| Summary: | <p>Abstract</p> <p>Background</p> <p><it>Polycomb-group genes </it>(<it>PcG</it>) encode proteins that maintain homeotic (<it>Hox</it>) gene repression throughout development. Conversely, <it>trithorax-group </it>(<it>trxG</it>) genes encode positive factors required for maintenance of long term <it>Hox </it>gene activation. Both kinds of factors bind chromatin regions called maintenance elements (ME). Our previous work has shown that <it>corto</it>, which codes for a chromodomain protein, and <it>dsp1</it>, which codes for an HMGB protein, belong to a class of genes called the <it>Enhancers of trithorax and Polycomb </it>(<it>ETP</it>) that interact with both <it>PcG </it>and <it>trxG</it>. Moreover, <it>dsp1 </it>interacts with the <it>Hox </it>gene <it>Scr</it>, the DSP1 protein is present on a <it>Scr </it>ME in S2 cells but not in embryos. To understand better the role of <it>ETP</it>, we addressed genetic and molecular interactions between <it>corto </it>and <it>dsp1</it>.</p> <p>Results</p> <p>We show that Corto and DSP1 proteins co-localize at 91 sites on polytene chromosomes and co-immunoprecipitate in embryos. They interact directly through the DSP1 HMG-boxes and the amino-part of Corto, which contains a chromodomain. In order to search for a common target, we performed a genetic interaction analysis. We observed that <it>corto </it>mutants suppressed <it>dsp1<sup>1 </sup></it>sex comb phenotypes and enhanced <it>Antp<sup>Scx </sup></it>phenotypes, suggesting that <it>corto </it>and <it>dsp1 </it>are simultaneously involved in the regulation of <it>Scr</it>. Using chromatin immunoprecipitation of the <it>Scr </it>ME, we found that Corto was present on this ME both in <it>Drosophila </it>S2 cells and in embryos, whereas DSP1 was present only in S2 cells.</p> <p>Conclusion</p> <p>Our results reveal that the proteins Corto and DSP1 are differently recruited to a <it>Scr </it>ME depending on whether the ME is active, as seen in S2 cells, or inactive, as in most embryonic cells. The presence of a given combination of ETPs on an ME would control the recruitment of either PcG or TrxG complexes, propagating the silenced or active state.</p>
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