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First published online 16 November 2005
doi: 10.1242/dev.02170

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FRIGIDA-ESSENTIAL 1 interacts genetically with FRIGIDA and FRIGIDA-LIKE 1 to promote the winter-annual habit of Arabidopsis thaliana

Robert J. Schmitz¹, Lewis Hong², Scott Michaels^2,* and Richard M. Amasino^1,2,

¹ Laboratory of Genetics, University of Wisconsin, Madison, WI 53706, USA
² Department of Biochemistry, University of Wisconsin, Madison, WI 53706, USA

View larger version (30K): [in a new window]   Fig. 1. Suppression of FRI-mediated late flowering by mutations in fes1. (A) Col FRI (left) and fes1-1 (right) grown in long days. The only observable phenotype associated with fes1 lesions is an inability to delay flowering. (B) Total leaf numbers when grown in both inductive (white bars) and non-inductive (black bars) photoperiods. fes1 mutants have a similar flowering-time phenotype to flc-3 in both conditions tested. fes1 mutants do not flower early in non-inductive photoperiods, unlike flm and maf2 mutants, suggesting that the suppression of late-flowering may be FLC specific. Error bars represent s.d. (C) fes1-2 lesions reduce steady-state levels of FLC mRNA.

View larger version (35K): [in a new window]   Fig. 2. fes1 lesions are not suppressors of late-flowering autonomous-pathway or photoperiod mutants. (A) fes1-4 completely suppresses FRI-mediated late flowering. fes1-4 is unable to suppress the late-flowering behavior of fld-3, fca-9, ld-1 and gi-2. Error bars represent s.d. (B) The suppression observed in Col FRI is due to a reduction in steady-state levels of FLC mRNA. No decrease in FLC mRNA is observed in the autonomous-pathway mutants fld-3 and ld-1. These data suggest two distinct mechanisms associated with promotion of FLC expression.

View larger version (29K): [in a new window]   Fig. 3. Schematic of the genomic structure and isolated lesions in FES1. fes1-1 and fes1-2 were isolated in a genetic screen for early flowering mutants in a Col FRI background. fes-1-3 and fes1-4 were isolated from the SALK T-DNA collection. FES1 contains a C-x8-C-x5-C-3x-H zinc finger. The closest four matches are represented in the alignment.

View larger version (23K): [in a new window]   Fig. 4. Genetic analyses between FRI, FRL1 and FES1. (A) fri;fes1 double mutants have the same flowering time as the parent plants do. Overexpression of FES1 is unable to delay the floral transition in a fri (Col) or frl1 (Col) genetic background. Overexpression of either FRI or FRL1 is suppressed by fes1 lesions. Error bars represent s.d. (B) Pathways that affect the expression of FLC and the FLC clade. These data provide evidence against a linear pathway, and favor a model in which FRI, FRL1 and FES1 form a complex to promote the expression of FLC.

View larger version (34K): [in a new window]   Fig. 5 . Vernalization acts downstream of FES1. (A) 35S::FES1 plants are completely responsive to vernalization. Error bars represent s.d. (B) Steady-state levels of FES1 mRNA are not affected by vernalization. NV, no vernalization; 10V, 10 days of vernalization; 40V, 40 days of vernalization; 40VT7, 40 days of vernalization plus 7 days return to warm growth conditions.

View larger version (125K): [in a new window]   Fig. 6. FES1 spatial expression pattern. (A) GUS fusions to FES1. GUS expression is mainly detected in the root and shoot apex and throughout the vascular system. (B) A close-up view of FES1::GUS expression in the shoot apex and vascular system. (C) A close-up view of FLC::GUS expression in the shoot apex and vascular system. (D) Nuclear expression pattern in the root of FES1::GUS.