ena23 zygotic/maternal mutant embryos display a wavy leading edge during dorsal closure, with defects in leading edge cell shape, a reduced rate of zippering and deep and persistent segmental grooves.
Approximately 90% of ena23 zygotic mutants exhibit virtually wild-type cuticles, whereas 8% display head holes.
Cultured primary neurons derived from ena23 and enaGC1/ena23 embryos show a significant reduction in the number of filopodia compared to control neurons. Mean filopodium length is reduced compared to wild type in these neurons.
24% of eggs derived from females carrying homozygous germline clones show a "dumpless" phenotype.
Egg chambers in females with homozygous germline clones have defects in the cytoplasmic filaments (the bundled cytoplasmic actin filaments extending from the cortex to nuclei). No defects in ring canal formation or growth are seen in mutant egg chambers. Some egg chambers contain multinucleate nurse cells.
Homozygous follicle cell clones do not usually cause significant disruptions in either epithelial organisation or in the assembly of cortical actin into follicle cells adherens junctions in stage 2-7 egg chambers. However, in later egg chambers, clones with reduced cortical actin and disruptions in epithelial integrity are seen.
Leading edge cells in embryos that are maternally and zygotically mutant for ena show a large decrease in average lamellipodial area and a striking decrease in filopodial number.
Homozygous clones that encompass the morphogenetic furrow do not result in a defect in cell constriction in the morphogenetic furrow.
ena23/enaGC1 embryos have reduced longitudinal axons in the central nervous system.
74% of zygotic ena23 mutant embryos have a wild-type cuticle, while 21% show misalignment/puckering along the dorsal midline.
Mature embryos that are both maternally and zygotically mutant for ena (ena23/enaGC1 embryos derived from females with homozygous ena23 germlines) proceed through gastrulation normally and have normal epithelial integrity. Segmental grooves are deeper than normal in these embryos and persist long after they should have regressed. The leading edge during dorsal closure is often uneven. Most of the embryos fail in head involution. Cells that should lead head involution appear to constrict far more than in wild type, nearly severing the head from the thorax.
Mature embryos that are both maternally and zygotically mutant for ena (ena23/enaGC1 embryos derived from females with homozygous ena23 germlines) show defects in the cuticle; 10% have a dorsal pucker, 37% have a hole in the head, 15% have both a dorsal pucker and a hole in the head and 28% have a large ventral hole.
Single cell γ neuron mutant clones in the mushroom body show drastic axon growth defects.
Homozygous embryos do not show midline crossing errors by axons in the central nervous system.
Mutant follicle cell clones lose cortical actin filaments from apical, basal and lateral sites.
96% of ISNb axons show a bypass phenotype in homozygous embryos.
Lethal in combination with enaGC1.