Scer\GAL4GMR.PU-mediated expression of Six4Scer\UAS.cCa moderately inhibits eye development.
Six4UAS.cCa/Scer\GAL4ey.PU is a suppressor of eye phenotype of so1
Scer\GAL4twi.PG, Six4UAS.cCa, eyaUAS.cBa has ventral oblique muscle cell phenotype
Scer\GAL4twi.PG, Six4UAS.cCa, eyaUAS.cBa has visceral trunk mesoderm phenotype
Scer\GAL4twi.PG, Six4UAS.cCa, eyaUAS.cBa has embryonic somatic muscle cell phenotype
Scer\GAL4twi.PG, Six4UAS.cCa, eyaUAS.cBa has mesoderm phenotype
Scer\GAL4twi.PG, Six4UAS.cCa, eyaUAS.cBa has fat body/gonad primordium phenotype
Scer\GAL4twi.PG, Six4UAS.cCa, eyaUAS.cBa has trunk mesoderm phenotype
Scer\GAL4ey.PU-mediated expression of Six4Scer\UAS.cCa significantly rescues the so1 eye phenotype.
Co-expression of eyaScer\UAS.cBa and Six4Scer\UAS.cCa in the twi domain, under the control of Scer\GAL4twi.PG strongly affects the mesoderm. Several cell types derived from the ventral and dorsolateral mesoderm expand. Greatly increased numbers of somatic gonadal precursors results in an enlarged gonad. There are also more fat body precursors, and these now extend into the dorsal region of the mesoderm, suggesting that dorsal cells have taken on more ventral fates. In contrast, derivatives of the dorsal mesoderm are disrupted. In stage 17 embryos no myosin-expressing cardioblasts are visible, while there are gaps in the pattern of dorsal muscles. Similarly, there are gaps in the visceral mesoderm at stage 12. In the ventral region of the somatic musculature, there are duplications of the ventral acute muscle (VA3), while the pattern of ventral oblique muscles is disrupted. The lateral somatic musculature also appears larger.