Necrosis and ethylene-inducing-like peptide patterns from crop pathogens induce differential responses within seven brassicaceous species

Plant Pathol. 2022 Dec;71(9):2004-2016. doi: 10.1111/ppa.13615. Epub 2022 Aug 5.

Abstract

Translational research is required to advance fundamental knowledge on plant immunity towards application in crop improvement. Recognition of microbe/pathogen-associated molecular patterns (MAMPs/PAMPs) triggers a first layer of immunity in plants. The broadly occurring family of necrosis- and ethylene-inducing peptide 1 (NEP1)-like proteins (NLPs) contains immunogenic peptide patterns that are recognized by a number of plant species. Arabidopsis can recognize NLPs by the pattern recognition receptor AtRLP23 and its co-receptors SOBIR1, BAK1, and BKK1, leading to induction of defence responses including the production of reactive oxygen species (ROS) and elevation of intracellular [Ca2+]. However, little is known about NLP perception in Brassica crop species. Within 12 diverse accessions for each of six Brassica crop species, we demonstrate variation in response to Botrytis cinerea NLP BcNEP2, with Brassica oleracea (CC genome) being nonresponsive and only two Brassica napus cultivars responding to BcNEP2. Peptides derived from four fungal pathogens of these crop species elicited responses similar to BcNEP2 in B. napus and Arabidopsis. Induction of ROS by NLP peptides was strongly reduced in Atrlp23, Atsobir1 and Atbak1-5 Atbkk1-1 mutants, confirming that recognition of Brassica pathogen NLPs occurs in a similar manner to that of HaNLP3 from Hyaloperonospora arabidopsidis in Arabidopsis. In silico analysis of the genomes of two B. napus accessions showed similar presence of homologues for AtBAK1, AtBKK1 and AtSOBIR1 but variation in the organization of AtRLP23 homologues. We could not detect a strong correlation between the ability to respond to NLP peptides and resistance to B. cinerea.

Keywords: brassica; grey mould; microbe/pathogen‐associated molecular pattern; necrosis and ethylene‐inducing peptide 1‐like proteins.