Burchard S, Paululat A, Hinz U, Renkawitz-Pohl R
Philipps-Universität, Marburg, FRG.
J Cell Sci. 1995 Apr;108 ( Pt 4):1443-54. doi: 10.1242/jcs.108.4.1443.
In a search for mutations affecting embryonic muscle development in Drosophila we identified a mutation caused by the insertion of a P-element, which we called not enough muscles (nem). The phenotype of the P-element mutation of the nem gene suggests that it may be required for the development of the somatic musculature and the chordotonal organs of the PNS, while it is not involved in the development of the visceral mesoderm and the dorsal vessel. Mutant embryos are characterized by partial absence of muscles, monitored by immunostainings with mesoderm-specific anti-beta 3 tubulin and anti-myosin heavy chain antibodies. Besides these muscle distortions, defects in the peripheral nervous system were found, indicating a dual function of the nem gene product. Ethyl methane sulfonate-induced alleles for the P-element mutation were created for a detailed analysis. One of these alleles is characterized by unfused myoblasts which express beta 3 tubulin and myosin heavy chain, indicating the state of cell differentiation.
在寻找影响果蝇胚胎肌肉发育的突变过程中，我们鉴定出一个由P因子插入引起的突变，我们将其命名为“肌肉不足”（nem）。nem基因的P因子突变表型表明，它可能是体壁肌肉组织和外周神经系统弦音器官发育所必需的，而它不参与内脏中胚层和背血管的发育。通过用中胚层特异性抗β3微管蛋白和抗肌球蛋白重链抗体进行免疫染色监测，突变胚胎的特征是部分肌肉缺失。除了这些肌肉畸变外，还发现了外周神经系统的缺陷，这表明nem基因产物具有双重功能。为了进行详细分析，我们创建了乙基甲磺酸诱导的P因子突变等位基因。其中一个等位基因的特征是未融合的成肌细胞，这些细胞表达β3微管蛋白和肌球蛋白重链，表明细胞分化状态。
