pntΔ88 mutant embryos show a significant increase in the overall number of cardioblasts (both generic and ostial cardioblasts), as compared to controls.
Oenocytes are completely absent in pntΔ88 homozygous stage 15 embryos, unlike in heterozygous or wild-type controls.
pntP1-82/pntΔ88 or pntP1-90/pntΔ88 mutant larval brains have a significant increase in the number of Asense-negative type II neuroblasts, but a significant decrease in the number of intermediate neural progenitors.
Adult midgut intestinal stem cell somatic MARCM clones homozygous for pntΔ88 display growth defects and never grow past the 2-cell stage. The rate of mitosis upon infection with Pseudomonas entomophila in the mosaic midgut is decreased compared to controls.
Supernumerary tracheal fusion cells are present in the dorsal trunk of pntΔ88 embryos.
Homozygous bract cells are never seen in somatic clones induced in the leg, while homozygous bristles are recovered.
Mutant embryos have gaps in the dorsal trunk. The tracheal cells of heterozygotes show moderate lack-of-migration defects in 44% of embryos, and show severe ectopic lack-of-migration defects in 15% of embryos.
pntΔ88/pnt1277 flies have rough eyes and show a loss of photoreceptor cells.
In control stage 15 embryos, the anterior and posterior lateral trunks (Lta and Ltp, respectively) from adjacent segments are joined. In contrast, gaps occur between the Lta and Ltp in stage 15 homozygous pntΔ88 embryos.
By stage 15, in control embryos, tracheal ganglionic cells and branches enter the ventral nerve cord (VNC) toward the central nervous system (CNS) midline. In contrast, in homozygous pntΔ88 embryos, tracheal ganglionic branches and cells rarely enter the VNC when present and are truncated, but in most cases are absent.
Homozygous pntΔ88 embryos show significant losses in the continuity of tracheal tubules (gaps and breaks) and constrictions in the dorsal trunk. Dorsal branch formation does not occur in some metameres in homozygous pntΔ88 mutants.
Homozygous pntΔ88 mutant fat body clones do not exhibit any mitochondrial phenotypes.
Many pntΔ88/pnt1277 ommatidia over- or under-rotate; the variance (s.d.) in degree of rotation is greater than in wild type in adult eyes.
Eggs derived from egg chambers containing complete homozygous follicle cell clones have a single thick dorsal appendages.
Eggs derived from females with mosaic pntΔ88 egg chambers have a single dorsal appendage.
pnt1277/pntΔ88 eye discs show polarity defects (6.7% of ommatidial clusters are inverted and 6% are symmetrical).
pnt1230/pntΔ88 eye discs show chirality defects in 26.4% of ommatidial clusters.
pntKG04968/pntΔ88 eye discs show chirality defects in 9.5% of ommatidial clusters.
pntΔ88 Minute clones in the eye disc fail to form the arcs and rosettes of cells in the morphogenetic furrow that are seen in wild-type eye discs. Some clones show small clusters of cells within the furrow while other clones contain no clustering.
The tracheal branches of pntΔ88 embryos do not show breaks.
Homozygous clones in the dorsal tracheal branches fail to develop as terminal cells.
pntΔ88 homozygous clones in the dorsal air sac primordium grow and normally but never contribute to the tip of the primordium.
In pntΔ88 stage 15 embryos, the genital disc precursor cells are completely missing.
In pntΔ88 embryos, migration of all primary tracheal branches is incomplete. pnt737/pntΔ88 transheterozygotes show a less severe phenotype in which nearly all branches are affected.
In mutant embryos midline glial cells fail to migrate in between the segmental commissure.
Only 23% of cuticles from pntΔ88 homozygous embryos show fusion of at least one pair of denticle belts.
Mutant embryos have ectopic cardioblasts that form enlarged hearts comprising disorganised rows of cardioblasts. The ectopic cardioblasts appear to be restricted to the posterior domain.
In pntΔ88 embryos, the anterior and posterior sensory fascicles are spaced further apart at the CNS-PNS transition zone compared with wild type.
In pntΔ88 mutant somatic clones in the 3rd instar eye disc, photoreceptors R2-R5 fail to undergo or differentiation. Within pntΔ88 mutant somatic clones there is a failure of G1 arrest in the furrow: all cells except R8s re-enter the cell cycle. However, many of these cells do not progress past G2 (in clones only about 40% of wild-type numbers of postmitotic cells are seen posterior to the furrow). Consequently, the mitotic index is reduced in these clones. Those cells entering mitosis in these clones, tend to do so later than in wild-type (more posterior to the furrow).
