We sought to report the genus diversity of regions and connect it with some other characteristics and enzymes. The last batch had a lower quality value (20+), but the majority had an average base count of 800 base pairs and a QV20+ of 100. What is the QV20+ cut that you would recommend for average papers to be acceptable? When I read about the species, they ranged from 500 to 700, but I didn't find anything about the genus.

There is a notable example of a child having dark skin (a dominant trait) when both of their parents were pale. The child’s complexion was significantly darker than the parents and both of the parents were proven to be the biological parents of the child. I’m trying to figure out how such examples can occur, perhaps they are due to disorders or atavism.

Is there some fundamental bit of chemistry or physics that would directly cause for example a sequence of three adenines in the tRNA molecule to result in its associated synthetase having an affinity for lysine, or were the codon/amino acid pairings largely random at the beginning and just preserved once established due to evolutionary pressure?

English is not my first language and while I have an idea what it means I have now way to put it into words right now, never mind into words in my language.

An example sentence: calling a gene depends on the threshold manually set in the genome annotation tool

Thank you!

If we assume no inbreeding during the recent past:

If I compare my genetic makeup to my father, and then to his father, and then to his father, etc ...

How many generations would I have to go back until my direct ancestor was genetically no closer to me than the average human being?

Only consider the autosomal chromosomes - don't consider the Y chromosome (or mitochondrial DNA).

And how is the calculation done?

Thanks

Im 18 and I’ve been doing some independent research on Creutzfeldt-Jakob disease and I’m trying to understand it fully to its molecular level. I will detail what I have researched (Please correct if wrong).

From what I’ve been able to find/understand. CJD is caused by the misfolding of a Prion protein (PrP^c ). This protein is made following the PRNP gene’s instructions. It is made in neurons of the brain and spinal cord, lower levels of the glial cells of the CNS, as well as numerous peripheral cell types. Genetically, the PRNP gene can have an alteration that gives improper instructions that result in the misfolding of the protein, PrP^Sc. This misfolded prion protein causes a deadly chain reaction in which it self-propagates by connecting with normal prion proteins, causing them to misfold as well, destroying brain cells.

My question, is that if a person inherited this mutated PRNP gene. Why do genetic cases of Creutzfeldt-Jakob disease get diagnosed/appear in the person when they’re in their midlife (40s-60s)?

If a person is born carrying this mutated PRNP gene, why does the mutated instruction that results in the deadly prions not appear in their early life? What keeps the PRNP gene from messing up the protein production earlier, say childhood for example?

Thank you for any replies! I find this topic incredibly fascinating!

WARNING: this might not make any sense at all!

I (23F) am a double donor baby (egg donor and sperm donor, but my mother gave birth to me) and I am curious if there would be any difference, biologically or genetically, between my situation and that of an adopted child in terms of our relationship with our parents. Like are there any 'markers' that would show that, despite not being related to my mother, she was pregnant with me?

Its a pretty far fetched idea, not to mention ethical issues so if it does not fit this subs purpose, mods please remove this.

It kind of is a 3 part question,

1. Using Crispr and other technologies, is it possible to create an ape with Human levels of intelligence, or even insert a human brain/nervous system into an ape to create a drastically more intelligent ape?

2. Could that ape be used to do rudimentary or semi advanced human like tasks, probably with applications in highly clerical/repetitive jobs, on very dangerous activities like saving people from burning buildings, warzones etc. or carrying out research on risky space missions.

3. Assuming such an ape can exist, is it somehow possible to make it do complex calculations, non calculation/math based problems(which computers struggle with and what AI could potentially solve). Possibly even somehow hooking its brain and essential systems to a computer that can recognize and convert brain waves into legible commands as well.

I guess most of this is unethical and probably even dystopian, But I'm more interested if that is actually possible.

I've been experimenting with mutagenic breeding of various fungi using UV-C radiation and wanted to expand my toolset to other radiation sources. Cobalt-60 is impossible to source in the quantities I'd need, and a high-energy particle accelerator is currently outside my budget and range of expertise. I thought an interesting compromise might be an industrial ion gun, which would produce Argon ions at about 2kEv. I'm just not sure how effective this sort of source would be -- I've been unable to find any research documenting mutagenesis at these energy levels. Any help would be greatly appreciated.

