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早期转录电路在光诱导的拟南芥幼苗中 PIF 介导的光形态建成抑制的逆转中的作用。

Definition of early transcriptional circuitry involved in light-induced reversal of PIF-imposed repression of photomorphogenesis in young Arabidopsis seedlings.

机构信息

Department of Plant and Microbial Biology, University of California-Berkeley, CA 94720, USA.

出版信息

Plant Cell. 2009 Nov;21(11):3535-53. doi: 10.1105/tpc.109.070672. Epub 2009 Nov 17.

Abstract

Light signals perceived by the phytochromes induce the transition from skotomorphogenic to photomorphogenic development (deetiolation) in dark-germinated seedlings. Evidence that a quadruple mutant (pifq) lacking four phytochrome-interacting bHLH transcription factors (PIF1, 3, 4, and 5) is constitutively photomorphogenic in darkness establishes that these factors sustain the skotomorphogenic state. Moreover, photoactivated phytochromes bind to and induce rapid degradation of the PIFs, indicating that the photoreceptor reverses their constitutive activity upon light exposure, initiating photomorphogenesis. Here, to define the modes of transcriptional regulation and cellular development imposed by the PIFs, we performed expression profile and cytological analyses of pifq mutant and wild-type seedlings. Dark-grown mutant seedlings display cellular development that extensively phenocopies wild-type seedlings grown in light. Similarly, 80% of the gene expression changes elicited by the absence of the PIFs in dark-grown pifq seedlings are normally induced by prolonged light in wild-type seedlings. By comparing rapidly light-responsive genes in wild-type seedlings with those responding in darkness in the pifq mutant, we identified a subset, enriched in transcription factor-encoding genes, that are potential primary targets of PIF transcriptional regulation. Collectively, these data suggest that the transcriptional response elicited by light-induced PIF proteolysis is a major component of the mechanism by which the phytochromes pleiotropically regulate deetiolation and that at least some of the rapidly light-responsive genes may comprise a transcriptional network directly regulated by the PIF proteins.

摘要

光信号被光敏色素感知后,会诱导暗萌发幼苗从暗形态建成向光形态建成(去黄化)的转变。缺乏四个光敏色素相互作用的 bHLH 转录因子(PIF1、3、4 和 5)的四重突变体(pifq)在黑暗中持续光形态建成的证据表明,这些因子维持暗形态建成状态。此外,光激活的光敏色素与 PIF 结合并诱导其快速降解,表明光受体在光暴露时逆转其组成性活性,从而启动光形态建成。在这里,为了确定 PIF 施加的转录调控和细胞发育模式,我们对 pifq 突变体和野生型幼苗进行了表达谱和细胞学分析。黑暗中生长的突变体幼苗表现出的细胞发育在很大程度上与在光照下生长的野生型幼苗相似。同样,在黑暗中生长的 pifq 突变体中缺失 PIFs 引起的 80%的基因表达变化,在野生型幼苗中通过延长光照也能正常诱导。通过比较野生型幼苗中快速光响应基因与 pifq 突变体中在黑暗中响应的基因,我们鉴定出一个富含转录因子编码基因的子集,这些基因可能是 PIF 转录调控的潜在主要靶点。总之,这些数据表明,光诱导的 PIF 蛋白水解引起的转录反应是光敏色素多效性调节去黄化的机制的主要组成部分,并且至少一些快速光响应基因可能构成直接受 PIF 蛋白调控的转录网络。

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