hb12 homo- or heterozygous mutants do not exhibit a rough eye phenotype.
hb12/+ does not cause any detectable change in the segmentation phenotype of homozygous maternal mutant Acsl1 embryos.
Mutant NB7-3 lineages (in segments A1 to A6) consist of two (20%) or three (80%) neurons at stage 13, but only two neurons at stage 15, The GW neuron appears not to survive to stage 15. In mutant embryos, the dorsal subset of the NB 7-1 derived neurons is missing in 97% of hemineuromeres: 80% showing a loss of two, 10% of one, and 7% of three cells. This missing cells are probably fpCC and/or the dorsal-most CQ neuron. aCC or pCC are missing in 39%, aCC and pCC in 11% and RP2 in 67% of mutant hemisegments.
In hbKM, hb12 animals, a duplication of interneuron 2 is seen at the expense of the first born 1/1G neurons. In these mutants the aCC and RP2 motorneurons fail to project their proper dorsal muscle target, suggesting a transformation of GMC-1 to a later born GMC fate. Mutants show a general reduction in the number of motorneuron projections, particularly to the dorsal muscles. Mutants lack the first born MM-CB glia at the midline.
Mutant larval cuticles lack all three thoracic segments and exhibit a large first abdominal segment. In presumptive cephalic regions, zygotic mutants lack elements of the labial segment, including the H piece and labial sense organs, and other head organs are severely disorganised.
The labial lobe is missing in mutant embryos.
When one copy of hbP1only is supplied zygotically (via the father) to hb12/hb15 embryos the A7/A8 fusion mutant phenotype is rescued. When one copy of hbP1only is supplied maternally both the A7/A8 and anterior labial and T1 segments are rescued; only T2 and T3 remain unrescued. When the maternal contribution of hbP1only is increased (three copies) 30% rescued embryos show only the maternal rescue of labial and T1 segments. Most show additional rescue of thoracic segments of mostly T3 character. 5-10% of embryos show rescue of all thoracic segments.
Homozygous embryos exhibit deletion of the third gnathal segment through the third thoracic segment, a deletion between the seventh and eighth abdominal belts and filzkorper defect. In(3R)hbD2/hb12 embryos exhibit only the posterior defect and filzkorper defect.
All thoracic segments and the most posterior gnathal segment are missing.
Nondefective in gonad assembly.
Reduction in salivary gland placode size corresponding to the reduced Scr expression domain.
The posterior gt domain is extended slightly toward the posterior and the anterior domain toward the anterior.
Suppression of tor13D embryos: increase in proportion of embryos that formed cuticle with denticles and decrease in proportion of embryos that formed empty sacs.
Narrowing of posterior gt expression domain is blocked and expression is seen in a new posterior domain during gastrulation and germ band extension.
Labial and thoracic segments missing, defects in abdominal segments 7 and 8.
The posterior abdomen is duplicated anteriorly in homozygous embryos derived from females with homozygous germ line clones. In addition, the naked cuticle of abdominal segment A7 and the denticle band of A8 are deleted.
Expression of the hbC20-hb construct in an hb12 genetic background causes fusion of abdominal segments 7 and 8 and defects in the second thoracic segment.
Thoracic structures (except the labial segment) and the eighth segment are missing. Posterior denticle belt is enlarged. Failure of head involution, floor of the pharynx protrudes.