I'm thrilled to share our new paper out today in @currentbiology.bsky.social! I teamed up with researchers at @harvardmed.bsky.social and the Smithsonian to study another historical American population using the 23andMe genetic database. 🧵 [1/9] Read it here: www.cell.com/current-biol...
www.cell.com
Population geneticists! Come work at 23andMe! New role just posted.
23andme.wd5.myworkdayjobs.com/23/job/Palo-...
Pretty wild: www.science.org/content/arti...
Happy to highlight new findings by Vanesa Getseva and Lin Poyraz about the sources of variation in germline mutation rates among humans: www.biorxiv.org/content/10.6...
Joint work with Anastasia Stolyarova and @ipsitaagarwal.bsky.social. 1/n
Why do people respond differently to GLP-1 weight-loss drugs? Genetics has the answer - provided in this genome wide association study led by @adamauton.bsky.social www.nature.com/articles/s41...
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www.nature.com/articles/d41...
This story is *really cool* - well worth a read. A great example of genealogical sleuthing with DNA. A huge congratulations to the amazing 23andMe, Smithsonian, and
Harvard teams. (I wasn’t involved with this study) www.cell.com/current-biol...
Éadaoin Harney
A nice “behind the paper” explainer here: communities.springernature.com/posts/unlock...
Were you inspired by our paper on the genetics of GLP-1 drug response? www.nature.com/articles/s41...
Want to make impactful discoveries with the world's best genetic dataset? We're hiring!
StatGen: tinyurl.com/ys4mvhej
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23andMe is looking for a quantitative scientist with extensive experience in population genetics and statistical modeling of human genetics data to join our R&D team. You will leverage your expert...
Genetic variants in GLP1R and GIPR, which encode targets of GLP-1-based medications, offer insights into why responses to these drugs vary and who might face adverse effects.
www.nature.com
People are born with variable numbers of de novo germline mutations (DNMs), depending primarily on the ages of their parents. To explore additional causes, we developed an approach to call DNMs from nucleotide differences between siblings in genomic regions inherited identical by descent from both parents. Applying it to whole genome sequences from 28,985 sibling pairs of diverse genetic ancestries present in the UK Biobank and All of Us datasets, as well as 2,330 trios, we identified >800K autosomal DNMs and characterized mutation phenotypes in 27,645 sets of parents. We found subtle shifts in the mutation spectrum but no differences in total DNM rates among genetic ancestry groups, or between smokers and non-smokers. Testing for associations between parental mutation phenotypes and their burden of loss-of-function and deleterious missense variants in a set of 180 DNA repair and maintenance genes, we discovered that disruptions in REV1 and LIG1 increase germline mutation rates, and thus that rare mutator alleles segregate in population cohorts. ### Competing Interest Statement The authors have declared no competing interest. NIH, R35 GM083098
Harney et al. analyze 49 genomes from 17th-century St. Mary’s City, Maryland. Using
an IBD-based approach, they identify connections to over 1.3 million living relatives,
enabling them to study the fo...
By pairing a rapid "research flywheel" with large-scale genomic data, 23andMe Research Institute scientists identified GLP1R and GIPR variants associated with some of the variability in individual res...
Identification of genetic variants associated with the efficacy and side effects of GLP1 medications could underpin development of precision medicine approaches in the treatment of obesity.