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A salt-regulated peptide derived from the CAP superfamily protein negatively regulates salt-stress tolerance in Arabidopsis

Title
A salt-regulated peptide derived from the CAP superfamily protein negatively regulates salt-stress tolerance in Arabidopsis
Author(s)
Chien, Pei-ShanNam, Hong GilChen, Yet-Ran
Issued Date
2015-08
Citation
Journal of Experimental Botany, v.66, no.17, pp.5301 - 5313
Type
Article
Author Keywords
Environmental regulationCAPnegative regulator of salt resistanceplant peptideproteolytic processsalinity
Keywords
ABSCISIC-ACIDCAPDROUGHT STRESSEnvironmental RegulationFUNCTIONAL-ANALYSISLARGE GENE LISTSMASS-SPECTROMETRYNegative Regulator of Salt ResistancePlant PeptidePlantsProteolytic ProcessSalinitySALINITY TOLERANCESIGNAL-TRANSDUCTION PATHWAYTHALIANATranscription Factor
ISSN
0022-0957
Abstract
High salinity has negative impacts on plant growth through altered water uptake and ion-specific toxicities. Plants have therefore evolved an intricate regulatory network in which plant hormones play significant roles in modulating physiological responses to salinity. However, current understanding of the plant peptides involved in this regulatory network remains limited. Here, we identified a salt-regulated peptide in Arabidopsis. The peptide was 11 aa and was derived from the C terminus of a cysteine-rich secretory proteins, antigen 5, and pathogenesis-related 1 proteins (CAP) superfamily. This peptide was found by searching homologues in Arabidopsis using the precursor of a tomato CAP-derived peptide (CAPE) that was initially identified as an immune signal. In searching for a CAPE involved in salt responses, we screened CAPE precursor genes that showed salt-responsive expression and found that the PROAtCAPE1 (AT4G33730) gene was regulated by salinity. We confirmed the endogenous Arabidopsis CAP-derived peptide 1 (AtCAPE1) by mass spectrometry and found that a key amino acid residue in PROAtCAPE1 is critical for AtCAPE1 production. Moreover, although PROAtCAPE1 was expressed mainly in the roots, AtCAPE1 was discovered to be upregulated systemically upon salt treatment. The salt-induced AtCAPE1 negatively regulated salt tolerance by suppressing several salt-tolerance genes functioning in the production of osmolytes, detoxification, stomatal closure control, and cell membrane protection. This discovery demonstrates that AtCAPE1, a homologue of tomato immune regulator CAPE1, plays an important role in the regulation of salt stress responses. Our discovery thus suggests that the peptide may function in a trade-off between pathogen defence and salt tolerance. © 2015 The Author.
URI
http://hdl.handle.net/20.500.11750/1568
DOI
10.1093/jxb/erv263
Publisher
OXFORD UNIV PRESS
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Appears in Collections:
Department of New Biology CBRG(Complex Biology Research Group) 1. Journal Articles

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