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Where does (retro)virus replication take place?
When a virus replicates, it has to create several copies of its genome to the "daughter viruses"? Where in the cell does this replication of the viral genome take place? And how?
In my book, they use HIV-viruses as an example, which I've understood is a retrovirus. The first steps they describe are attachment, entry and uncoating, which I understand. Then, the next step is integration, which they say start with that the RNA translates to DNA and the new DNA strand works as a template to create a dsDNA. dsDNA is then integrated in the host cells genome, and then after that the transcription and translation of virus protein can start. What I don't understand is when the replication of RNA strands take place? After the synthesis of protein, there is the assembly, where the protein and RNA build up new viruses. Where does the RNA come from? Does the replication take place before the integration? Or when the DNA is integrated in the host cell genome, at the same time as the protein synthesis?
For other types of virus, they say that the genome replicates by a "rolling circle mechanism"? Where does that take place? In the cytoplasm? In those cases, isn't the viral genome integrated in the host cells genome at all? They just use the host cells polymerase, ribosomes etc.? Is retro viruses the only viruses that integrates in the genome?
This became kind of long, but to summarize my questions:

Retroviruses: Where and how does the replication of the RNA take place? Before or during integration of the host cell genome?
Where does the replication of genome of other viruses (that use the rolling circle mechanism) take place? In the cytoplasm?

Welcome to SE Biology.  I have no idea what your book is, but it has given you a limited and distorted view of viruses. There is a wide spectrum of viruses, with different sorts of genome — DNA, RNA, single and double-stranded, linear, circular and segmented. How and where they replicated differs accordingly. Retroviruses are a strange hybrid, and rolling-circle replication only applies to small circular viruses, so these seem an odd choice for a text. Read the general Wikipedia article and specific articles for viruses of interest…

…This should provide you with answers.  If there is a particular aspect you do not understand, then you need to show that you have done some research in crafting a question about that specific problem. At the moment your question is several questions based on false premises. And rather than just asking questions, try to think about and rationalize the problem. Ask whether a virus uses its own replicative enzyme or that of the host. If it uses the host DNA polymerase, it needs to be in the nucleus to replicate. If not, it may not — although other considerations come into play with retroviruses.

First Question:
Integration is essential for retroviruses, otherwise cDNA isn‘t transcribed efficiently into RNA (viral genome). Eucaryotic transcription requires multiple factors that are only present in the nucleus and work best when associated to genomic DNA (host). Retroviruses also lack an RNA-dependent RNA polymerase, which would replicate viral genome in the cytosol.
Craige & Bushman 2012:

Integration of a DNA copy of the viral genome into a host cell chromosome is an essential step in the retroviral replication cycle (Varmus et al. 1989; Coffin et al. 1997).

Textbook like reference Ref 1, Ref 2

The viral DNA is transported across the nucleus, where the HIV protein integrase integrates the HIV DNA into the host’s DNA. The host’s normal transcription machinery transcribes HIV DNA into multiple copies of new HIV RNA. Some of this RNA becomes the genome of a new virus, while the cell uses other copies of the RNA to make new HIV proteins.

For more details see Dutilleul et al. 2020

Once randomly integrated into the host cellular genome, HIV-1 gene expression is mainly regulated at the transcriptional level by hijacking the cellular RNA polymerase II (RNAPII) machinery. HIV-1 transcription initiates at the U3/R junction in the 5′-long terminal repeat (5′LTR) and is regulated by cellular transcription factors […]

So Replication happens after insertion of cDNA (complementary DNA, product of reverse transcription and second strand synthesis) into the host genome in the nucleus. Then transcription factors can bind the promoter and initiate elongation.
Second Question:
For DNA- viruses, some require integration into host genome, too. Interestingly, non-integrated viral DNA can populate the nucleus as dormant (circular) episomes (see viral latency, De Leo et al. 2020). Non-integrating DNA viruses often bring a DNA-dependent DNA polymerase and can replicate in the cytosol.
(If interested, see this review on viral polymerases that enable replication of viral genomes in the cytosol Choi 2016)
About Rolling Circle Replication:
Rolling circle replication is mainly found in procaryotic viruses (Phages). For eucaryotic viruses, rolling circle is pretty rare. The Geminivirus however, is one example of a non integrating DNA virus that replicates by rolling circle within the nuclei of plants. It seems that it relies heavily on nuclear factors for efficient DNA-Replication Castellano et al 1999

@markur - There are varying definitions of "schoolroom knowledge". To me, much of medicine is "schoolroom knowledge", and as a molecular biologist, much of biochemistry is "schoolroom knowledge". On this site, answers are expected to be supported regardless of your level of education, so that others may evaluate your answer on its merits, not simply on your say-so. There is no argument from authority (well, one can make a case for that from sources, but research is better.)

@anongoodnurse I've removed my comment. The answer still seems a bit misleading to me (e.g.: part 2 talks about DNA viruses only, but then quotes a passage that's broader than that) but I think that's mostly from the misdirection and multiplicity of questions in the original post, as pointed out by David in other comments.

@BryanKrause - I see. I edited that part on polymerases to appear more as a side-note. I think it‘s a cool review that helps understand viral lifecycles in general.


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Plant cell question in age 12 science test Part II
I'm a parent and I think the teacher had been a bit harsh with marking most of these questions but can someone help me answer the very last question on the paper please (where someone has written SP against it). Is the answer mitochondria?

As I already mentioned in the other post, questions like this are not generally useful for others because it is not really about a scientific query. The annotations/diagrams are not from a well known book/journal or other such published sources and therefore it is more about having an understanding with the teacher. Moreover, this would be considered a "homework" as per our site standards and such questions are expected to have some research effort from the asker.

what did the teacher say the answer was?

HI WYSIWYG I wasn't ignoring you - I didn't see your previous posts in time - I was too busy writing this one out :) But I won't post any more like this now - if anything I might post a question if I've tried many other avenues first together showing where I've checked.

To Vance I don't know as it was part of a test as I don't think the teacher went over all the answers.

No problem. You can even use the chat if you have quick questions.

I would grade alike. The subject might be considered advanced for 12 years old (I would assume the teacher is respecting the program) but the answers that are counted as wrong are quite obviously wrong.

The question is off-topic here as it is not about science but about teaching. If you happen to have doubts on how to deal with how the grade affects your kid, you might want to ask a question on parenting.SE.

I will decide what is off topic as I posted the original question I had trouble with.

The community decides what is off topic, not you @masterSQL

Or you either !!  Am I not the community as well then? Or does my opinion count for less or something?

@MasterSQL rg255 is right. You get to decided what is on topic in so much as you can post whatever you feel like posting. Higher rep users can go through questions and nominate questions for closing due to being off topic. If enough nominations are made, the question is closed (This is what rg255 means when they say "the community decides").

So, to go through the question in total:
(a) Part A nucleus is correct, but Part B ist the cytosol/cytoplasm, as the line does not stop at the border, but goes through it and ends in the gray part of the cell.
(b) For part C, it is the same problem as in your first question. Yes, the picture may be a plant cell, however, upon this drawing one cannot differentiate a mitochondrium from a chloroplast. In my opinion, a good teacher should have marked this answer as correct, even if he/she wanted to hear the other possibility. Part D is correct.
(c) 'Photosynthesis takes place here': Photosynthesis takes place in the chloroplasts. Mitochondria would have been correct, if the teacher would have asked for the respiratory chain or for the often in school simplified powerhouses of the cell.
'Many of the cell's chemical reactions take place here': I think, the teacher wanted to hear the cytosol as answer.

Hi SeRe I very appreciate your answer, thank you. I think if the very last question had said 'Jelly-like material surrounding the nucleus of a cell; chemical reactions take place here' then it would have given the pupils a better clue so yes the answer is cytoplasm. Thanks again.

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Heteroduplex and Products of cleavage of Holliday Junction (Resolution)
In homologous recombination (Holliday model), the last process i.e resolution can occur in two ways (horizontl and vertical cuts) leading to formation of either "splice" or crossover products or "patch" or non-crossovers product (as shown in the image).
The two possible products confuse me with what are crossovers. I could not understand why the "patch" product (Fig. (g) in the image) is called a non-crossover. Is it because one strand of both the homologous helices are same?
Also please do explain what is the hetero-duplex in this model?

Hello @SanjuktaGhosh.
My question did come out to be a duplicate. My apologies.
The question you linked is exactly what I wanted to know. I read your answer to the same. But I still couldn't understand the concept. Can you please elaborate on the complimentary part?
Thank you.

Yeah. I'll. Give me some time. I'll elaborate as soon as I have some time.

I'm done explaining my answer you may go through it now.

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Human Blood vessels,
Why is blood drawn from veins? Is it because veins have a large lumen? Or is it because the blood is flowing at a lower pressure and makes discharge easier? Is it safer to draw blood from veins?

If you draw blood from arteries,it will spout out because the arterial blood flows at some pressure. Moreover, it is too hard to stick a needle because arteries consist of thick blood walls.


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Why are there few four legged bugs?
I may be biased, and will delete if I'm wrong, but why are there so many more insects when compared to quad bugs?

What is the question exactly? Afaik, there are no invertebrates with 2 pairs of legs only. Is the question why, while we see that 2 pairs of legs is a successful bodyplan in vertebrates?

By "bugs" you mean insects, right? All insects have six legs (some may be reduced). Arachnids have eight legs. You can see this answer for some explanation on why six legs may be favourable to many insects. In general, it is not easy to reason out "why" something happened. Many times evolutionary choices are just random.

