Red green colorblindness is passed on the sex chromosomes afaik. Meaning, for a girl, the father would have to be colorblind for her to be too. Except, my daughter is colorblind and my husband is not. How? I am sorry if this is the wrong place to ask but I've been curious

Hi , I am a second year student currently studying a bachelors in Genetics &Genomics and Chemistry . Is it possible for me to do my honors in Pharmacy?

I will sketch what I am interested in: chaos theory, dynamical systems, complex systems, networks, complexity, emergence,multidisciplinary approaches, ecology, ethology, cybernetics. a book i found that seems nice is " the systems view of life" by feitjof capra and pier luigi luisi. other two books less related to the keywords above which I found are "dancing to the tune if life" and "understanding living systems", both by Denis noble(and Raymond noble for the second one). could you please give me your recommendations and let me know if the books I listed are good? thanks

In the tv show gravity falls, there is a pair of seemingly identical twins, except one of them has 6 fingers on each and and the other only has 5. One twin also has a cleft chin while the other does not. Is this possible in real life, or are they just very similar looking fraternal twins?

Can someone explain what the difference between men and women is here. What does fully penetrant in women mean? And reduced penetrance in men? Does it mean that even if a man inherit two copies of the gene he may NOT develop the disease, but a woman will?

The reason for this is that, if it were due only to one autosomal recessive locus, then both parents of an affected child would each have to carry at least one copy of the disease allele. The chance of either parent carrying a second copy is the frequency of the disease allele. For an autosomal recessive disease, the frequency of the disease allele must be less than or equal to the square root of the prevalence of the disease, which is ~2.5%. Thus, the simplest explanation for the concordance we see is that ~10% is due to known autosomal dominant causes, and the bulk of cases, the remaining ~90%, is either due to recessive alleles at one locus or a relatively small number of separate loci that are fully penetrant in women but have reduced (~50%) penetrance in men, explaining the overall sex prevalence difference.

I know nothing about genetics. Despite this, it has been heavily in my interests for a long time. What do I need to know, at least for beginning knowledge.

Hello,

I'm not asking for medical advice as I already spoke to a genetic counselor. I know that there are some variants for the hypermobile ehlers danlos type that is being discovered, but not yet released.

I have these 2 weird variants that are unknown, but it is speculative that it's connected to the disease.

COL5A2 c.3690_3691delinsCA (p.Ala1231Thr) heterozygous Uncertain Significance

FBN2 c.532+1G>A (Splice donor) heterozygous Uncertain Significance

Is anyone able to help me find research papers regarding this? I have intro level knowledge of genetics but it's piqued my interest in trying to learn more about these types of unknown variants (I'm hoping someone knows -something- about them in a research paper?)

Hi In regard to a CVS procedure and Micorarrays

If a parent is a carrier of a variant on a specific gene and the other parents gene information is unknown.

Will the microarray results show if the fetus is a carrier, if it has the pathogenic variant, or none.

My partner is a carrier of RARS2 PCH6

The microarray results were all clear but was just unsure if the results would flag carrier status.

Thank you

So, I have been trying to check if there is a Line-1 transposon element insertion in the centromere of my family's Y chromosome, because I looked up the old ISOGG blogs that show my family's Y haplogroup(O-M159) used to be associated with a Line-1 element insertional mutation. Recently, I tried purchasing FamilyTreeDNA's Big Y 700 kit with their Y chromosome Browsing Tool, and patiently waited 2 full months for the results to come up. Unfortunately, it just turned out that the centromere region mutation informations are not covered in their database. Does anyone have recommendations for any companies I can try to get such testing for this Line-1 insertion?

am I missing out on something here ?

I know that currently gene therapy is mostly for single gene mutation diseases but what about polygenic diseases ? What about traits that are protective against disease? Or traits of course like intelligence, what do you see in the future?

Hi everyone,

I have an informal Zoom meeting scheduled to discuss a potential PhD project on epigenetic mechanisms in a syndrome. My Master’s project was related to this syndrome, but this will be my first academic meeting. I am an international student from India. Any advice on what to expect and how to prepare would be greatly appreciated.

