MOF-Regulated acetylation of MSL-3 in the Drosophila dosage compensation complex
MOF-Regulated acetylation of MSL-3 in the Drosophila dosage compensation complex
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DOI：
10.1016/s1097-2765(03)00140-0
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发表时间：
2003-05-01
期刊：
影响因子：
16
通讯作者：
Akhtar, A
中科院分区：
文献类型：
--
作者：
Buscaino, A;Köcher, T;Akhtar, A
剂量补偿确保了X连锁基因在男性和女性中的平等表达。在果蝇中，平衡是通过雄性X染色体的超转录实现的。这一过程需要一个含有剂量补偿复合体(DCC)的RNA/蛋白质。在这里，我们使用单个DCC组件的RNA干扰来定义施耐德细胞中复杂组装的顺序。我们发现，MOF与MSL-3的相互作用导致MSL-3在其一个染色域附近的单个赖氨酸残基上发生特异性乙酰化。我们观察到MSL-3在X染色体上的定位是RNA依赖的和乙酰化敏感的。我们发现MSL-3的乙酰化状态决定了它与roX2 RNA的相互作用。此外，我们还发现RPD3与MSL-3相互作用，并且MSL-3可以被RPD3复合体脱乙酰化。我们认为，MSL-3的调节乙酰化可能为剂量补偿复合体沿男性X染色体的扩散提供了机制解释。
Dosage compensation ensures equal expression of X-linked genes in males and females. In Drosophila, equalization is achieved by hypertranscription of the male X chromosome. This process requires an RNA/ protein containing dosage compensation complex (DCC). Here we use RNA interference of individual DCC components to define the order of complex assembly in Schneider cells. We show that interaction of MOF with MSL-3 leads to specific acetylation of MSL-3 at a single lysine residue adjacent to one of its chromodomains. We observe that localization of MSL-3 to the X chromosome is RNA dependent and acetylation sensitive. We find that the acetylation status of MSL-3 determines its interaction with roX2 RNA. Furthermore, we find that RPD3 interacts with MSL-3 and that MSL-3 can be deacetylated by the RPD3 complex. We propose that regulated acetylation of MSL-3 may provide a mechanistic explanation for spreading of the dosage compensation complex along the male X chromosome.