Brassinosteroids Promote Seed Germination

Abstract

Seed germination of Arabidopsis thaliana, Nicotiana tabacum, and of parasitic angiosperms (Orobranche and Striga species) is determined by the balance of forces between the growth potential of the embryo and the mechanical restraint of the micropylar testa and/or endosperm tissues. Brassinosteroids (BR) and gibberellins (GA) promote seed germination of these species and counteract the germination-inhibition by abscisic acid (ABA). Severe mutations in GA biosynthetic genes in Arabidopsis, such as ga1-3, result in a requirement for GA application to germinate, but germination in this phenotype can also be rescued by BR. Germination of both the BR biosynthetic mutant det2–1 and the BR-insensitive mutant bri1-1 is more strongly inhibited by ABA than is germination of wild type. In contrast to GA, BR does not release tobacco photodormancy; i.e. seed germination in darkness remains blocked. BR promotes germination of nonphotodormant tobacco seeds, but did not appreciably affect the induction of class I s-1,3-glucanase (sGlu I) in the micropylar endosperm. BR and GA promote tobacco seed germination by distinct signal transduction pathways and distinct mechanisms. Xyloglucan endo-transglycosylase (XET) enzyme activity accumulates in the embryo and the endosperm of germinating tobacco seeds and this appears to be partially controlled of BR. GA and light seem to act in a common pathway to release photodormancy, whereas BR does not release photodormancy. Induction of sGlu I in the micropylar endosperm and promotion of release of ‘coat-imposed’ dormancy seem to be associated with the GA-dependent pathway, but not with BR signaling. It is proposed that BR promote seed germination by directly enhancing the growth potential of the emerging embryo in a GA-independent manner.