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CLAVATA1控制不同的信号输出,通过两步转录补偿环缓冲茎尖干细胞增殖。

CLAVATA1 controls distinct signaling outputs that buffer shoot stem cell proliferation through a two-step transcriptional compensation loop.

作者信息

Nimchuk Zachary L

机构信息

Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States of America.

Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States of America.

出版信息

PLoS Genet. 2017 Mar 29;13(3):e1006681. doi: 10.1371/journal.pgen.1006681. eCollection 2017 Mar.

DOI:10.1371/journal.pgen.1006681
PMID:28355208
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5371295/
Abstract

The regulation of stem cell proliferation in plants is controlled by intercellular signaling pathways driven by the diffusible CLAVATA3 (CLV3p) peptide. CLV3p perception is thought to be mediated by an overlapping array of receptors in the stem cell niche including the transmembrane receptor kinase CLV1, Receptor-Like Protein Kinase 2 (RPK2), and a dimer of the receptor-like protein CLV2 and the CORYNE (CRN) pseudokinase. Mutations in these receptors have qualitatively similar effects on stem cell function but it is unclear if this represents common or divergent signaling outputs. Previous work in heterologous systems has suggested that CLV1, RPK2 and CLV2/CRN could form higher order complexes but it is also unclear what relevance these putative complexes have to in vivo receptor functions. Here I use the in vivo regulation of a specific transcriptional target of CLV1 signaling in Arabidopsis to demonstrate that, despite the phenotypic similarities between the different receptor mutants, CLV1 controls distinct signaling outputs in living stem cell niches independent of other receptors. This regulation is separable from stem cell proliferation driven by WUSCHEL, a proposed common transcriptional target of CLV3p signaling. In addition, in the absence of CLV1, CLV1-related receptor kinases are ectopically expressed but also buffer stem cell proliferation through the auto-repression of their own expression. Collectively these data reveal a unique in vivo role for CLV1 separable from other stem cell receptors and provides a framework for dissecting the signaling outputs in stem cell regulation.

摘要

植物中干细胞增殖的调控由可扩散的CLAVATA3(CLV3p)肽驱动的细胞间信号通路控制。CLV3p的感知被认为是由干细胞微环境中的一系列重叠受体介导的,包括跨膜受体激酶CLV1、类受体蛋白激酶2(RPK2)以及受体样蛋白CLV2和CORYNE(CRN)假激酶的二聚体。这些受体的突变对干细胞功能有定性相似的影响,但尚不清楚这是否代表共同或不同的信号输出。先前在异源系统中的研究表明,CLV1、RPK2和CLV2/CRN可能形成高阶复合物,但这些假定的复合物与体内受体功能有何关联也不清楚。在这里,我利用拟南芥中CLV1信号特定转录靶点的体内调控来证明尽管不同受体突变体之间存在表型相似性,但CLV1在活的干细胞微环境中独立于其他受体控制着不同的信号输出。这种调控与由WUSCHEL驱动的干细胞增殖是可分离的,WUSCHEL是CLV3p信号的一个假定共同转录靶点。此外,在没有CLV1的情况下,CLV1相关的受体激酶异位表达,但也通过自身表达的自动抑制来缓冲干细胞增殖。这些数据共同揭示了CLV1与其他干细胞受体不同的独特体内作用,并为剖析干细胞调控中的信号输出提供了一个框架。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a470/5371295/dc6135cdab8b/pgen.1006681.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a470/5371295/e0d0c7cd830c/pgen.1006681.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a470/5371295/de7a301a6c55/pgen.1006681.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a470/5371295/4399436ed822/pgen.1006681.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a470/5371295/3f4fe9332f83/pgen.1006681.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a470/5371295/8715b90401dc/pgen.1006681.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a470/5371295/dc6135cdab8b/pgen.1006681.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a470/5371295/e0d0c7cd830c/pgen.1006681.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a470/5371295/de7a301a6c55/pgen.1006681.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a470/5371295/4399436ed822/pgen.1006681.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a470/5371295/3f4fe9332f83/pgen.1006681.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a470/5371295/8715b90401dc/pgen.1006681.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a470/5371295/dc6135cdab8b/pgen.1006681.g006.jpg

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