Transmission rate of Dp(1;f)J21A through females to progeny is 28%, Klp3A mutation strongly decreases transmission. Mutation also decreases transmission of Dp(1;f)1B, Dp(1;f)25A and Dp(1;f)10B.
Over 90% eggs laid do not hatch into larvae, of these over 80% contain sperm tails so the primary block in development must occur after fertilisation. The large majority undergo very few if any nuclear divisions. In the terminal state the presumptive female pronucleus remains associated with the other 3 products of female meiosis in a single polar body. The male pronucleus remains separated a considerable distance from this polar body. Although the gonomeric spindle cannot be formed in these conditions a bipolar spindle is established around the haploid paternal genome. A significant minority of embryos develop past this point and display mitotic defects (disorganised spindles, unequal spacing of nuclei and free centrosomes). At gastrulation these embryos display a range of apparently nonspecific defects accompanied by cellular degradation. Examination of the cuticles reveals variable defects in cuticle formation and incomplete segmentation. Some rare embryos escape and hatch into larvae, almost all of these develop into normal adults. Adult male and female escapers are recovered in equal proportions. None of these adults are aneuploid for the X or 4th chromosome suggesting chromosome segregation during meiosis in eggs is generally regular.
Heterozygotes with Df(1)63e4 are viable but female sterile (exhibit a maternal effect lethal egg phenotype) and male semi-sterile. Hemizygous males exhibit low fertility, well over half of the males are completely sterile, the remainder exhibit variable fertility.
Embryonic defects detectable at preblastoderm stages.
In eggs laid by double homozygous Hira185b, Klp3A3 mothers, the single centrally located nucleus has abnormally condensed chromatin. The male stock often displays an elongated protrusion of chromatin extending towards a free aster (as seen in embryos laid by Klp3A3 mothers), sometimes forming a hemispindle.
Klp3A3 is rescued by Klp3A+tSCA9
Klp3A3 is rescued by Klp3A+tSCA9
Fertility and cytological phenotypes are rescued by Klp3A+tSCA9.