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Association of cytochrome b 5 with ETR 1 ethylene receptor signaling through RTE 1 in A rabidopsis
Author(s) -
Chang Jianhong,
Clay John M.,
Chang Caren
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.12401
Subject(s) - mutant , endoplasmic reticulum , arabidopsis , ethylene , bimolecular fluorescence complementation , gene isoform , receptor , microbiology and biotechnology , wild type , chemistry , biochemistry , biology , yeast , gene , catalysis
Summary Ethylene plays important roles in plant growth, development and stress responses, and is perceived by a family of receptors that repress ethylene responses when ethylene is absent. Repression by the ethylene receptor ETR 1 depends on an integral membrane protein, REVERSION TO ETHYLENE SENSITIVITY 1 ( RTE 1), which acts upstream of ETR 1 in the endoplasmic reticulum ( ER ) membrane and Golgi apparatus. To investigate RTE 1 function, we screened for RTE 1‐interacting proteins using the yeast split‐ubiquitin assay, which yielded the ER ‐localized cytochrome b 5 ( C b5) isoform D . Cb5s are small hemoproteins that perform electron transfer reactions in all eukaryotes, but their roles in plants are relatively uncharacterized. Using bimolecular fluorescence complementation (Bi FC ), we found that all four ER ‐localized Arabidopsis C b5 isoforms (AtCb5–B, ‐C, ‐D and ‐E) interact with RTE 1 in plant cells. In support of this interaction, atcb5 mutants exhibited phenotypic parallels with rte1 mutants in Arabidopsis. Phenotypes included partial suppression of etr1–2 ethylene insensitivity, and no suppression of RTE 1‐independent ethylene receptor isoforms. The single loss‐of‐function mutants atcb5–b , ‐ c and ‐ d appeared similar to the wild‐type, but double mutant combinations displayed slight ethylene hypersensitivity. Over‐expression of AtCb5–D conferred reduced ethylene sensitivity similar to that conferred by RTE 1 over‐expression, and genetic analyses suggested that A t C b5– D acts upstream of RTE 1 in the ethylene response. These findings suggest an unexpected role for C b5, in which C b5 and RTE 1 are functional partners in promoting ETR 1‐mediated repression of ethylene signaling.