4.7 Article

A viral protein orchestrates rice ethylene signaling to coordinate viral infection and insect vector- mediated transmission

期刊

MOLECULAR PLANT
卷 15, 期 4, 页码 689-705

出版社

CELL PRESS
DOI: 10.1016/j.molp.2022.01.006

关键词

arboviruses; ethylene signaling; host-virus-vector interaction; SRBSDV; OsRTH2; OsEIL2

资金

  1. National Natural Science Foundation of China [31871928, 31671993]
  2. Guangdong Special Branch Plan for Young Talent with Scientific and Technological Innovation [2019TQ05N158]
  3. Pearl River S&T Nova Program of Guangzhou [201906010093]
  4. Research and Development Project in Major Fields of Guangdong [2019B020238001]
  5. Guangdong Provincial Innovation Team for General Key Technologies in Modern Agricultural Industry [2019KJ133]

向作者/读者索取更多资源

This study reveals the molecular mechanism of transmission of the Southern rice black-streaked dwarf virus (SRBSDV), finding that the SRBSDV-encoded P6 protein regulates rice ethylene signaling to coordinate viral infection and transmission. In early infection, P6 interacts with OsRTH2 to activate ethylene signaling and enhance virus proliferation, repelling the insect vector. In late infection, P6 enters the nucleus and interacts with OsEIL2 to suppress ethylene signaling, attracting the insect vector for viral transmission.
Arthropod-borne viruses cause serious threats to human health and global agriculture by rapidly spreading via insect vectors. Southern rice black-streaked dwarf virus (SRBSDV) is the most damaging rice-infecting virus that is frequently transmitted by planthoppers. However, the molecular mechanisms underlying its propagation in the host plants and epidemics in the field are largely unknown. Here, we showed that the SRBSDV-encoded P6 protein is a key effector that regulates rice ethylene signaling to coordinate viral infection and transmission. In early SRBSDV infection, P6 interacts with OsRTH2 in the cytoplasm to acti-vate ethylene signaling and enhance SRBSDV proliferation; this also repels the insect vector to reduce infestation. In late infection, P6 enters the nucleus, where it interacts with OsEIL2, a key transcription factor of ethylene signaling. The P6-OsEIL2 interaction suppresses ethylene signaling by preventing the dimerization of OsEIL2, thereby facilitating viral transmission by attracting the insect vector. Collectively, these findings reveal a novel molecular mechanism by which an arbovirus modulates the host defense system to promote viral infection and transmission.

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