Human MutS and FANCM complexes function as redundant DNA damage sensors in the Fanconi Anemia pathway
The Fanconi Anemia (FA) pathway encodes a DNA damage response activated by DNA
damage-stalled replication forks. Current evidence suggests that the FA pathway initiates
with DNA damage recognition by the FANCM complex (FANCM/FAAP24/MHF). However,
genetic inactivation of FANCM in mouse and DT40 cells causes only a partial defect in the
FA pathway activation, suggesting the existence of redundant DNA damage sensors. Here
we show that the MutS homologs function in this capacity. A RNAi screen revealed that …
damage-stalled replication forks. Current evidence suggests that the FA pathway initiates
with DNA damage recognition by the FANCM complex (FANCM/FAAP24/MHF). However,
genetic inactivation of FANCM in mouse and DT40 cells causes only a partial defect in the
FA pathway activation, suggesting the existence of redundant DNA damage sensors. Here
we show that the MutS homologs function in this capacity. A RNAi screen revealed that …