Abstract
ABA plays important roles in the maintenance of seed dormancy. In Arabidopsis, fus3 mutant seeds fail to undergo dormancy. Several studies have shown that FUS3 positively regulates ABA biosynthesis. However, little is known about the molecular mechanisms underlying this process. To this end, we mutagenized a transgenic line in which ectopic expression of FUS3 could be artificially induced by estrogen and screened for novel mutants defective in FUS3-imposed growth arrest at seedling stages. Among the identified mutants, fga2 showed reduced seed dormancy and resistance to a GA biosynthesis inhibitor, paclobutrazol. Interestingly, the hypocotyls of fga2 seedlings were dramatically elongated when FUS3 was ectopically induced. To further investigate whether FGA2 might act in the regulation of ABA biosynthesis downstream of FUS3, map-based cloning of FGA2 is being carried out. Based on these results, we will discuss possible functions of FGA2 and FUS3 in the regulation of ABA biosynthesis during seed development.