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dc.contributor.authorWeiberg, Arneen_US
dc.contributor.authorWang, Mingen_US
dc.contributor.authorLin, Feng-Maoen_US
dc.contributor.authorZhao, Hongweien_US
dc.contributor.authorZhang, Zhihongen_US
dc.contributor.authorKaloshian, Isgouhien_US
dc.contributor.authorHuang, Hsien-Daen_US
dc.contributor.authorJin, Hailingen_US
dc.date.accessioned2014-12-08T15:32:15Z-
dc.date.available2014-12-08T15:32:15Z-
dc.date.issued2013-10-04en_US
dc.identifier.issn0036-8075en_US
dc.identifier.urihttp://dx.doi.org/10.1126/science.1239705en_US
dc.identifier.urihttp://hdl.handle.net/11536/22682-
dc.description.abstractBotrytis cinerea, the causative agent of gray mold disease, is an aggressive fungal pathogen that infects more than 200 plant species. Here, we show that some B. cinerea small RNAs (Bc-sRNAs) can silence Arabidopsis and tomato genes involved in immunity. These Bc-sRNAs hijack the host RNA interference (RNAi) machinery by binding to Arabidopsis Argonaute 1 (AGO1) and selectively silencing host immunity genes. The Arabidopsis ago1 mutant exhibits reduced susceptibility to B. cinerea, and the B. cinerea dcl1 dcl2 double mutant that can no longer produce these Bc-sRNAs displays reduced pathogenicity on Arabidopsis and tomato. Thus, this fungal pathogen transfers "virulent" sRNA effectors into host plant cells to suppress host immunity and achieve infection, which demonstrates a naturally occurring cross-kingdom RNAi as an advanced virulence mechanism.en_US
dc.language.isoen_USen_US
dc.titleFungal Small RNAs Suppress Plant Immunity by Hijacking Host RNA Interference Pathwaysen_US
dc.typeArticleen_US
dc.identifier.doi10.1126/science.1239705en_US
dc.identifier.journalSCIENCEen_US
dc.citation.volume342en_US
dc.citation.issue6154en_US
dc.citation.spage118en_US
dc.citation.epage123en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.department生物資訊及系統生物研究所zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.contributor.departmentInstitude of Bioinformatics and Systems Biologyen_US
dc.identifier.wosnumberWOS:000325126100059-
dc.citation.woscount44-
Appears in Collections:Articles