Larval muscle 4 neuromuscular junctions in dia⁵ heterozygotes do not show significant changes in synaptic bouton number, as compared to controls.

There is an increase in the frequency of clone splitting in the dia⁵ mutant 'loser' cells when dia⁵ mutant clones are generated in the wild type pupal notum, compared with wild type clones in wild type tissue. The loser clones show reduced compactness over time.

The four cells within mutant sensory organ precursors develop in correct number and position in large homozygous clones in the leg, but the socket cell protrusions which are normally seen in wild type are significantly suppressed and disorganised. Bracts are not induced adjacent to the mutant sensory organs in these large clones.

Embryos lacking both maternal and zygotic dia function which are grown at 18[o]C and then shifted to 25[o]C for analysis during dorsal closure undergo dorsal closure more slowly than normal and have defects in epidermal sheet alignment. The mutant leading edge cells form both filopodia and lamellipodia. Filopodial number is decreased, filopodial length is increased and lamellipodial area is increased.

Apical F-actin in the trachea disappears in mutant embryos, while residual F-actin is retained in the adherens junctions.

Pupal eye epithelial adherens junctions are unaffected in dia⁵ MRCM clones. dia⁵ clones that are shifted to the non-permissive temperature for 30 hours before dissection do not exhibit any effect on the adherens junctions.

Actin pseudocleavage furrow extension is significantly impaired in all embryos maternally mutant for dia⁵. In some cases, most actin remain in caps during metaphase in dia⁵ mutants, but more frequently actin is located in weak rings.

Heterozygotes do not exhibit any gross defects in external bristle morphology.

Compared to controls, heterozygous mutants show a reduced response to an auditory stimulus mimicking flies' courtship song.

Embryos derived from dia⁵ homozygous female germline clones and which have a paternally derived copy of dia⁺ have defects in ventral furrow formation; first, a subset of cells that should apically constrict fail to do so, and second, as some cells invaginate, they pull on neighbouring cells, which become massively multinucleate, rather than stretching towards the midline as occurs in wild-type embryos. Adherens junctions are normal in these embryos at the end of gastrulation.

Adherens junctions form and cortical F-actin and myosin are not grossly disrupted at the end of gastrulation in embryos derived from dia⁵ homozygous female germline clones and which are also zygotically mutant for dia (dia²/dia⁵). However, although the initial assembly of adherens junctions occurs, maintenance of adherens junctions is defective in these embryos, and adherens junction destabilisation is accompanied by cortical blebbing on the basolateral cortex.

Embryos derived from dia⁵ homozygous female germline clones which and which are also zygotically mutant for dia (dia²/dia⁵) have abnormal cell protrusions that extend from the amnioserosa cells during dorsal closure. Dorsal closure is defective, with cell misalignment as the epidermal sheets meet at the dorsal midline.

Homozygous cells in the morphogenetic furrow (in clones that encompass the morphogenetic furrow) fail to undergo apical constriction.

dia⁵ follicle cell clones exhibit cytokinesis defects in the presence of a normal actin cortex. During early oogenesis, these clones retain a rectangular shape, do not flatten, and the underlying cyst bulges out. Late clones show no outward bulging over the growing oocyte and maintain a normal cell shape, with the exception that the cells are bigger because of the absence of cytokinesis.

In mid-cellularisation embryos derived from dia⁵ germline clones, the furrow canals are considerably enlarged compared to wild-type and are filled with large cytoplasmic blebs. Interruptions in the regular F-actin array (a hexagonal array is normally evident in surface views) are seen in these embryos and a variable proportion of the forming cells contain multiple nuclei.

Embryos derived from dia⁵ germ-line clones have severe cellularization defects.

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

dia⁵ causes larval and pupal lethality. Only about 3% of embryos derived from homozygous female germline clones hatch. Defects in these embryos first appear at nuclear cycle 11. Abnormalities in nuclear and actin cytoskeletal organisation affects almost two-thirds of all fertilised embryos at cycles 11-13 and a higher percentage at later stages. The area of the embryo affected varies considerably between embryos. 100% of embryos fail to form pole cells. More than 95% of embryos are grossly defective at gastrulation (despite the fact that half the embryos have received a wild-type copy of dia paternally). A wide range of cuticle defects, including a failure in head involution, loss of head structures, reduction or absence of denticle bands and incomplete formation of the cuticle are seen. Severe structural changes in the actin cytoskeleton compared to wild type are manifested after nuclear cycle 11 in embryos derived from homozygous female germline clones. Formation of the hexagonal actin arrays is disrupted during prophase and metaphase and there is an absence of actin staining between the metaphase nuclei, indicating that the metaphase furrow fails to form. Nuclei in the mutant embryos frequently show abnormal spacing and in some cases fuse in subsequent nuclear cycles. Nuclei are frequently found displaced into the interior of the embryo although the centrosomes remain at the surface. In embryos derived from homozygous female germline clones there is a variable defect in the organisation of both actin- and microtubule-based structures during cellularisation. In the least severe cases, the cellularisation furrow is absent between some nuclei, without any noticeable defect in morphology or positioning of nuclei or microtubule structure. In more severely affected embryos, actin staining is absent at the furrow canals and irregular at some regions of the cortex. Surface regions that lack any organised actin show abnormalities in the positioning of nuclei and microtubule baskets. Centrosomal behaviour is abnormal in these regions. Formation and growth of the cytoplasmic buds occurs normally at the posterior pole of embryos derived from homozygous female germline clones. The buds never cleave to produce pole cells (as occurs in wild-type embryos). Rather, they regress in synchrony with the buds covering the rest of the embryonic cortex. Buds reform at the posterior pole at each nuclear cycle, but do not undergo cytokinesis. In some embryos, the number and size of the somatic buds are abnormal. Unlike the somatic nuclei, the posterior pole nuclei fail to initiate cellularisation.

dia[+]/dia⁵ is a suppressor | partially of decreased size | adult stage phenotype of Scer\GAL4^A9, Shrm^A.UAS

dia[+]/dia⁵ is a suppressor | partially of visible | adult stage phenotype of Scer\GAL4^A9, Shrm^A.UAS

dia⁵ is a suppressor of abnormal neuroanatomy phenotype of LIMK1^UAS.Tag:HA, Scer\GAL4^ey-OK107

dia[+]/dia⁵ is a suppressor | partially of wing phenotype of Scer\GAL4^A9, Shrm^A.UAS

dia[+], zip[+], dia⁵, zip¹ is a suppressor of embryo | embryonic stage 5 phenotype of Scer\GAL4^{VP16.mat.αTub67C}, step^HMS00365

dia[+], zip[+], dia⁵, zip¹ is a suppressor of furrow canal phenotype of Scer\GAL4^{VP16.mat.αTub67C}, step^HMS00365

dia⁵ is a suppressor of adult mushroom body phenotype of LIMK1^UAS.Tag:HA, Scer\GAL4^ey-OK107

dia[+]/dia⁵ is a non-suppressor of embryonic/larval neuromuscular junction | larval stage phenotype of DAAM^Ex68

dia[+]/dia⁵ is a non-suppressor of NMJ bouton | larval stage phenotype of DAAM^Ex68

dia[+]/dia⁵ is a non-suppressor of larval LL1 motor neuron | larval stage phenotype of DAAM^Ex68

dia[+]/dia⁵ is a non-suppressor of embryo | embryonic stage 5 phenotype of Scer\GAL4^{VP16.mat.αTub67C}, step^HMS00365

dia[+]/dia⁵ is a non-suppressor of furrow canal phenotype of Scer\GAL4^{VP16.mat.αTub67C}, step^HMS00365