@Joce I wanted to know why six legged invertebrates are more successful than their four legged counterparts

@WYSIWYG Insects have six legs, and I want to know why is four not evolutionarily better for them

I don't see how this is a dupe


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Why do we need to close eyes to sleep?
Out of all our sensory organs, we need to stop taking signals explicitly only from eyes in order to sleep. Even interestingly, those who are not able to receive signals from eyes (i.e., the visually challenged people) also need to close their eyes in order to sleep. I wonder what is the relation of closing eyes with sleeping. I think the reason might be related to the state of the muscles related to the eyes. Of course, even if it were the case that one could keep her eyes open while sleeping, the brain would stop paying attention to the signals received by the eyes -- just like the brain stops paying much attention to the signals received by the nose or the ears while sleeping even if these organs are not physically closed or prevented from receiving signals. But in the case of the eyes, they are physically closed while sleeping,  which makes me curious.

Possible duplicate of Why do our eyes close when we sleep.

Unlike our underwater ancestors, land animals have evolved eye lids or nictitating membranes to protect our eyes and keep them moist periodically by blinking. During the sleep state, closing our lids protects the eyes from drying out and getting damaged while unconscious.  In addition to the lids themselves blocking light stimulus (not totally), our eyes also roll back to attenuate light stimulation.  Fish also sleep and don't need eyelids to do so, thus closing eyes is not a prerequisite for the sleep state.
Textbook Source: Butler, Ann B.; Hodos, William (2 September 2005). Comparative Vertebrate Neuroanatomy: Evolution and Adaptation. John Wiley & Sons. p. 215. ISBN 978-0-471-73383-6.


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Why does low redox potential mean less oxygen?
I often see statements about adding reducing agents like cysteine to anaerobic medium to decrease the amount of the dissolved oxygen.
However, I am not sure why.
I am wondering if it is because under the low redox potential conditions, dissolved molecular oxygen is easily reduced, is that correct?
If so, what is the oxygen reduced to? H2O?
For example, I am not sure of the rationale for the following statement?

The higher the redox potential is, the higher the oxygen dissolved in the media will be.

https://biology.stackexchange.com/a/52439/72932

Thank you very much for your comments. I did not quite understand the original purpose of adding reducing agents (to lower the redox potential) and the concomitant results (to reduce the contaminated oxygen).

@Beginner - I think that lot of people have applied different amounts of reducing agents to their culture and have found the best concentration enabling best viability simply by trial and error. One can speculate why certain concentrations are toxic while others support growth, however most of the time, culturing conditions are configured empirically. Usually people are simply happy that it just works for once. Here, we did lay out somewhat of a basis that there might be a "redox-sweet-spot" that is capable of reducing O2 in culture medium while minimizing H2O2 production.

You‘re partially correct. Adding reducing agents will cause $O_2$ to be converted to $H_2O_2$, as thiol groups are turning from $SH$ to $S$-$S$ (forming dimers). In a second reaction, further thiols may reduce $H_2O_2$ to $H_2O$, (but H2O2 also may react with $SH$ to form toxic byproducts like thiooxides $SO$).
Intermediates (like $H_2O_2$ or $O_2^-$) might get reduced to $H_2O$ by subsequent reactions with thiol groups, Enzymes or spontaneous dismutation (Kiley & Stolz 2004, Aires et al. 2008)

$O_2$ + 2 $SH$ -> $H_2O_2$ + $S$-$S$

$H_2O_2$ + 2 $SH$ -> 2 $H_2O$ + $S$-$S$  (see NG et al. 2007, DTT Assay Wang et al. 2018)

However, while the first reaction is very probable, the second reaction is less probable (some even argue that it is too unlikely to have an effect)
The second reaction might depend on concentration. Usually cell culturing protocols are designed by trial and error. So it’s based on testing multiple concentrations to find out the amount that yields the highest culture viability. I can only speculate that e.g. the right concentration hits a sweet-spot. That sweet-spot might lie between production of toxic thiooxide ($SO$) and oxygen reduction. But that depends on a lot of factors like organism and other culturing conditions.
Cell Cultures are in Generally too Oxidative; Reducing Agents might Help no Matter the Exact Reaction Path
Oxygen is a general problem in many cell cultures (Jagannathan et al. 2017). Even for human cell cultures, 20% $O_2$ is not physiological and introduces a background of oxidative stress (it even increases mutation rate).
To describe aggressive oxidative features of oxygen, it's useful to use the more generalized term „reactive oxygen species“ (ROS) instead of "oxygen", since redox potential doesn‘t care which exact compound acts as an electron donor. By referring to ROS, it‘s not necessary to keep track of exact oxygen-compounds.
The main point is that in the end, some biomolecule gets damaged by oxidation and the probability for that increases with high $O_2$ -levels. Hence, reducing agents could increase viability by scavenging any kind of oxidative species from the medium. And it makes sense to assume that one of the end products might be $H_2O$.

„the higher the potential, the higher the dissolved oxygen in medium“.

I think the wording is misleading, since high redox potential is a consequence of oxygen being present, not the other way around (as that would imply something like high redox potential attracting atmospheric oxygen into water). I speculate that the author meant that dissolved (organic) compounds tend to release $O_2$ (or rather any reactive oxygen species (ROS)) more often in an oxidative milieu.

I added "ultimately" in the first line to imply a possible reaction chain. Also, I don't think that sophisticated biochemistry is necessary, since in the presence of excessive thiol groups each oxygen-intermediate should be reduced subsequently by further thiol groups. It's not stated explicitly in the literature, but in my own experience,  adding DTT to reverse transcription reactions is good practice to protect RNA from oxidation damage. No other biochemistry needed.

first: O2 + 2 SH -> H2O2 +S2, second: H2O2 + 2 SH -> 2 H2O +S2 ... Where's the problem?

@user338907 -  how probable is H2O2 + 2 SH leading to -SOH compared to 2 H2O +S2? In fact, thiol groups do remove hydrogen peroxide NG et al. 2007  ... I think you might have gotten sidetracked here...

Yes I am claiming just that, and so do all scientist using the DTT assay to determine oxidative potentials Ref: H2O2 removes DTT. Ref2. No enzymes need. Again, in the context of this question reducing agents are added in excess, so the occasional formation of thiooxides does not prevent overall reduction of little Oxygen. I could ask a question on SE chemistry though, if enzymes are required for thiols to reduce H2O2

Ok, so 4 mM cysteine is too much, since it causes toxic side reactions. So you claim the ONLY product of thiols is H2O2?  So why do people add cysteine to their media? Could it be that less cysteine (than 4 mM) is actually favorable, since thiol oxidation is rarer than H2O2 reduction, and (like everything in chemistry) is dependent on concentration..?

Ok I changed my answer. Congrats, it‘s ugly and unconcise now. Please note that OP asked for reducing agents in general and what scientists aim to turn O2 into. (With emphasis on AIM. If what you‘re saying is correct, thousands of scientists are using a  wrong protocol). You‘re way too focused on thiol details which confuses the main message.

Thank you very much for your detailed explanation and discussions!

No problem. Remember to accept your favorite answer, if it answered your question.

Of course, I accepted your great answer!

However, I am still unsure how the concentration determines the probability of the second reaction.
"so 4 mM cysteine is too much, since it causes toxic side reactions."
I do not think 4 mM cysteine is harmful to bacteria (I lost its reference) because about 0.5g/L L-cysteine (about 3mM) is usually added to medium (an example is Whitaker et al. 2017).
Moreover, Karunatilaka et al. 2013 added 8mM L-cysteine. ("The 8 mM L-cysteine in the minimal media compensates for slow leakage of oxygen over time.")

@user338907 - Thanks for combining both praise and critique, it helps me get most of your input! — I‘m having trouble extracting the core message of your info. Could you summarize a bit? I mean, it‘s clear that 20% oxygen atmosphere IS a problem for ALL cell cultures. We in our lab solve that by adding selenocysteine (common culture protocols actually exclude Selenium, which is bad since it‘s needed to deal with oxidative stress in eukaryotes; I could look up the reference if you wish). Maybe there‘s no need to fully exclude oxygen, but just to reduce it a little to increase culture viability?

I‘ve edited the answer to focus on reducing agents to be something like a scavenger to remove oxidative species in general, not just H2O2. It could be misleading to isolate exact reaction paths. I mean we are talking about culture medium, a mixture of amino acids, glucose, growth factors, maybe even serum. Oxygen will definitely react not just with thiols but produce multiple different uncharacterized (hence no literature reference) oxidized molecules, inactivating their function or react as an oxidant themselves. These random intermediates could be countered by adding reducing agents, no?

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Genotype vs Alleles - What's the difference?
I have searched through various websites, however, I am still rather confused with the difference between 'genotype' and 'alleles' since each site seems to be contradicting another site.
I would be much grateful if someone could please give me a concise and clear differentiation between 'genotype' and 'alleles'.

This question is duplicated a lot on this page (e.g. this), but since this is a re-occuring issue and I didn't find a reasonable AND concise  answer on this site (or at least concise enough for my taste :P), I'm just gonna answer it here.

Please note that opinions on the exact wording of the following can differ a lot. You will have to find one for yourself that works best for you.
Gene = An element within the DNA/Genome with function(s)
Allele = A subtype of a gene with (or without) altered function(s) (due to function-changing mutation(s))

Every individual has two homologous versions (not exact copies) of every gene. 1 version on each chromosome (don't confuse with sister chromatids). This allows two versions (alleles) of the same gene to be present at the same time.
1 allele is from mama, 1 allele is from papa. Both alleles often have a similar known functions, although they're rarely exact copies (unless your parents are siblings).
If two alleles have the same function, they may or may not be summarized as the same allele, depending on the aim of the study or how well the function of each mutation is characterized. Most textbook examples work with alleles with very defined functions ("wildtype vs. white").
A whole population of individuals has the same exact numbers of genes as a single individual (A human has just as many genes as the species humans). But the population has a multitude of alleles for each gene, while a single individual can have max two alleles per gene.

