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TaPIMP2,小麦中一种病原诱导的 MYB 蛋白,有助于宿主抵抗由旋孢腔菌引起的普通根腐病。

TaPIMP2, a pathogen-induced MYB protein in wheat, contributes to host resistance to common root rot caused by Bipolaris sorokiniana.

机构信息

The National Key Facility for Crop Gene Resources and Genetic Improvement, Institute of Crop Science, Chinese Academy of Agricultural Sciences, Beijing, 100081, China.

出版信息

Sci Rep. 2017 May 11;7(1):1754. doi: 10.1038/s41598-017-01918-7.

DOI:10.1038/s41598-017-01918-7
PMID:28496196
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5431884/
Abstract

MYB transcription factors (TFs) have been implicated in various biology processes in model plants. However, functions of the great majority of MYB TFs in wheat (Triticum aestivum L.) have not been characterized. The soil-borne fungal pathogens Bipolaris sorokiniana and Rhizoctonia cerealis are the causal agents of important destructive diseases of wheat. Here, the TaPIMP2 gene, encoding a pathogen-induced MYB protein in wheat, was isolated through comparative transcriptomic analysis, and its defensive role was studied. TaPIMP2 was proved to localize in nuclei. TaPIMP2 responded in a different extent and speed upon infections of B. sorokiniana or R. cerealis. TaPIMP2 displayed different expression patterns after exogenous application of phytohormones, including abscisic acid, ethylene, and salicylic acid. Silencing of TaPIMP2 repressed resistance of wheat cultivar Yangmai 6 to B. sorokiniana, but did not alter resistance of wheat line CI12633 to R. cerealis. TaPIMP2 overexpression significantly improved resistance to B. sorokiniana rather than R. cerealis in transgenic wheat. Moreover, TaPIMP2 positively modulated the expression of pathogenesis-related genes, including PR1a, PR2, PR5, and PR10. Collectively, TaPIMP2 positively contributes to wheat resistance to B. sorokiniana possibly through regulating the expression of defense-related genes, and TaPIMP2 plays distinct roles in defense responses to different fungal infection.

摘要

MYB 转录因子(TFs)已被牵涉到模式植物的各种生物学过程中。然而,小麦(Triticum aestivum L.)中绝大多数 MYB TF 的功能尚未得到表征。土传真菌病原体双极镰刀菌和禾谷丝核菌是小麦重要破坏性疾病的病原体。本研究通过比较转录组分析,分离了小麦中一个编码病原菌诱导 MYB 蛋白的 TaPIMP2 基因,并研究了其防御作用。证明 TaPIMP2 定位于细胞核内。TaPIMP2 在受到双极镰刀菌或禾谷丝核菌感染时,其响应的程度和速度不同。TaPIMP2 在受到外源植物激素(包括脱落酸、乙烯和水杨酸)处理后,表现出不同的表达模式。TaPIMP2 的沉默抑制了小麦品种扬麦 6 对双极镰刀菌的抗性,但不改变小麦品系 CI12633 对禾谷丝核菌的抗性。TaPIMP2 的过表达显著提高了转基因小麦对双极镰刀菌的抗性,而不是对禾谷丝核菌的抗性。此外,TaPIMP2 还能正向调控病程相关基因(如 PR1a、PR2、PR5 和 PR10)的表达。综上所述,TaPIMP2 通过调控防御相关基因的表达,正向促进小麦对双极镰刀菌的抗性,而在防御不同真菌侵染时,TaPIMP2 发挥着不同的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/12d2d6096233/41598_2017_1918_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/8d7388c8d190/41598_2017_1918_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/68d8211380f6/41598_2017_1918_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/2923803d1d62/41598_2017_1918_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/3b635bdc0048/41598_2017_1918_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/fa360d07479e/41598_2017_1918_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/7ac76761021f/41598_2017_1918_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/20ad7e993988/41598_2017_1918_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/12d2d6096233/41598_2017_1918_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/8d7388c8d190/41598_2017_1918_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/68d8211380f6/41598_2017_1918_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/2923803d1d62/41598_2017_1918_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/3b635bdc0048/41598_2017_1918_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/fa360d07479e/41598_2017_1918_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/7ac76761021f/41598_2017_1918_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/20ad7e993988/41598_2017_1918_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3fd/5431884/12d2d6096233/41598_2017_1918_Fig8_HTML.jpg

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