Ying Li , Xipan Wang , Kaijie Shang , Na Xu , Ting Zhang , Hongmei Liu , Shumei Zhou , Changxiang Zhu , Chenchen Wang

Abstract

Rice stripe virus (RSV) causes substantial rice (Oryza sativa) yield losses and poses a serious threat to agricultural production. Auxin is a pivotal hormone in orchestrating the antagonism between plant growth and defense. Conversely, pathogen manipulation of auxin signaling promotes disease and inhibits plant growth, but how this hormone influences immunity is not fully understood. Here, we report that RSV infection results in dwarfism and short crown roots in rice and reduces the sensitivity of rice plants to NAA. The RSV-encoded nonstructural protein 3 (NS3) interacts with Aux/IAA repressor protein OsIAA25, disrupting its degradation by the auxin receptor transport inhibitor response 1 (OsTIR1). Additionally, NS2 and NS3 can form heterodimers to enhance the ability to stabilize OsIAA25. Plants overexpressing OsIAA25 or OsIAA25P98L, a single-amino-acid substitution of leucine for proline at position 98, exhibit growth and development defects similar to RSV-infected plants and increased susceptibility to RSV infection. By contrast, OsIAA25 knockout plants display an opposite phenotype, indicating that OsIAA25 positively regulates RSV infection. Thus, our findings establish a mechanism by which RSV proteins guide virus infection and affect plant growth by interfering with the auxin signaling pathway through their interaction with rice OsIAA25.

Paper Linkage:https://doi.org/10.1093/plphys/kiag080