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GhKWL1 上调了 …… 的表达,但其功能受到与病原菌效应蛋白 VdISC1 结合的抑制。

GhKWL1 Upregulates but Its Function Is Impaired by Binding with VdISC1, a Pathogenic Effector of .

机构信息

Biotechnology Research Center, Southwest University, No. 2 Tiansheng Road, Beibei, Chongqing 400716, China.

出版信息

Int J Mol Sci. 2021 Jul 8;22(14):7328. doi: 10.3390/ijms22147328.

DOI:10.3390/ijms22147328
PMID:34298948
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8306359/
Abstract

Verticillium wilt, caused by , is a devastating disease for many important crops, including cotton. Kiwellins (KWLs), a group of cysteine-rich proteins synthesized in many plants, have been shown to be involved in response to various phytopathogens. To evaluate genes for their function in resistance to Verticillium wilt, we investigated KWL homologs in cotton. Thirty-five genes () were identified from the genome of upland cotton (). Among them, GhKWL1 was shown to be localized in nucleus and cytosol, and its gene expression is induced by the infection of . We revealed that GhKWL1 was a positive regulator of . Silencing of resulted in a decrease, whereas overexpression led to an increase in resistance of transgenic plants to Verticillium wilt. Interestingly, through binding to GhKWL1, the pathogenic effector protein VdISC1 produced by could impair the defense response mediated by GhKWL1. Therefore, our study suggests there is a GhKWL1-mediated defense response in cotton, which can be hijacked by through the interaction of VdISC1 with GhKWL1.

摘要

黄萎病是由 引起的,是许多重要作物(包括棉花)的毁灭性病害。凯林蛋白(KWLs)是一组在许多植物中合成的富含半胱氨酸的蛋白质,已被证明参与了对各种植物病原体的反应。为了评估基因在抗黄萎病中的功能,我们研究了棉花中的 KWL 同源物。从陆地棉()基因组中鉴定出 35 个 基因()。其中,GhKWL1 被证明定位于细胞核和细胞质中,其基因表达受 的感染诱导。我们揭示了 GhKWL1 是 的正调控因子。 的沉默导致抗性下降,而过表达导致转基因植物对黄萎病的抗性增加。有趣的是, 通过与 GhKWL1 结合, 产生的致病性效应蛋白 VdISC1 可以破坏 GhKWL1 介导的防御反应。因此,我们的研究表明,棉花中存在 GhKWL1 介导的防御反应, 可以通过 VdISC1 与 GhKWL1 的相互作用来劫持该反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea10/8306359/3f53203f1064/ijms-22-07328-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea10/8306359/25df51cd97de/ijms-22-07328-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea10/8306359/5cf11eac8aeb/ijms-22-07328-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea10/8306359/9d570f6a5dc0/ijms-22-07328-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea10/8306359/52f71282b591/ijms-22-07328-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea10/8306359/95e7dcdb1a6f/ijms-22-07328-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea10/8306359/3f53203f1064/ijms-22-07328-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea10/8306359/25df51cd97de/ijms-22-07328-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea10/8306359/5cf11eac8aeb/ijms-22-07328-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea10/8306359/9d570f6a5dc0/ijms-22-07328-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea10/8306359/52f71282b591/ijms-22-07328-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea10/8306359/95e7dcdb1a6f/ijms-22-07328-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea10/8306359/3f53203f1064/ijms-22-07328-g006.jpg

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