Single cell γ neuron mutant clones in the mushroom body do not show axon growth defects.

Germ-line clones of Sop2^R337st lead to relatively mild defects in nurse cell dumping: late stage oocytes are abnormally small, while late stage nurse cells are abnormally large. The diameter and shape of ring canals is compromised.

Homozygous Sop2^R337st embryos (created as germ-line clones) appear relatively normal through division 10 to 10, but show spindle interactions and chromosome segregation errors that increase in frequency during divisions 12 and 13. However no defects are seen in the spacing of interphase nuclei. Occasionally, free centrosomes are observed in these embryos. However, the vast majority of interphase nuclei have a normal complement of centrosomes, and there does not appear to be any effect on centrosome association with the nuclear envelope. In wild-type embryos interphase actin caps form on mitotic exit, and expand through interphase, merging to form pseudo-cleavage furrows by the following mitosis. In Sop2^R337st embryos (created as germ-line clones) pronounced actin caps do assemble on mitotic exit, but these caps do not expand, actin remains loosely organised over the nuclei, and furrow assembly fails - only superficial rings of actin are seen. The Sop2^R337st mutation does not block blastoderm cellularisation.

The spacing and morphology of nuclei is abnormal in cycle 12-13 blastoderm Sop2^R337st germ-line clone embryos. By cycle 14, these embryos show abnormal accumulation of nuclei internally. The actin cytoskeletons of Sop2^R337st germ-line clone embryos are also abnormal at these stages: the network of metaphase furrows between adjacent spindles characteristic of wild-type embryos fails to form properly, and there is a general depletion of actin above each spindle throughout the division cycle. These defects are accompanied by a general decrease in filamentous actin levels, although cell cycle-dependent fluctuations in filamentous actin levels persist.