📣 Two ERC-funded positions are available in the lab! If you are interested in exploring the mechanisms underlying mutation, we’d love to hear from you.

PhD: shorturl.at/Oc04N
Postdoc: shorturl.at/1ShHB

RPs and shares would be greatly appreciated!
🧪🧬🖥️ #ScienceJobs #PostdocJobs

In sum, it appears that the fine-scale recombination landscape of a species reflects a tug of war between competing signals, the outcome of which is lopsided in mammals (and in species lacking PRDM9 altogether), but more even in snakes and potentially many other vertebrates. 22/n

(ii) Hotspots associated with PRDM9 binding sites, which are short-lived, and show only a small increase in GC* at corn snake hotspots in the corn snake lineage. 20/n

However, in contrast to all mammals with PRDM9 studied to date, in corn snakes, recombination rates are also increased near promoter-like features. The effects of promoter-like features are separable and largely independent from those of PRDM9 binding. 18/n

We therefore complement our analysis of LD patterns along the genome of 24 corn snakes with that of crossovers in pedigrees from two nuclear families of five kids each. Using both approaches, we find evidence that PRDM9 directs meiotic recombination in this species. 16/n

Resequencing the PRDM9 zinc finger, we find an immense diversity of alleles & putative binding sites in corn snakes. A possible implication is that no one PRDM9 allele was long-lived enough to leave much of a footprint in linkage disequilibrium (LD) or divergence data. 15/n