Abstract. 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 GA4, the brassinosteroid (BR)
brassinolide (BL) did not release photodormancy of dark-imbibed photodormant
seeds. Brassinolide promoted seedling elongation and germination of non-photodormant
seeds, but did not appreciably affect the induction of class I ß-1,3-glucanase
(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 GLU I induction. Promotion of endosperm
rupture by BL was dose-dependent and 0.01 µM BL was most effective.
Brassinolide and GA4 promoted abscisic acid (ABA)-inhibited dark-germination
of non-photodormant seeds, but only GA4 replaced light in inducing
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 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 GLU I-independent manner.
Key words: Abscisic acid, Brassinosteroid, Gibberellin, ß-1,3-Glucanase,
Photodormancy, Seed germination
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