Genotype = A summary of genes and/or alleles per gene of an individual.

"Small differences among alleles of the same gene contribute to each person’s unique characteristics." (from thoughtco)

Phenotype = The observable functions/properties of an individual that are determined by its genotype

An allele is a variant of a gene, while a genotype is an (arbitrarily) specified combination of alleles, mostly stating the homo- or heterocygous presence or absence of certain mutation(s) in a certain gene or combination of genes. E.g. Genotype A: Gene A (wild-type allele | mutant allele), gene B (wild-type allele | wild-type allele).

According to a format guide,  https://samtools.github.io/hts-specs/VCFv4.1.pdf:

Allele is representing single genetic haplotypes

Genotype is an assignment of alleles for each chromosome of a single named sample at a particular locus.

(A haplotype is a group of genes within an organism that was inherited together from a single parent. The word "haplotype" is derived from the word "haploid," which describes cells with only one set of chromosomes, and from the word "genotype," which refers to the genetic makeup of an organism. A haplotype can describe a pair of genes inherited together from one parent on one chromosome, or it can describe all of the genes on a chromosome that were inherited together from a single parent. This group of genes was inherited together because of genetic linkage)
(For human genome,  a haplotype is defined as the combination of alleles for different polymorphisms that occur on the same chromosome, and for any given stretch of chromosomal DNA an individual will have two haplotypes, although at a population level there may be numerous haplotypes for any given stretch of chromosomal DNA.)

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DNA as a data storage medium: how many GB can a human genome store?
DNA molecules may be the digital storage medium of the future. I was looking at how much data you could fit if you would synthesize a DNA molecule the size of a human genome.
So DNA base molecules are represented by A, C, T, G and they are always found in pairs (so A connected to T and C connected to G). One such pair is called a basepair. The human genome contains ~3 billion of those basepairs (i.e. 6 billion bases). Now you mostly read about assigning two bits to every base, so A = 00, C = 01, G=10, T = 11. Then you could say a basepair stores 4 bits e.g. AT = 0011. BUT there are only 4 possible basepairs: AT and CG and the reverse, so TA and GC. This AT,TA,GC,CG system could then again be represented by only 2 bits for every pair.
Assuming the latter, a human genome contains 2 bits/basepair*3 billion basepairs = 6 billion bits. Divide by 8 billion to convert to GB, so a human genome could store 0.75 GB.
Now in case of digital DNA storage a part of the molecules needs to be used for error correction, indexing, etc. To account for this ‘overhead’ you can conservatively assume that only 50% of the total storage can be used for the data storage, which would result in 0.375GB.
Now in the whitepaper of the ‘DNA data storage alliance’ backed by Twist, Microsoft, etc. (https://dnastoragealliance.org/dev/wp-content/uploads/2021/06/DNA-Data-Storage-Alliance-An-Introduction-to-DNA-Data-Storage.pdf Page 20) they come to a different result: they assume 2 bits per base, but as 50% is needed for overhead, they say every base stores 1 bit, so 2 bits per basepair AFTER accounting for overhead (above I concluded 2 bits per basepair before accounting for overhead). The total storage then becomes 2 bits/basepair *  3 billion basepairs = 6 billion bits. Divide by 8 billion and we get 0.75GB can be stored in the human genome after we account for overhead. According to this line of thought the full human genome would have a size of 1.5GB (?). General consensus on the internet seems to be that the full human genome stores 0.75GB.
Who’s right??

Thanks! I used 50% overhead because they mention it in the paper. So know Im thinking the following: every base in a sequence stores 2 bits. We ignore the complementary strand as it basically stores the same information but ‘reversed’ but it does help in molecular structure. Then there only 3B 2 bit bases in the 3B basepairs that are or interest for storage. So 6B bits * 0.8% overhead = 0.6GB . If I use 50% overhear I get to 375MB again. Idk if this makes sense at all? Is it true the complementary strand doesn’t add info per se? (Srry this is not my field)

I removed my comments and posted an answer with the same information.

different but related: DNA as a digital storage medium; sequences algorithmically avoided for safety reasons (or should be)?

You are confusing the sequences with the pairs. AC is a completely possible sequence, and it will connect to a sequence of TG on the other strand of the double helix. Basically, everything in one strand is repeated with the complementary base pairs in the other one. This is why they say you have 50% overhead - the double helix requires everything to be represented twice.
The 50% you are already paying also provides the physical robustness of the double helix molecular structure, so you can probably get by with less overhead than with other solutions, since this already provides some resilience against single-bit errors.
Both sources agree that the capacity is 0.75GB and then whatever you need for additional error checking or other overhead you need to subtract from that.
As a benchmark, network transmissions under good conditions add about 20% overhead (so approx 10 bits per byte for parity checks, occasional retries, etc) but I would hesitate to come up with a concrete number without empirical experimentation. Off the cuff, maybe 10% redundancy would be good for reconstructing the occasional damaged sequence (look at Hamming codes etc). But the question is then what reliability you are hoping to achieve. Again, the raw storage capacity is 0.75 GB, and you use it as you see fit for your specific application.
Furthermore, it's unclear why you use the human genome as a yardstick for anything. You can't replace information in a human's genes with random information you want to store and still end up with a human cell. And as a carrier of information, a human is rather inefficient; quick Duck Duck Going gives me a number of 30 trillion cells per human, all carrying the same information in their DNA. The genome of the rice plant contains many more base pairs, anyway. But as the paper you link to emphasizes, you do not need living organisms to carry the DNA you want to store information in (nor could you, realistically).

Thanks for the answer/following up on my comment! To touch on your last comment; I was also looking at sequencing costs of DNA storage, and commonly you find the human genome is the benchmark (e.g. 600$ to sequence the full genome) - I wanted to convert this to $/GB

The much more expensive operation (I assume) would be getting the bits there in the first place, though of course, the cost of reading them will be a factor, too.

The 0.75 GB (assuming 2 bits per nucleotide) is correct as far as I know. But I think I can add some additional context. Typically, I point people to this Nature Review from 2019 for a nice overview of the field.
In theory the genome could store that amount of information. But it doesn't make sense to consider aspects such as error correction because it is not currently possible to encode digital data into nucleic acids on that scale in vivo. Typically, in vivo data storage applications are typically in the form of either cellular recording or use CRISPR–Cas to insert short nucleic acid sequences.
Conversely, in vitro data storage has been considered the most practical form of encoding digital data into DNA. In Table 1 you can see some of the most notable demonstrations of in vitro DNA data storage. You can see the strand lengths are limited to less than 200 nucleotides, which is about the current limits of synthetic capacity. The sequencing (read) technologies are maturing faster than the synthesis (write) costs which is among the current bottlenecks. Larger datasets need to be synthesized independently in strand segments and reconstructed from mixed data pools.
If you wanted to come up with $/GB value for the sequencing of the human genome as a fun thought experiment, you could make the simplifying assumptions (2 bits per nt) and call it a day. But to calculate a more realistic number for arbitrary storage of nucleic acid data on the order of the human genome would be much more complex. The experiment itself would also not be trivial or cheap.
Though to be honest I didn't read through your whitepaper, and it looks to be more recent from 2021. Maybe progress has been made I'm not aware of since it's not my area of expertise.
Hopefully that adds something worthwhile to the discussion.


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Why do flies and fruit flies exhibit two distinctive (but not exclusive) flying patterns?
I live near a forest with a canal, and often see fruit flies, they also sometimes come in our house and occasionally feed on bits of fruit. Also, sometimes I meet regular house flies here and there, and also in the city I commute to.
I noticed that most fruit flies and alike most often fly in circular shaped trajectories in the air, their curvature of flight contains bends, as if they were riding an invisible rollercoaster all the time. Their flight can be faster or slower, centered around a lamp fixture or near my face eventually, but most importantly, circa 80% of the time I see them flying in this fashion. Also, this is the way I see regular flies flying around, in 99% of cases.
On the other hand, in roughly 20% of cases when I see fruit flies flying, they fly in straight lines, with abrupt and sharp changes in their direction. This is usually (but not necessarily) slower than their rollercoaster way of flying, and it can also be varied regarding how often they change direction abruptly. However, this "sharp" way of flying is extremely rare in case of the house fly, I have only seen it two times actually, so let's say it happens in 1% of house flies.
What are these distinct flying styles? What is their cause?
Are both styles natural and should occur in healthy fruit flies, and house flies as well? Then why is it much rarer in case of house flies? Isn't the "sharp" style a result of some infection around these animals?
Those house flies that I saw flying in the "sharp" pattern were rather slow anyway, and I saw them in/near my home. Does it occur more rarely in cities?
Thank you for any helping answers, I am very curious!


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Has there ever been a published experiment to take a viral "census" of a human subject's blood?
Has there ever been a published experiment to take a viral "census" of a human subject's blood?
By a "census", I mean to identify every active virus in the subject's blood with some probability.
So, for example, we can imagine taking different samples of blood, diluting them, then taking the dilution and using it to innoculate a lawn of hemocytes. Presumably, different viruses would make different plaques, so they could be separated, isolated and identified. By doing different combinations of dilutions, one could I suppose make a table or curve that would show the probability of detection of a given virus based on its concentration in the blood. Thus, at the end of the experiment the researcher could state, "I have isolated all the viruses in the subject's blood having a concentration above X with a probability of Y." Obviously, this would require hundreds of samples and thousands of innoculations to achieve an accurate census.
Has anyone published a study like this?

