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I am delighted to share new work with Simon Myers (www.biorxiv.org/content/10.6...), on how genetic variants that influence binding patterns of PRDM9 and slow down the repair of meiotic double-strand breaks impact mammalian spermatogenesis and fertility. 1/n

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

Arc Institute’s “MULTI-evolve” learns a classical additive model, not epistasis. Preprint (w/ Gian Marco Visani and Aayush Verma): www.biorxiv.org/content/10.6... Blog: dewitt-lab.github.io/posts/2026-0...

Now published: journals.plos.org/plosbiology/...

The Ly Lab is recruiting two #postdocs to study intercellular DNA transfer. Join us to tackle fundamental questions at the intersection of genome instability, cell-cell communication, and cancer evolution. Please share! 🙏 Full posting: cri.utsw.edu/careers/

Very pleased with the response and still have spots & funding especially for students/postdocs. Sign up soon before it gets full. If you are working at or wanting to learn about the intersection of functional biology and ecology/evolution, you would get a lot of it! www.grc.org/function-of-...

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

Arc Institute’s “MULTI-evolve” learns a classical additive model, not epistasis.

dewitt-lab.github.io

Accounting for recurrent mutation in the frequency spectrum of rare alleles https://www.biorxiv.org/content/10.64898/2026.05.29.728884v1

Mutation rates per generation are strikingly similar across germlines of animals and across at least one somatic cell type, suggesting a key role for natural selection in shaping mutation rates. This ...