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Elife. 2020 Mar 24;9. pii: e53753. doi: 10.7554/eLife.53753. [Epub ahead of print]

CCR4, a RNA decay factor, is hijacked by a plant cytorhabdovirus phosphoprotein to facilitate virus replication.

Author information

1
College of Biological Sciences, China Agricultural University, Beijing, China.
2
State Key Laboratory of Agro-Biotechnology, China Agricultural University, Beijing, China.
3
College of Plant Protection, China Agricultural University, Beijing, China.
4
Department of Plant Pathology, College of Plant Protection, Shandong Agricultural University, Tai'an, China.

Abstract

Carbon catabolite repression 4 (CCR4) is a conserved mRNA deadenylase regulating posttranscriptional gene expression. However, regulation of CCR4 in virus infections is less understood. Here, we characterized a pro-viral role of CCR4 in replication of a plant cytorhabdovirus, Barley yellow striate mosaic virus (BYSMV). The barley (Hordeum vulgare) CCR4 protein (HvCCR4) was identified to interact with the BYSMV phosphoprotein (P). The BYSMV P protein recruited HvCCR4 from processing bodies (PBs) into viroplasm-like bodies. Overexpression of HvCCR4 promoted BYSMV replication in plants. Conversely, knockdown of the small brown planthopper CCR4 inhibited viral accumulation in the insect vector. Biochemistry experiments revealed that HvCCR4 was recruited into N-RNA complexes by the BYSMV P protein and triggered turnover of N-bound cellular mRNAs, thereby releasing RNA-free N protein to bind viral genomic RNA for optimal viral replication. Our results demonstrate that the co-opted the CCR4-mediated RNA decay facilitates cytorhabdovirus replication in plants and insects.

KEYWORDS:

infectious disease; microbiology; plant biology; viruses

PMID:
32207684
DOI:
10.7554/eLife.53753
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Conflict of interest statement

ZZ, QG, XF, ZD, DG, WX, QC, JQ, YY, CH, YW, XY, DL, XW The authors declare that no competing interests exist.

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