When I was studying genetic markers and the bandings on chromosomes, I had myself partially lost.

Though I am familiar with the nomenclature of genetic markers, I am unfamiliar with what the decimal points refer to. For instance, -q25.2 or -q23.3 attached to the numeral (autosome chromosome) or character (sex chromosome) of the chromosome. I am just not understanding the .#.

To ask another question, what do each of the band marks refer to or represent? Do these band marks refer to a certain trait or gene?

Is it possible to calculate the Fst of a population dataset containing subpopulations when all that is given is the observed heterozygosity?

I'm not going to post it yet, but I have a potentially world altering theory about genetics. I'm a guy with 0 creditintials, and I think that's one of the reasons this might be huge.

I suspect yall have been on the right track mostly, but not 100% I've avoided reading anything myself about genetics because I like approaching a problem with a blank slate, so my thought process isn't poisoned by another's ideas.

I have been thinking for years about how genetics relates to one problem, and I had a bit of an epiphany about how genetics relates to literally all of the strife and chaos going on in the world at the moment.

Today might be the day the world starts to heal.

If your car's is broken and wont drive, would you spend time polishing the windows or fixing the doors? Of course; Neither. You’d go straight for the engine, right? Some things simply have more impact than others — especially when it comes to longevity.

Trends in health range from eating algae with some even suggesting you should eat Ashwagandha all the way to decoding our DNA. Think about it this way: not smoking will probably add more years to your life than taking a daily Ashwaganda or algae. Now of course these are not mutually exclusive, you can both not smoke and eat the right supplements. But following this argument there are billions of things we have to do to increase our longevity, supplements, treatments, therapies and so forth.

Let’s shift the conversation to what is high impact, and therefore genetic conditions. If you look at the statistics, it is crazy. For example, familial hypercholesterolemia affects 1 in 250 people, over 90% are undiagnosed and unfourtnantly the first symptom may very well be a heart attack at your 40s. There are more heart conditions that have the same statistic all the way to hereditary cancer?

My question is, why are we so focused on so much small things and not our own stepping stones of life, DNA? I am working with monogenic diseases, ask me anything.

Basically the title

I've never met my uncle before, but I often feel energetic and have the need to just jump around the house like an idiot just because I can. (espescially if there's music) Apparently my uncle used to love jumping and running everywhere when he was younger, too.

My brother used to rest in the womb the same way my grandma slept. I wonder if it's correlated or just coincidences?

I am O- My parents were O+ and O- so all good. My kids dad is A+, now not one of 3 of my kids is exactly same as either of us but a mix. Eldest A- then middle and last O+ is that normal they all got mixed up? The A- caused most issues for him, cannot explain why something to do with my blood. Lost 4 pregnancies after 3rd I would think they would have given RH needle though.

Hi, is my privacy actually safe when I use 3rd party apps to analyze my genome? I had my DNA sequenced on Sequencing and have only used them to ananlyze my genome. Thinking about using one of their partners. What should I do?

if I look more like and have more characteristics of my mother then I have more of her DNA? But if I where to have a child with a man him having more of his fathers DNA, could there be a possibility that our child comes out looking like more of (the mothers) fathers side even tho I’m more made up like my mother? Correct me if I’m wrong in anyway and the science behind it I’m very interested

Just wondering if trainees would like to meet informally in groups and go around Denver!

Not sure why these groups don’t exist, but I would love to meet more genetic enthusiasts!

"Does exome sequencing offer consistent coverage and depth across both coding and non-coding regions?

Hi, I'm a master student in bioinformatics and I have a strong computer science background but a really poor biological background (i.e. I've never studied microbiology, embryology, histology...). I have a good bases in genetics, could anyone recommend me some resources/books on genetics (not just human) and immune genetics? Thanks so much in advance

It can get pretty expensive to keep getting small segments of my genome tested while not necessarily offering new direction to consider subsequent other sorts of testing, or treatment that might help.

My question is if 30x full genome sequencing would capture all the snp I want, so that if a Dr wonders if I have a variant of CYP21A2 that is associated with congenital adrenal hyperplasia (cah), that can be looked up readily, or even to actively scan through in case there are any strong genetic associations like having HLA-DQB1*06:02 ?

Or is this flexibility of a full genome sequencing unreasonable or impractical?

I

Hello! I have a male cat that is orange with white on his face, paws, and belly. I did a basepaws DNA test for him and everything made sense except for his coat color. The report said that he inherited two copies of a CA deletion in the ASIP gene, from my understanding a mutation of that type would lead to a solid coat color that is likely black. I am not super familiar with cat genetics but from my understanding it is not possible for a male cat to have two copies of that mutation and not be solid or black. So I was just wondering how this was possible? If it helps i originally fostered him with his mother and brothers, so I know what they looked like. His mother was a dilute tortie (grey and beige), one of his brothers was solid gray with white patches, one was a gray tabby, and one was identical to him beige and white. Thank you!

Hello, I recently got my DNA data from ancestry and was wondering if there are any free tools for analyzing the data for genetic health risks. I’ve seen a couple options but it’s hard to know which ones are valid.

https://preview.redd.it/cszt89gev9yd1.jpg?width=1536&format=pjpg&auto=webp&s=1937fa365f04e21a7b1f40ae16e86b1d750613fc

I'm reading research articles trying to find SNP associated with a disease and all the SNP are denoted with word rs, what does this mean ? And how to I find the location of this SNP in a genomic database?

