| The floral transition is one of the most important changes during the plant life cycle. In Arabidopsis, FRIGIDA (FRI) and FLOWERING LOCUS C (FLC) are the two major loci which confer the late-flowering behavior of winter annual accessions. FLC is a major floral repressor and a point of convergence of FRI, vernalization and autonomous pathways. A late-flowering line containing both FRI and FLC was mutagenized and a screen for early flowering plants was performed. Here, isolation and characterization of five suppressors of the FRI-mediated late-flowering phenotype are reported. Three lesions affect flowering and also leaf morphology while two lesions specifically affect flowering. We show that in Arabidopsis, genes that encode Cap-binding Proteins, ABH1 (Abscisic Acid Hypersensitive) and AtCBP20 (Cap-Binding Protein 20), affect flowering and leaf morphology. Lesions in ABH1 suppress the late-flowering in a FRI-specific pathway by reducing FLC levels. AtCBP20 and another locus which affects leaf morphology, named FS385 (FRI Suppressor 385), also suppress late-flowering by reducing FLC levels. A lesion in a gene named FS28, which is related to FRI, at both nucleotide and protein sequence, suppresses the late-flowering phenotype in a FRI-specific way; fs28 does not suppress late-flowering of the autonomous pathway mutants ld and fpa and the photoperiod pathway mutant gi. The final FRI suppressor was identified as a mutation named fs40, that behaves as a single recessive locus in Col. All suppressors isolated confer early-flowering by reducing FLC expression levels. We propose that regulation of the flowering time conferred by FRI and FLC is controlled by multiple genes, some of which act specifically in flowering and act through FRI while others also affect other developmental processes. |
