The Rice Stripe Virus p2 Interacts With Lsm1 and Disrupts the Lsm1-Lsm4 Complex to Facilitate the Viral infection

Processing bodies (P-bodies) play central roles in RNA metabolism and in the regulation of viral infection. However, whether they function during infection by negative-strand RNA viruses, and how such viruses manipulate P-body activities, remain largely unclear. Here, we showed that the p2 protein encoded by rice stripe virus (RSV), a segmented negative-strand RNA virus, interacted with Lsm1, a core subunit of the Lsm1-7 complex responsible for decapping-dependent 5'-3' mRNA decay in P-bodies. Genetic analyses in rice and Nicotiana benthamiana demonstrated that Lsm1 negatively regulates RSV infection. Mechanistically, p2 binds a 17-amino-acid motif at the N terminus of OsLsm1 and competitively disrupts its association with OsLsm4, thereby impairing Lsm1-7 complex assembly. Consequently, RSV infection impairs P-body-mediated mRNA decay activity, as evidenced by the delayed turnover of marker transcripts (EXPL1 and SEN1). Our work suggests that P-bodies constitute a post-transcriptional barrier that restricts RSV infection. RSV overcomes this barrier by deploying p2 to associate with Lsm1 and weaken Lsm1-Lsm4 complex assembly. This counterdefence strategy allows RSV to modulate host RNA decay pathways to its advantage.