SHA1, a novel RING finger protein, functions in shoot apical meristem maintenance in Arabidopsis
SHA1, a novel RING finger protein, functions in shoot apical meristem maintenance in Arabidopsis
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DOI：
10.1111/j.1365-313x.2007.03062.x
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发表时间：
2007-05-01
期刊：
影响因子：
7.2
通讯作者：
Ikeda, Akira
中科院分区：
文献类型：
--
作者：
Sonoda, Yutaka;Yao, Shan-Guo;Ikeda, Akira
胚后植物生长依赖于功能性的茎顶端分生组织（SAM），该分生组织为新的气生器官的持续发育提供细胞。然而，SAM是如何在营养发育过程中动态维持的，在很大程度上还不清楚。我们在这里报告的一个新的SAM维护突变体，sha1-1（茎尖分生组织逮捕1-1），在成人阶段表现出主要SAM缺陷型的表征。SHA1基因编码一种新的环指蛋白，并在茎尖中表达最强烈。我们发现，在sha1-1突变体中，初级SAM在幼年营养阶段正常发育，但进入成年营养阶段后，细胞层结构变得混乱，导致功能失调的SAM不能启动花原基。sha1-1 SAM完全终止于野生型开始抽苔的阶段，产生具有主花序缺陷表型的成年植株。这些观察结果表明，SHA1，一个假定的E3连接酶，需要通过控制适当的细胞组织的胚后SAM维护。
Post-embryonic plant growth is dependent on a functional shoot apical meristem (SAM) that provides cells for continuous development of new aerial organs. However, how the SAM is dynamically maintained during vegetative development remains largely unclear. We report here the characterization of a new SAM maintenance mutant, sha1-1 (shoot apical meristem arrest 1-1), that shows a primary SAM-deficient phenotype at the adult stage. The SHA1 gene encodes a novel RING finger protein, and is expressed most intensely in the shoot apex. We show that, in the sha1-1 mutant, the primary SAM develops normally during the juvenile vegetative stage, but cell layer structure becomes disorganized after entering the adult vegetative stage, resulting in a dysfunctional SAM that cannot initiate floral primordia. The sha1-1 SAM terminates completely at the stage when the wild-type begins to bolt, producing adult plants with a primary inflorescence-deficient phenotype. These observations indicate that SHA1, a putative E3 ligase, is required for post-embryonic SAM maintenance by controlling proper cellular organization.