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首页> 外文期刊>Nucleic Acids Research >dSAP18 and dHDAC1 contribute to the functional regulation of the Drosophila Fab-7 element.
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dSAP18 and dHDAC1 contribute to the functional regulation of the Drosophila Fab-7 element.

机译：dSAP18和dHDAC1有助于果蝇Fab-7元件的功能调节。

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摘要

It was described earlier that the Drosophila GAGA factor [Trithorax-like (Trl)] interacts with dSAP18, which, in mammals, was reported to be a component of the Sin3-HDAC co-repressor complex. GAGA-dSAP18 interaction was proposed to contribute to the functional regulation of the bithorax complex (BX-C). Here, we show that mutant alleles of Trl, dsap18 and drpd3/hdac1 enhance A6-to-A5 transformation indicating a contribution to the regulation of Abd-B expression at A6. In A6, expression of Abd-B is driven by the iab-6 enhancer, which is insulated from iab-7 by the Fab-7 element. Here, we report that GAGA, dSAP18 and dRPD3/HDAC1 co-localize to ectopic Fab-7 sites in polytene chromosomes and that mutant Trl, dsap18 and drpd3/hdac1 alleles affect Fab-7-dependent silencing. Consistent with these findings, chromatin immunoprecipitation analysis shows that, in Drosophila embryos, the endogenous Fab-7 element is hypoacetylated at histones H3 and H4. These results indicate a contribution of GAGA, dSAP18 and dRPD3/HDAC1 to the regulation of Fab-7 function.
机译：先前已经描述过，果蝇GAGA因子[Trithorax-like（Trl）]与dSAP18相互作用，据报道，dSAP18在哺乳动物中是Sin3-HDAC协同阻遏物复合物的组成部分。提出GAGA-dSAP18相互作用有助于对位胸复合体（BX-C）的功能调节。在这里，我们显示Trl，dsap18和drpd3 / hdac1的突变等位基因增强了A6-to-A5转化，表明对A6处Abd-B表达的调节有贡献。在A6中，Abd-B的表达是由iab-6增强子驱动的，该增强子通过Fab-7元件与iab-7绝缘。在这里，我们报告GAGA，dSAP18和dRPD3 / HDAC1共定位到多烯染色体中的异位Fab-7位点，并且突变体Tr1，dsap18和drpd3 / hdac1等位基因影响Fab-7依赖性沉默。与这些发现一致，染色质免疫沉淀分析表明，在果蝇胚胎中，内源性Fab-7元素在组蛋白H3和H4处被低乙酰化。这些结果表明GAGA，dSAP18和dRPD3 / HDAC1对Fab-7功能的调节。

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