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首页> 外文期刊>Epigenetics & Chromatin >Male X-linked genes in Drosophila melanogaster are compensated independently of the Male-Specific Lethal complex
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Male X-linked genes in Drosophila melanogaster are compensated independently of the Male-Specific Lethal complex

机译:果蝇中雄性X连锁基因的补偿独立于雄性特异性致死复合体

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Background In organisms where the two sexes have unequal numbers of X-chromosomes, the expression of X-linked genes needs to be balanced not only between the two sexes, but also between X and the autosomes. In Drosophila melanogaster, the Male-Specific Lethal (MSL) complex is believed to produce a 2-fold increase in expression of genes on the male X, thus restoring this balance. Results Here we show that almost all the genes on the male X are effectively compensated. However, many genes are compensated without any significant recruitment of the MSL-complex. These genes are very weakly, if at all, affected by mutations or RNAi against MSL-complex components. In addition, even the genes that are strongly bound by MSL rely on mechanisms other than the MSL-complex for proper compensation. We find that long, non-ubiquitously expressed genes tend to rely less on the MSL-complex for their compensation and genes that in addition are far from High Affinity Sites tend to not bind the complex at all or very weakly. Conclusions We conclude that most of the compensation of X-linked genes is produced by an MSL-independent mechanism. Similar to the case of the MSL-mediated compensation we do not yet know the mechanism behind the MSL-independent compensation that appears to act preferentially on long genes. Even if we observe similarities, it remains to be seen if the mechanism is related to the buffering that is observed in autosomal aneuploidies.
机译:背景技术在两个性别的X染色体数目不相等的生物中,不仅需要在两个性别之间而且还要在X和常染色体之间平衡X连锁基因的表达。在果蝇中,男性特异性致死(MSL)复合物被认为可使男性X上的基因表达增加2倍,从而恢复了这种平衡。结果在这里我们表明,雄性X上几乎所有基因都得到了有效补偿。然而,许多基因被补偿而没有MSL-复合物的任何显着募集。这些基因受到针对MSL复杂成分的突变或RNAi的影响非常微弱。此外,即使与MSL牢固结合的基因也依赖于MSL复合物以外的机制进行适当的补偿。我们发现,长的,无处不在的表达的基因倾向于较少依赖MSL-复合物进行补偿,而距高亲和力位点远的基因则倾向于根本不结合或非常弱地结合复合物。结论我们得出的结论是,大多数X连锁基因的补偿是由MSL独立机制产生的。类似于MSL介导的补偿的情况,我们尚不了解独立于MSL的补偿背后似乎优先作用于长基因的机制。即使我们观察到相似性,其机制是否与常染色体非整倍性中观察到的缓冲作用有关,还有待观察。

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