Vincent Pagès

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

The paper shows that the RecBC complex protects nascent DNA from degradation by ExoI during lesion bypass, ensuring efficient repair of single-stranded DNA gaps.

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 that a unique secondary contact of Pol IV with the processivity clamp enhances its ability to perform translesion synthesis past strong replication blocks.

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 that the presynaptic phase is crucial for modulating lesion tolerance pathways in E. coli, with defects leading to reduced HDGR and increased TLS.

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.

The paper shows that proximity of replication-blocking lesions in E. coli increases error-prone TLS usage, independent of SOS activation, but additive with SOS mutagenic effects.

This paper identifies a non-catalytic role of RecBCD in stabilizing blocked replication forks during homology directed gap repair and translesion synthesis.