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.