2.8 +/- 0.3% of homozygotes survive to adulthood. Escapers have a cleft in the dorsal midline of the thorax. The phenotype varies in severity from nearly normal, through a midline devoid of bristles to a cleft notum.
Src42AJp45 has lethal | recessive phenotype, enhanceable by hep[+]/hepr75
Src42AJp45 has lethal | recessive phenotype, enhanceable by bsk2/bsk[+]
Src42AJp45 has lethal | recessive phenotype, enhanceable by Btkk05610/Btkk00206
Src42AJp45 has lethal | recessive phenotype, suppressible by pucE69/puc[+]
Src42AJp45/Src42A[+], p130CAS1 has partially lethal - majority die | embryonic stage phenotype
Src42AJp45 has adult thorax | dorsal phenotype, enhanceable by hep[+]/hepr75
Src42AJp45 has adult thorax | dorsal phenotype, suppressible by pucE69/puc[+]
p130CAS1 homozygous mutants in combination with either Fak56DCG1 heterozygous or homozygous mutants yield no viable adult offspring. The Fak56DCG1/Fak56DCG1; p130CAS1/+ genotype significantly reduces the viability of adults. Analysis of the double homozygous mutant lethal phenotype indicates that most (95%) of the embryos do not hatch. The few escapers survive to pupal stages, but do not emerge.
In contrast to either Fak56DCG1 or p130CAS1 homozygotes, onnly 5% of double mutants produce cuticles and almost all observed cuticles are marked by dorsal and/or ventral holes, indicating dorsal closure defects. Additionally, double mutant cuticles exhibit fused or missing denticle belts, a phenotype never observed in Fak56DCG1 homozygotes alone.
Approximately 29% of Src42AJp45/+; p130CAS1/p130CAS1 double mutants emerge as adults.
The lethality of homozygotes is dominantly enhanced by hepr75 or bsk2 and dominantly suppressed by pucE69. The severity of the dorsal cleft phenotype is dominantly enhanced by hepr75 and dominantly suppressed by pucE69. Btk29Ak00206/Btk29Ak05610 enhances the lethality of Src42AJp45.
Excision of the P-element reverts the semi-lethality and cleft thorax phenotype.