SCARk13811 mutant cells in mosaic follicular epithelia exhibit a non-cell-autonomous defect in trailing edge retraction, as wild type cells directly ahead of SCARk13811 mutant cells exhibit significantly elongated basal surfaces.
SCARk13811 mutant embryos that lack both the zygotic and maternal SCAR gene products (derived from females containing homozygous germline clones mated to homozygous males) display a duplication of the RP2 neuron in one hemisegment and have one missing in the contralateral segment. Embryos are also seen in which RP2 neurons fail to migrate from their location of formation.
SCARk13811 mutant embryos show a partial loss of myoblast fusion at stage 14 and, unlike in wild type, enlarged actin foci persist at stage 15. The percentage of F-actin foci that are invasive and the depth of invasion are both comparable to wild type. These phenotypes are seen when just the zygotic contribution is removed, or when both the maternal and zygotic gene products are absent.
Homozygous SCARk13811 embryos exhibit a weak myoblast fusion defect. Unfused myoblasts are visible. Dorsal closure seems incomplete in these embryos.
SCARk13811 germline clone embryos, with reduced maternal and zygotic SCAR contributions exhibit a severe myoblast fusion defect, with increased numbers of free myoblasts and thinner muscles. SCARk13811 mutants show a dramatic increase in the size and number of actin foci.
The spacing and morphology of nuclei is abnormal in cycle 12-13 blastoderm SCARK13811 germ-line clone embryos. By cycle 14, these embryos show dramatic abnormal accumulation of nuclei internally. The actin cytoskeletons of SCARK13811 germ-line clone embryos are also abnormal at these stages. This is particularly clear during metaphase when, in the majority of embryos, actin accumulates in aberrant structures positioned above individual spindles, rather than forming a network of metaphase furrows between adjacent spindles, as in wild-type. These defects are accompanied by a general decrease in filamentous actin levels, although cell cycle-dependent fluctuations in filamentous actin levels persist. CNS axon morphology in SCARK13811 homozygous embryos is normal. However, in SCARK13811 homozygous embryos from SCARK13811 germ-line clone mothers, gaps appear in both longitudinal and commissural bundles (93% of segments, n = 242). In extreme cases, a severe depletion of all axon bundles occurs (46% of segments). At a lower frequency, these embryos exhibit defects in commissure fasciculation and separation (18% of segments), and medial (13%) or lateral (9%) displacement of axons.