The role of EBS in the repression of flowering in Arabidopsis Manuel Piñeiro1, Concepción Gómez-Mena1, José M. Martínez-Zapater1, and G. Coupland2 1 Centro Nacional de Biotecnología. Campus de la U. Autónoma de Madrid, Cantoblanco. 28049, Madrid. Spain. 2John Innes Centre. Colney Lane, NR4 7UH. Norwich. UK Mutations in the EARLY BOLTING IN SHORT DAYS (EBS) gene of Arabidopsis cause an early flowering phenotype, especially under non-inductive photoperiods (short days –SD). Genetic analyses demonstrated that the early flowering phenotype of ebs mutants requires both the activity of the FT gene and gibberellic acid (GA) biosynthesis. In addition to early flowering, the flowers of ebs mutants show overexpression of floral organ identity genes such as AGAMOUS, APETALA3 and PISTILATA. We have recently identified the EBS locus. The predicted aminoacid sequence of the protein suggests that EBS could be part of a protein complex that is involved in the regulation of gene expression by modulating chromatin structure. To understand how EBS participates in the regulation of the floral transition we have generated transgenic lines overexpressing the gene. These lines show an early flowering phenotype, similar to that caused by loss-of-function mutations in the EBS gene. This phenotype is consistent with the hypothesis of EBS being part of a protein complex. The accumulation of the EBS product in 35S::EBS lines could alter the correct formation of the complex, interfering with its normal function. Since EBS is likely to act as a transcriptional regulator, we have analysed the effect of the ebs mutations on the expression of several genes known to be involved in the control of flowering time in Arabidopsis. The results obtained demonstrate that the FT gene is prematurely upregulated in ebs mutants grown under SD, whereas the expression of other key genes in the regulation of flowering time and GA biosynthesis is not affected in ebs mutants, indicating that the repression of flowering by EBS is mediated by its effect on FT expression. Our progress in understanding the molecular mechanism of EBS function will be discussed.