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果蝇的头部退化缺陷基因在程序性细胞死亡中发挥作用。

The head involution defective gene of Drosophila melanogaster functions in programmed cell death.

作者信息

Grether M E, Abrams J M, Agapite J, White K, Steller H

机构信息

Howard Hughes Medical Institute, Department of Brain and Cognitive Sciences, Cambridge, Massachusetts, USA.

出版信息

Genes Dev. 1995 Jul 15;9(14):1694-708. doi: 10.1101/gad.9.14.1694.

Abstract

Deletions of chromosomal region, 75C1,2 block virtually all programmed cell death (PCD) in the Drosophila embryo. We have identified a gene previously in this interval, reaper (rpr), which encodes an important regulator of PCD. Here we report the isolation of a second gene in this region, head involution defective (hid), which plays a similar role in PCD. hid mutant embryos have decreased levels of cell death and contain extra cells in the head. We have cloned the hid gene and find that its expression is sufficient to induce PCD in cell death defective mutants. The hid gene appears to encode a novel 410-amino-acid protein, and its mRNA is expressed in regions of the embryo where cell death occurs. Ectopic expression of hid in the Drosophila retina results in eye ablation. This phenotype can be suppressed completely by expression of the anti-apoptotic p35 protein from baculovirus, indicating that p35 may act genetically downstream from hid.

摘要

染色体区域75C1、2的缺失几乎阻断了果蝇胚胎中所有的程序性细胞死亡(PCD)。我们在这个区间内鉴定出了一个先前的基因——收割者(rpr),它编码PCD的一个重要调节因子。在此我们报告在该区域分离出的第二个基因——头部内卷缺陷(hid),它在PCD中发挥类似作用。hid突变胚胎的细胞死亡水平降低,头部含有多余的细胞。我们克隆了hid基因,发现其表达足以在细胞死亡缺陷突变体中诱导PCD。hid基因似乎编码一种新的410个氨基酸的蛋白质,其mRNA在胚胎中发生细胞死亡的区域表达。hid在果蝇视网膜中的异位表达导致眼睛消融。杆状病毒抗凋亡p35蛋白的表达可完全抑制这种表型,这表明p35可能在hid的遗传下游起作用。

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