A bacterial effector targets host plasmodesmata to promote pathogen virulence in plants
K. AUNG (1), S. He (1) (1) Michigan State University, U.S.A.

The Arabidopsis-Pseudomonas syringae pv. tomato (Pst) DC3000 pathosystem has been extensively studied to elucidate basic principles underlying plant-microbe interactions. Previous studies have led to a model in which plants and pathogens battle to activate/suppress defense signaling within infected host cells; however, whether bacteria also modulate host cell-to-cell communication between infected and adjoining non-infected host cells is unknown. Recent reports demonstrated that plants induce the closure of plasmodesmata (PD) as part of a defense response against bacterial infection. PD is a membrane-lined channel, which connects adjacent cells in plants to facilitate cell-to-cell communication. To overcome plant defense, Pst DC3000 injects 36 virulence effector proteins into plant cells to subvert host immunity. Using live cell imaging, we discovered that Pst DC3000 effector protein HopO1-1 is targeted to the PD in Arabidopsis. Expression of HopO1-1 in Arabidopsis leads to an increase in PD-dependent molecular flux between plant cells. HopO1-1 is physically associated with Arabidopsis PD-located proteins (PDLP5 and PDLP7); both PDLPs are involved in plant immunity against bacterial infection. Consistent with its putative ADP-ribosyltransferase activity, we showed that HopO1-1 is an active enzyme. Moreover, deletion of hopO1-1 from Pst DC3000 genome leads to a significant defect in bacterial proliferation upon infection and greatly reduces distal spreading when the bacteria are inoculated locally. The finding raises the exciting possibility that bacterial pathogens deliver effectors such as HopO1-1 to modulate host cell-to-cell communication to facilitate initial infection and distal spreading of bacteria.

Abstract Number: P7-154
Session Type: Poster