The dodo mutant resembles Egfr- and hs-CF2. dodo was originally identified by genomic sequencing and transcript mapping (Maleszka, 1996). To reveal phenotypes associated with loss-of-function mutations without preset screening criteria, small overlapping chromosomal deletions were generated (Maleszka, 1996) that uncovered the entire dodo transcription unit in addition to two flanking genes: penguin (pen) and fli-I. The dodo-null genotype was confirmed by Northern blot analysis. The trans-heterozygous deletion mutant is lethal but viability can be restored by replacing the genomic copy of fli-I with a transgene (Maleszka, 1996). The resulting trans-heterozygotes lacking both the dodo and pen transcription units are viable and the surviving adult females permit the examination of possible oogenic phenotypes, particularly those associated with the MAPK signaling defects in the follicle cells. Initial examination showed a ventralized eggshell phenotype that was consistent but of low penetrance (35% at 25°C), ranging in expressivity from fused dorsal appendages to no appendages at all. Because the deletion mutant (in the background of the fli-I transgene) is also null for the gene pen, it was necessary to determine whether or not the ventralized phenotype is the result of dodo deletion. To this end it was shown that the phenotype can be rescued almost completely by supplying an exogenous dodo transgene under the transcriptional control of a heat-shock promoter in a dose-dependent manner (Hsu, 2001).
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date revised: 30 June 2001
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