The ATM-Dependent DNA Damage Response Acts as an Upstream Trigger for Compensation in the fas1 Mutation during Arabidopsis Leaf Development
The ATM-Dependent DNA Damage Response Acts as an Upstream Trigger for Compensation in the fas1 Mutation during Arabidopsis Leaf Development
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DOI：
10.1104/pp.113.216796
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发表时间：
2013-06-01
期刊：
影响因子：
7.4
通讯作者：
Tsukaya, Hirokazu
中科院分区：
文献类型：
--
作者：
Hisanaga, Tetsuya;Ferjani, Ali;Tsukaya, Hirokazu
在叶片发育过程中，细胞数量的减少通常会导致细胞大小的增加。这种称为补偿的现象表明，某些系统协调细胞增殖和细胞扩张，但这是如何在分子水平上调节的仍不清楚。拟南芥Fugu2突变体表现出典型的补偿表型。在这里，我们报告了FUGU2基因编码FASCIATA1(FAS1)，它是染色质组装因子1的P150亚基。为了揭示Fas1突变是如何导致代偿的，我们进行了微阵列分析，发现许多参与DNA损伤反应的基因在Fas1中上调。我们的遗传分析进一步表明，Fas1中DNA损伤反应的激活和伴随的细胞数量的减少依赖于突变的共济失调毛细血管扩张(ATM)，而不是ATM和Rad3相关的。运动学分析表明，细胞周期的延迟导致Fas1的细胞数量减少，ATM的丧失部分恢复了这一表型。一致地，Fas1的细胞大小表型和高倍体表型也被ATM抑制，支持ATM依赖的DNA损伤反应导致这些表型。综上所述，这些数据表明，依赖于ATM的DNA损伤反应在Fas1中作为上游触发器，延迟细胞周期，促进进入内周期，导致代偿细胞扩张。
During leaf development, a decrease in cell number often triggers an increase in cell size. This phenomenon, called compensation, suggests that some system coordinates cell proliferation and cell expansion, but how this is mediated at the molecular level is still unclear. The fugu2 mutants in Arabidopsis (Arabidopsis thaliana) exhibit typical compensation phenotypes. Here, we report that the FUGU2 gene encodes FASCIATA1 (FAS1), the p150 subunit of Chromatin Assembly Factor1. To uncover how the fas1 mutation induces compensation, we performed microarray analyses and found that many genes involved in the DNA damage response are up-regulated in fas1. Our genetic analysis further showed that activation of the DNA damage response and the accompanying decrease of cell number in fas1 depend on ATAXIA TELANGIECTASIA MUTATED (ATM) but not on ATM AND RAD3 RELATED. Kinematic analysis suggested that the delay in the cell cycle leads to a decrease in cell number in fas1 and that loss of ATM partially restores this phenotype. Consistently, both cell size phenotypes and high ploidy phenotypes of fas1 are also suppressed by atm, supporting that the ATM-dependent DNA damage response leads to these phenotypes. Altogether, these data suggest that the ATM-dependent DNA damage response acts as an upstream trigger in fas1 to delay the cell cycle and promote entry into the endocycle, resulting in compensated cell expansion.