Kurada P, White K
Cutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Charlestown 02129, USA.
Cell. 1998 Oct 30;95(3):319-29. doi: 10.1016/s0092-8674(00)81764-x.
Activation of Ras inhibits apoptosis during Drosophila development. Genetic evidence indicates that Ras antiapoptotic activity in the developing eye is regulated by the Drosophila EGF receptor and operates through the Raf/MAPK pathway. Decreased activity of this pathway enhances, and increased activity suppresses, apoptosis induced by ectopic expression of the cell death regulators reaper (rpr) and head involution defective (hid). In addition, ectopic activation of the Ras/MAPK pathway in the developing embryo and in the developing eye suppresses naturally occurring apoptosis and regulates the transcription of the proapoptotic gene hid. Null alleles of hid recapitulate the antiapoptotic activities of Ras/MAPK, providing genetic evidence that downregulation of hid is an important mechanism by which Ras promotes survival.
在果蝇发育过程中，Ras的激活可抑制细胞凋亡。遗传学证据表明，发育中的眼睛里Ras的抗凋亡活性受果蝇表皮生长因子受体调控，并通过Raf/丝裂原活化蛋白激酶（MAPK）信号通路发挥作用。该信号通路活性降低会增强，而活性增加则会抑制由细胞死亡调节因子收割者（rpr）和头部内卷缺陷（hid）异位表达所诱导的细胞凋亡。此外，在发育中的胚胎和眼睛里，Ras/MAPK信号通路的异位激活可抑制自然发生的细胞凋亡，并调节促凋亡基因hid的转录。hid的无效等位基因重现了Ras/MAPK的抗凋亡活性，这提供了遗传学证据，表明hid的下调是Ras促进细胞存活的重要机制。
