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First published online 22 February 2006
doi: 10.1242/dev.02301
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1 Departamento de Genética Molecular de Plantas, Centro Nacional de
Biotecnología, C/ Darwin 3, Madrid 28049, Spain.
2 Departamento de Biotecnología, Instituto Nacional de
Investigación y Tecnología Agraria y Alimentaria, Ctra. de A
Coruña, km 7, Madrid 28040, Spain.
3 Plant Science Institute, Department of Biology, University of Pennsylvania, PA
19104, USA.
Author for correspondence (e-mail:
jarillo{at}inia.es)
Accepted 17 January 2006
We have characterized Arabidopsis esd1 mutations, which cause early flowering independently of photoperiod, moderate increase of hypocotyl length, shortened inflorescence internodes, and altered leaf and flower development. Phenotypic analyses of double mutants with mutations at different loci of the flowering inductive pathways suggest that esd1 abolishes the FLC-mediated late flowering phenotype of plants carrying active alleles of FRI and of mutants of the autonomous pathway. We found that ESD1 is required for the expression of the FLC repressor to levels that inhibit flowering. However, the effect of esd1 in a flc-3 null genetic background and the downregulation of other members of the FLC-like/MAF gene family in esd1 mutants suggest that flowering inhibition mediated by ESD1 occurs through both FLC-and FLC-like gene-dependent pathways. The ESD1 locus was identified through a map-based cloning approach. ESD1 encodes ARP6, a homolog of the actin-related protein family that shares moderate sequence homology with conventional actins. Using chromatin immunoprecipitation (ChIP) experiments, we have determined that ARP6 is required for both histone acetylation and methylation of the FLC chromatin in Arabidopsis.
Key words: Flowering time, Floral repression, Chromatin remodelling, Arabidopsis
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