Homozygous females show reduced fecundity, laying 7.4 +/- 1.5 eggs/20 hours (compared to 46.0 +/- 3.3 eggs/20 hours for wild-type females). MED311/Df(3R)Z1 females also show reduced fecundity, laying 3.2 +/- 0.4 eggs/20 hours.
Only 2.1% of embryos laid by homozygous females mated to wild-type males hatch.
Only 3.2% of embryos laid by MED311/Df(3R)Z1 females mated to wild-type males hatch.
91.6% of embryos laid by MED311/MED3121 females mated to wild-type males hatch.
The majority of embryos laid by homozygous or MED311/Df(3R)Z1 females (independent of paternal genotype) show severe morphological defects beyond stage 8.
Embryos derived from homozygous females mated to wild-type males reach the cellular blastoderm stage, but begin to display severe defects upon gastrulation. The proctodeal invagination, transverse furrow, stomodeal invagination and the cephalic furrow do form in the mutant embryos. However, the mitotic domains are missing or completely mislocalised in the mutant embryos and coincide with abnormal morphology. The formation of the posterior pole cells appears unaffected in the mutant embryos, but shortly after their formation, cells at the anterior and posterior pole start to delaminate toward the interior of the embryo. Abnormal cell ingression is seen at the anterior-dorsal region of the embryo. Cells associated with the migrating polar plate behave abnormally, resulting in severe deformations at the posterior-dorsal region of the embryo. During later stages, abnormal migration and degeneration at the poles results in cell loss.
A small proportion of embryos laid by homozygous females hatch, and some of these larvae progress through development and produce adult escapers. 33.7% of adult escapers derived from homozygous females mated to wild-type males have abdominal segmentation defects and 45.6% of adult escapers derived from homozygous females mated to homozygous males have abdominal segmentation defects. Defects in both sexes include incomplete tergite separation and additional tergites (13.4%), distinct patches of pigment in the abdominal epidermis (14.3%) and abnormally positioned sternites. Haltere development is disrupted in 10.6% of cases.
MED311/Df(3R)Z1 and MED311/MED311 adults derived from heterozygous parents do not develop significant abdominal defects.
MED311/MED31[+] is a non-enhancer of visible | maternal effect | dominant phenotype of skdL7062
MED311 has adult epidermis | maternal effect phenotype, enhanceable by skdL7062/skd[+]
MED311/MED31[+] is a non-enhancer of adult abdomen | maternal effect phenotype of skdL7062
When MED311/MED311 females are crossed to skdL7062/+ males, 54.7% of the MED311/skdL7062 adult progeny have abdominal defects, indicating that zygotic skdL7062 enhances the MED311 phenotype.
No increase in abdominal segmentation defects is seen in the adult progeny of MED311/skdL7062 females compared to the defects of the progeny of skdL7062/+ females, indicating that MED311 is not an enhancer of skdL7062 when maternally supplied.
