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Pathogenesis‐related protein 4b interacts with leucine‐rich repeat protein 1 to suppress PR 4b‐triggered cell death and defense response in pepper
Author(s) -
Hwang In Sun,
Choi Du Seok,
Kim Nak Hyun,
Kim Dae Sung,
Hwang Byung Kook
Publication year - 2014
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.12400
Subject(s) - pathogenesis , leucine rich repeat , leucine , microbiology and biotechnology , cell , programmed cell death , pepper , chemistry , biology , immunology , biochemistry , receptor , amino acid , apoptosis , food science
Summary To control defense and cell‐death signaling, plants contain an abundance of pathogen recognition receptors such as leucine‐rich repeat ( LRR ) proteins. Here we show that pepper ( Capsicum annuum ) LRR 1 interacts with the pepper pathogenesis‐related ( PR ) protein 4b, PR 4b, in yeast and in planta . PR 4b is synthesized in the endoplasmic reticulum, interacts with LRR 1 in the plasma membrane, and is secreted to the apoplast via the plasma membrane. Binding of PR 4b to LRR 1 requires the chitin‐binding domain of PR 4b. Purified PR 4b protein inhibits spore germination and mycelial growth of plant fungal pathogens. Transient expression of PR 4b triggers hypersensitive cell death. This cell death is compromised by co‐expression of LRR 1 as a negative regulator in Nicotiana benthamiana leaves. LRR 1 / PR 4b silencing in pepper and PR 4b over‐expression in Arabidopsis thaliana demonstrated that LRR 1 and PR 4b are necessary for defense responses to Pseudomonas syringae pv. tomato and Hyaloperonospora arabidopsidis ( Hpa ) infection. The mutant of the PR 4b Arabidopsis ortholog, pr4 , showed enhanced susceptibility to Hpa infection. Together, our results suggest that PR 4b functions as a positive modulator of plant cell death and defense responses. However, the activity of PR 4b is suppressed by interaction with LRR 1.