Cp1902 germ-line clone embryos have a severe axial-expansion defect; at nuclear cycle 7-8 the nuclei remain clustered toward the anterior of the embryo.
Cp1902, Cp1902/Df(3R)P280-NR27 and Cp1901/Cp1902 mutants show some larval mortality, but approximately half the mutants survive until late pupal stages, dying as pharate adults. Cp1902 larval brains show no obvious mitotic defects and the eyes, wings and cuticle of pharate adults appear normal, showing that tissue organization is not affected by a major defect in mitosis. Additionally, there are no observable meiotic defects in Cp1902 larval testes.
Cp1902 has cleavage nucleus phenotype, suppressible by sqhE20.E21
Cp1902 has cleavage nucleus phenotype, non-suppressible by sqhRLC.GFP(S65T)
Expression of one copy of the sqhE20.E21 transgene partially restores axial expansion in Cp1902 germ-line clone embryos. However, expression of one copy of the wild-type sqhT:Avic\GFP transgene does not rescue this defect.
Cp1902 is rescued by Cp190Ubi-p63E.PB
Df(3R)P280-NR27/Cp1902 is rescued by Cp190Ubi-p63E.PB
Cp1902 is rescued by Cp190Ubi-p63E.PB
Cp1902 is partially rescued by Cp190ΔM.Ubi-p63E
Cp1902 is partially rescued by Cp190ΔM.Ubi-p63E
Expression of the Cp190ΔM.Ubi-p63E transgene fails to rescue the axial-expansion defect of Cp1902 flies.
The Cp190ΔM.Ubi-p63E transgene rescues the lethality of Cp1902 mutants so that ~80% of flies survive to adulthood. However, these adults are unhealthy and only survive for a few days.