Here's a deep sequencing paper characterizing the DNA virome of human blood. I'm not sure if anyone has attempted viral "Culturomics" work for viruses. https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1006292

You wouldn’t try to isolate viruses, this being the 21st century.  You’d perform metagenomics analysis, which is much more sensitive.
That’s been done several times.  Two examples:

Anellovirus and pegivirus C (GBV‐C) were detected among these donors. None of them were found solely in donors with abnormal liver enzyme. Anellovirus was highly prevalent (93.3%) and the co‐infection with multiple genera (alpha, beta, and gammatorquevirus) were more common in the donors with normal ALT values in comparison to those with elevated ALT ...

—-Full annotation of serum virome in Chinese blood donors with elevated alanine aminotransferase levels

Anelloviruses were detected in each of the 10 plasma pools. Human pegivirus A (HPgV; GB virus type C) sequences were identified in eight of the 10 pools, more than 90% of which belong to Genotype 2. The recently described human HPgV2 in Flaviviridae was not detected. A small number of sequence reads of human papillomavirus were also detected in three pools. In one pool, two different gemycircularvirus genomes were identified and fully sequenced.

—-Viral nucleic acids in human plasma pools

I don't see what this has to do with a viral census. In my copy of Fields Virology (6th Edition) there is no mention of "metagenomic analysis" so I don't know what that is.

Metagenomics


text:
How do animals contain and dispose of bacterial endotoxins (lipopolysaccharides)?
Gram negative bacteria naturally release endotoxins which are lipopolysaccharide molecules. These molecules are toxic to many eukaryote cells, including macrophages. My question is how animal organisms locate, isolate, contain these toxic molecules. For example, if a lipopolysaccharide attaches to a macrophage, thus neutralizing it, does this actually kill the macrophage or just render it inert? In any case, the ineffective macrophage must now be removed as waste. How does that occur?
In the Wikipedia article on endotoxin it reads "Normal human blood serum contains anti-LOS antibodies..." without further describing them. I find this statement strange because normally when I think of antibodies, I think of them attacking cells or organisms, not individual molecules like lipopolysaccharides. What are these anti-LOS antibodies and how do they function?

There are a lot of questions in this post. I went ahead and answered what I read as the central question, but you should consider making separate posts for your other questions re: macrophage killing, dead macrophage clearance, anti-LOS antibodies, etc.

There are too many questions embeded here to cover in a single answer. I'll summarize and answer what I interpret to be the "central" question.

How do animals A) locate, B) isolate, and C) contain/eliminate bacterial endotoxins?

LPS in the blood stream is rapidly bound by LPS-binding protein (LBP) and localized to the liver for detoxification and excretion (1).
A) LBP recognizes and binds the Lipid-A region of the LPS molecule (2),
B) At this point LPS is released from bacterial cell membrane and sequestered into complexes with high-density lipoprotein (HDL). This is also the stage at which free LPS can activate CD14+ monocytes, triggering an acute inflammation response (3). However, additional HDL reduces monocyte activation, suggesting that these complexes inactivate LPS by "isolating" it from CD14 (4).
C) Finally, the LPS-HDL complex is taken up by the liver, either into Kupffer Cells (~25%) or liver sinusoidal endothelial cells (~75%), where enzymatic inactivation of LPS occurs either by dephosphorylation of the phosphates or deacetylation of the primary acyl components of lipid A (5)
Given the hydrophobic characteristics of LPS lipid-A and the fact that it's processed in the liver, I suspect that LPS and its metabolites are eliminated from the body via excretion into the bile ducts, but I haven't found a reference in the literature to confirm that suspicion.
References:

Wassenaar and Zimmermann, Eur J Microbiol Immunol. 2018 Sep 28; 8(3): 63–69.
Tobias et al., J Biol Chem. 1989 Jun 25;264(18):10867-71.
Vesy et al., Infect Immun. 2000 May; 68(5): 2410–2417.
Flegel et al, Infect Immun. 1989 Jul; 57(7): 2237–2245.
Yao et al. J Immunol. 2016 Sep 15; 197(6): 2390–2399.


text:
Why are monarch butterflies attracted to particular flowers but not others?
I have a "Purple Emperor Butterfly Bush" (Buddleia davidii 'Purple Emperor') and sure enough it does attract butterflies.
I have seen monarch butterflies using it, which confuses me, because I thought that monarch butterflies only fed from milkweed.
What makes this type of bush a substitute for the milk weed, but not other flowers?

It's the Monarch caterpillars that only feed on milkweed. Adult Monarchs, like many butterflies, feed on the nectar from flowers. https://www.fs.fed.us/wildflowers/pollinators/Monarch_Butterfly/habitat/index.shtml


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

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

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

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

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

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

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

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

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


text:
Does a bird nest out of its breeding range?
I have a book by the Audubon Society on building bird houses and for each bird they show a breeding, wintering and all year range.
Do the birds only breed in their breeding range, or in both breeding and all-year range?
For example, the northern flicker is shown as breeding in Canada, but its all-year range is in the United States. So, am I wasting my time building a bird house for a northern flicker in the United States which is south of the breeding range, but inside the all-year range?

An all-year range for a bird species is obviously a range where a population exists year round, and since birds generally breed each year, there will be individuals of the species breeding within this range.  Precisely speaking, this is part of the breeding range of the species, but maps of bird ranges commonly call this range the all-year range, and will reserve the term "breeding range" for that part of the range map where birds breed but are not present during part of the year.  This is helpful since it communicates which times of the year the birds can be expected to be present.
Because in temperate zones summer is the time when breeding most always occurs, maps commonly show the summer-only breeding range in a warm color such as red. For migratory species, a range where they spend the winter but do not remain during the breeding season is usually shown in a cool color such as blue.  Typically such maps will show the year-round range in a combination of these two colors, e.g. purple.  (Some maps also show a migratory range, where birds transit but do not stay for long periods, in some other color.)


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Why are there fewer ospreys in upper New England?
I have a book by the Audubon Society on building bird houses. In this book the chapter on ospreys shows their breeding range to include Canada and then a pocket around the Connecticut and New York coasts, but no upper New England (Massachusetts, New Hampshire and Maine).
This corresponds to my own experience. I have seen a lot of Osprey nests in Connecticut, but they seem much rarer in Massachusetts and New Hampshire. Why is this?
If the answer was that they prefer a warmer climate, then it makes no sense because they have a widespread breeding range in parts of Canada that are colder than New England.


text:
Why chemical synapses are more common?
Reading into the types of synapses I found out that there are two types of them; electrical and chemical.

chemical synapses use neurotransmitters to transmit impulses, are slower than electrical synapses and are much more common.
electrical synapses use electricity, transmit faster and are rare in our system.

My intuition says, "Shouldn't faster impulses mean a more efficient mode of transport of information and hence be more dominant/common?" Granted, the neurotransmitters help transmitting complex impulses, but is that not possible with electrical synapses?

Electrical synapses are hardly synapses at all, they allow the connected cells to share some components of their cytoplasm.
This really makes them more like one "super cell" rather than individual processing units. The circuits that use these synapses are often inhibitory circuits that reduce the collective activity of a large group of local neurons together. It works for that purpose, but if every cell in the brain is connected that way, you'd just have two states: everything "on" and everything "off". A single bit of information isn't very useful computationally.
Chemical synapses are very accessible to regulation. The strength of specific synapses can be changed by either releasing more transmitter or having more receptors. Receptors with different affinity can respond differently to different firing patterns. Different released chemical signals can cause different effects at the same or different locations. There can be inhibition as well as excitation.
Speed isn't everything.


text:
Is it physically impossible for a male Anopheles mosquito to bite?
I know that malaria is spread through female Anopheles mosquitos as they require a blood meal to survive and that male ones do not bite and they survive off of nectar, etc.
But is it physically impossible for a male Anopheles mosquito to bite an organism infected with malaria?
If it is physically possible, then doesn't that imply that there can be a chance, albeit a small one, that they can have Plasmodium in their gut?

Just making sure - physically possible and therefore plasmodium or physically impossible and therefore no chance of plasmodium?

@bob1 I want to know if it is physically possible and therefore plasmodium.

It is physically possible to kick a football on the surface of Mars. Does that help you know whether or not there are footballs on Mars?

Thanks - the wording was confusing with the physically impossible one one line and the no words indicating either way on the next.


text:
TMPRSS2 Primer Design
I am trying to design a primer for TMPRSS2 PCR reaction. However, this gene is in reverse position like in the picture I'll show.
From the nucleotide sequence I got from NCBI, should I reverse the sequence and start designing the primer, or do you have any other solution? Thank you!

Welcome to the site. Please take a [tour] and visit the [help] for more information about the site and what we do here, as well as about good questions and answers. Can you please specify if you aim to amplify genomic DNA or coding sequence only (e.g. off RNA/cDNA).

If your goal is simply PCR amplification than it makes no difference whether you flip the sequence or not: By convention the 'forward' primer refers to the primer that is designed against the anti-sense strand and your 'reverse' primer is designed so it is complementary to the sense strand. In practice however the PCR reaction obviously doesn't care what we call the primers, it will amplify the region that is encompassed by them, producing double-stranded DNA fragments that are indistinguishable regardless if the sequence/design was flipped or not.

Thanks for your answer. I am considering to use the original sequence (unflipped) retrieved from NCBI RefSeq to cover the whole region I'd like to amplify.


text:
Are psilocybin/psilocyn the only psychoactive compounds in psychoactive mushrooms?
Psilocybe cubensis is the most common psychedelic mushroom, and its active ingredients are psilocin and psilocybin (which is converted to psilocin in the body).
There are other psychedelic mushrooms, such as psilocybe cyanescens, psilocybe mexicana, and amanita muscaria, as well as many others. Are there any other psychoactive compounds in mushrooms other than psilocybin and psilocin?
I found this page but wonder if it is exhaustive: https://en.wikipedia.org/wiki/List_of_psychoactive_plants,_fungi,_and_animals?wprov=sfti1

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

In particular, a Google search in the US for list of psychoactive compounds in mushrooms gives 8 different compounds, and there may be more.

