Winfried Edelmann

This study shows that a mammalian-specific domain of MSH5 is essential for converting licensed DSB repair intermediates to designated class I crossovers during meiosis.

The paper shows DNA2 and MSH2 work together to remove G4 structures at telomeres, preventing replication issues and telomere instability.

This study shows that DNA mismatch repair-deficient mouse fibroblasts can tolerate high mutation burdens in vitro without significant growth effects, revealing mutation-driven population changes and negative selection.

This study shows that reducing MSH3 in Huntington's disease mouse models prevents somatic CAG repeat expansion but does not accelerate disease onset, suggesting somatic expansion may not be required for pathogenesis.

The paper defines resected DSB structures in mouse spermatocytes, identifies ATM as a key regulator of resection, and shows PRDM9-dependent chromatin remodeling at recombination sites.

This study uses single-cell whole-genome sequencing to analyze mutational landscapes in Msh2-deficient mouse fibroblasts, revealing elevated SNVs and INDELs with distinct mutational signatures.

This study shows that a functional MutSγ complex is required for all crossovers in mammalian meiosis, even though class II crossovers were thought to be MutSγ-independent.