P-111 - Bacterial eﬀector hopAM1 ac vity reconfigures ETI responses.

Wednesday, July 16, 2025

13:30 - 15:15

Location: Confex Hall 3

Effector Interference Mechanisms

Presenting Author(s)

NK

Nestoras Kargios, PhD

University of Warwick
COVENTRY, England, United Kingdom

Author(s)

JS

John Sidda

University of Warwick
Coventry, England, United Kingdom
AF

Alice Flint

University of Warwick
COVENTRY, England, United Kingdom
AB

Adam Bayless

Colorado State University
Fort Collins, Colorado, United States
MN

Marc Nishimura

Professor
Colorado State University
Fort Collins, Colorado, United States
VN

Vardis Ntoukakis

University of Warwick
COVENTRY, England, United Kingdom
LS

Lijiang Song

University of Warwick
Coventry, England, United Kingdom
MG

Murray Grant

University of Warwick
Coventry, England, United Kingdom

Plant disease resistance (R) proteins comprise of two main classes of nucleotide-binding and leucine-rich repeat (LRR) domains, distinguished by either an N-terminal coiled-coil domain (CNL) or a Toll Interleukin 1 Receptor domain (TNL). Recently, it has been shown that the TIR domain of TNLs exhibits NADase activity, leading to the production of a novel nucleoside variant of cyclic ADP ribose, referred to as 2’cADPR. The functional NADase activity is crucial for initiating the hypersensitive response through an EDS1 (Enhanced Disease Susceptibility 1)-dependent pathway. Pseudomonas syringae pv. tomato DC3000 (Pst) utilizes 36 effectors which collaborate in suppressing host immunity, including two copies of the hopAM1 T3SS effector. Both HopAM1-1 and HopAM1-2 possess a TIR domain but produce 3’cADPR. It was previously shown that 3’cADPR plays a role in suppressing immunity to Pst. Here, we explored the impact of HopAM1 on ETI dynamics and outcomes, in both Col-0 and mutants lines compromising TNL signalling. Using whole plant image techniques, chlorophyll fluorescence and biophoton imaging, we show different impacts of HopAM1 function on both CNL and TNL signalling and attempt to rationalise these altered ETI dynamics using various resistance signalling mutants. We further demonstrate that TIR v-cADPR derived metabolite with isomers produced by the activity of TNLs and hopAM1 could play a role in altering plant immune responses.