Patterning defects of the 18304 mutant and oskar dependence of the phenotype
| Genotype . | Wild type . | Haed defect . | Bicaudal . | Posterior group . | No cuticle development* . |
|---|---|---|---|---|---|
| W1118 | 95 | 0 | 0 | 0 | 5 |
| 18304 germline clone | 21 | 21 | 29 | 0 | 29 |
| 18304/Df(3L)ri-XT106 | 12 | 34 | 32 | 0 | 22 |
| 18304/E1 | 20 | 25 | 36 | 0 | 19 |
| oskar346/oskar166 | 0 | 0 | 0 | 70 | 30 |
| 18304, oskar346/Df(3L)ME107, oskar166 | 0 | 0 | 0 | 30 | 70 |
| Genotype . | Wild type . | Haed defect . | Bicaudal . | Posterior group . | No cuticle development* . |
|---|---|---|---|---|---|
| W1118 | 95 | 0 | 0 | 0 | 5 |
| 18304 germline clone | 21 | 21 | 29 | 0 | 29 |
| 18304/Df(3L)ri-XT106 | 12 | 34 | 32 | 0 | 22 |
| 18304/E1 | 20 | 25 | 36 | 0 | 19 |
| oskar346/oskar166 | 0 | 0 | 0 | 70 | 30 |
| 18304, oskar346/Df(3L)ME107, oskar166 | 0 | 0 | 0 | 30 | 70 |
The patterning defects of the 18304 mutant in different genetic backgrounds were evaluated by examination of embryonic cuticles and were quantified. More than 200 embryos of each genotype were analyzed. The phenotypes of embryos derived from 18304 in trans to three deficiencies (Df(3L)ri−XT106, Df(3L)ri−XT1 and Df(3L)ME107) were virtually identical, and the result obtained from Df(3L)ri−XT106 is shown. The behavior of E1 was indistinguishable from that of the deficiencies, suggesting that E1 is a null allele of the 18304 locus.
About 30% of oskar346/oskar166 embryos did not develop cuticle, presumably because of second-site mutations accumulated in the stocks. This population was 70% in 18304, oskar double mutants. Of the 18304, oskar double mutant embryos that developed cuticle, 100% completely lacked an abdomen - the oskar phenotype. The suppression of posterior structure formation in the 18304, oskardouble mutant embryos indicates that the patterning defects in the 18304 mutant are caused by oskar activity alone.