Abstract
ABA plays vital roles in the maintenance of seed dormancy. In Arabidopsis, fus3 seeds fail to undergo dormancy. 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 those, line 2-44 showed reduced induction of CRC and At2S3 by exogenous ABA, in the presence of FUS3, indicating that line 2-44 has a defect in ABA-sensitivity. Moreover, the mutant had reduced dormancy during seed development. Interestingly, however, dry mature seeds were hypersensitive to ABA upon germination. These observations suggest that the product of causative gene of the mutant may function on ABA sensitivity through different mechanisms between developing and dry mature seeds. To further explore the molecular roles of the product of the causative gene, map-based cloning of line 2-44 is being carried out. Based on these results, we will discuss the possible functions of the gene product in the regulation of embryo growth arrest and dormancy, and seed germination.
