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Drosophila architectural protein CTCF is not essential for fly survival and is able to function independently of CP190
Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms ( IF 2.6 ) Pub Date : 2021-07-24 , DOI: 10.1016/j.bbagrm.2021.194733
Olga Kyrchanova 1 , Natalia Klimenko 2 , Nikolay Postika 3 , Artem Bonchuk 1 , Nikolay Zolotarev 3 , Oksana Maksimenko 2 , Pavel Georgiev 3
Affiliation  

CTCF is the most likely ancestor of proteins that contain large clusters of C2H2 zinc finger domains (C2H2) and is conserved among most bilateral organisms. In mammals, CTCF functions as the main architectural protein involved in the organization of topology-associated domains (TADs). In vertebrates and Drosophila, CTCF is involved in the regulation of homeotic genes. Previously, it was found that null mutations in the dCTCF gene died as pharate adults, which failed to eclose from their pupal case, or shortly after hatching of adults. Here, we obtained several new null dCTCF mutations and found that the complete inactivation of dCTCF appears is limited mainly to phenotypic manifestations of the Abd-B gene and fertility of adult flies. Many modifiers that are not associated with an independent phenotypic manifestation can significantly enhance the expressivity of the null dCTCF mutations, indicating that other architectural proteins are able to functionally compensate for dCTCF inactivation in Drosophila. We also mapped the 715–735 aa region of dCTCF as being essential for the interaction with the BTB (Broad-Complex, Tramtrack, and Bric a brac) and microtubule-targeting (M) domains of the CP190 protein, which binds to many architectural proteins. However, the mutational analysis showed that the interaction with CP190 was not important for the functional activity of dCTCF in vivo.



中文翻译:

果蝇结构蛋白 CTCF 对果蝇生存不是必需的,并且能够独立于 CP190 发挥作用

CTCF 是包含大簇 C2H2锌指结构域 (C2H2)的蛋白质的最可能祖先,并且在大多数双侧生物体中是保守的。在哺乳动物中,CTCF 作为参与拓扑相关域 (TAD) 组织的主要结构蛋白起作用。在脊椎动物和果蝇中,CTCF 参与同源基因的调节。以前,发现dCTCF基因中的无效突变在pharate 成虫时死亡,这些成虫未能从它们的蛹壳中或在成虫孵化后不久死亡。在这里,我们获得了几个新的空dCTCF突变,发现dCTCF的完全失活主要限于Abd-B 的表型表现成蝇的基因和生育能力。许多与独立表型表现无关的修饰符可以显着增强无效dCTCF突变的表达能力,表明其他结构蛋白能够在功能上补偿果蝇中的dCTCF 失活。我们还绘制了 dCTCF 的 715-735 aa 区域作为与 BTB(Broad-Complex、Tramtrack 和 Bric a brac)和 CP190 蛋白的微管靶向 (M) 域相互作用所必需的区域,CP190 蛋白与许多结构域结合蛋白质。然而,突变分析表明,与 CP190 的相互作用对于 dCTCF在体内的功能活性并不重要。

更新日期:2021-08-10
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