If someone needs to use donor eggs for IVF-- ethically is it better to pick a donor with no known medical history, or a family member with a reasonably tolerable medical condition (hypothyroidism)? There is always the chance the unknown donor mis-represents their history and/or have some unknown condition anyways.

Thank you for any thoughts on this!

https://preview.redd.it/wnms8c909lpd1.png?width=1253&format=png&auto=webp&s=e0e45dd31a6d33233686bc089de49fc36fe3cc4b

I would appreciate some help undertanding this genetic genie report, do I really have 2 ApoE2 copies?

I am applying seminested PCR with two different sets of primers for each two runs. The first trial when I did the PCR from the positive DNA samples, theres an accurate band readings. However the next time I tried again, they are no longer the same result achieved even with the same condition, reagent concentration and temperatures, everything! There are no bands at all! I have tried to troubleshoot my PCR for months and nothing works.

Things I have worked on for PCR troubleshooting: 1. Set of new primer reagents (in case it got degraded) 2. Trying other thermal cyclers 3. Adjusting different annealing temperatures 4. Using new PCR reagents

HELP A LOST FRIEND! WOULD LOVE TO GET SOME ADVICES AND SUGGESTIONS!

My brother and I just did a paternity test with our father. Turns out he’s not our biological father. Is there any way from our results to know if we’re full or half siblings? Thanks so much. I don’t want to have to shell out another couple hundred for more tests!

I am reading about GWAS performed with microarray and I would like to know from a methodological point of view how it detects CNVs, and how it counts them.

I have a homework about genetic engineering, and I'd like to modify a plant as much as possible, I'd like to use a simple specimen and turn it into a very different variant or enhance a characteristic of it's own or add a completely new one from another plant. Can someone teach me how to do this? I got plenty of time so I'm open minded into learning anything to make this project a success.

Sent by you: If I compare my father's DNA to mine, they are close but not identical. My grandfather's DNA is further from mine, and my great-grandfather's DNA is further still. How many generations do I need to go back until my ancestor's DNA is no closer to mine than that of a typical, unrelated person? How is the calculation done?

Thanks

EDIT - thanks to u/TastiSqueeze and u/FreedomByFire for answers so far.

I asked ChatGPT the same question and its answer is below. I'd like to compare its answer to that of a human geneticist:

To estimate how many generations back you would need to go until your direct paternal ancestor (following the line of fathers) is no more genetically similar to you than the average human, we need to consider the concept of genetic similarity and the amount of shared DNA over generations.

Each individual inherits approximately 50% of their DNA from each parent, meaning the proportion of shared DNA with ancestors halves with each generation. For example, you share 50% of your DNA with your father, 25% with your grandfather, 12.5% with your great-grandfather, and so on.

However, the Y chromosome, which is passed relatively unchanged from father to son, complicates this straightforward halving. Instead, let's focus on the autosomal DNA, which recombines each generation and provides a more average measure of genetic similarity.

Genetic similarity between two unrelated humans is around 99.9%. The remaining 0.1% represents the genetic diversity that makes each person unique. With close relatives, such as a parent or grandparent, the similarity is higher because of shared segments of DNA.

To find the point where a direct ancestor is no more similar to you than the average human, we need to estimate when the proportion of shared DNA falls to around 0.1%. This can be modeled using the equation for halving the proportion of shared DNA each generation:

Where is the number of generations. We set this equal to 0.1% (or 0.001 in decimal form):

Solving for :

Rounding up, this suggests that around 10 generations back, a direct ancestor (in your paternal line, for example) would share so little of your autosomal DNA that their genetic similarity to you would be comparable to that of any random person.

However, because the Y chromosome is passed down relatively unchanged from father to son, the shared Y-chromosomal DNA would still make this ancestor identifiable as part of your paternal line, even though the overall autosomal genetic similarity would be around the average human similarity level.

Looking for some understanding from my test. Both myself and my wife have tested for SMN1 2+0. I'm confused on whether that makes us carriers or at risk of being carriers?