UAS regulatory sequences drive expression of a short inverted repeat.
Maternal expression of CrkHMC03964 under the control of Scer\GAL4VP16.mat.αTub67C leads to near complete embryonic lethality; most embryos exhibit morphological defects, which can be denticle belt deletion or fusion, ventral or dorsal holes, severe pattern disruption, or cuticle fragments; frequently there are also germband retraction defects. Nuclear division cycle 10 proceeds relatively normally, though pseudocleavage furrows appears less continuous; by nuclear division cycle 11, spindle defects are more frequent, with a most embryos showing cases of colliding neighboring spindles and half of embryos showing regions with nuclear loss; by nuclear division cycle 12, all embryos show multiple spindle collisions and regions of nuclear loss. At cellularization, nuclei are less uniform in shape ("bottle-shaped" rather than oval) and misaligned, and their actin rings are less uniform, while the yolk channels are uneven in size, and some abnormally enlarged. At nuclear division cycles 10-12, the pseudocleavage furrow invagination is significantly shallower and the actin cap expansion is reduced, as compared to controls. By stage 15, almost half of embryos show CNS defects, most having mild axon patterning defects (inappropriate midline crossing of axons as well as loss of commissural or longitudinal axons in some segments) and some having severe nervous system patterning disruption; most embryos with strong CNS defects also have strong defects in the overlying epidermis, ranging from epidermal holes to strong disruptions to the epidermal pattern.