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Pathology of the Adult Cneter Nervous System Induced by Genetic Inhibition of Programmed Cell Death in Drosophila Pupae

机译:果蝇P程序性细胞死亡的遗传抑制诱导成人中枢神经系统的病理。

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In the spinster (spin) mutant of Drosophila melanogaster, the extent of programmed cell death (PCD) in the abdominal ganglion 6 h after puparium formation (APF) is significantly reduced. The shortening of the abdominal ganglion, which is normally completed 48 h APF, does not occur. After eclosion, neurodegeneration accompanied by accumulation of atuofluorescent materials is manifested in the central nervous system (CNS) of the spin mutant. The materials accumulated in the spin-mutant CNS contain a substance that is immunopositive to an antibody against GM2 ganglioside. Halving the dosage of three cell death genes, rpr, grim, and hid, blocks shortening of the abdominal ganglion and induces neurodegeneration accompanied by accumulation of autofluorescent materials in the adult CNS. These observations suggest that the primary action of the spin mutations is to reduce the extent of PCD 6 h APF, which concomitantly leads to a failure in shortening of the abdominal ganglion and to neurodegeneration of the adult CNS. Arch. Insect Biochem. Physiol.
机译:在果蝇的纺锤体(spin)突变体中,形成(APF)后6 h,腹部神经节中程序性细胞死亡(PCD)的程度显着降低。腹神经节缩短通常不会在APF 48小时内完成。脱落后,在自旋突变体的中枢神经系统(CNS)中表现出伴随变性的荧光物质堆积的神经变性。在自旋突变CNS中积累的物质包含对GM2神经节苷脂抗体具有免疫阳性的物质。将三个细胞死亡基因rpr,grim和hid的剂量减半,可以阻止腹部神经节的缩短,并诱导神经变性,并伴随着成人CNS中自身荧光物质的积累。这些观察结果表明,自旋突变的主要作用是减少PCD 6 h APF的程度,从而导致腹神经节缩短失败和成人CNS的神经变性。拱。昆虫生化。生理学。

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