A single region of the Phytophthora infestans avirulence effector Avr3b functions in both cell death induction and plant immunity suppression

Abstract

As a destructive plant pathogen, Phytophthora infestans secretes diverse host-entering RxLR effectors to facilitate infection. One critical RxLR effector, PiAvr3b, not only induces effector-triggered immunity (ETI), which is associated with the potato resistance protein StR3b, but also suppresses pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI). To date, the molecular basis underlying such dual activities remains unknown. Based on phylogenetic analysis of global P. infestans isolates, we found two PiAvr3b isoforms that differ by three amino acids. Despite this sequence variation, the two isoforms retain the same properties in activating the StR3b-mediated hypersensitive response (HR) and inhibiting necrosis induced by three PAMPs (PiNpp, PiINF1, and PsXeg1) and an RxLR effector (Pi10232). Using a combined mutagenesis approach, we found that the dual activities of PiAvr3b were tightly linked and determined by 88 amino acids at the C-terminus. We further determined that either the W60 or the E134 residue of PiAvr3b was essential for triggering StR3b-associated HR and inhibiting PiNpp-and Pi10232-associated necrosis, while the S99 residue partially contributed to PTI suppression. Additionally, nuclear localization of PiAvr3b was required to stimulate HR and suppress PTI, but not to inhibit Pi10232-associated cell death. Our study revealed that PiAvr3b suppresses the plant immune response at different subcellular locations and provides an example in which a single amino acid of an RxLR effector links ETI induction and cell death suppression.

The Phytophthora parasitica effector AVH195 interacts with ATG8, attenuates host autophagy, and promotes biotrophic infection

“…S1). AVH153 expresses its cell death-inducing activity in tobacco, but not in N. benthamiana , similar to what has been observed for AVR3b [ 25 ]. We therefore used N. tabacum instead of N. benthamiana for transient expression in our cell death studies.…”

The Botrytis cinerea transglycosylase BcCrh4 is a cell death‐inducing protein with cell death‐promoting and ‐suppressing domains

“…The two domains probably compete for the same plant target since co‐infiltration of BcCrh4 75–126 with BcCrh4 22–41 and suppresses the induction of cell death and plant immune responses. Inhibition of the plant immune responses is a common mode of action of microbial effectors (Gu et al, 2023; Wang et al, 2022); however at this point, we are unable to determine whether the fungus actually uses the BcCrh4 75–126 domain to suppress PTI.…”

“…Inhibition of the plant immune responses is a common mode of action of microbial effectors (Gu et al, 2023;Wang et al, 2022); however at this point, we are unable to determine whether the fungus actually uses the BcCrh4 75-126 domain to suppress PTI.…”

Population Dynamics of Phytophthora infestans in Egypt Reveals Clonal Dominance of 23_A1 and Displacement of 13_A2 Clonal Lineage

“…Studying such molecular interactions are helpful to unravel the primary molecular mechanisms of resistance against late blight [ 62 ]. Similar to other oomycetes, the most studied effector AVR genes in P. infestans belong to the RxLR group due to the presence of a common RxLR domain [ 63 ]. Two commonly studied effector genes AVR2 and AVR2-like that related to resistance genes in the differential set were selected to study their presence or absence in eleven 23_A1 genotyped isolates from Egypt.…”