Buying time: FASCIATA1 deficiency rescues wee1 plants from replication stress by delaying mitosis.
Buying time: FASCIATA1 deficiency rescues wee1 plants from replication stress by delaying mitosis.
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DOI:
10.1093/plphys/kiab256
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发表时间:
2021-08-03
期刊:
影响因子:
7.4
通讯作者:
Tulin F
中科院分区:
文献类型:
--
作者:
Tulin F
Cells have a remarkable ability to faithfully duplicate and segregate the genome, even when replication is challenged by various types of DNA damage. The fidelity of chromosome segregation relies on the DNA damage response (DDR), a checkpoint system that activates DNA repair genes and blocks cell cycle progression until the damage is repaired. The checkpoint kinase WEE1 has emerged as a core component in the plant DDR, mainly from studies in Arabidopsis (Arabidopsis thaliana). In this issue of Plant Physiology, Eekhout et al. investigate how both WEE1-dependent and-independent signaling pathways contribute to completion of DNA replication in the presence of stress. In plants, as in other eukaryotes, two closely related sensor kinases, ATAXIA TELANGIECTASIA MUTATED (ATM) and ATM AND RAD3-RELATED (ATR), initiate DNA damage signaling (Figure 1). ATM is responsible for processing doublestranded breaks, a particularly dangerous type of DNA damage that must be repaired before the cell enters mitosis. ATR is more broadly required for sensing extended tracts of single-stranded DNA, a common consequence of replication stress during S phase. Downstream of ATM/ATR, the two pathways converge on the master regular SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1), which is a direct substrate of ATM and responsible for transcriptional activation of a broad range of DNA repair and cell cycle genes (Ogita et al., 2018). Inactivation of SOG1 generally blocks both ATM-and ATR-dependent signaling (Figure 1) with severe consequences for DNA damage tolerance and genome stability (Yoshiyama et al., 2009).
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影响因子:
7.4
作者:
Eekhout, Thomas;Dvorackova, Martina;De Veylder, Lieven
通讯作者:
De Veylder, Lieven
影响因子:
11.6
作者:
Kalhorzadeh, Pooneh;Hu, Zhubing;De Veylder, Lieven
通讯作者:
De Veylder, Lieven
影响因子:
11.6
作者:
Cools, Toon;Iantcheva, Anelia;De Veylder, Lieven
通讯作者:
De Veylder, Lieven
影响因子:
7.2
作者:
Ogita, Nobuo;Okushima, Yoko;Umeda, Masaaki
通讯作者:
Umeda, Masaaki
影响因子:
56.9
作者:
WEINERT, TA;HARTWELL, LH
通讯作者:
HARTWELL, LH