Newly formed spectrosomes in primordial germ cells of stage 11-12 dppH46 embryos are similar in size and morphology to wild-type of the same age. In older embryos, differences are readily apparent and the spectrosomes in dppH46 primordial germ cells fall into three classes. Primordial germ cells in the first class (39%) resemble wild-type and have a single large spherical spectrosome. The second class (28%) display either small diffusely stained spectrosomes or several small fragmented spectrosomes. In the third and final class (33%), primordial germ cells have no spectrosome and can be deformed and irregular in appearance.
dppH46 mutant embryos occasionally show fusion of the embryonic denticle belts.
dppH46 exhibit a phenotype in the development of the dorsal head. The dorso-median strip of epidermis that normally separates the placodes is absent and replaced by hyperplastic placodes in stage 12 embryos.
dppH46 clones generated in the wing at 22-26 hours after pupariation (AP), using the Minute technique, have no effect on venation when they are limited to one surface of the wing. When there is overlap between dppH46 clones on the dorsal and ventral surfaces, there is no consistent cell-autonomous disruption of the posterior crossvein (PCV) within regions of overlap. However, a slight disruption of the posterior end of the PCV, largely outside the region of the clone, has been observed in one case. When overlapping clones cover the region of the fourth longitudinal vein normally intersected by the PCV, the anterior of the PCV can be disrupted.
The corpus cardiacum is normal in size in mutant embryos, but shows defects in migration.
In stage-15 dppH46 mutant embryos, the lymph gland, cardioblasts and pericardial nephrocytes fail to develop from the cardiogenic mesoderm.
The average number of crystal cells per embryo is significantly reduced in homozygous stage 13-14 embryos compared to wild type.
In dppH46 homozygotes cycle 14 mitotic domains 1 and 5 are fused across the midline, and domain 3 is absent.
Ventral denticle belts cover the whole epidermis in mutant embryos.
Head midline epidermis does not form in mutant embryos, with both midline and dorsolateral regions showing characteristics of lateral neuroectoderm. Optic lobe and Bolwig's organ are absent. The dorsal head ectoderm is "invaded" by protocerebral neuroblasts.
Homozygous clones in the wing have no effect on the posterior cross vein (PCV) unless both dorsal and ventral surfaces are homozygous ("double-sided" clones). Double-sided clones that cover half the PCV show loss of the vein in the mutant clone up to or within 2 to 3 cells of the clone boundary. Vein L4 can also be truncated in clones.
The hindgut of mutant embryos is significantly shorter than that of wild-type embryos. Incorporation of BrdU in the large intestine is abolished in mutant embryos.
Gnathal morphology is severely disrupted in mutant embryos.
The cuticle of homozygous embryos consists only of ventral epidermis. This phenotype is not altered if the embryos are derived from homozygous dl1 females. brkM68; dppH46 sna18 Df(2R)twi quadruple mutant embryos secrete cuticles showing partial transformation of ventral into dorsal epidermis.
Gonadal mesoderm development is largely unaffected in mutants. Germ cells do not migrate from endoderm to mesoderm, presumably due to the gastrulation defects.
Embryos are strongly ventralised and germ band extension is abnormal.
Fat body precursor cells do develop in dppH46 embryos.
Homozygous clones induced in first instar larvae produce abnormalities in the dorsal side of the leg. Pattern elements from the dorsal side are missing. Occasional defects in the ventral side of the leg are also seen.
Suppresses the majority of pattern defects caused by Pka-C1H2 clones in the wing, notum, halteres and antennae and partially suppresses defects in the ventral regions of the leg.
Dominant lethality greater than 50%. Homozygous and transheterozygous embryos were examined with respect to 25 cuticular markers, results demonstrate a graded requirement for dpp along the dorso-ventral axis.
Strong ventralised phenotype. Rings of ventral denticle belts differentiate around the entire dorsoventral axis, almost no dorsal hairs are seen and the antennal and maxillary sense organs are missing. Defective movements of the germ band: due to loss of the amnioserosa and because the dorsalmost cells have acquired the lateral fate of the dorsal ectoderm. Dorsal cell fates are deleted and ventrolateral mitotic domains are expanded.
Ventralized embryos: rings or patches of ventral denticles along dorsoventral axis. Disruption of germ band extension that leads to the invagination of posterior segments into the interior of the embryo.
Fail to complete germ band extension, die with strong ventralized phenotype and no dorsal derived epidermis.
Homozygotes have a ventralized embryonic phenotype: normally ventral epidermal pattern elements are present ventrally and dorsally.