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Plant and Cell Physiology, 2003, Vol. 44, No. 6 555-564
© 2003 Oxford University Press

Arabidopsis TERMINAL FLOWER 2 Gene Encodes a Heterochromatin Protein 1 Homolog and Represses both FLOWERING LOCUS T to Regulate Flowering Time and Several Floral Homeotic Genes

Toshihisa Kotake1,4,5, Shinobu Takada2,4, Kenji Nakahigashi2, Masaaki Ohto3,6 and Koji Goto1,2,7

1 Research Institute for Biological Sciences, Okayama, 716-1241 Japan
2 CREST, Japan Science and Technology Corporation
3 National Institute for Basic Biology, Okazaki, 444-8585 Japan

Floral transition should be strictly regulated because it is one of the most critical developmental processes in plants. Arabidopsis terminal flower 2 (tfl2) mutants show an early-flowering phenotype that is relatively insensitive to photoperiod, as well as several other pleiotropic phenotypes. We found that the early flowering of tfl2 is caused mainly by ectopic expression of the FLOWERING LOCUS T (FT) gene, a floral pathway integrator. Molecular cloning of TFL2 showed that it encodes a protein with homology to heterochromatin protein 1 (HP1) of animals and Swi6 of fission yeast. TFL2 protein localizes in subnuclear foci and expression of the TFL2 gene complemented yeast swi6 mutants. These results suggested that TFL2 might function as an HP1 in Arabidopsis. Gene expression analyses using DNA microarrays, however, did not show an increase in the expression of heterochromatin genes in tfl2 mutants but instead showed the upregulation of the floral homeotic genes APETALA3, PISTILLATA, AGAMOUS and SEPALLATA3. The pleiotropic phenotype of the tfl2 mutant could reflect the fact that TFL2 represses the expression of multiple genes. Our results demonstrate that despite its homology to HP1, TFL2 is involved in the repression of specific euchromatin genes and not heterochromatin genes in Arabidopsis.

4 These authors contributed equally to this work.

5 Present address: Faculty of Science, Saitama University, Saitama, 338-8570 Japan

6 Present address: Section of Plant Biology, Division of Biological Sciences, University of California, Davis, CA 95616, U.S.A.

7 Corresponding author: E-mail, kgoto{at}v004.vaio.ne.jp; Fax, +81-866-56-9454.


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