Table 1. Phenotypic strength of selected vab-1 mutations and molecular lesions.
| Allele | Mutagen | Embryonic lethality (%) | Larval lethality (%) | Adult, Vab (%) | Adult, non-Vab (%) | WT sequence | Mutant sequence | Effect |
|---|---|---|---|---|---|---|---|---|
| Strong | ||||||||
| e2027(null) | SPO | 58.2 | 31.3 | 8.9 | 2.5 | — | 74-bp deletion, removing first 7 bp of exon 5 | — |
| e721 | EMS | 58.2 | 29.3 | 11.4 | 1.0 | ACG | ATG | ATG codon in 5′-UTR |
| ok1699 | UV | 53.4 | 20.7 | 23.9 | 2.0 | — | 1016-bp deletion of exon 5 | — |
| ju220 | UV/TMP | 45.4 | 15.0 | 34.6 | 5.1 | — | Exon 1 rearrangement | — |
| ju307 | EMS | 41.9 | 27.2 | 29.1 | 1.8 | GAA | AAA | E62K |
| Intermediate | ||||||||
| ju275 | EMS | 18.0 | 7.3 | 65.0 | 9.8 | GCG | GTG | A245V |
| Weak | ||||||||
| zd118 | EMS | 13.8 | 7.5 | 24.6 | 54.0 | TGG | TGA | W934opal |
| ju426 | EMS | 13.6 | 2.1 | 55.3 | 28.9 | TGG | TGA | W934opal |
| e118(kd) | EMS | 10.1 | 8.6 | 45.6 | 35.8 | — | 326-bp deletion in exon 10 | — |
| ju306 | ENU | 1.7 | 1.4 | 32.4 | 64.4 | GTC | GAC | V220D |
| qa2211 | EMS | 1.5 | 1.1 | 18.7 | 78.7 | GGA | GAA | G256E |
Three new alleles were characterized as genetically null based on phenotypic strength and molecular lesions: ju220 is a rearrangement of unknown structure that affects exon 1, encoding the start codon and signal sequence; ok1699 is a 1016-bp deletion of exon 5, which encodes part of the ephrin binding domain and the cysteine-rich domain in the extracellular domain; and ju307 results in the same missense alteration (E62K) as the previously described ju8 (George et al. 1998). The previously unsequenced null allele e721 creates a premature ATG in the vab-1 5′-untranslated region; translation from this out-of-frame upstream ORF likely interferes with translation from the native vab-1 ATG. Three new alleles result in missense alterations in the extracellular cysteine-rich domain, providing mutational evidence for the importance of this domain.