Yes, there are multiple psychoactive compounds, including norpsilocin, baeocystin, norbaeocystin, and aeruginascin. Ergot and Fly-Argaric have different substances.
A lot of mushrooms contain ergot alkaloids to defend against nematodes and bacteria.
Alkaloids contain Nitrogen. They have biological effects like neurotransmission, circulation, hormonal, immuno-stimulant (lion's mane, chaga mushroom), immuno-depressant.
The psylocin group are very similar isomers:
Norpsilocin (4-HO-NMT) is tryptamine alkaloid recently discovered in 2017 in the psychedelic mushroom Psilocybe cubensis. It is hypothesized to be a dephosphorylated metabolite of baeocystin. Norpsilocin was found to be a full agonist of 5-HT2A receptor. It is also more potent than psilocin.
Baeocystin is a zwitterionic alkaloid and analog/derivative of psilocybin, and is reported to have similar strength and pharmacology.
Norbaeocystin is a N-demethylated derivative of baeocystin. phosphorylated derivative of 4-hydroxytryptamine. The latter is notable as a positional isomer of serotonin, which is 5-hydroxytryptamine.
Fly-argaric is also psychoactive via muscimol and ibotenic acid, a neurotoxin converting to muscimol after ingestion. Read the wiki page to find out the uses.
Lion's mane also changes neurotransmission..
To find current research, I suggest googling "neurotransmission funghi" and "funghi neurotoxin".
Flying is not the only measure of helicopters and planes, there's also landing, ground control, maintenance, cost, atmospheric events, efficiency and cargo events.

What does the last sentence add to your post?

@AliceD This friendly reminder disguised as an analogy might be referring to 'What goes up must come down' or 'No effect without side-effects'..


text:
What is H-activation vs. O-activation in the context of cellular respiration?
I was reading this article on Albert Szent-Gyorgyi and on page 7 there's this statement:

Now, I thought myself capable of tackling a biochemical problem. I
embarked on biological oxidations. At that time a violent controversy raged
between O. Warburg and H. Wieland and their followers. The former thought
that oxygen activation was the most essential feature of respiration, while
Wieland put H-activation in the fore.

This Wikipedia article states that in biochemistry, activation is where biologically active molecules acquire the ability to perform their biological function. What does this mean in the context of the above statement?

Warburg-Wieland Controversy
In the years immediately preceding the 1925 publication by Keilin of his seminal papers on the cytochromes, a fierce controversy between Warburg and Wieland was in full flow regarding the nature of biological oxidation (Manchester, 1998).
H-Activation
Wieland and coworkers considered what we would call dehydrogenases were the key to understanding biological oxidation, and that these enzymes 'activated' hydrogen atoms in substrates such as succinate, passing them to a suitable acceptor. In other words they considered removal of hydrogen atoms, catalyzed by dehydrogenases, as central, and that these enzymes act as hydrogen activators.
To this end, they often used a Thunberg apparatus, where the the reduction of the dye methylene blue to a colourless form in the presence of tissue extracts and (for example) succinate could be followed anaerobically. Allowing oxygen to enter the system inhibited the colour change.
As pointed out by Manchester (1998), a key tenet of this mechanism is that oxygen does not directly combine with the organic substrate, and that oxygen atoms are not incorporated into CO2.
The adherents to H-activation were well aware of the role O2 played in respiration, but considered this to be passive, analogous to what happens when O2 is allowed enter a Thunberg apparatus and accepts electrons from colourless (reduced) methylene blue. That is, they saw no requirement for oxygen activation.
Enzymes and 'Specific Activation'
The term 'activation' may require comment, with regards to enzyme catalysis. It was not uncommon in the early days of enzymology to consider an enzyme as 'activator' of a substrate, in the sense of making it more reactive. As late as 1979, for example, Dixon and Webb (1979, p4), defined an enzyme as "a protein with catalytic power due to its power of specific activation" (and argue that cytochrome C should not be considered an enzyme because it acts as a carrier and not by activating any other substance).
O-Activation
Warburg, almost universally accepted as one of the great biochemists, but also renowned for his vituperative attacks† on those who did not agree with his ideas (see Gratzer, 1992) was very dismissive of H-activation, which he considered unnecessary and misleading (Hartree, 1963)
Instead, Warburg proposed that all cells have an iron-containing respiratory enzyme, Atmungsferment, (respiratory ferment) which, in conjunction with unspecific surface forces, is responsible for adding oxygen to organic molecules (Keilin, 1966; Hartree, 1963; Manchester, 1998). Thus, Warburg considered oxygen activation as key to understanding respiration.
The Atmungsferment system had one great advantage: it was inhibited by low concentrations of cyanide, a known inhibitor of cellular respiration (Keilin, 1966).
Resolution of the Conflict.
As related by Manchester (1998) and Szent-Gyorgyi (1963), a key experiment that lead the recognition that both H-activation and O-activation are required for respiration was performed by Szent-Gyorgyi.  He showed that succinate oxidation by minced tissue extracts could be inhibited by cyanide, but that respiration could be restored by addition of methylene blue. That oxygen activation was necessary could be inferred from inhibition by low concentrations of cyanide (interpreted as knocking out 'O2 activation') but "the dye restored respiration, replacing O2 activation. It was reduced by activated H and then reoxidized spontaneously" (Szent-Gyorgyi, 1963).
But in this regard, the contributions of Keilin, in particular his (re)discovery of the cytochromes, were also critical.  Hartree (1963) argues that Keilin's work had two great effects on the elucidation of the mechanism of biological oxidation.
Firstly, the recognition that haem-containing cytochromes were reversibly oxidized and reduced in respiration was a seminal discovery.  Among other things, this allowed Warburg to deduced that Atmungsferment contains heme and is inhibited by CO. (We now recognise that a key component of Atmungsferment is cytochrome oxidase).
Secondly, Keilin's experiments lead to the development of the concept of the respiratory redox chain.
To be fair to Warburg, he did concede in his 1931 Nobel lecture that H-activation precedes O-activation: "It must, therefore, be concluded that activation of the combustible substance in the breathing cell precedes the attack of the ferment iron; this corresponds with 'hydrogen activation' as postulated in the theory of Wieland and Thunberg" (Warburg, 1931).
Furthermore, although he originally thought that Atmungsferment catalyzes the direct transfer of oxygen to substrate, he conceded that it is possible "that the iron that reacts with the molecular oxygen does not directly oxidize the activated combustible substances, but that it exerts its effects indirectly through still other iron compounds - the three non-autoxidizable cell haemins of MacMunn, which occur in living cells according to the spectroscopic observations of MacMunn and Keilin, and which are reduced in the cell under exclusion of oxygen" (Warburg, 1931, emphasis is mine).
† Warburg was incensed by the 1927 award of the Nobel prize to Wieland (for work on bile acids) and wrote to his sister that the award had little significance, having been awarded by 'a gang of drunken Swedes' (Gratzer, 1992).
Dixon, Malcolm, Webb, Edwin C. Thorne, C.J.R, Tipton, Keith F. (1979) Enzymes 3rd Edition Longmans, [Available at the internet archive)
Gratzer, W (1992) Warburg's wars Nature 356, 640-641
Hartree, E. F. (1963) David Keilin (1887-1963) Biochem. J. 89, 1-5
Keilin, D. (1925) On cytochrome, a respiratory pigment, common to animals, yeast, and higher plants. Proc. R. Soc. Lond. B. 98, 312–339
Keilin, D. (1966) The History of Cellular Respiration and Cytochrome. Cambridge University Press
Manchester, Keith L. (1998) Albert Szent-Gyorgyi and the unravelling of biological oxidation. Trends Biochem. Sci. 23, 37-40, 1998
Mann, T. (1964) David Keilin (1887-1963) Biogr. Mem. Fellows. R. Soc.  10, 183–205
Szent-Gyorgyi (1963) Lost in the Twentieth Century Annu. Rev. Biochem 32, 1-15
Warburg, O. (1931) The Oxygen-Transferring Ferment of Respiration. Nobel Lecture

The answer to this question is to be found in an extensive biography of Warburg published by The Royal Society of London in 1972, written by his former pupil and fellow Nobel laureate, Hans A. Krebs.
The reasons that this is/was difficult to find is that searches for Warburg bring up dozens of papers about the Warburg Effect, and O-, H-activation are obsolete terms reflecting a stage in the study of mitochondrial oxidation (although mitochondria, as such hadn’t been discovered — they were the active components in the particulate fractions used) in which the various haem components of the electron transport chain were in the course of being unravelled. To quote from the publication, starting on p. 648:

Warburg’s next major undertaking was the elucidation of the mechanism of action of the ‘hydrogen activating enzyme’ in biological material. It had been known from the work of Thunberg, Wieland and others, beginning in
the first decade of this [the 20th] century, that biological material contains enzymes which catalyse the reduction of methylene blue (and similar synthetic dyes) or nitrophenols to colourless compounds by a variety of substances like succinate, malate, citrate, lactate or glutamate. The common feature of these substances is their ability to donate hydrogen atoms and undergo ‘de-hydrogenation’. Such experiments indicated that O2, the physiological hydrogen acceptor in the process of combustion, can be replaced by other acceptors. During the 1920s it was intensely argued whether the catalytic activation of oxygen, as studied by Warburg, or the catalytic activation of the hydrogen atoms of the substrates, as studied by Thunberg and by Wieland, was the essential feature of biological oxidations. At the earlier stages of the discussion Warburg dismissed the concept of the activation of hydrogen because the experiments of Thunberg and others on which it was based, involved non-biological oxidising agents such as methylene blue or nitrophenols. He scathingly stated that the oxidation of organic material by derivatives of nitric acid or synthetic dyes is of no biological interest. But he did not properly appreciate that although methylene blue is not a naturally occurring compound, the reactions which Thunberg had studied were enzyme-catalysed processes. Eventually, however, Warburg became impressed by the enzymic nature of the methylene blue reduction when E. S. G. Barron demonstrated some methylene blue experiments on red cells to him personally in 1929 while visiting the Johns Hopkins Medical School at Baltimore.

