Brassinosteroids and gibberellins promote tobacco seed germination by distinct pathways

Seed germination of Nicotiana tabacum L. cv. Havana 425 is determined by th e balance of forces between the growth potential of the embryo and the mech anical restraint of the micropylar endosperm. In contrast to the gibberelli n GA(4), the brassinosteroid (BR) brassinolide (BL) did not release photodo rmancy of dark-imbibed photodormant seeds. Brassinolide promoted seedling e longation and germination of nonphotodormant seeds, but did not appreciably affect the induction of class I beta -1,3-glucanase (beta GLU I) in the mi cropylar endosperm. Brassinolide, but not GA4, accelerated endosperm ruptur e of tobacco seeds imbibed in the light. Brassinolide and GA4 promoted endo sperm rupture of dark-imbibed non-photodormant seeds, but only GA4 enhanced beta GLU I induction. Promotion of endosperm rupture by BL was dose-depend ent and 0.01 muM BL was most effective. Brassinolide and GA4 promoted abscs ic acid (ABA)-inhibited dark-germination of non-photodormant seeds, but onl y GA4 replaced light in inducing beta GLU I. These results indicate that BR s and GAs promote tobacco seed germination by distinct signal transduction pathways and distinct mechanisms. Gibberellins and light seem to act in a c ommon pathway to release photodormancy, whereas BRs do not release photodor mancy. Induction of beta GLU I in the micropylar endosperm and promotion of release of 'coat-enhanced' dormancy seem to be associated with the GA-depe ndent pathway, but not with BR signalling. It is proposed that BRs promote seed germination by directly enhancing the growth potential of the emerging embryo in a GA- and beta GLU I-independent manner.