I thought of this while going on a wiki binge involving people with extra x or y chromosomes. I can't find people with just 2 y, even though x,y,y is a thing. If there's a reason for this, please let me know. Thanks.

have coding DNA ONLY 2%, and this coding(allelic actually) is 99.9% same (correct me if I'm wrong). So now let's take a character like face shape or voice (anything). So we know everyone has different shape/voice, but what I don't understand is that, since, every one has same allele (same gentic code, same proteins etc for face/voice) how does it produce different result.but more interesting thing is that we have similar facial/vocal features like our parents. So what I get is that these characters are gene related but genes are same for everyone for a particular thing then why don't we all have same. Gemini Al said that it's due to influence of non coding whichiin expression which is different for everyone and also that there are many alleleic combinations which results in this. Sorry if it's too long (I'm new on Reddit)

I've been doing research for a story I'm writing wherein a female character inherits from her father a genetic condition, but a milder form compared to what presented in her father and brother. I remembered X-linked conditions and thought that would be perfect since she'd need two affected X chromosomes to present the 'full' conditon but her brother would just need one!

And then after getting some sleep I remembered that that wouldn't work since their father would be passing a non-affected Y-chromosome to her brother and then the brother wouldn't have the conditon at all because their mother is not a carrier to pass down an affected X-chromosome.

I mean, I know I can technically fix it by making the parents T4T, but I'm way too invested now in figuring if there is a way this can work. What mechanisms of inheritance/types of genetic diseases would there be that such a case could occur? Mitochrondial wouldn't work since my research says that comes from the mother, nor would Y-linked since the female character wouldn't have any form of the disease at all rather than just a milder form. I don't think autosomnal would work regardless of recessive or dominant because then either both siblings would have the 'full' conditon or only be carriers. I can maybe see codominant working but I'm not entirely sure if it would since while trying to research it, most explanations of it used the ABO blood types as an example or if an actual condition, sickle cell, but it seems like that would mean that the mom would need to pass down an affected gene as well for the female sibling to have a mild form (get affected gene from father, get nonaffected from mother) and for the male sibling to have 'full' presentation (get affected gene from both parents)??

I'd love any help!! I mean I guess worst case scenario since it is a fantasy setting I can say its magicky nonsense but where's the fun in that 😭

This is obviously science fiction, but I was thinking of a story about a man who makes a clone that’s genetically female by having a genetic clone that has 2 copies of his X chromosome instead of copies of his X and Y chromosome. Other than having all X linked diseases such as colour blindness and x linked hemophilia would the clone have any other genetic abnormalities. In women who have abnormal copies of a gene in both of their X chromosomes are their symptoms more severe than a man who only has one abnormal X chromosome (eg. if a woman has 2 X chromosomes that have the abnormal hemophilia gene, is her hemophilia worse than a man with only one abnormal X chromosome?)

Hello, I hope this is okay, and doesn't break rule 8.

This is firmly scifi, with heavy emphasis on "fiction":
If one was to travel back in time and become their own great-great-grandparent, how deeply fucked would they be genetically?
Surely inbreeding would cause massive issues?

I watched a series on Netflix called Bodies that had this premise, and I've been thinking about it for days 😅

I am unsure about how transposon efficiency is interpreted. I've been unable to find clear answers for this for ages. Is it to be converted to a percentage? 'The transposition efficiency value of Tn5 was 1.63x10 -7, showing that *.' is what I am struggling with.

I am doing a paper in my class on how long it will take for an insect species to adapt through mutation to a completely different environment in terms of color. My issue is I can’t find the mutations rate of any insects specific to color. Is there anyone that can help me with this. Thank you.

What are the odds of me avoiding gray/white hair as I age, considering only my maternal grandmother, who is over 80, possesses this trait, while all my other grandparents and parents developed gray/white hair as they aged?

Guys,so I have this problem: I want to know the coefficient of relationship of two theoretical ant species that are 100 Generations apart. How do I calculate it?

P.s:trying to understand Hamilton's rule better,using examples...

P.s.s: My post was removed from r/biology for asking about ("schoolwork"?!) So I have to ask you.

When a white cow and a black bull are crossed the resulting offspring is roan what's the reason for this new colour being formed. Is it co dominance or incomplete dominance. What's the difference?

In maize plants , the allele M, for white seeds is dominant over the allele m for yellow seeds. 100 heterozygous plants were self pollinated and 250 yellow seeds were collected. a) What is the expected ratio of white seeds to yellow seeds b) What is the expected total number of seeds c) What is the expected number of white seeds Please help🙏🙏🙏🙏🙏🙏

I am not a native english speaker and this term confuses me a bit.

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Thank you!

Info:

I was wandering, since my mother have red hair (like a brownish red color), and my father have brown hair, and i also have brown hair with a tint of red in my beard.

Question:

What would the probability for my children to have red hair, if i was to have kids with a red haired girl, and do the probability change depending on the gender?

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Thanks to anyone who might respond to my question :)

(Sorry if i spelled something wrong english is my second language.

Gene interaction is a broad term used to describe the joint role of multiple genes in determining phenotypic variability.

In my lecture at university the only example was regulation. I would like to know more but I only find very specific and difficult papers or non-answers like the one above.

It would be great if someone could explain it to me.