To cut to the punch-line, having abandoned his previous dogmatic position, Warburg went on to identify the riboflavin component (co-enzyme) of the ‘yellow enzyme’ involved, in which the oxidation and reduction is indeed the addition and removal of hydrogen.

Returning finally to the actual question, “what was meant by ‘activation’?”, it was the (re)conversion of the the cofactors (Fe in the cytochromes, the pyridine ring in NAD and NADP, and the flavin ring in FAD) to their higher oxidation state. This differs from the current use of the term activation, e.g. for amino acids in amino acyl tRNAs, or acetate in acetylCoA, where the negative free energy  change from breaking a linkage in the activated form drives the formation of a bond with another molecule. However, as redox half-reactions involve calculable free energy changes, it is perhaps ultimately not so different.

you carry this site


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Codon alignment via Python?
I have pairs of coding DNA sequences which I wish to perform pairwise codon alignments via Python, I have "half completed" the process.
So far..

I retrive pairs of orthologous DNA sequences from genbank using Biopython package.
I translate the orthologous pairs into peptide sequences and then align them using EMBOSS Needle program.

I wish to..

Transfer the gaps from the peptide sequences into the original DNA sequences.

Question
I would appreciate suggestions for programs/code (called from Python) that can transfer gaps from aligned peptide sequence pairs onto codons of the corresponding nucleotide sequence pairs. Or programs/code that can carry out the pairwise codon alignment from scratch.

Why don't you simply align the nucleotide sequences in the first place? Just use any alignment software.

Codon alignments serve a purpose, only this way you can obtain values of non-synonymous (dN) and synonymous (dS) rates of mutation.. which can then be used to obtain the dN/dS ratio used to infer selection

You can do that easily enough from the DNA sequence, no need to translate. Just align and read the codons from the alignment. You seem to be complicating your life needlessly. That said, this is probably too computer geeky for this site and you would be better off asking on biostars.

Anyway, I would simply create a hash (a dict I believe they're called in Python) that links each amino acid to its codon. Then, once you have your alignment, read it and use the dict to translate back to the original codons inserting the gaps as you find them.

This question appears to be off-topic because it is about programming and not biology. Bioinformatics questions are on topic here if they are about the underlying concepts, you are asking a very technical issue whose answer will be code.

Good point on the "too technical", hmm although I have seen various technical questions regarding software as well as lab protocol. Also if I did indeed use DNA alignments wouldn't I get overlapping codons due to gap sizes that are not a multiple of 3? I am doing codon alignments as it is standard procedure for dN/dS analysis - here is an explanation: http://www.hiv.lanl.gov/content/sequence/CodonAlign/codonalign_explanation.html

I am quite familiar with it, thanks :). I did my PhD on comparative genomics and reconstructing evolutionary histories, I've done more alignments than I care to remember. You need to know whether two codons are synonymous or not in order to get the dN/dS but not necessarily to translate them, it's just an easy way to check. Anyway, using my dict suggestion this is pretty trivial. Feel free to @ping me in [chat] if you need more help with it.

Store the genetic code in a dictionary; Use some default codon for each amino acid use --- for a gap denoted in the peptide sequence by -.
The way to do it in python is:
gcode={}
gcode['M']='ATG'
gcode['-']='---'
... and so on
Then split the input sequence ans look up for each letter in the dictionary

The basic process would be (in pseudocode, I don't know python well enough, I'm a Perl geek):
$seq1=ATGCCAGGCTGA
$seq2=ATGGGACCATAA;
for ($i=0;$i<length($seq1);$i++){
   codons1[$i]=amino_acid
}
for ($i=0;$i<length($seq2);$i++){
       codons2[$i]=amino_acid
}

At this point you will have two arrays or hashes or tuples or dicts or whatever holding the amino acid that corresponds to each codon position of the input seqs. You go and do your translation and dS/dN thing and you can then use these lists to map back to the original nucleotides:
for ($i=0;$i<length($ProteinSseq1);$i++){
  print codons1[$i]
}

You will need to adapt this to deal with codons correctly (i++ will only increment by one, you need to extract the triplets) and then to read the gaps but these are all programming issues that have nothing to do with the biological side of things.


text:
Indian snake ID
I saw this snake being attacked on the ground by a dog and it escaped up a tree with amazing rapidity. Can anyone help with the ID? It was maybe nearly a metre long. Seen in Rajasthan.

Quite hard to ID without being able to see the pattern on the dorsal side.


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Did predators evolve eyes first?
I'm an engineer and biology is my weakest point, so please forgive if this question is dumb.
Lately I've been wondering, "Why do animals that have eyes tend to have exactly 2 of them?" The closest related answer I can find is that 2 eyes provide depth perception. However:

That answer really only answers why animals have more than 1 eye; it doesn't say why animals have 2 (as opposed to 3, or more); and
Depth perception can only explain animals near the top of the food chain - wolves, bears, humans - but not animals closer to the middle of the food chain - penguins, squirrels, or fish.

Predators typically have depth perception. Prey typically do not, even if they still have 2 eyes. I'm painting an entire kingdom in broad strokes, and obviously there are exceptions. Big sharks are pretty close to the top of the food chain, but they don't seem to have depth perception. (If they can turn their eyes 90 degrees forward they might get depth perception, but only over a narrow range. I mention this because I read a statement that animals with eyes on the sides of their heads have more depth perception, but I don't see how that can be true.)
This shortcoming of depth perception can be overcome if predators evolved vision first, and then some of their descendants evolved into predators while others evolved into prey.
So here's my question:
Did (near) apex predators evolve vision first? Or, is there any evidence to suggest that that's what happened?

2 eyes, one on each side of the head allows perception of a 360-view. This is common in prey animals.

Additionally: Prey animals also need some food, take penguins for example. They need to fish, in order to be successful, they need 3D information. Also this is very useful for perception of their environment.

Bilateral symmetry is pretty ancient, and 2 eyes may just be a natural consequence of that. It's likely useful enough that both predators and prey can get advantages from it.

2?  eyes have evolved many many times. When eyes first show up in the fossil record a lot of things have them some have 2 some have 5

"Why do animals that have eyes tend to have exactly 2 of them?" I think this is a wrong assumption. Most species probably have a different number than 2. Did you know that bees, flies, and wasps typically have five, not two, eyes?

Your focus on depth perception seems very terrestrial-centric. It is less important if you do not need to leap and the types of animals with the first vision would have been aquatic.

I'm also no biologist, but equivalent to the question about two eyes probably is the question about (most) animals being symmetric. Also it seems I recently discovered that hornets have three smaller eyes on the top of their heads (see also http://www.hornissenschutz.de/grbilder/ocellen3.htm); why three? ;-)

"I read a statement that animals with eyes on the sides of their heads have more depth perception, but I don't see how that can be true." I think what you read was regarding hammerhead sharks. Their elongated head shape gives them better depth perception than other sharks that have eyes on both sides of their head. (https://science.fau.edu/shark_lab/pdfs/mtk09.pdf#:~:text=Several%20factors%20that%20influence%20the%20evolution%20of%20the,and%20is%20consistent%20with%20the%20%E2%80%98enhanced%20binocularfield%E2%80%99%20hypothesis.)

Short answer
Complex eyes may have evolved first in predator species, specifically in box jellyfish. Trilobites are another group of animals where complex eyes may have evolved first. The trilobites covered a vast range of species in many different flavors, with variable life styles and variable diets.
Background
The biggest question here is what is vision? If you call the sensation of light vision, then vision evolved perhaps 1.5 billion years ago (Williams, 2016) as a mechanism of phototaxis in unicellular, photosynthesizing microorganisms (prokaryotes); phototaxis being the moving towards light (Jekely, 2009). Also negative phototaxis existed early, as a protective mechanism against too much illumination. The present day relatives, tiny single celled algae, even have what you can call eyes, namely orange-colored eyespots (Fig. 1). These pigments, however, do not collect light, but block it to give direction to light. From there on evolution of vision becomes a much more complicated matter and can fill libraries.
Nonetheless, I think that's exactly what you are interested in since you are talking apex predators, i.e., I reckon, multicellular creatures, perhaps even with furry or feathered coats and clawed paws. If that is what you are looking for in terms of vision, we are further down on the path of visual evolution.
Cnidarians such as the box jelly fish are relatively primitive species that feature eyes (Fig. 2) and are thought to have appeared in the Precambrian Period between 635 and 541 million years ago. The trilobytes, marine arthropods, also featured relatively complex eyes (Fig. 3) and first appeared around 521 mln years ago. I think, from a quick search, that these taxa are among the first to have featured complex eyes (Williams, 2016). Both the cnidaria and trilobites (why I keep on typing trilobytes, I must be geeked) are considered predators, but trilobites may also have been detritus feeders, scavengers or even filter feeders. The cnidaria have their hallmark nettle cells with which they can paralyze their prey. Since the Cnidaria precede the trilobites, and are considered predators, I reckon we can hypothesize that complex eyes evolved first in predator species, although some attribute the first eyes to the trilobites.
References
- Jekely, Philos Trans R Soc Lond B Biol Sci (2009); 364(1531): 2795–808
- Williams, Eye (2016); 30(2): 173–8

Fig. 1. Eye spots in Euglena cells. source: ThoughtCo

Fig. 2. Eyes in a box jellyfish. source: box jellyfish

Fig. 3. Trilobite fossil showing its insect like eyes. source: Museum fur Naturkunde, Berlin

These images are great nightmare material.

