all of whom are apparently tall/antennae, e.g. dominant characters one supposes), whose apparently random mating yields the F2 generation (with the 4 types you are counting). In the absence of other information, one supposes that the non-parental types are dwarf-antennae and tall-no antennae. Is that correct? Do your numbers really add up? Do you know the F0 (parental) types? Check again.