Loss of FAS1 function reveals rescue of an aberrant intra-S-phase checkpoint by the G2/M checkpoint regulator SOG11[OPEN]

Abstract

ABSTRACTThe WEE1 and ATR kinases represent important regulators of the plant intra-S-phase checkpoint, as evidenced by the hypersensitivity ofWEE1KOandATRKOroots to replication inhibitory drugs. Here, we report on the identification of a defective allele of theFASCIATA1(FAS1) subunit of the chromatin assembly factor 1 (CAF-1) complex as a suppressor ofWEE1- or ATR-deficient plants. We demonstrate that lack ofFAS1activity results in the activation of an ATM- and SOG1-mediated G2/M-arrest that makes the ATR and WEE1 checkpoint regulators redundant. This ATM activation accounts for telomere erosion and loss of ribosomal DNA described for thefas1plants. Knocking outSOG1in thefas1 wee1background restores replication stress sensitivity, demonstrating that SOG1 plays a prominent role as secondary checkpoint regulator in plants that fail to activate the intra-S-phase checkpoint.One-Sentence SummaryLack of the chromatin assembly factor-1 subunit FAS1 results in a DNA damage response that overrules the need for replication checkpoint activators.