Importantly, cnidarians have more than 2 eyes. Having 2 eyes is more a consequence of bilateral symmetry as all animals with bilateral symmetry have approximately 2 of everything.

@BryanKrause very wrong, some of the first bilaterally symmetric animals with eyes have 5 eyes, 3 eyes, or 2 eyes.

@BryanKrause Yes, and there many examples of extant bilaterally symmetric animals with > 2 eyes, eg many spiders have 8. Eyes have evolved independently something like 22 times, so there is vast variety that eludes simple generalizations.

great, now I want a 100 trilobyte drive...

Mostly a great answer, but Euglena are no more the "present day relatives" of photosynthetic prokaryotes than we are.

AliceD's answer is great but just to address your points 1 and 2.

Eyes are expensive. From a study on fish loosing their vision in caves.

The cost of vision was calculated to be 15% of resting metabolism for a 1-g fish, decreasing to 5% in an 8.5-g fish as relative eye and brain size declined during growth.

Why would prey animals/middle of the chain animals not want depth perception? Squirrels certainly need it for their acrobatics!

Finally, from this answer, you don't always need two eyes/overlapping vision to get depth perception.

I was told by a coworker who had lens replacement eye surgery that he was told that he would be really hungry for a while since his brain would be unaccustomed to processing all the extra visual detail. And he said the doctor was correct. Apparently it far surpasses the clarity he had with glasses.

Eyes evolved multiple independent times in convergent evolution.
Almost all the vertebrates have eyes. Those few that doesn't lost their eyes through evolution and live in deep ocean of in caves where there is no light.
Going back from vertebrates into other chordates, we note that tunicates have very simple eyes in their larval stage and lose them as adults. So, it is likely that the common ancestor of vertebrates and tunicates already had eyes. Going back into the evolutionary tree, lancelets have very simple eyes and have more than two, so it is here that things start to get interesting.
Going further back into the evolution tree, we look into other deuterostomes, where we find equinodermatas and hemichordatas, which does not have eyes.
So, the common ancestor of all chordates should have primitive eyes. Those became more complex as they evolved until the appearance of the first fish.
Parallel to that, in convergent evolution, Panarthopodas (arthopodes, tardigrades and onychophora) also developed eyes and some mollusca too. So, eyesight evolved at least three times (likely much more) independently in the animal kingdom except if this was a crazy result of horizontal gene transfers (which is possible due to participation of viruses and parasites doing strange things, but still unlikely).
Also, some jellyfishes also have eyes and some nematodes and annelids also sense light, but they have no eyesight yet.
Let's focus on chordates. The primitive eyed chordate probably had a very poor and simple vision, like lancelets do today, and likely fed on plancton and detritus living in the late Eadiacaran or early Cambrian, it could also eat small invertebrates. The line between sensing light and having true eyesight is blurry, but it was crossed somewhere by an early chordate. Also, the animal kingdom was very poorly developed at those times. So, it was in fact a predator, but not in the sense that you were thinking, it was not anything similar to apex predators we have today, since even a herbivore animal is also a predator of plants. Also, the apex predator at the time were probably jellyfish, which never developed eyesight because they lack brains, only having very simple and rudimentary nerve networks.
In fact, a couple of years ago I had read out somewhere (don't remember where though) that one hypothesis about what triggered the Cambrian explosion was the evolution of eyesight in animals starting an arms race. This could make many animals orders coevolving really fast or become extinct, and even plants would also quickly evolve spines, toxins and thick protective coats against better herbivores, leading to a Cambrian world much different than the previous Eadiacaran world.
So, no, the eyes didn't evolved into a predator because it was a predator. The first eyed animals had very poor eyesight without any depth perception. It likely evolved firstly to avoid the sun, or to locate the sun and floating algae, avoid dangers (including predators) and to better locate food (which is not the same thing as hunting, since searching for cabbage is not what people would call as hunting). But once it developed, it started to evolve quickly both for predators and prey.
After the first fishes appeared in mid-Cambrian, those who tended to be prey needed to scan the environment better to detect, evade and hide from predators and they did that by gradually moving their eyes to the sides of the head. Those who were predators, needed to attack the prey precisely in order to ensure it won't escape, evolving better depth perception with binocular vision which is better done by having both eyes in the front of the skull. Invertebrates with eyesight did roughly the same thing. So neither the evolved first, they both co-evolved together. Or if one did evolved first, it was by a very small margin. Also, since the first sighted animals had very poor eyesight, they could not perceive depth, that only came after some reasonable eyesight was evolved.
Also, flying animals, even when being prey, also needed very good depth perception without losing panoramic vision, which they attained by having very specific head shapes. But this only happened much later, roughly into late Silurian or early to middle Devonian for insects, into the late Jurassic for pterodactyls, into the middle Cretaceous for birds and middle or late Eocene for bats.
Animals and plants without eyesight were limited in developing toxins, poisons, carapaces and spines as a defense, but some sighted animals needed to develop those too as protection from predation.
A few references
https://www.jstor.org/stable/1311112
https://royalsocietypublishing.org/doi/10.1098/rspb.2014.1729
https://evolution-outreach.biomedcentral.com/articles/10.1007/s12052-008-0085-0
https://www.nhm.ac.uk/discover/eyes-on-the-prize-evolution-of-vision.html
https://www.nature.com/articles/srep02751
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3783037/
https://www.sciencedirect.com/science/article/pii/S2667242122000203

The reference link dump format isn't very useful to someone hoping to better understand aspects of your answer. Better to connect specific statements to specific points made.

@BryanKrause I just joined this community today, I am still not used to the style of this one. I will try to edit that though.

Understood, I appreciate your efforts very much, I think it'll be an excellent answer especially for your first contribution here.

@VictorStafusa-BozoNaCadeia if you click the edit link on either mine or AliceD's answers you'll see how we've linked specific points to references. You can do that yourself when you edit your answer by highlighting a piece of text, then clicking the "link" button in the editor, and then pasting the link. You'll end up with a hyperlink on the text you highlighted.

For example you might link within the body of your post to a popularized account of the role of eyesight theorized to connect the Cambrian explosion to brain development, or link to peer reviewed scientific literature on the subject.  Help your Readers by describing what they might expect to find by following your links.


text:
How does a trait become heritable?
How does a trait become associated with genetic loci?
It is possible for a previously negligible trait to become heritable.
For example, some phenotypes are under sexual selection, but clearly were not always under sexual selection (such as the Peacock's plumage).
How do traits like this become heritable?
If a parent favors offspring with traits that the parent shares, would this cause these traits to become heritable?

Ok, I see why this was closed, but this is a valid question. For example, see: https://en.wikipedia.org/wiki/Sexy_son_hypothesis https://en.wikipedia.org/wiki/Fisherian_runaway

The whole question is based on the assumption that it makes sense to talk about genetic trait, while it is actually a little bit undefined. The closest existing concept you might want to read about is the concept of heritability. Please see my comments in your text and especially the links on heritability.

Evolutionary psychology and genetics how does a trait become genetic

I don't understand why you are talking about evolutionary psychology in your title. The rest of the post seems unrelated.
As you have received a downvote which might be related to your title, I have now edited your title.

How does a trait become genetic?

It is unclear by what you mean here. But you should probably read about the post Why is a heritability coefficient not an index of how “genetic” something is?.

If a trait is passed down from parent to offspring how is it made that the trait is passed along as heritable.

Again, this is unclear. From the above link post, if at least part of the variation for a phenotypic trait is caused by genetic variation, then the trait is heritable (heritability differs from zero). If a trait is heritable, then parents and offspring will tend to look alike (see Why does the slope of parent-offspring regression equal the heritability in the narrow sense?).

If a woman is similar to her mother and she is sexually selected on this basis. Would this make the trait become genetic?

I don't understand why you are talking about sexual selection here.
Note that selection act on population, selecting specific genetic variants. Talking about an individual being selected just mean that the individual is carrying the genetic variant that is associated with higher fitness in the population.
Note also, that without heritability, there is no selection. You should have a look at Lewontin recipe, for example at the post How does Darwinian Evolution work?.

Parent favors Offspring with traits that they have that are similar to their own selves.

Do they? In humans? In other species? It would require a reference to really what process you are referring to and whether it is actually true.

Would this make it genetic?

Again, this is unclear unfortunately.

How a trait becomes heritable is a topic in evolutionary psychology, which is probably why they're mentioning it.


text:
Why are there only 3 types of data (0,1,2 ) in some GWAS tables?
I am wondering about the format of raw genotyping data in a GWAS article published on 21 December 2023, the supplementary data contains a table named "Diversity_genotyping_raw" (inside Supplementary Data 1), which is shown below:

The table contains samples as the leftmost column, with the Affymetrix array variant specifiers as the top row.
It seems to be the single nucleotide polymorphisms among the varieties used in the experiment.
My question is: why are there only $3$ types of data ($0,1,2$) in this table, while there are $4$ nucleotide types?

@David I've edited it a bit to see if it might help the question

@BigMistake — That's good. That's how SE is supposed to work, allowing questions to be improved by editing. Thank you. I'll delete my previous comments.