The arrangement of glial cells is irregular in the central nervous system of mutant embryos.
The second mitotic wave is absent in pntΔ88 clones in the eye. The cells are arrested in G2.
Despite the absence of secondary and tertiary tracheal branches in pntΔ88 mutant embryos, the tip cells of migrating branches in these embryos have numerous filpodia as in wild-type.
pntΔ88 mutant embryos have an estimated 85 cells in each Malpighian tubule cell (as opposed to about 125 in wild-type).
Homozygous embryos show some loss of VA2 muscle precursor cells (81% of hemisegments contain VA2 precursor cells).
The size of the primary branches of the tracheal system is largely unaffected in mutant embryos.
Formation of eve-expressing progenitors in the mesoderm is variably reduced in mutant embryos. The formation of eve-expressing pericardial cells and muscle DA1 is reduced in mutant embryos.
Heterozygotes have wild-type wings.
The third midgut chamber is greatly reduced in size in homozygous embryos. The central and posterior constrictions that form this chamber form normally, but are located more closely together than in the wild-type gut. 85% of embryos fail to form the anterior constriction completely; the constriction initiates at its normal site but does not significantly constrict the midgut. Elongation of gastric caecae is not seen in these embryos. The number of visceral mesoderm (VM) cells in the third midgut chamber is reduced compared to wild-type, while the first, second and fourth midgut chambers contain normal numbers of cells. Defects in VM cell segregation are seen immediately after the stage 12 mitosis, producing a junction in the central midgut. By stage 16, VM cells are often scattered around the surface of the midgut, in contrast to the ordered files of cells seen in wild-type embryos. pnt05484Δ33/pntΔ88 and pnt07825Δ78/pntΔ88 embryos have wild-type midgut development.
Homozygous embryos have a reduced number of cells in both the anterior and posterior Malpighian tubules compared to wild-type embryos.
The central nervous system (CNS) is narrower than normal and the commissures are thicker than normal and incompletely separated in pntΔ88 embryos.
Exit glial cells fail to extend cellular processes to properly ensheath the two nerve bundles. pnt ttk double mutant flies display an additive CNS phenotype combining characteristics of both phenotypic traits.
The Bolwig's nerve defasciculates and becomes misrouted during its growth from P1 to P2. The aberrant BN branches grow on the surface of the optic lobe anlagen and their endings reach various ectopic positions during mid-stage 16.
Segmental commissures are fused in mutant embryos.
pnt2/pntΔ88 embryos exhibit subtle ventral defects. Leg and eye/antenna pnt2/pntΔ88 mutant discs can be in vivo cultured. Wing and haltere discs cannot.
Segmental commissures appear fused in homozygous embryos. 90% of the ommatidia in pntΔ88/pnt1277 flies lack the R7 photoreceptor and/or some outer photoreceptor cells.
pntΔ88/pntT6 combination is viable, 25% ommatidia are missing R7 cells.
Eggs laid by mosaic females (generated using Scer\FRT/Scer\FLP1 recombination system) that have a clone of mutant follicle cells in the dorsal-anterior region or a clone that covers the entire follicle cell layer exhibit a single broad dorsal appendage 4 times wider than a wild type appendage. This is not a fusion of the two appendages but cells from the middle region taking on an appendage-producing cell fate. The majority of these eggs hatch and develop into fertile adults. Eggs from females with a germline homozygous for pntΔ88 do not exhibit defects in the dorsal appendages or any discernible embryonic phenotype.
Heterozygotes with pnt1277 lack one to three photoreceptor cells in most ommatidia. The R7 precursor can be rescued by pnt P2 transcript expressed by sev enhancers but the mutant phenotype is enhanced by pntT151A.Scer\UAS expressed by sev enhancers.
Mutants show fused commissures and disrupted trachea. Longitudinal glia do not form the typical flat sheet on the dorsal side of the CNS, but cells of rounded appearance are evident, partly sitting on top of one another. Some of these cells have glial-type morphology, with lobulated nuclei, that nevertheless fail to flatten and ensheath the longitudinal connectives.
CNS and tracheal phenotype.