Karim F D, Chang H C, Therrien M, Wassarman D A, Laverty T, Rubin G M
Howard Hughes Medical Institute, University of California, Berkeley 94720-3200, USA.
Genetics. 1996 May;143(1):315-29. doi: 10.1093/genetics/143.1.315.
Cell-fate specification of the R7 photoreceptor cell is controlled by the sevenless receptor tyrosine kinase (SevRTK) and Ras1, the Drosophila homologue of mammalian H-ras, K-ras and N-ras oncogenes. An activated form of Ras1 expressed under control of the sevenless enhancer/promoter (sev-Ras1V12) induces production of supernumerary R7 photoreceptor cells, which causes the eye to become rough in appearance. To isolate mutations in genes functioning downstream of Ras1, we carried out a screen for dominant suppressors and enhancers of this rough eye phenotype. Approximately 850,000 mutagenized flies were screened, and 282 dominant suppressors and 577 dominant enhancers were isolated. Mutations in the Drosophila homologues of Raf, MEK, MAPK, type I Geranylgeranyl Transferase and Protein Phosphatase 2A were isolated, as were mutations in several novel signaling genes. Some of these mutant genes appear to be general signaling factors that function in other Ras1 pathways, while one seems to be more specific for photoreceptor development. At least two suppressors appear to function either between Ras1 and Raf or in parallel to Raf.
R7光感受器细胞的细胞命运特化由七less受体酪氨酸激酶（SevRTK）和Ras1控制，Ras1是哺乳动物H-ras、K-ras和N-ras癌基因的果蝇同源物。在七less增强子/启动子（sev-Ras1V12）控制下表达的活化形式的Ras1诱导产生额外的R7光感受器细胞，这会使眼睛外观变得粗糙。为了分离在Ras1下游起作用的基因中的突变，我们对这种粗糙眼表型的显性抑制子和增强子进行了筛选。大约筛选了850,000只诱变果蝇，分离出了282个显性抑制子和577个显性增强子。分离出了果蝇Raf、MEK、MAPK、I型香叶基香叶基转移酶和蛋白磷酸酶2A同源物中的突变，以及几个新的信号基因中的突变。这些突变基因中的一些似乎是在其他Ras1途径中起作用的一般信号因子，而其中一个似乎对光感受器发育更具特异性。至少有两个抑制子似乎在Ras1和Raf之间起作用，或者与Raf平行起作用。
