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Abstract:
To identify new naturally occurring genetic variants affecting flowering time, we have crossed dominant mutants to a panel of wild Arabidopsis thaliana accessions. We started with dominant alleles of FWA, which encodes a homeodomain transcription factor. Its epigenetic allele, fwa, causes late flowering phenotype. We crossed fwa-2 mutants with 22 relatively early flowering natural accessions and monitored flowering time of the F1 plants. Most F1 plants showed an increment of 50 to 100% in total leaf number compared to that of parental accessions. However, the F1 derived from a cross between fwa-2 and Ll-2 accession produced an extremely late flowering phenotype. A control cross showed that the late flowering phenotype was not fwa-2 dependent, since the F1 between two the early flowering accessions Ler, the parent of fwa-2, and Ll-2 also flowered late. Crossing Ll-2 with different FRI FLC combinations (e.g., fri flc-3, FRI flc-3, or fri FLC), as well as sequencing the FRI gene from Ll-2, suggested that a functional FRI allele from Ll-2 causes late flowering in the F1 by activating the weak FLC allele of Ler. In addition to delayed flowering, we observed aerial rosettes in the latest plant derived from a backcross of the F1 into Ler. Such a phenotype has previously been shown by Grbic and colleagues to be conferred by synergistic activation of FLC by ART1 and FRI loci in the Sy-0 ecotype. Furthermore, the FLG locus, which has been mapped as a QTL between the Cvi and Ler accessions by Koornneef, Alonso-Blanco and colleagues, also enhances FLC action. We have started to examine possible candidate genes with known effects on flower development in this region, including the HUA2 locus identified by Chen and coworkers. We observed that the late flowering phenotype co-segregates with the HUA2 allele from Ll-2. Sequencing revealed changes at amino acid level in the HUA2 allele of Ll-2 compared to Columbia. We are now testing whether the dominant HUA2 allele of Ll-2 accession modulates flowering phenotype and aerial rosette formation by acting through the FRI/FLC pathway.
