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一种与内体相互作用并促进SHORT-ROOT 转录因子运动的必需蛋白。

An essential protein that interacts with endosomes and promotes movement of the SHORT-ROOT transcription factor.

机构信息

Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.

出版信息

Curr Biol. 2011 Sep 27;21(18):1559-64. doi: 10.1016/j.cub.2011.08.013. Epub 2011 Sep 15.

Abstract

Plant cells can communicate through the direct transport of transcription factors [1-7]. One of the best-studied examples of this phenomenon is SHORT-ROOT (SHR), which moves from the stele cells into the endodermis and root tip of Arabidopsis, where it specifies endodermal cell identity and stem cell function, respectively [8-10]. In the endodermis, SHR upregulates the transcription factors SCARECROW (SCR) [2] and JACKDAW (JKD), which in turn inhibit movement of SHR from the endodermis [11]. Although much is known about the regulatory pathways that mediate expression and activity of SHR [1, 8-14], little is known about the factors that promote its movement or the movement of other transcription factors. We have identified a novel protein, SHORT-ROOT INTERACTING EMBRYONIC LETHAL (SIEL), that interacts with SHR, CAPRICE (CPC), TARGET OF MONOPTEROUS 7 (TMO7), and AGAMOUS-LIKE 21 (AGL21). Null alleles of SIEL are embryonic lethal. Hypomorphic alleles produce defects in root patterning and reduce SHR movement. Surprisingly, both SHR and SCR regulate expression of SIEL, so that siel/scr and siel/shr double mutants have extremely disorganized roots. SIEL localizes to the nucleus and cytoplasm of root cells where it is associated with endosomes. We propose that SIEL is an endosome-associated protein that promotes intercellular movement.

摘要

植物细胞可以通过转录因子的直接运输进行通讯[1-7]。这种现象的一个研究得最好的例子是SHORT-ROOT(SHR),它从中柱细胞移动到拟南芥的内皮层和根尖,在那里它分别指定内皮层细胞的身份和干细胞功能[8-10]。在内皮层中,SHR 上调转录因子 SCARECROW(SCR)[2]和 JACKDAW(JKD),这反过来又抑制 SHR 从内皮层的运动[11]。尽管人们对介导 SHR 表达和活性的调控途径了解很多[1,8-14],但对促进其运动或其他转录因子运动的因素知之甚少。我们已经鉴定出一种新的蛋白质,SHORT-ROOT INTERACTING EMBRYONIC LETHAL(SIEL),它与 SHR、CAPRICE(CPC)、MONOPTEROUS 7 的靶蛋白(TMO7)和 AGAMOUS-LIKE 21(AGL21)相互作用。SIEL 的缺失等位基因是胚胎致死的。功能减弱的等位基因导致根模式缺陷,并减少 SHR 的运动。令人惊讶的是,SHR 和 SCR 都调节 SIEL 的表达,因此 siel/scr 和 siel/shr 双突变体的根极不规则。SIEL 定位于根细胞的细胞核和细胞质,在那里它与内体相关联。我们提出 SIEL 是一种与内体相关的蛋白,可促进细胞间运动。

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