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

Development 132, 5471-5478 (2005)
Published by The Company of Biologists 2005
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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 Michaels2,* and Richard M. Amasino1,2,{dagger}

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

{dagger} Author for correspondence (e-mail: amasino{at}biochem.wisc.edu)

Accepted 13 October 2005

Studies of natural variation have revealed that the winter-annual habit of many accessions of Arabidopsis is conferred by two genes, FRIGIDA (FRI) and FLOWERING LOCUS C (FLC), whose activities impose a vernalization requirement. To better understand the mechanism underlying the winter-annual habit, a genetic screen was performed to identify mutants that suppress the late-flowering behavior of a non-vernalized winter-annual strain. We have identified a locus, FRIGIDA-ESSENTIAL 1 (FES1), which, like FRI, is specifically required for the upregulation of FLC expression. FES1 is predicted to encode a protein with a CCCH zinc finger, but the predicted sequence does not otherwise share significant similarity with other known proteins. fes1 is a complete suppressor of FRI-mediated delayed flowering, but has little effect on the late-flowering phenotype of autonomous-pathway mutants. Thus, FES1 activity is required for the FRI-mediated winter-annual habit, but not for the similar phenotype resulting from autonomous-pathway mutations. Epistasis analysis between FES1, FRI and another specific suppressor of FRI-containing lines, FRIGIDA-LIKE 1 (FRL1), indicates that these genes do not function in a linear pathway, but instead act cooperatively to promote the expression of FLC.

Key words: Winter annuals, FLOWERING LOCUS C (FLC), FRIGIDA (FRI), Flowering time, CCCH zinc finger




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