BACKGROUND dADD1 and dXNP proteins are the orthologs in Drosophila melanogaster of the ADD and SNF2 domains, respectively, of the ATRX vertebrate's chromatin remodeler, they suppress position effect variegation phenotypes and participate in heterochromatin maintenance. RESULTS We performed a search in human cancer databases and found that ATRX protein levels were elevated in more than 4.4% of the samples analyzed. Using the Drosophila model, we addressed the effects of over and under-expression of dADD1 proteins in polytene cells. Elevated levels of dADD1 in fly tissues caused different phenotypes, such as chromocenter disruption and loss of banding pattern at the chromosome arms. Analyses of the heterochromatin maintenance protein HP1a, the dXNP ATPase and the histone post-translational modification H3K9me3 revealed changes in their chromatin localization accompanied by mild transcriptional defects of genes embedded in heterochromatic regions. Furthermore, the expression of heterochromatin embedded genes in null dadd1 organisms is lower than in the wild-type conditions. CONCLUSION These data indicate that dADD1 overexpression induces chromatin changes, probably affecting the stoichiometry of HP1a containing complexes that lead to transcriptional and architectural changes. Our results place dADD1 proteins as important players in the maintenance of chromatin architecture and heterochromatic gene expression.

中文翻译：

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dADD1错误表达在染色质组织和转录中的分子效应。

背景技术dADD1和dXNP蛋白分别是果蝇果蝇中ATRX脊椎动物的染色质重塑剂的ADD和SNF2结构域的直向同源物，它们抑制位置效应的变异表型并参与异染色质的维持。结果我们在人类癌症数据库中进行了搜索，发现在超过4.4％的分析样本中ATRX蛋白水平升高。使用果蝇模型，我们解决了polyTene细胞中dADD1蛋白过度表达和表达不足的影响。苍蝇组织中dADD1的水平升高会引起不同的表型，例如色中心破坏和染色体臂上条带模式的丧失。异染色质维持蛋白HP1a的分析，dXNP ATPase和组蛋白翻译后修饰H3K9me3揭示了它们染色质定位的变化，并伴随着嵌入异色区的基因的轻度转录缺陷。此外，在无效的dadd1生物中异染色质嵌入基因的表达低于野生型条件。结论这些数据表明dADD1的过表达诱导了染色质的改变，可能影响了HP1a含有导致转录和结构变化的复合物的化学计量。我们的结果将dADD1蛋白作为维持染色质结构和异色基因表达的重要参与者。在无效的dadd1生物中，异染色质嵌入基因的表达低于野生型条件。结论这些数据表明dADD1的过表达诱导了染色质的改变，可能影响了HP1a含有导致转录和结构变化的复合物的化学计量。我们的结果将dADD1蛋白作为维持染色质结构和异色基因表达的重要参与者。在无效的dadd1生物中，异染色质嵌入基因的表达低于野生型条件。结论这些数据表明dADD1的过表达诱导了染色质的改变，可能影响了HP1a含有导致转录和结构变化的复合物的化学计量。我们的结果将dADD1蛋白作为维持染色质结构和异色基因表达的重要参与者。