Towards a molecular understanding of
vernalization: A genetic analysis of pleiotropic
regulators of the flowering-time switch FLC
Steven van Nocker* and Callista Ransom
Program in Plant Breeding/Genetics and Department of Horticulture, Michigan State University, East Lansing, MI 48824, U.S.A.
*Corresponding author: S. van Nocker, 390 Plant and Soil Science Building. Phone: 1-517-432-7133. Fax: 1-517-353-0890.
A central question in developmental biology is how programs of gene expression are maintained or altered following cell division. The phenomenon of vernalization (promotion of flowering by extended growth in the cold) provides fertile ground for probing this question. Elegant experiments by Wellensiek and others have demonstrated that the vernalized state can be both perceived and transmitted mitotically, hallmarks of an epigenetic mechanism. More recently it was shown that a major effect of vernalization in Arabidopsis thaliana is the transcriptional silencing of the MADS-box flowering repressor gene FLOWERING LOCUS C (FLC). The mechanism by which this silencing becomes established is mostly unknown. To gain additional insight, we identified a class of early-flowering mutant designated vernalization independence (vip) in which FLC RNA is not expressed to detectable levels. This class is represented by at least 7 loci, none of which appear to correspond to previously identified genes affecting flowering. Members of the vip mutant class also display similar developmental pleiotropy, including FLC-independent effects on flowering time and floral defects potentially related to ectopic expression of the floral regulator AGAMOUS. Our results to date suggest that the VIP genes function as components of a common mechanism. The identity of the VIP4 protein as the plant homolog of a yeast transcriptional coactivator component suggests that this mechanism could play a direct role in gene expression. One possible scenario is that the VIP genes encode components of a transcriptional coactivator that is recruited to FLC, or an upstream FLC activator, by vernalization-downregulated transcription factor(s).