PICKLE is a repressor in seedling de-etiolation pathway

PICKLE is a repressor in seedling de-etiolation pathway
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PICKLE 是幼苗去黄化途径的阻遏物

DOI:
10.4161/psb.25026
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发表时间:
2013-08
影响因子:
2.9
通讯作者:
景艳军
景艳军
中科院分区:
生物学4区
文献类型:
--
作者:
景艳军

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光在幼苗脱黄化过程中起着重要作用,在脱黄化过程中,光显著抑制下胚轴的生长,促进子叶的开放以及叶绿素和花青素的合成。在光感知之后,光感受器用于抑制光信号传导的两个主要分支,PIF和COP 1-HY 5。我们最近确定PKL/EPP 1,染色质重塑因子,作为一个新的组件在调节光介导的下胚轴生长。在这项研究中,我们发现EPP 1与SPA 1相加抑制幼苗脱黄化。此外,与野生型相比,cop 1突变体的下胚轴区域中EPP 1的表达特异性下调。我们进一步发现,EPP 1显著抑制HY 5的蛋白质和转录水平,但反之亦然,表明HY 5作用于EPP 1的下游。因此,我们提出了一个模型,其中EPP 1定义了一个新的阻遏物,并介导了一个独特的信号通路的光形态建成。
Light plays a vital role in seedling de-etiolation during which it remarkably inhibits hypocotyl growth and promotes cotyledon opening and the synthesis of chlorophyll and anthocyanin. After light perception, photoreceptors act to repress two main branches of the light signaling, PIFs and COP1-HY5. We recently identified PKL/EPP1, a chromatin remodeling factor, as a new component in regulating light-mediated hypocotyl growth. In this study, we found that EPP1 acts additively with SPA1 to repress seedling de-etiolation. Moreover, the expression of EPP1 is downregulated specifically in the hypocotyl region of the cop1 mutant compared with that of the wild type. We further found that EPP1 drastically inhibits both the protein and transcript levels of HY5, but not vice versa, indicating that HY5 acts downstream of EPP1. We thus propose a model in which EPP1 defines a new repressor and mediates a distinct signaling pathway of photomorphogenesis.
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