4.7 Article

A fijiviral nonstructural protein triggers cell death in plant and bacterial cells via its transmembrane domain

期刊

MOLECULAR PLANT PATHOLOGY
卷 24, 期 1, 页码 59-70

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WILEY
DOI: 10.1111/mpp.13277

关键词

cell death; fijivirus; transmembrane domain; viral nonstructural protein

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The P9-2 protein of Southern rice black-streaked dwarf virus (SRBSDV) has been found to induce cell death in both bacterial and plant cells. Its localization to the plasma membrane (PM) is essential for its cell death-inducing ability. The central transmembrane hydrophobic domain and specific amino acid residues play important roles in the induction of cell death by P9-2. This study also suggests that the nonstructural protein of fijiviruses may trigger cell death by targeting conserved cellular factors or via a highly conserved mechanism.
Southern rice black-streaked dwarf virus (SRBSDV; Fijivirus, Reoviridae) has become a threat to cereal production in East Asia in recent years. Our previous cytopathologic studies have suggested that SRBSDV induces a process resembling programmed cell death in infected tissues that results in distinctive growth abnormalities. The viral product responsible for the cell death, however, remains unknown. Here P9-2 protein, but not its RNA, was shown to induce cell death in Escherichia coli and plant cells when expressed either locally with a transient expression vector or systemically using a heterologous virus. Both computer prediction and fluorescent assays indicated that the viral nonstructural protein was targeted to the plasma membrane (PM) and further modification of its subcellular localization abolished its ability to induce cell death, indicating that its PM localization was required for the cell death induction. P9-2 was predicted to harbour two transmembrane helices within its central hydrophobic domain. A series of mutation assays further showed that its central transmembrane hydrophobic domain was crucial for cell death induction and that its conserved F90, Y101, and L103 amino acid residues could play synergistic roles in maintaining its ability to induce cell death. Its homologues in other fijiviruses also induced cell death in plant and bacterial cells, implying that the fijiviral nonstructural protein may trigger cell death by targeting conserved cellular factors or via a highly conserved mechanism.

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