A new loss-of-function allele 28y reveals a role of ARGONAUTE1 in limiting asymmetric division of stomatal lineage ground cell
A new loss-of-function allele 28y reveals a role of ARGONAUTE1 in limiting asymmetric division of stomatal lineage ground cell
复制标题
一个新的功能丧失等位基因 28y 揭示了 ARGONAUTE1 在限制气孔谱系地面细胞不对称分裂中的作用
DOI：
10.1111/jipb.12154
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发表时间：
2014-06-01
影响因子：
11.4
通讯作者：
Le, Jie
中科院分区：
文献类型：
--
作者：
Yang, Kezhen;Jiang, Min;Le, Jie
在拟南芥中，气孔是通过一系列分裂产生的，包括不对称分裂和对称分裂。分生组织样母细胞的不对称分裂产生两个子细胞，即较小的分生组织样母细胞和较大的姐妹细胞，即气孔谱系基细胞（SLGC）。气孔系基底细胞可以分化成表皮铺层细胞，但有可能不对称分裂，间隔分裂，产生卫星分生组织。肽配体和TOO MANY MOUTHS（TMM）和ERECTA家族受体调节气孔谱系的起始、活性和间隔分裂的方向。本文报道了一个自然突变体28 y的气孔密度和气孔指数增加。使用图位克隆，我们确定了ARGONAUTE 1（AGO 1）突变是28年表型的原因。对气孔谱系细胞的延时追踪表明，28年的气孔过量生产是由SLGCs过度的不对称间隔分裂引起的。进一步的遗传学结果表明，AGO 1作用于TMM的下游，并负调控SPCH转录本，但以油菜素类固醇非依赖的方式。AGAMOUS-LIKE 16（AGL 16）在28 y突变体中的上调表明AGO 1是限制AGL 16介导的气孔间隔分裂所必需的，这是除了配体-受体信号传导模块之外的一种miRNA途径。
In Arabidopsis thaliana L., stomata are produced through a series of divisions including asymmetric and symmetric divisions. Asymmetric entry division of meristemoid mother cell produces two daughter cells, the smaller meristemoid and the larger sister cell, a stomatal lineage ground cell (SLGC). Stomatal lineage ground cells can differentiate into epidermal pavement cells but have the potential to divide asymmetrically, spacing divisions, to create satellite meristemoids. Peptide ligands and TOO MANY MOUTHS (TMM) and ERECTA family receptors regulate the initiation of stomatal lineages, activity, and orientation of spacing divisions. Here, we reported that a natural mutant 28y displayed an increased stomatal density and index. Using map-based cloning, we identified mutation in ARGONAUTE1 (AGO1) as the cause of 28y phenotypes. Time-lapse tracing of stomatal lineage cells reveals that stomatal overproduction in 28y is caused by the excessive asymmetric spacing division of SLGCs. Further genetic results demonstrated that AGO1 acts downstream of TMM and negatively regulates the SPCH transcripts, but in a brassinosteroid-independent manner. Upregulation of AGAMOUS-LIKE16 (AGL16) in 28y mutants suggests that AGO1 is required to restrict AGL16-mediated stomatal spacing divisions, an miRNA pathway in addition to ligand-receptor signaling modules.