The muscleblind gene participates in the organization of Z-bands and epidermal attachments of Drosophila muscles and is regulated by Dmef2
The muscleblind gene participates in the organization of Z-bands and epidermal attachments of Drosophila muscles and is regulated by Dmef2
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DOI：
10.1006/dbio.1997.8833
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发表时间：
1998-03-15
影响因子：
2.7
通讯作者：
Baylies, MK
中科院分区：
文献类型：
--
作者：
Artero, R;Prokop, A;Baylies, MK
我们报告了muscleblind（mbl）的胚胎表型，这是最近描述的一种参与成年小眼终末分化的果蝇基因。 mbl 是一种核蛋白，在胚胎晚期在咽部、内脏和躯体肌肉、腹神经索和幼虫感光系统中表达。研究的所有三个 mbl 等位基因均表现出致命表型，并在 17 期胚胎或一龄幼虫时死亡。这些幼虫部分瘫痪，腹部典型地收缩，并且缺乏肌肉条纹。我们对躯体肌肉系统的分析表明，肌肉的模式建立正确，并且它们形成形态正常的突触。然而，超微结构分析揭示了肌肉终末分化的两个缺陷：无法区分肌节中的 Z 带，以及表皮附着部位的细胞外肌腱基质减少。未能区分这两种结构可以解释部分瘫痪和腹部收缩表型。对 Dmef2 突变体或异位表达 Dmef2 的胚胎中 mbl 表达的分析将 mbl 置于生肌分化程序中 Dmef2 功能的下游。因此，mbl 可能在肌肉终末分化中执行两个 Dmef2 依赖性过程中发挥关键作用。 (C) 1998 年学术出版社。
We report the embryonic phenotype of muscleblind (mbl), a recently described Drosophila gene involved in terminal differentiation of adult ommatidia. mbl is a nuclear protein expressed late in the embryo in pharyngeal, visceral, and somatic muscles, the ventral nerve cord, and the larval photoreceptor system. All three mbl alleles studied exhibit a lethal phenotype and die as stage 17 embryos or first instar larvae. These larvae are partially paralyzed, show a characteristically contracted abdomen, and lack striation of muscles. Our analysis of the somatic musculature shows that the pattern of muscles is established correctly, and they form morphologically normal synapses. Ultrastructural analysis, however, reveals two defects in the terminal differentiation of the muscles: inability to differentiate Z-bands in the sarcomeric apparatus and reduction of extracellular tendon matrix at attachment sites to the epidermis. Failure to differentiate both structures could explain the partial paralysis and contracted abdomen phenotype. Analysis of mbl expression in embryos that are either mutant for Dmef2 or ectopically express Dmef2 places mbl downstream of Dmef2 function in the myogenic differentiation program. mbl, therefore, may act as a critical element in the execution of two Dmef2-dependent processes in the terminal differentiation of muscles. (C) 1998 Academic Press.