heterozygous embryos do not show obvious dorsal closure defects, as compared to controls.
An average of 0.6 PGCs remain outside the midgut in embryos from mothers carrying one copy of shg2
, with 29% of embryos exhibiting a phenotype.
embryos have abnormal gonads that exhibit both somatic gonadal precursor cluster fusion defects and compaction defects.
homozygous embryos do not progress to 1st instar larval stage due to moderate (49%) to severe (42% and 9%) defects in the embryonic head and ventral cuticle.
heterozygotes do not exhibit a visible phenotype nor a reduction in viability.
Cell attachments in the tracheal branches of shg2
mutant embryos are loosened and broken in several places, and adherens junctions appear diffuse and discontinuous. These phenotypes are more severe in the unicellular dorsal branch than the multicellular dorsal trunk.
mutant embryos display disorganised nervous systems, but the nervous system is not hyper-neuralised.
embryos show defective branch fusion and interruptions in the tubes. The tracheal cells have a rounded shape and tracheal branches tend to break. The accumulation of cortical actin is decreased in the tubules relative to controls.
Posterior spiracles in shg2
zygotic mutant embryos fail to invaginate. This invagination failure is not due to problems of cell elongation.
mutants exhibit disrupted head and, to varying degrees, ventral epidermis. Approximately 4.5% of shg2
mutants are apparently wild-type. The majority (approximately 55%) of these mutants exhibit a fragmentary ventral cuticle phenotype. Approximately 11.4% of mutants exhibt holes in their embryonic ventral cuticle. Approximately 13.7% of shg2
mutants exhibit a dorsal cuticle phenotype.
52% of shg2
embryos show defective cardiac cell alignment. This phenotype is recessive.
mutant embryos show disorganization of epithelial tissues in the head and the ventral epidermis.
homozygous embryos gonad compaction is sometimes initiated, but often does not proceed to completion. The three clusters of somatic gonadal precursors (SGPs) from parasegments (PS) 10-12 are able to associate correctly with one another, and with germ cells, to form a cohesive group. However, these cells often remain loosely associated and spread over more than one parasegment, rather than compacting tightly in PS10. In the most severe cases, compaction from PS10-12 to PS10 appears completely blocked. In weaker examples, compaction is initiated but not completed, resulting in partially compacted and misshapen gonads. Phenotypes are weaker these embryos (3% severe, 50% weak, n=36) than in shgg317
Mutant embryos are unable to form trachea and in some cases to complete tracheal fusion at the adherens junction. At segment boundaries where fusion does not occur. F-Actin containing fusion tracks are absent.
Homozygous mutant embryos show holes in the ventral cuticle.
The gonadal mesoderm fails to fully coalesce into an embryonic gonad in mutant embryos.
The optic placode does not invaginate in mutant embryos and remains at the surface. The placode cells lose contact and dissociate. Loss of epithelial integrity and an increase in cell death is seen in the head epidermis, resulting in partial or full exposure of the brain in late mutant embryos. Cells of the optic lobe and Bolwig's organ do not differentiate structurally.
When homozygous somatic clones are made in the thoracic epithelium, mutant cells have a smaller apical surface than their wild-type neighbours. Apical-basal polarity is defective in these cells.
embryos have tracheal defects; dorsal trunk cell fusion is blocked.
Homozygous female germ line clones give rise to egg chambers with misplaced oocytes in 46% of cases. This phenotype is apparent in the germarium; although region 2b cysts usually have a wild-type arrangement of germ cells in homozygous germ line clones, the oocyte never protrudes into the follicle cell layer when the cyst enters region 3, and frequently occupies a lateral position. The oocyte is misplaced in 23% of mosaic cysts which contain a homozygous clone that includes the follicle cells at the posterior of the cyst. The misplaced oocyte lies adjacent to the wild-type follicle cells in these mosaic cysts. The oocyte is correctly localised in mosaic cysts where the homozygous clone includes only lateral or anterior follicle cells.
Germline clones generate mutant germ cells that are not adherent to each other, nor to the follicle epithelium. Mutation has no effect on the number of germ cells or on their positioning in the egg chamber. Border follicle cells never enter the nurse cell cluster and instead remain stuck in the follicle cell layer. Border cells retain their motility but do not reach their target position. Also the onset of centripetal follicle cell migration is slightly delayed. These follicle cells often take the wrong pathway, causing defects in cytoplasm transport into the oocyte, nurse cell regression and gross distortion of the egg shape and structure. No fertilised eggs are obtained.
transheterozygotes exhibit lack of head skeleton, loss of ventral cuticle and the appearance of holes in the lateral cuticle.
Intermediate embryonic tracheal phenotype.
Class III allele: lacks most of the head and ventral epidermis. In germ-line clones, no eggs are recovered.
Mutants show gross disorganization of epithelial tissues in the head, ventral epidermis, Malpighian tubules and tracheal ducts. Malpighian tubule tip cells are present and differentiate into neurons, as in wild type. Tracheal tip cells are also present. Phenotype is alleviated by shghs.PU
The principal midgut epithelial cells spread over the visceral mesoderm but do not become columnar, they maintain a rounded to cuboidal shape, and do not form a monolayer. At later stages (stage 14-17) the principle midgut epithelial cells become attached to the visceral mesoderm and gradually adopt a more wild type appearence. By the time the embryos are fully differentiated, no difference from wild type can be seen.