Deletion of nucleotides 1651 and 1652, causing a frameshift at amino acid residue E205 and producing a stop codon 60 nucleotides further downstream.
Deletion of 2 G residues, causing a frameshift at amino acid residue E205 and producing a stop codon 60 nucleotides further downstream.
scu4058 homozygote mutants display delay in pupariation compared to heterozygote sibling controls and although majority of the mutant animals does pupariate eventually, they all fail to eclose and survive to adulthood. High proportion of scu4058 mutants also show pupal case defects - incomplete or failed spiracle eversion or do not form compact pupal cases at all but rather larval-like cases.
scu4058 homozygous mutants display mitochondrial morphology defects in larval brain neuroblasts: the mitochondria are larger and swollen and often have ring-like shape.
scu4058 shows an early lethal phase during embryogenesis, followed by a major period of lethality around the onset of metamorphosis. The number of homozygous clones produced in the adult cuticle is reduced compared to the wild-type controls in twin mosaic analysis. Testis size is reduced in males examined before the onset of lethality. Spermatocytes are organised into smaller groups of cells than normal in pupal testes, and sperm bundles are not seen. The number of mitochondria in the cytoplasm of the spermatocytes is reduced.
Individuals die as embryos or pupae. Interruption of the longitudinal nerve tracts at the level of the fourth abdominal neuromere and he defect in fasciculation of the nerves of the last abdominal neuromere. Heterozygotes have a Sh phenotype.
Male lethality is completely rescued by scu+t2.4.
Somatic clonal analysis indicates that scu+ activity is required for cell survival and that this requirement is cell autonomous. The degree of reduction of testis size varies in the following order: scu174 > scu4058 > scuS152 > scu3127.
Mutation in the haplo-lethal (HL) region of the Sh complex.
Mutation within the haplo-lethal (HL) region of the Sh complex.