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过表达野生型 IAA15 导致生长素稳态失调，从而影响根干细胞的分化和向重力性。

Perturbation of auxin homeostasis by overexpression of wild-type IAA15 results in impaired stem cell differentiation and gravitropism in roots.

机构信息

State Key Laboratory of Hybrid Rice, College of Life Sciences, Wuhan University, Wuhan, Hubei, China.

出版信息

PLoS One. 2013;8(3):e58103. doi: 10.1371/journal.pone.0058103. Epub 2013 Mar 5.

DOI:10.1371/journal.pone.0058103
PMID:23472140
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3589423/
Abstract

Aux/IAAs interact with auxin response factors (ARFs) to repress their transcriptional activity in the auxin signaling pathway. Previous studies have focused on gain-of-function mutations of domain II and little is known about whether the expression level of wild-type Aux/IAAs can modulate auxin homeostasis. Here we examined the perturbation of auxin homeostasis by ectopic expression of wild-type IAA15. Root gravitropism and stem cell differentiation were also analyzed. The transgenic lines were less sensitive to exogenous auxin and exhibited low-auxin phenotypes including failures in gravity response and defects in stem cell differentiation. Overexpression lines also showed an increase in auxin concentration and reduced polar auxin transport. These results demonstrate that an alteration in the expression of wild-type IAA15 can disrupt auxin homeostasis.

摘要

Aux/IAAs 与生长素响应因子 (ARFs) 相互作用，抑制生长素信号通路中它们的转录活性。以前的研究集中在结构域 II 的功能获得性突变上，而对于野生型 Aux/IAAs 的表达水平是否可以调节生长素稳态知之甚少。在这里，我们通过异位表达野生型 IAA15 来研究生长素稳态的干扰。还分析了根向重力性和干细胞分化。转基因系对外源生长素的敏感性较低，表现出低生长素表型，包括对重力反应的失败和干细胞分化的缺陷。过表达系也表现出生长素浓度的增加和极性生长素运输的减少。这些结果表明，野生型 IAA15 表达的改变会破坏生长素稳态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d6f/3589423/0b141e6bbce9/pone.0058103.g010.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d6f/3589423/b7e779b1491c/pone.0058103.g009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d6f/3589423/5e4a28e9cb83/pone.0058103.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d6f/3589423/0fc6b87eb21b/pone.0058103.g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d6f/3589423/0b141e6bbce9/pone.0058103.g010.jpg

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