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SAUR17 and SAUR50 Differentially Regulate PP2C-D1 during Apical Hook Development and Cotyledon Opening in Arabidopsis
The Plant Cell ( IF 10.0 ) Pub Date : 2020-12-01 , DOI: 10.1105/tpc.20.00283
Jiajun Wang 1 , Ning Sun 1 , Fangfang Zhang 1 , Renbo Yu 1 , Haodong Chen 1 , Xing Wang Deng 2, 3 , Ning Wei 4
Affiliation  

Following germination in the dark, Arabidopsis (Arabidopsis thaliana) seedlings undergo etiolation and develop apical hooks, closed cotyledons, and rapidly elongating hypocotyls. Upon light perception, the seedlings de-etiolate, which includes the opening of apical hooks and cotyledons. Here, we identify Arabidopsis Small Auxin Up RNA17 (SAUR17) as a downstream effector of etiolation, which serves to bring about apical hook formation and closed cotyledons. SAUR17 is highly expressed in apical hooks and cotyledons and is repressed by light. The apical organs also express a group of light-inducing SAURs, as represented by SAUR50, which promote hook and cotyledon opening. The development of etiolated or de-etiolated apical structures requires asymmetric differential cell growth. We present evidence that the opposing actions of SAUR17 and SAUR50 on apical development largely result from their antagonistic regulation of Protein Phosphatase 2C D-clade 1 (PP2C-D1), a phosphatase that suppresses cell expansion and promotes apical hook development in the dark. SAUR50 inhibits PP2C-D1, whereas SAUR17 has a higher affinity for PP2C-D1 without inhibiting its activity. PP2C-D1 predominantly associates with SAUR17 in etiolated seedlings, which shields it from inhibitory SAURs such as SAUR50. Light signals turn off SAUR17 and upregulate a subgroup of SAURs including SAUR50 at the inner side of the hook and cotyledon cells, leading to cell expansion and unfolding of the hook and cotyledons.



中文翻译:


SAUR17 和 SAUR50 在拟南芥顶钩发育和子叶开放过程中差异调节 PP2C-D1



在黑暗中发芽后,拟南芥( Arabidopsis thaliana )幼苗经历黄化并发育出顶钩、闭合的子叶和快速伸长的下胚轴。一旦感知到光,幼苗就会脱黄,包括顶钩和子叶的张开。在这里,我们将拟南芥小生长素上RNA17SAUR17 )确定为黄化的下游效应子,其作用是形成顶端钩和闭合子叶。 SAUR17在顶钩和子叶中高度表达,并受到光的抑制。顶端器官还表达一组光诱导SAUR ,以SAUR50为代表,促进钩和子叶的打开。黄化或去黄化顶端结构的发育需要不对称的差异细胞生长。我们提供的证据表明,SAUR17 和 SAUR50 对顶端发育的相反作用很大程度上是由于它们对蛋白磷酸酶 2C D-clade 1 (PP2C-D1) 的拮抗调节,蛋白磷酸酶 2C D-clade 1 (PP2C-D1) 是一种抑制细胞扩张并在黑暗中促进顶端钩发育的磷酸酶。 SAUR50 抑制 PP2C-D1,而 SAUR17 对 PP2C-D1 具有更高的亲和力,但不抑制其活性。 PP2C-D1 主要与黄化幼苗中的 SAUR17 结合,从而保护其免受 SAUR50 等抑制性 SAUR 的影响。光信号关闭SAUR17并上调SAUR的一个亚群,包括钩和子叶细胞内侧的SAUR50 ,导致钩和子叶细胞扩张和展开。

更新日期:2020-12-04
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