Brassinosteroids and gibberellins promote tobacco seed germination by distinct pathways

Seed germination of Nicotiana tabacum L. cv. Havana 425 is determined by the balance of forces between the growth potential of the embryo and the mechanical restraint of the micropylar endosperm. In contrast to the gibberellin GA(4), the brassinosteroid (BR) brassinolide (BL) did not release photodormancy of dark-imbibed photodormant seeds. Brassinolide promoted seedling elongation and germination of nonphotodormant seeds, but did not appreciably affect the induction of class I beta -1,3-glucanase (beta GLU I) in the micropylar endosperm. Brassinolide, but not GA4, accelerated endosperm rupture of tobacco seeds imbibed in the light. Brassinolide and GA4 promoted endosperm rupture of dark-imbibed non-photodormant seeds, but only GA4 enhanced beta GLU I induction. Promotion of endosperm rupture by BL was dose-dependent and 0.01 muM BL was most effective. Brassinolide and GA4 promoted abscsic acid (ABA)-inhibited dark-germination of non-photodormant seeds, but only GA4 replaced light in inducing beta GLU I. These results indicate that BRs and GAs promote tobacco seed germination by distinct signal transduction pathways and distinct mechanisms. Gibberellins and light seem to act in a common pathway to release photodormancy, whereas BRs do not release photodormancy. Induction of beta GLU I in the micropylar endosperm and promotion of release of 'coat-enhanced' dormancy seem to be associated with the GA-dependent 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.