Department of Plant Biotechnology and Bioinformatics, Ghent University, 9052 Gent, Belgium.
Center for Plant Systems Biology, VIB, 9052 Gent, Belgium.
Plant Physiol. 2021 Aug 3;186(4):1893-1907. doi: 10.1093/plphys/kiab201.
The WEE1 and ATM AND RAD3-RELATED (ATR) kinases are important regulators of the plant intra-S-phase checkpoint; consequently, WEE1KO and ATRKO roots are hypersensitive to replication-inhibitory drugs. Here, we report on a loss-of-function mutant allele of the FASCIATA1 (FAS1) subunit of the chromatin assembly factor 1 (CAF-1) complex that suppresses the phenotype of WEE1- or ATR-deficient Arabidopsis (Arabidopsis thaliana) plants. We demonstrate that lack of FAS1 activity results in the activation of an ATAXIA TELANGIECTASIA MUTATED (ATM)- and SUPPRESSOR OF GAMMA-RESPONSE 1 (SOG1)-mediated G2/M-arrest that renders the ATR and WEE1 checkpoint regulators redundant. This ATM activation accounts for the telomere erosion and loss of ribosomal DNA that are described for fas1 plants. Knocking out SOG1 in the fas1 wee1 background restores replication stress sensitivity, demonstrating that SOG1 is an important secondary checkpoint regulator in plants that fail to activate the intra-S-phase checkpoint.
WEE1 和 ATM 以及 RAD3 相关（ATR）激酶是植物内 S 期检查点的重要调节因子；因此，WEE1KO 和 ATRKO 根对复制抑制药物高度敏感。在这里，我们报告了染色质组装因子 1 (CAF-1) 复合物 FASCIATA1 (FAS1) 亚基的功能丧失突变体等位基因，该等位基因抑制了 WEE1 或 ATR 缺陷拟南芥 (Arabidopsis thaliana) 植物的表型。我们证明，缺乏 FAS1 活性会导致 ATAXIA TELANGIECTASIA MUTATED (ATM) 和 SUPPRESSOR OF GAMMA-RESPONSE 1 (SOG1) 介导的 G2/M 期阻滞的激活，从而使 ATR 和 WEE1 检查点调节剂冗余。这种 ATM 激活解释了 fas1 植物中描述的端粒侵蚀和核糖体 DNA 丢失。在 fas1 wee1 背景中敲除 SOG1 恢复了复制应激敏感性，表明 SOG1 是植物中未能激活内 S 期检查点的重要次级检查点调节剂。
