EIN3 and PIF3 Form an Interdependent Module That Represses Chloroplast Development in Buried Seedlings
EIN3 and PIF3 Form an Interdependent Module That Represses Chloroplast Development in Buried Seedlings
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EIN3 和 PIF3 形成一个相互依赖的模块，抑制埋地幼苗叶绿体的发育
DOI：
10.1105/tpc.17.00508
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发表时间：
2017-12-01
期刊：
影响因子：
11.6
通讯作者：
Shi, Hui
中科院分区：
文献类型：
--
作者：
Liu, Xiaoqin;Liu, Renlu;Shi, Hui
在埋藏的幼苗中，叶绿体在黄化体阶段被阻止，但它们在幼苗出现时迅速成熟。通过整合土壤诱导的信号，包括压力和缺乏光，叶绿体分化停止，尽管这些信息如何收敛到调节细胞决策的细节仍然不清楚。在这里，我们确定了一个相互依赖的转录模块，整合了机械压力和黑暗信号控制叶绿体发育拟南芥。乙烯不敏感3（EIN 3）是乙烯信号传导途径中的主要转录因子，在机械压力下被激活，突变会导致在黑暗中早期发育成黄化体，并在光照下发生严重的光漂白。遗传学研究表明EIN 3抑制原生质体分化需要光敏色素相互作用因子3（PIF 3），一种黑暗稳定的bHLH转录因子。EIN 3和PIF 3直接相互作用并形成一个相互依赖的模块，以抑制大多数光捕获复合体（LHC）基因的表达;即使一个LHC过表达也可能导致病原体的过早发育。EIN 3-PIF 3转录模块通过相互依赖地共同占据LHC基因的启动子而协同地停止叶绿体发育。因此，我们的研究结果定义了一个转录调控模块，并提供了多个土壤诱导的信号协同调节叶绿体发育的机制见解。
In buried seedlings, chloroplasts are arrested at the etioplast stage, but they rapidly mature upon emergence of the seedling. Etioplast-chloroplast differentiation is halted through the integration of soil-induced signals, including pressure and the absence of light, although the details on how this information converges to regulate cellular decisions remain unclear. Here, we identify an interdependent transcription module that integrates the mechanical pressure and darkness signals to control chloroplast development in Arabidopsis thaliana. Mutations of ETHYLENE-INSENSITIVE3 (EIN3), the primary transcription factor in the ethylene signaling pathway that is activated in response to mechanical pressure, cause early development of etioplasts in the dark and severe photobleaching upon light exposure. Genetic studies demonstrate that repression of etioplast differentiation by EIN3 requires PHYTOCHROME INTERACTING FACTOR3 (PIF3), a darkness-stabilized bHLH transcription factor. EIN3 and PIF3 directly interact and form an interdependent module to repress the expression of most LIGHT HARVESTING COMPLEX (LHC) genes; overexpressing even one LHC could cause premature development of etioplasts. The EIN3-PIF3 transcription module synergistically halts chloroplast development by interdependently co-occupying the promoters of LHC genes. Thus, our results define a transcriptional regulatory module and provide mechanistic insight on the concerted regulation of chloroplast development by multiple soil-induced signals.