Yes, that's an interesting question. The short answer is that most variants only have two alleles, and even though you can be heterozygous at a position in two different ways, both of these result in the same genotype.
We can have A, T, C, or G at a position.
Since there are two chromosomes, we could have many genotypes: AT, AC, AG, CG, GC, etc. However, most of the base pairs in all mammal species are the same. Only a small fraction have even one alternate allele. That is, most positions just have one letter in them in all humans (and animals), and there isn't any other letter anywhere in the population to make an alternate genotype. However, sometimes there is this extra letter available in the population. This is what we call a "variant." Since this is somewhat rare for there to be a variant at a position, it is even rarer that there are more than one variants at a single position. GWASs therefore usually only consider the case where there is one variant. That is, there are two possibilities for the DNA "letter" at that position.
Let's imagine these are C and T. The possible genotypes are C C, C T, T C, and T T.
T C and C T are the same genotype, because they both have 1 C and 1 T.
This means that there are three unique genotypes for the case where there are two variants. This is where the 0, 1, 2 coding comes from. 1 refers to the heterozygotic position (C T or T C, in our example).
In reality, it is possible to have more than two variants. These are called multiallelic sites, and they are not uncommon, but they are rare enough to not be worth the trouble of including in GWAS, so they are either excluded or split up into multiple alleles, each with two variants. There is some work on modeling these more effectively.

Thank you very much for your answer. This leads to another question: why is it that in some database (for example https://www.ncbi.nlm.nih.gov/genbank/), only one nucleotide sequence is included while there are 2 chromosomes?

@anonymous67 Look at BLAST. When dealing with different species, or the whole genome of a species, it's easier just to have one copy as the variants are rare. It's just a choice. Some databases don't require variants for the analyses which require alternate alleles


text:
How do insects survive the winter?
I had an interesting discussion today in which the question arose how insects survive in the winter. Since they need a high enough external temperature to be active, this seems a bit difficult in the winter. With frost they should completely freeze and I don't think they will survive this. Do they rely on eggs laid in the fall (which have to survive freezing temperatures as well) or do they employ other techniques for that?

As there are many insects, there are also a number of different strategies. As you already said, insects depend on the temperature of the environment and cannot produce enough heat with their metabolism. The major strategies are:

Migration,
Communal living
Cold tolerance (by means of antifreeze proteins)

Only some of the insects can opt for " Migration" , those which are big enough to travel long distances. A good examples for this migration of insects is the monarch butterfly which migrates from summer habitat in the north-eastern US and southern Canada to Mexico in the fall. Using this strategy, the insects avoid life-threatening temperatures.
"Communal living" helps insects to get over the winter, as the colony produces enough heat to survive. A prominent example are bees, which maintain relatively high temperatures in their hives; another would be ants.
"Antifreeze proteins" are also employed by a few. Some insects contain special proteins or glycerol in their hemolymph (the equivalent to blood) which either prevents it from freezing and/or prevents the formation of ice crystals which destroy the cells. An example for such an animal would be the New Zealand Mountain Stone Weta which can stay frozen for months until the temperature gets high enough for living again. Some insects go into some kind of winter sleep, in which they survive the cold temperatures. Their living cycle is synchronized with the seasons of the year.
The answer is based on this and this article, have a look for further information and references.

The above answer is perfectly correct...except it deals with mainly ectothermic insects...now there are some endothermic insects as well..& many of them adopt this following curious technique to elevate their body temperature....
Here the hawkmoth's capacity to elevate their body temperature depends on their powerful flight muscles which generate large amount of heat during when operating. The insects use shivering to warm off before they take flight..they contract their flight muscles in synchrony before flight, so that only slight wing movements occur but considerable heat is produced. Chemical reactions , & hence cellular respiration speed up their warmed-up flight motors enabling them to fly during cold days & even during night....

Also some endothermic moths take help of 'time-trusted' countercurrent heat exchanger, that helps to maintain a high temperature in thorax...where majority of flight muscles are located...thus maintaining a constant temp. of about 30 degree celcius at the body core when the outside temperature is,sometimes ,even near subzero...

Also...this particular mechanism is applied by insects & animals...ectotherms & endotherms alike...
Introduction of cholesterol in the cell membrane thus hindering solidification at low temperture by disrupting the regular packing of phospholipids...

please don't just copy and paste from a source, especially if you are not crediting them (http://insects.about.com/od/adaptations/p/wintersurvival.htm) see the help pages on how to write a good answer

Sorry...I'm changing my answer...& this time it's not a copy-paste...

Well, these are some nice pictures, but your answer has nothing to do with the actual question. Do insects use this mechanism survive the winter? As far as I know, they don't. If you want to correct minor issues in an answer, please use the comment function.

@Hav0k , just look up the highlighted points...


text:
What does `knee atlas` means in an IEEE's paper?
I am referring an IEEE's paper for my project which has a term called knee atlas, I am not getting the exact meaning of this term, does they mean it a processed image or something else? I am working in matlab and here is the paragraph of IEEE's paper:

Six atlases were derived from 3-D DESS WE series from six subjectswith visually normal knee images ... The series for three of these atlases were selected from the public release OAI image dataset 0.D.1 and three were from the baseline pilot study. Trained human observers created the knee MRI atlases using manual segmentation.

Could you link the article or provide a full reference? An excerpt out-of-context is difficult to interpret. For example, we might need to know what OAI means.

The knee atlas is an MRI generated with the intent of identifying anatomical features, much like this.


text:
Where can I find DNA Sequence data for colon cancer
I am a computer scientist studying pattern recognition, and I am hoping to do some supervised learning on colon cancer.  Unfortunately, I'm having a heck of a time finding DNA data in the following format.
Benign DNA (Adenoma?)     Malignant DNA (Carcinoma?)
A                         A
A                         A
T                         G
G                         G
C                         C

So I just need two columns (don't care if it goes down for 3 billion records/ amino acids): one with the good DNA and one with the bad.
Is there anywhere I can find data in that specific format?

Did you checkout dcc.icgc.org? I think unlikely that someone will have the data formatted precisely the way you described, but you should be able to reformat it to suit your analysis pipeline. What you can download from there is a VCF file which only lists the positions in the tumour where it differs from the Normal so if you really want the entire genome file you would need to start with the human reference sequence, and change the sites to match the annotations in the VCF file. N.B. the will not have a comparison between a benign and a malignant. just tumour vs. normal

You may try the data for "Colon Adenocarcinoma" made by the TCGA project:
http://gdac.broadinstitute.org/runs/analyses__2015_04_02/reports/cancer/COAD/
The file with mutations called by the tumor against a matched normal,
http://gdac.broadinstitute.org/runs/analyses__2015_04_02/reports/cancer/COAD/MutSigNozzleReport2.0/COAD-TP.final_analysis_set.maf
What you need are column 11, 12 and 13. Column 11 is the reference allele (your so-call good DNA). For each row, the alternative allele (bad DNA) is column 12 if column 12 does not equal column 11, otherwise it is column 13. -- It would be a piece of cake to make by coding :)
In case you are interested, column 16 and 17 are the tumor and normal sample IDs.

THANK YOU!!!  This is exactly what I need, and thank you for making the field references easy.  I'm using R to extract the .maf format, so I very much appreciate how much easier your answer makes the data understanding.  Thank you as well for the insight into columns 16 and 17.  Really, very helpful, thank you.

You're most welcome! Here is more information about the .maf file, https://www.biostars.org/p/69222/ , though it might be a bit biology intensive.

One quick question about that data: a couple of the alleles (records for the alleles) have more than one letter.  Do you know what that is about?  Just want to know if I should record it as an A, T, G, or a C.  Thank you so much again.

Those are indels (insertions or deletions) that involve multiple nucleotides. The rest are so-called SNVs, single nucleotide variations. Splitting and merging over indels/SNVs is a common practice in data analysis.


text:
Has perturbation theory been applied to mutation process frameworks?
For example, imagine this Feynman diagram:

This is analogous to mutational homoplasy.
When comparing haplotypes, there are many possible tree topologies. Under maximum parsimony, we ignore suboptimal tree paths which certainly occur sometimes in reality. For example, imagine the following two haplotypes:
1: C A T T G
2: C A T A A
There are two mutations that make these different.
Maximum parsimony may infer this intermediate, not directly observed haplotype:
C A T A G
If we move from 1 to 2, the tree looks like:
C A T T G --> C A T A G --> C A T A A
However, the following is also possible:
C A T T G --> C A T A G --> C A T T G --> C A T A G
Or:
C A T T G --> C A T T C --> C A T A C --> C T T A C --> C A T A C --> C A T A C --> C A T A G
The not-directly-observed haplotype is analogous to the virtual particle. The directly observed haplotypes are the non-virtual particles. One could construct Feynman diagrams that look similar except have haplotypes instead of particles.
It is possible to imagine that some less-likely haplotypes actually are more harmonious with the observations. It seems that perturbation theory may help.
I don't have completely formalized thoughts on this. I am wondering if this has actually been used before to make a mutation process framework (e.g., an improvement to the infinite alleles model).

@David Thanks, fixed. I try to follow the rules but I don't know what all of them are yet

No problem. The way SE works as a question and answer site is a bit hard to fathom initially, but I hope you persist as your expertise can clearly be of benefit. One key thing is that it is not a discussion site with a dialogue between someone with a question and someone who has an answer. The questions are supposed to be of use generally (and some of them are), discoverable by web searches. And that is why you find reference to the OP (original poster), acknowledging that a question may be edited and that it doesn't "belong" to whoever posted it, but the group in general.

this is basically the argument behind maximum likelihood tree inference. Parsimony can lead to a lot of issues, as argued in the classic Felsenstein paper (linked).
Here is a brief paper discussing a particular improvement to the max likelihood method for tree inference in which substitution rates among sites are allowed to vary, which is another critical factor affecting tree topology estimation in a ML framework that can lead to the different mutational paths you show. I think it's a good entry point showing the value of ML over parsimony in incorporating multiple possible mutational paths with different interpretations (topologies).
If you are talking purely about cases in which the infinite alleles model isn't appropriate, I wrote a review on this topic a few years ago (see box 1 for some mutational paths very similar to the one that you present).
I am not sure how perturbation analysis fits into this or what the Feynman diagram means.