Seed dormancy and germination are complex traits that are controlled by many genes. Four mutants in Arabidopsis thaliana exhibiting a reduced dormancy phenotype, designated rdo1, rdo2, rdo3, and rdo4, have been characterized, both genetically and physiologically. Two of these mutants, rdo1 and rdo2, have been described before, the other two represent novel loci. The mutants mapped on chromosome 1 (rdo3), chromosome 2 (rdo2 and rdo4), and chromosome 3 (rdo1). None of these loci has been related to dormancy before. All four mutants show pleiotropic effects in the adult plant stage, which are different for each mutant. None of the mutants is deficient in ABA. Compared to Ler (wild-type), ABA sensitivity is not altered either, thereby excluding the possibility that ABA is involved in causing the reduced dormancy phenotype. The GA requirement was studied by using the GA biosynthesis inhibitor paclobutrazol, and genetically by generating double mutants with the GA-deficient mutant ga1-3. The results obtained by these two methods were comparable for all but one mutant: rdo1. In a GA-deficient background, rdo1, rdo2 and rdo3, all show sensitivity to GA between that of ga1-3 and ga1-3 aba1. However, when using paclobutrazol rdo1 exhibited the same sensitivity as rdo4 and wild-type. Analysis of double mutants among the rdo mutants revealed a very complex and inconsistent pattern.
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http://dx.doi.org/10.1034/j.1399-3054.2002.1150415.x | DOI Listing |
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