Mesoderm invagination is delayed (mesoderm breadth is significantly reduced), posterior midgut is variably affected (the anterior movement of pole cells due to posterior midgut invagination and tissue extension is defective) and ectoderm extension is significantly reduced in Gγ1^N159/Gγ1^N159 embryos (germline clones) compared to controls.

Gustatory receptor neurons bearing Gγ1^N159 mutants exhibit normal responses to water, high (300mM) and low (30mM) concentrations of salt. However, these neurons show lower nerve responses to 10-300mM sucrose.

Gγ1^N159 mutants which lack both zygotic and maternal Gγ1⁺ function exhibit abnormal gastrulation. The apical-basal polarity of the mutant epithelial cell is virtually normal, but the spindle orientation is randomised, causing divisions at oblique angles or parallel to the surface in the mutant neuroblasts. In addition, these embryos exhibit characteristic anterior and posterior holes. In contrast to wild-type, Gγ1^N159 mutant neuroblasts in embryos that lack both zygotic and maternal Gγ1⁺ function cleave into nearly equal-sized daughter cells. Microtubule structures in the mutant neuroblasts are nearly symmetric and develop well from both centrosomes throughout mitosis. The cell-size ratio of the ganglion mother cell and the neuroblast is approximately doubled compared to wild-type.

Mutant neuroblasts in embryos derived from germline clones mostly divide into equal-sized daughters.