Myrigalone A Inhibits Lepidium sativum Seed Germination by Interference with Gibberellin Metabolism and Apoplastic Superoxide Production Required for Embryo Extension Growth and Endosperm Rupture

0374859 - ÚEB 2012 RIV JP eng J - Journal Article
Oracz, K. - Voegele, A. - Tarkowská, Danuše - Jacquemoud, D. - Turečková, Veronika - Urbanová, Terezie - Strnad, Miroslav - Sliwinska, E. - Leubner-Metzger, G.
Myrigalone A Inhibits Lepidium sativum Seed Germination by Interference with Gibberellin Metabolism and Apoplastic Superoxide Production Required for Embryo Extension Growth and Endosperm Rupture.
Plant and Cell Physiology. Roč. 53, č. 1 (2012), s. 81-95. ISSN 0032-0781. E-ISSN 1471-9053
R&D Projects: GA AV ČR KAN200380801; GA MŠMT ED0007/01/01; GA ČR GD522/08/H003
Keywords : Embryo cell extension growth * Endoreduplication * Endosperm rupture * Gibberellin metabolism * Lepidium sativum * Myrica gale * Phytotoxicity * Reactive oxygen species
Subject RIV: EF - Botanics
Impact factor: 4.134, year: 2012

Myrica gale L. (sweet gale) fruit leachate contains myrigalone A (MyA), a rare C-methylated dihydrochalcone and putative allelochemical, which is known to be a phytotoxin impeding seedling growth. We found that MyA inhibited Lepidium sativum L. seed germination in a dose-dependent manner. MyA did not affect testa rupture, but inhibited endosperm rupture and the transition to subsequent seedling growth. MyA inhibited micropylar endosperm cap (CAP) weakening and the increase in the growth potential of the radical/hypocotyl region (RAD) of the embryo, both being key processes required for endosperm rupture. We compared the contents of abscisic acid (ABA) and gibberellins in the tissues and found that the major bioactive forms of gibberellin in L. sativum seed tissues were GA(4) and GA(6), while GA(8) and GA(13) were abundant inactive metabolites. MyA did not appreciably affect the ABA contents, but severely interfered with gibberellin metabolism and signaling by inhibiting important steps catalyzed by GA3 oxidase, as well as by interfering with the GID1-type gibberellin signaling pathway.
Permanent Link: http://hdl.handle.net/11104/0207675