Whereas wild-type adult midgut progenitor cells (AMPs) form many large clusters, few AMP clusters are found in late larval vn10567 and vn10567/vnγ7 mutant midguts.
Most vn10567/vnγ7 mutants die as pharate adults.
Lineage analysis of marked clones reveals that vn10567/vnγ7 mutants display a failure of proliferation of AMPs during early larval stages, although the number of AMPs generated initially during embryogenesis is not different between mutants and wild-type controls. The size of the few remaining AMP clusters in vn10567/vnγ7 mutants is relatively normal, suggesting that the late phase of AMP proliferation is largely unaffected in these mutants.
Expression of vnScer\UAS.cSa in larval enterocytes driven by Scer\GAL4Myo31DF-NP0001 not only rescues the adult midgut progenitor cell phenotype of vn10567 mutants, but it also causes ectopic AMP cell proliferation.
Border cells still migrate dorsally when all dorsal follicle cells are mutant for vn10567 in females containing homozygous clones.
Shows very mild midgut phenotype. vn10567/Df(3L)γ3 causes lack of midgut constrictions and failure of elongation of gastric caeca.
A significant number of somatic muscle fibres show multiple, mis-guided membrane extensions at their leading edges. The DA1 muscle precursor is sometimes missing.
Abnormal muscle phenotype. Myotubes of mutant embryos are elongated and continuously send filopodia in random directions.