PT  - JOURNAL ARTICLE
AU  - Eekhout, Thomas
AU  - Dvorackova, Martina
AU  - Garcia, José Antonio Pedroza
AU  - Dadejova, Martina Nespor
AU  - Kalhorzadeh, Pooneh
AU  - Van den Daele, Hilde
AU  - Vercauteren, Ilse
AU  - Fajkus, Jiri
AU  - De Veylder, Lieven
TI  - Loss of FAS1 function reveals rescue of an aberrant intra-S-phase checkpoint by the G2/M checkpoint regulator SOG1<sup>1[OPEN]</sup>
AID  - 10.1101/2021.02.22.432330
DP  - 2021 Jan 01
TA  - bioRxiv
PG  - 2021.02.22.432330
4099  - http://biorxiv.org/content/early/2021/02/23/2021.02.22.432330.short
4100  - http://biorxiv.org/content/early/2021/02/23/2021.02.22.432330.full
AB  - The WEE1 and ATR kinases represent important regulators of the plant intra-S-phase checkpoint, as evidenced by the hypersensitivity of WEE1KO and ATRKO roots to replication inhibitory drugs. Here, we report on the identification of a defective allele of the FASCIATA1 (FAS1) subunit of the chromatin assembly factor 1 (CAF-1) complex as a suppressor of WEE1- or ATR-deficient plants. We demonstrate that lack of FAS1 activity 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 the fas1 plants. Knocking out SOG1 in the fas1 wee1 background 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 Summary Lack of the chromatin assembly factor-1 subunit FAS1 results in a DNA damage response that overrules the need for replication checkpoint activators.