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通过靶向致病性和发育基因对稻瘟病进行宿主诱导基因沉默以控制该病。

Host induced gene silencing of by targeting pathogenicity and development genes to control rice blast disease.

作者信息

Wang Mengying, Dean Ralph A

机构信息

Fungal Genomics Laboratory, Department of Entomology and Plant Pathology, Center for Integrated Fungal Research, North Carolina State University, Raleigh, NC, United States.

出版信息

Front Plant Sci. 2022 Aug 11;13:959641. doi: 10.3389/fpls.2022.959641. eCollection 2022.

DOI:10.3389/fpls.2022.959641
PMID:36035704
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9403838/
Abstract

Rice blast disease caused by the hemi-biotrophic fungus is the most destructive disease of rice world-wide. Traditional disease resistance strategies for the control of rice blast disease have not proved durable. HIGS (host induced gene silencing) is being developed as an alternative strategy. Six genes () that play important roles in pathogenicity and development of were chosen for HIGS. HIGS vectors were transformed into rice calli through -mediated transformation and T0, T1 and T2 generations of transgenic rice plants were generated. Except for , HIGS transgenic rice plants challenged with showed significantly reduced disease compared with non-silenced control plants. Following infection with of HIGS transgenic plants, expression levels of target genes were reduced as demonstrated by Quantitative RT-PCR. In addition, treating with small RNA derived from the target genes inhibited fungal growth. These findings suggest RNA silencing signals can be transferred from host to an invasive fungus and that HIGS has potential to generate resistant rice against .

摘要

由半活体营养型真菌引起的稻瘟病是全球水稻最具毁灭性的病害。传统控制稻瘟病的抗病策略尚未证明具有持久性。宿主诱导基因沉默(HIGS)正在被开发为一种替代策略。选择了六个在该真菌致病性和发育中起重要作用的基因用于HIGS。通过农杆菌介导的转化将HIGS载体导入水稻愈伤组织,并产生了T0、T1和T2代转基因水稻植株。除了一个基因外,与未沉默的对照植株相比,用该真菌挑战的HIGS转基因水稻植株表现出显著降低的病害。用HIGS转基因植物的该真菌感染后,定量RT-PCR证明靶基因的表达水平降低。此外,用来自靶基因的小RNA处理该真菌可抑制其生长。这些发现表明RNA沉默信号可以从宿主转移到入侵真菌,并且HIGS有潜力产生抗该真菌的抗性水稻。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1314/9403838/3a117169b89c/fpls-13-959641-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1314/9403838/3e59efc75fd1/fpls-13-959641-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1314/9403838/f690f4712c6c/fpls-13-959641-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1314/9403838/3a117169b89c/fpls-13-959641-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1314/9403838/73c29b0e46d2/fpls-13-959641-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1314/9403838/177d93f032f3/fpls-13-959641-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1314/9403838/ecdbef559c1b/fpls-13-959641-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1314/9403838/b75c6124bd2e/fpls-13-959641-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1314/9403838/af98f9a92a66/fpls-13-959641-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1314/9403838/3e59efc75fd1/fpls-13-959641-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1314/9403838/f690f4712c6c/fpls-13-959641-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1314/9403838/3a117169b89c/fpls-13-959641-g008.jpg

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