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BIG 通过拟南芥根中的 SCR/SHR 途径调节干细胞生态位和分生组织发育。

BIG Modulates Stem Cell Niche and Meristem Development via SCR/SHR Pathway in Arabidopsis Roots.

机构信息

State Key Laboratory of Hybrid Rice, Department of Plant Sciences, College of Life Sciences, Wuhan University, Wuhan 430072, China.

Hubei Hongshan Laboratory, Wuhan 430070, China.

出版信息

Int J Mol Sci. 2022 Jun 17;23(12):6784. doi: 10.3390/ijms23126784.

DOI:10.3390/ijms23126784
PMID:35743225
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9224481/
Abstract

BIG, a regulator of polar auxin transport, is necessary to regulate the growth and development of Arabidopsis. Although mutations in the gene cause severe root developmental defects, the exact mechanism remains unclear. Here, we report that disruption of the gene resulted in decreased quiescent center (QC) activity and columella cell numbers, which was accompanied by the downregulation of () gene expression. BIG affected auxin distribution by regulating the expression of PIN-FORMED proteins (PINs), but the root morphological defects of mutants could not be rescued solely by increasing auxin transport. Although the loss of gene function resulted in decreased expression of the and genes, genetic interaction assays indicate that this is not the main reason for the root morphological defects of mutants. Furthermore, genetic interaction assays suggest that BIG affects the stem cell niche (SCN) activity through the SCRSCARECROW (SCR)/SHORT ROOT (SHR) pathway and BIG disruption reduces the expression of and genes. In conclusion, our findings reveal that the gene maintains root meristem activity and SCN integrity mainly through the SCR/SHR pathway.

摘要

BIG 是极性生长素运输的调节剂,对于调控拟南芥的生长和发育是必需的。尽管 基因的突变会导致严重的根发育缺陷,但确切的机制仍不清楚。在这里,我们报告称, 基因的破坏导致静止中心(QC)活性和中柱细胞数量减少,同时伴随着 ()基因表达的下调。BIG 通过调节 PIN 蛋白(PINs)的表达来影响生长素的分布,但仅仅通过增加生长素运输并不能挽救 突变体的根形态缺陷。尽管 基因功能的丧失导致 和 基因的表达减少,但遗传相互作用分析表明,这不是 突变体根形态缺陷的主要原因。此外,遗传相互作用分析表明,BIG 通过 SCRSCARECROW(SCR)/SHORT ROOT(SHR)途径影响干细胞龛(SCN)活性,并且 BIG 破坏会降低 和 基因的表达。总之,我们的研究结果表明, 基因主要通过 SCR/SHR 途径维持根分生组织的活性和 SCN 的完整性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2de/9224481/b846bd86fde4/ijms-23-06784-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2de/9224481/aab06f7ca74a/ijms-23-06784-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2de/9224481/9c4247b73097/ijms-23-06784-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2de/9224481/081a2e136249/ijms-23-06784-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2de/9224481/e2464c4e92b1/ijms-23-06784-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2de/9224481/0a96958e8bba/ijms-23-06784-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2de/9224481/b846bd86fde4/ijms-23-06784-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2de/9224481/aab06f7ca74a/ijms-23-06784-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2de/9224481/9c4247b73097/ijms-23-06784-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2de/9224481/081a2e136249/ijms-23-06784-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2de/9224481/e2464c4e92b1/ijms-23-06784-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2de/9224481/0a96958e8bba/ijms-23-06784-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2de/9224481/b846bd86fde4/ijms-23-06784-g006.jpg

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