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. The numbers of pericardial cells is about half that of wild-type.
Lethality acts early and in the first larval instar.
Lethality occurs during the embryonic and larval stages. Dorsal localization of LCh5 in 1-2 segments per embryo.
pntS012309 is a non-enhancer of dorsal vessel wall cell phenotype of pnr1
pntS012309 is a non-enhancer of dorsal vessel wall cell phenotype of pnrVX6
pntS012309 is a non-enhancer of embryonic pericardial cell phenotype of pnrVX6
pntS012309 is a non-suppressor of dorsal vessel wall cell phenotype of pnr1
pntS012309 is a non-suppressor of embryonic pericardial cell phenotype of pnrVX6
pntS012309 is a non-suppressor of dorsal vessel wall cell phenotype of pnrVX6
pnrVX6, pntS012309 double mutant embryos lack cardioblasts and pericardial cells and are phenotypically indistinguishable from pnrVX6 embryos. In pnr1, pntS012309 embryos local overproduction of cardioblasts are seen as seen in pnr1 embryos.
pntS012309 is rescued by Scer\GAL4twi.PG/pntP2.UAS
pntS012309 is not rescued by Scer\GAL4twi.PG/pntP1.UAS
Analysis of excess cardioblast phenotype provides an allelic series:pntS012309, pnt2 > pntRR112, pntrM254 > pntΔ88, pnt07825.
Δ2-3 induced reversion demonstrates the insertion is responsible for the lethal phenotype.