首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Cooperative functions of the reaper and head involution defective genes in the programmed cell death of Drosophila central nervous system midline cells
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Cooperative functions of the reaper and head involution defective genes in the programmed cell death of Drosophila central nervous system midline cells

机译:果蝇中枢神经系统中线细胞的程序性细胞死亡中收割者和头部对合缺陷基因的协同功能

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摘要

In Drosophila, the chromosomal region 75C1–2 contains at least three genes, reaper (rpr), head involution defective (hid), and grim, that have important functions in the activation of programmed cell death. To better understand how cells are killed by these genes, we have utilized a well defined set of embryonic central nervous system midline cells that normally exhibit a specific pattern of glial cell death. In this study we show that both rpr and hid are expressed in dying midline cells and that the normal pattern of midline cell death requires the function of multiple genes in the 75C1–2 interval. We also utilized the P[UAS]/P[Gal4] system to target expression of rpr and hid to midline cells. Targeted expression of rpr or hid alone was not sufficient to induce ectopic midline cell death. However, expression of both rpr and hid together rapidly induced ectopic midline cell death that resulted in axon scaffold defects characteristic of mutants with abnormal midline cell development. Midline-targeted expression of the baculovirus p35 protein, a caspase inhibitor, blocked both normal and ectopic rpr- and hid-induced cell death. Taken together, our results suggest that rpr and hid are expressed together and cooperate to induce programmed cell death during development of the central nervous system midline.
机译:在果蝇中,染色体区域75C1-2至少包含三个基因,即收割者(rpr),头部向内缺陷(hid)和严酷,它们在激活程序性细胞死亡中具有重要功能。为了更好地了解这些基因如何杀死细胞,我们利用了一组定义明确的胚胎中枢神经系统中线细胞,这些细胞通常表现出特定的神经胶质细胞死亡模式。在这项研究中,我们显示rpr和hid均在垂死的中线细胞中表达,中线细胞死亡的正常模式需要在75C1-2间隔中具有多个基因的功能。我们还利用P [UAS] / P [Gal4]系统靶向rpr的表达并将其隐藏到中线细胞中。单独表达rpr或hid不足以诱导异位中线细胞死亡。然而,rpr和hid的表达一起迅速诱导异位中线细胞死亡,这导致具有异常中线细胞发育突变体的轴突支架缺陷特征。杆状病毒p35蛋白(一种半胱天冬酶抑制剂)的中线靶向表达可阻断正常和异位rpr和hid诱导的细胞死亡。两者合计,我们的结果表明 rpr hid 一起表达,并合作诱导中枢神经系统中线发育过程中的程序性细胞死亡。

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