Nucleotide substitution: G?A.
Amino acid replacement: W2154term.
This nonsense mutation is predicted to result in an expressed protein that lacks 80% of the wild-type protein sequence.
Truncation of at least the C-terminus.
egg chamber & actin filament | maternal effect | germ-line clone
follicle cell & nucleus | somatic clone
nurse cell & cytoplasm | maternal effect | germ-line clone
nurse cell & nucleus | maternal effect | germ-line clone
oocyte & nucleus | maternal effect | germ-line clone
Msp-300sz75 homozygotes are semi-lethal (approximately 30% of the expected genotypes survive).
Msp-300sz75 mutants are viable and have no obvious defects in the eye. The external eyes and the retinal tissue are indistinguishable from wild-type.
Homozygous Msp-300sz75 females exhibit a completely penetrant dumpless phenotype and sterility.
Msp-300sz75 is not homozygous lethal.
Msp-300sz75/+ females with Msp-300sz75 homozygous germ-line clones lay a reduced number of eggs compared to wild type. The majority of such eggs are significantly shorter than wild-type eggs with short dorsal appendages and a subset have a severely shrunken appearance. All of these eggs show abnormal development.
Msp-300sz75 egg chambers that develop from Msp-300sz75 germ-line clones show a severe disruption in cytoplasmic dumping of the nurse cells. Following this abnormal dumping, the nuclei of nurse cells and the oocyte become mislocalized. While 92% of late egg chambers show mislocalized nurse cell nuclei, 4% display a severe version of the phenotype in which nurse cell nuclei invade the oocyte and become arranged in a line. Additionally, during and following the cytoplasmic dumping stage, the egg chambers show a disruption of actin organization. Actin bundle-like microfilaments are formed, but do not extend far enough from the plasma membrane to form actin-cages around the nuclei. The number of ring canals is reduced during the dumping stage, from an average of 15 in wild type to an average of 6 in the mutant.
Follicle cell nuclei display slight defects in their positions and shapes in Msp-300sz75 follicle cell clones.
Muscle phenotype; overall shape of each myotube is defective and they do not reach their epidermal attachment sites. Defects in the somatic musculature leads to severe impairment of muscle function resulting in inability to hatch from the chorion. Visceral and heart muscle are not affected. Stage 15 and stage 16 Msp-300sz75 LanA9-32 double mutant embryos exhibit complete disruption of the muscle pattern.
CAP49e, Msp300sz75 has increased cell number | embryonic stage phenotype
Msp300sz75, scb01288 has increased cell number | embryonic stage phenotype
Msp300sz75, WASp3 has increased cell number | embryonic stage phenotype
CAP49e, Msp300sz75 has embryonic cardioblast | increased number phenotype
Msp300sz75, scb01288 has embryonic cardioblast | increased number phenotype
Msp300sz75, WASp3 has embryonic cardioblast | increased number phenotype
The dumpless and sterility phenotype of Msp-300sz75 females are not complemented by Dp(2;1)B19.
This allele has been described as embryonic lethal. However, the lethality of the original Msp-300sz75 chromosome is due to a second mutation, not the Msp-300sz75 allele.