Damage on plants activates Ca2+-dependent metacaspases for release of immunomodulatory peptides
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
ID 4638427
Author(s) Hander, Tim; Fernandez-Fernandez, Alvaro D.; Kumpf, Robert P.; Willems, Patrick; Schatowitz, Hendrik; Rombaut, Debbie; Staes, An; Nolf, Jonah; Pottie, Robin; Yao, Panfeng; Goncalves, Amanda; Pavie, Benjamin; Boller, Thomas; Gevaert, Kris; Van Breusegem, Frank; Bartels, Sebastian; Stael, Simon
Author(s) at UniBasel Boller, Thomas
Hander, Tim
Merker, Sebastian
Schatowitz, Hendrik
Year 2019
Title Damage on plants activates Ca2+-dependent metacaspases for release of immunomodulatory peptides
Journal Science
Volume 363
Number 6433
Pages / Article-Number 1301-+
Mesh terms Amino Acid Sequence; Arabidopsis, immunology; Arabidopsis Proteins, metabolism; Calcium, metabolism; Cysteine Endopeptidases, metabolism; Cytosol, enzymology; Immunomodulation; Oligopeptides, metabolism; Plant Immunity; Protein Precursors, metabolism
Abstract Physical damage to cells leads to the release of immunomodulatory peptides to elicit a wound defense response in the surrounding tissue. In Arabidopsis thaliana, the plant elicitor peptide 1 (Pep1) is processed from its protein precursor, PRECURSOR OF PEP1 (PROPEP1). We demonstrate that upon damage, both at the tissue and single-cell levels, the cysteine protease METACASPASE4 (MC4) is instantly and spatiotemporally activated by binding high levels of Ca2+ and is necessary and sufficient for Pep1 maturation. Cytosol-localized PROPEP1 and MC4 react only after loss of plasma membrane integrity and prolonged extracellular Ca2+ entry. Our results reveal that a robust mechanism consisting of conserved molecular components links the intracellular and Ca2+-dependent activation of a specific cysteine protease with the maturation of damage-induced wound defense signals.
ISSN/ISBN 0036-8075
edoc-URL https://edoc.unibas.ch/86917/
Full Text on edoc No
Digital Object Identifier DOI 10.1126/science.aar7486
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/30898901
ISI-Number WOS:000462016400043
Document type (ISI) Journal Article

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