Katarzyna H. Masłowska

This study identifies Rad51 mutations that shift post-replication repair pathway usage from homologous recombination to alternate pathways by affecting fork protection.

This study examines how the timing of lesion bypass during DNA replication affects mutagenesis, showing that TLS at certain lesions occurs post-replicatively and competes with DA, reducing mutagenicity.

This study shows Rad5 has opposite roles in DNA damage tolerance: promoting error-free bypass via PCNA ubiquitination and enabling error-prone TLS by recruiting Rev1.

The paper shows TLS is locally controlled by PCNA ubiquitination at individual lesions, not globally induced by genotoxic stress.

The paper introduces a method to insert modified DNA into the yeast genome and shows how DNA damage tolerance is regulated by inhibiting homologous recombination.