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Título

Repression by TTK69 of GAGA-mediated Activation Occurs in the Absence of TTK69 Binding to DNA and Solely Requires the Contribution of the POZ/BTB Domain of TTK69

Autor Pagans, Sara; Piñeyro, David ; Kosoy, Ana; Bernués, Jordi ; Azorín, Ferran
Fecha de publicación 3-dic-2004
EditorAmerican Society for Biochemistry and Molecular Biology
Citación Journal of Biological Chemistry 279(11): 9725-9732 (2004)
Resumentramtrack 69 (TTK69) is known to repress GAGA-mediated activation of the eve promoter in S2 cells. Here, we show that repression by TTK69 occurs in the absence of bona fide TTK69-binding sites on the template, indicating that it does not require the binding of TTK69 to DNA. Consistent with this interpretation, the POZ/BTB domain of TTK69, which does not bind DNA, is sufficient for repression. Moreover, a fusion protein in which the POZ/BTB domain of GAGA is replaced by that of TTK69 is not capable of activating the eve promoter but efficiently represses GAGA-dependent activation. Repression involves GAGA-TTK69 interaction because TTK69 is not capable of repressing basal transcription. Most probably, GAGA-TTK69 interaction occurs at the promoter because GAGA·TTK69 complexes are fully competent in binding DNA in vitro. Our results also show that repression by TTK69 of GAGA-dependent activation of the eve promoter is not mediated by any of the co-repressors known to interact with TTK69 (dMi2 or C-terminal binding protein) or by trichostatin A-sensitive histone deacetylases. Altogether, these observations strongly suggest that the binding of TTK69 prevents the interaction of GAGA with the transcription machinery and, therefore, compromises its activation potential
Versión del editorhttp://dx.doi.org/10.1074/jbc.M313200200
URI http://hdl.handle.net/10261/112480
DOI10.1074/jbc.M313200200
ISSN0021-9258
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