hepr75 mutant clones in sensory neurons in adult wing do not display any defects in injury-induced axon degeneration (following an axotomy, the severed axons are cleared away normally).
hepr75 mutant clones do not affect photoreceptor differentiation or survival.
hepr75 neuroblast clones in mushroom bodies show axonal degeneration, though the main observable phenotype is overextension of axons.
Single cell hepr75 clones in mushroom bodies show a low frequency of axon breaks.
83.8% of hepr75 pupae show wing eversion defects 6 hours after puparium formation (eversion is complete at this time in wild-type animals); 31% have partially everted wings and 52.8% show a complete failure of disc eversion. 12.7% have leg eversion defects.
The basement membrane of wing discs is not degraded in hepr75 pupae which fail to evert their wing discs.
hepr75 follicle cell clones cease mitotic division too early, resulting in clones that contain a lower number of cells than their respective twin spots.
Homozygous hepr75 mutants exhibit a low level of ventral-to-dorsal R axon misrouting.
Wing disc fusion during thoracic closure is inhibited in hepr75 mutants, while dorsal closure is not affected. Wing discs of hepr75/+ females that are cut and left to regenerate are usually healed after 24 hours. In contrast, wounded wing discs of hepr75/Y males fail to heal, even after 7 days. In wild-type wing discs, wound healing is accomplished by the formation of an actin rich cable and filopodia for zipping epithelial edges together. In hepr75/Y mutants, wounds show an actin-rich area only at the wound vertex and not throughout the rest of the wound, and filpodial protrusions are much reduced compared to wild type. Additionally, peripodial epithelial cells do not elongate toward the wound edge, a process that occurs in wild-type wound healing.
Transplanted fragmented leg discs show a large reduction in transdetermination, compared to wild-type leg discs.
Mutant embryos show no defects in the initiation of mesoderm spreading.
Shortly after pupariation begins in wild-type flies, the wing discs move so that their peripodial side is in apposition with the larval epidermis. In 40% of hepr75 homozygotes, this apposition fails. In wild-type flies, appositions is proceeded by fusion of peripodial/stalk cells and larval epidermis, followed by eversion of the disc through a steadily enlarging hole in the fused peripodial epithelium / larval epidermis and then spread over the surrounding larval epidermis before fusing to adjacent discs. 50% of hepr75 homozygotes fail to complete this eversion and everted disc fails to spread. The remaining 10% of hepr75 homozygotes, the discs fail to fuse to adjacent discs.
During dorsal closure in hepr75 mutant embryos the embryonic leading edge cells lack filopodia and lamellipodia. Unlike wild-type no actin cable is visible in the leading edge cells of conventionally (formaldehyde/PBS) fixed embryos, although some evidence for a reduced actin cable can be seen in embryos fixed in the presence of phalloidin, and in live embryos. Very late in the process of closure, the epidermis and the amnioserosa detach from each other in these mutants.
The cuticles of embryos laid by hep1/hepr75 mothers crossed to hep1 hemizygous males display classic dorsal closure phenotypes (a large dorsal hole of variable size). The prominent actin cable seen in leading edge cells during dorsal closure in wild-type embryos is much reduced in these mutants.
Eggs derived from females with homozygous clones in the follicle cells show a strong reduction of the dorsal appendages (DA) with an accompanying expansion of their bases. The DA defects can either be partial or complete and symmetrical, depending on the size and location of the clones in the follicle cells. The micropyle is sometimes reduced in size with a more blunted aspect than normal. Abnormal stage 14 egg chambers with shortened anterior ends are seen in females with homozygous follicle cell clones. The centripetal and border follicle cells migrate normally in egg chambers that have either partially or completely mutant follicle cells. Homozygous germline clones do not produce (or only very rarely) dorsal appendage defects.
Embryos laid by hepr75/hep1 mothers (with hep1/Y fathers) abort dorsal closure early. The epithelium sweeps forward as normal and only fails at the onset of zippering. No signs of the normal actin based protrusions from leading edge cells at any stage during dorsal closure are seen. Fusion of opposing fronts also fails and segmental stripes are misaligned.
Wing discs of maternally recued homozygous hepr75 animals, unlike wild-type, remain in their initial position in the pre-pupa, they do not spread, and in many cases disc eversion does not take place. There is a compacting of the actin cytoskeleton at the leading edge. No filopodia appear to be generated from the imaginal epithelium, and imaginal cells are progressively pulled together, causing bunching of the epidermis.
hepr75/Y mutant eye discs show bristle mislocalisation and abnormal pigment cells shapes.
Discs dissected from L3 larvae are delayed in their development, reduced in size, and malformed or misfolded. Dissected pupae reveal one consistent and major defect: the absence or aberrant spreading and fusion of the two lateral wing discs. In some cases eversion does take place, in the absence of disc fusion. In viable hepr39/hepr75 transheterozygotes wing disc morphogenesis can proceed almost normally, with occasional unilateral defects. Gut and larval tissues are extruded on account of the failure of closure of the thorax in the mutant pupae. Eye antenna discs can fuse but the head does not form. Leg discs evert and fuse though their shape is abnormal. hepr75/hep1 adult females show mutant cleft thorax and bristle defects.
Transheterozygous embryos with hep1 display a dorsal open phenotype caused by lack of thoracic and abdominal cuticle. The head is very disorganised, the cephalopharyngeal skeleton is reduced to mouth hooks. Homozygous germline clones produce a similar dorsal open and head phenotype.