Investigating redundant roles by Myosin XI-K, Myosin XI-2 and CHUP1 during Cauliflower mosaic virus infection of Arabidopsis thaliana
J. SCHOELZ (1), C. Angel (2), A. Rodriguez (1), Y. Zhang (1), P. Harries (3), R. Nelson (4) (1) University of Missouri, U.S.A.; (2) Cenicafe, Colombia; (3) Pittsburgh State University, U.S.A.; (4) The Samuel Roberts Noble Foundation, U.S.A.

The P6 effector of Cauliflower mosaic virus (CaMV) is a multifunctional virus protein that forms inclusion bodies (IBs) in infected cells. P6 IBs have the capacity to interact with and move in association with microfilaments, and several studies now suggest that P6 IBs may utilize microfilaments to deliver virions to plasmodesmata for movement to adjacent cells. To investigate the mechanism for intracellular movement of P6 IBs, we have utilized yeast two hybrid and co-immunoprecipitation assays to identify candidate host proteins that interact with P6, coupled with inoculation of CaMV virions to T-DNA knockouts of Arabidopsis thaliana. Previous studies have shown that P6 interacts with CHUP1, a plant protein that contributes to chloroplast movement on microfilaments, and CaMV infections of chup1 T-DNA knockout plants are delayed relative to wild type Col-0 plants. We have now extended our analysis of T-DNA knockouts to include several myosins. CaMV local lesion appearance was delayed in myosin xi-2, xi-K and chup1 T-DNA knockout plants, but no delay was observed in the viii-A and viii-B knockout lines, relative to Col-0. CaMV infections were delayed further with each of the double knockouts (chup1/xi-2, xhup1/xi-k, xi-k/xi-2) as well as for the triple knockout (chup1/xi-2/xi-k). This study suggests that CHUP1, Myosin XI-2, and Myosin XI-K may be functionally redundant in contributing to intracellular movement of CaMV P6 IBs for delivery of virions to plasmodesmata.

Abstract Number: P7-209
Session Type: Poster