Tomato chlorosis virus-encoded p22 suppresses auxin signaling to promote infection via interference with SKP1-Cullin-F-boxTIR1 complex assembly.

Abstract

Phytohormone auxin plays a fundamental role in plant growth and defense against pathogens. However, how auxin signaling is regulated during virus infection in plants remains largely unknown. Auxin/indole-3-acetic acid (Aux/IAA) is the repressor of auxin signaling and can be recognized by an F-box protein transport inhibitor response 1 (TIR1). Ubiquitination and degradation of Aux/IAA by SKP1-Cullin-F-boxTIR1 (SCFTIR1 ) complex can trigger auxin signaling. Here, with an emerging important plant virus worldwide, we showed that tomato chlorosis virus (ToCV) infection or stable transgenic overexpression of its p22 protein does not alter auxin accumulation level but significantly decreases the expression of auxin signaling responsive genes, suggesting that p22 can attenuate host auxin signaling. Further, p22 could bind the C-terminal of SKP1.1 and compete with TIR1 to interfere with the SCFTIR1 complex assembly, leading to a suppression of Aux/IAA degradation. Silencing and over-expression assays suggested that both NbSKP1.1 and NbTIR1 suppress ToCV accumulation and disease symptoms. Altogether, ToCV p22 disrupts the auxin signaling through destabilizing SCFTIR1 by interacting with the C-terminal of NbSKP1.1 to promote ToCV infection. Our findings uncovered a previously unknown molecular mechanism employed by a plant virus to manipulate SCF complex-mediated ubiquitin pathway and to reprogram auxin signaling for efficient infection. This article is protected by copyright. All rights reserved.