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Mef2 Interacts with the Notch Pathway during Adult Muscle Development in Drosophila melanogaster

机译:Mef2在果蝇的成年肌肉发育过程中与缺口途径相互作用。

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摘要

Myogenesis of indirect flight muscles (IFMs) in Drosophila melanogaster follows a well-defined cellular developmental scheme. During embryogenesis, a set of cells, the Adult Muscle Precursors (AMPs), are specified. These cells will become proliferating myoblasts during the larval stages which will then give rise to the adult IFMs. Although the cellular aspect of this developmental process is well studied, the molecular biology behind the different stages is still under investigation. In particular, the interactions required during the transition from proliferating myoblasts to differentiated myoblasts ready to fuse to the muscle fiber. It has been previously shown that the Notch pathway is active in proliferating myoblasts, and that this pathway is inhibited in developing muscle fibers. Furthermore, the Myocyte Enhancing Factor 2 (Mef2), Vestigial (Vg) and Scalloped (Sd) transcription factors are necessary for IFM development and that Vg is required for Notch pathway repression in differentiating fibers. Here we examine the interactions between Notch and Mef2 and mechanisms by which the Notch pathway is inhibited during differentiation. We show that Mef2 is capable of inhibiting the Notch pathway in non myogenic cells. A previous screen for Mef2 potential targets identified Delta a component of the Notch pathway. Dl is expressed in Mef2 and Sd-positive developing fibers. Our results show that Mef2 and possibly Sd regulate a Dl enhancer specifically expressed in the developing IFMs and that Mef2 is required for Dl expression in developing IFMs.
机译:果蝇中的间接飞行肌肉(IFM)的肌发生遵循明确的细胞发育方案。在胚胎发生过程中,指定了一组细胞,即成年肌肉前体(AMPs)。这些细胞将在幼虫阶段变成增生的成肌细胞,然后产生成年IFM。尽管已经很好地研究了该发育过程的细胞方面,但仍在研究不同阶段背后的分子生物学。特别地,在从增殖的成肌细胞到分化成肌细胞的过渡过程中所需的相互作用准备融合到肌纤维上。先前已经表明,Notch途径在增殖的成肌细胞中有活性,并且该途径在发育的肌纤维中被抑制。此外,心肌细胞增强因子2(Mef2),前庭(Vg)和扇形(Sd)转录因子对于IFM发育是必需的,而Vg是分化纤维中Notch通路抑制所必需的。在这里,我们检查了Notch和Mef2之间的相互作用以及Notch通路在分化过程中受到抑制的机制。我们表明,Mef2能够抑制非成肌细胞中的Notch途径。先前针对Mef2潜在目标的屏幕将Delta识别为Notch途径的组成部分。 D1在Mef2和Sd阳性显影纤维中表达。我们的结果表明,Mef2和可能的Sd调节在发育中的IFM中特异性表达的D1增强子,并且在发展中的IFM中D1表达需要Mef2。

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