Med4 mutants exhibit defects in R axon projection and lamina morphology. Such defects are only observed when large clones are generated in the posterior-dorsal or ventral domains, which presumably include glial cell progenitors. Clones in other regions, such as the outer proliferation center, lamina or medulla, do not result in R-axon targeting defects.
Lethal in transheterozygous combination with MedD5.
Med4/Df(3R)Kpn-A embryos sometimes have abnormal gastric caeca and midgut morphology. Med2/Med4 embryos show a partial loss of the second midgut constriction.
Homozygous third larval instar have variably reduced central nervous systems.
Lethality occurs during larval and pupal stages.
Med4/Med2 is a suppressor of embryonic midgut constriction 1 phenotype of Scer\GAL4how-24B, dppUAS.cSa
Med4/Med2 is a suppressor of embryonic midgut constriction 3 phenotype of Scer\GAL4how-24B, dppUAS.cSa
Med4, dpphr4/dpp[+] has cephalopharyngeal skeleton phenotype
Med4/Med[+], dpphr4 has cephalopharyngeal skeleton phenotype
The combination Med2/Med4 usually restores the first and third midgut constrictions in embryos expressing dppScer\UAS.cSa under the control of Scer\GAL4how-24B.
Maternal lethal interaction with dpphr4 is due to a loss of dorsal-most fates in the embryos, demonstrated by loss of amnioserosa cells. dpphr4/dpp+;Med4/Med+ embryos have a partially involuted head skeleton. Embryos exhibits a 'tail up' phenotype, the posterior most structures are pointed more vertically and there is more curvature to the abdominal segments.