MYB3R-mediated active repression of cell cycle and growth under salt stress in Arabidopsis thaliana
MYB3R-mediated active repression of cell cycle and growth under salt stress in Arabidopsis thaliana
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盐胁迫下MYB3R介导的细胞周期和生长主动抑制
DOI：
10.1007/s10265-020-01250-8
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发表时间：
2021
影响因子：
2.8
通讯作者：
Ito Masaki
中科院分区：
文献类型：
--
作者：
Okumura Toru;Nomoto Yuji;Kobayashi Kosuke;Suzuki Takamasa;Takatsuka Hirotomo;Ito Masaki
在环境胁迫下，植物被认为是主动抑制生长以节约资源，并改变其分配以获得对胁迫的耐受性。虽然许多研究已经发现了应对压力和获得耐受的精确机制，但对压力下调节生长抑制的机制还不是很清楚。目前还不清楚哪些与细胞周期控制相关的特定基因参与了主动生长抑制。在这里，我们证明了中等盐胁迫下植物生长的减少是由MYB3R转录因子介导的，这些转录因子已经被认为对G2/M特异基因的转录进行正向和负向调节。我们的全基因组基因表达分析显示，在盐胁迫下，拟南芥G2/M特异性基因普遍下调。重要的是，MYB3R阻遏物的突变导致的MYB3R抑制物的丢失显著且普遍地缓解了这种下调。因此，在缺乏MYB3R阻滞剂的突变体中，拟南芥植物在盐胁迫下的生长表现显著恢复。这种生长恢复涉及到细胞增殖的改善，这可能是由于延长和加速了细胞增殖，这在一定程度上是由于根分生组织扩大和CyCB1；1-GUS阳性细胞数量的增加。我们的倍体分析进一步表明，在盐胁迫下，细胞周期在G2期的进展被推迟，这种延迟可以通过MYB3R阻滞剂的丧失而恢复。盐胁迫下，MYB3R激活子和抑制子在mRNA和蛋白水平的表达变化均不显著。这一观察结果表明，盐胁迫下MYB3R介导的生长抑制的新机制不同于其他胁迫条件下的机制，如DNA损伤和高温。
Under environmental stress, plants are believed to actively repress their growth to save resource and alter its allocation to acquire tolerance against the stress. Although a lot of studies have uncovered precise mechanisms for responding to stress and acquiring tolerance, the mechanisms for regulating growth repression under stress are not as well understood. It is especially unclear which particular genes related to cell cycle control are involved in active growth repression. Here, we showed that decreased growth in plants exposed to moderate salt stress is mediated by MYB3R transcription factors that have been known to positively and negatively regulate the transcription of G2/M-specific genes. Our genome-wide gene expression analysis revealed occurrences of general downregulation of G2/M-specific genes in Arabidopsis under salt stress. Importantly, this downregulation is significantly and universally mitigated by the loss of MYB3R repressors by mutations. Accordingly, the growth performance of Arabidopsis plants under salt stress is significantly recovered in mutants lacking MYB3R repressors. This growth recovery involves improved cell proliferation that is possibly due to prolonging and accelerating cell proliferation, which were partly suggested by enlarged root meristem and increased number of cells positive for CYCB1;1-GUS. Our ploidy analysis further suggested that cell cycle progression at the G2 phase was delayed under salt stress, and this delay was recovered by loss of MYB3R repressors. Under salt stress, the changes in expression of MYB3R activators and repressors at both the mRNA and protein levels were not significant. This observation suggests novel mechanisms underlying MYB3R-mediated growth repression under salt stress that are different from the mechanisms operating under other stress conditions such as DNA damage and high temperature.