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GLYCINE‐RICH RNA‐BINDING PROTEIN1 interacts with RECEPTOR‐LIKE CYTOPLASMIC PROTEIN KINASE1 and suppresses cell death and defense responses in pepper ( Capsicum annuum )
Author(s) -
Kim Dae Sung,
Kim Nak Hyun,
Hwang Byung Kook
Publication year - 2015
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.13105
Subject(s) - biology , bimolecular fluorescence complementation , microbiology and biotechnology , programmed cell death , rna interference , rna , small interfering rna , gene silencing , rna silencing , gene , biochemistry , apoptosis
Summary Plants use a variety of innate immune regulators to trigger cell death and defense responses against pathogen attack. We identified pepper ( Capsicum annuum ) GLYCINE‐RICH RNA‐BINDING PROTEIN1 (CaGRP1) as a RECEPTOR‐LIKE CYTOPLASMIC PROTEIN KINASE1 (CaPIK1)‐interacting partner, based on bimolecular fluorescence complementation and coimmunoprecipitation analyses as well as gene silencing and transient expression analysis. CaGRP1 contains an N‐terminal RNA recognition motif and a glycine‐rich region at the C‐terminus. The CaGRP1 protein had DNA‐ and RNA‐binding activity in vitro . CaGRP1 interacted with CaPIK1 in planta . CaGRP1 and CaGRP1–CaPIK1 complexes were localized to the nucleus in plant cells. CaPIK1 phosphorylated CaGRP1 in vitro and in planta . Transient coexpression of CaGRP1 with CaPIK1 suppressed the CaPIK1 ‐triggered cell death response, accompanied by a reduced CaPIK1 ‐triggered reactive oxygen species (ROS) burst. The RNA recognition motif region of CaGRP1 was responsible for the nuclear localization of CaGRP1 as well as the suppression of the CaPIK1 ‐triggered cell death response. CaGRP1 silencing in pepper conferred enhanced resistance to Xanthomonas campestris pv vesicatoria ( Xcv ) infection; however, CaPIK1 ‐silenced plants were more susceptible to Xcv . CaGRP1 interacts with CaPIK1 and negatively regulates CaPIK1 ‐triggered cell death and defense responses by suppressing ROS accumulation.