So I’ve read several times from different sources that humans cannot technically be melanistic, there are melanism-like disorders, but no true melanism. I was wondering why? Do we just lack the pattern gene that causes true melanism (ik we don’t have many pattern genes that cause different mutations in other animals so that was the only reason I could think of for why we lack the mutation)

How accurate are the genetic testing for cancer at the hospital? Do you have to retake them down the road?

Our final project has opened for my genetics class, but I am unsure if I should stick with the topic I have been playing with or if I should find a new one. The supposed objective of the project (it’s been unclear so far) is to find a gene of interest in a particular species that is not very well studied and design our own research around the minimal research that does already exist. I really want to specialize in fish veterinary medicine one day, so I tried to focus on a fish species specifically. I originally chose SLC24A5, which is a gene on the 18th chromosome of zebrafish (Danio rerio) which acts upstream of/within eye pigmentation, melanocyte differentiation, and melanocyte migration, and potentially other things. I wasn’t having a ton of luck finding ideas so I’d love some recommendations! Should I stick with what I have, or are there any cool ideas out there that might be fun to research?? TIA

Hello everyone,

I just read an article suggesting that de Novo gene creation could occurs from intergenic DNA.

In the article this is justified by a lack of homology of a lot of "orphan genes" with current databases. Knowing that the scientific community is far from having sequenced the DNA of all existing species, do you know what evidence would allow us to believe in this specific theory of gene creation that implies hypothesis which naively seem to me more unlikely to occurs than hgt with viruses present everywhere in the environment ? Sorry if my question seems stupid.

If a specific male pattern hair loss autosome is present in 2 males, assuming similar environmental, lifestyle, and hormonal conditions, can the hair loss affect them differently?

Family tree background:

-Grandfather: X chromosome or maternal autosome

-Father: X chromosome or autosome from either parent

-Mother's side of family: Absent

My father and paternal grandfather both have male pattern hair loss. My grandfather's father did not have male pattern hair loss, so my grandfather (and his similarly male-pattern-balding-affected half brother of the same mother and different father, who too did not have male pattern hair loss), inherited male pattern hair loss either through their mother's X chromosome or autosomes. My father had male pattern hair loss, there isn't really any evidence to rule out anything except for that it cannot be from the Y chromosome given his paternal grandfather did not have male pattern hair loss. Nobody in my mother's side of family has any sign of hair loss at all so I will just rule that out.

My paternal grandfather's, my father's, and my hair loss patterns:

Grandfather:

-Started at age 34, thinning of corners and crown with everything else being relatively thick.

-At age 53, he had a mature hairline but his hair down the middle of his scalp was essentially just thin overall but no specific recession or hairline.

-Completely bald by age 60

Father:

-Started at age 20, recession of corners and general thinning of the frontal forelock but dense crown.

-Currently age 53, his frontal forelock is close to peach fuzz, his hairline is essentially on the middle of his scalp but his crown is still relatively dense.

Myself:

-Started at age 14, barely noticeable recession of right corner of hairline

-Currently age 16, my right corner of my hairline is probably about 1cm more recessed than my left corner (could be my hair styling acting some mild tension alopecia), and the area in my right corner that recessed has thin peach fuzz hair. My left corner is barely recessed and is what you would call a "juvenile hairline" while my right corner has recessed to where you could call a "mature hairline". My hairline's recession looks more like something found in my mother's side of family, where it stops at a mature hairline by the time they were in their early 20s.

Given how my father and grandfather were experiencing hair loss so differently, I was wondering if it was still possible for them to share the same autosomal hair loss gene which can be then passed on to me or if they were both just so unlucky to receive an X chromosome from their mothers containing hair loss genetics?

Hello I am in my last year of Bachelors and currently writing a thesis. I need some help in interpreting the data that I got after sequencing, making graphs and everything. I will be looking for homozygosity regions. My supervisor isn’t much of help and I couldn’t find anything on YouTube.

I am having trouble with a homework question regarding silencers. The question is:

"A reporter construct contains lacZ under the control of a core promoter, an enhanced, and a silencer. If the sequence of the silencer is deleted, but all other elements of the construct are normal, what is the most likely impact of the silencer deletion on expression of the lacZ reporter gene?"

So I was under the impression that silencers need repressors in order to silence a gene. Is this true? In that case, I don't believe that expression of the lacZ reporter gene will change since there isn't a repressor

OK, so when miosis occurs in prophase one, all homologous chromosomes cross over, sharing genetic information with the adjacent chromatid. That still leaves two of the four chromatids solely with maternal or paternal DNA. Is it POSSIBLE that when the gametes form one of the gametes will have ONLY maternal and paternal DNA? As in none of the chromatids that ended up in the gamete had crossed over AND they are ALL from either one of the parents (maternal or paternal chromatids). FURTHER, what happens if you were fertilised from two gametes of JUST the maternal or paternal gametes? would you not be a half-sibling to both your parents? I'm sorry. Finals are going crazy.

I'm going as an MSc candidate and it's my first time. Im interested in research, but also in networking and trying to find a job when I graduate. If anyone has advice on how to maximize how I spend my time at this conference let me know! (Also, does anyone know the dress code for the trainee dinner? Business or Formal?)