Deletion of the Pvf2 promoter and five of six exons in Pvf3. Generated by FLP-mediated recombination between the two progenitor insertions (P{XP}Pvf2^d00645 and PBac{WH}Pvf3^f04842).

Imprecise excision of P{XP}Pvf2^d00645 and PBac{WH}Pvf3^f04842 generates a 35kb deletion that uncovers the 3' genomic sequence of Pvf3 and the 5' genomic sequence of Pvf2.

Df(2L)Pvf2-3/Df(2L)Pvf2-3 as well as Df(2L)Pvf2-3/Df(2L)BSC291 mutants are embryonic lethal and display hemocyte distribution defects: Hemocytes are completely absent from the germband of stage 12 mutant embryos and posterior hemocytes are missing in stage 13 embryos, while abnormal aggregations of hemocytes appear in the head. The passage of hemocytes through ventral nerve cord as they populate the ventral midline is also largely absent.

Unlike in wild-type, anterior hemocytes of Df(2L)Pvf2-3/Df(2L)Pvf2-3 stage 13 embryos form dense aggregates having engulfed numerous apoptotic corpses (indicating increased phagocytic activity) and the hemocyte numbers are significantly decreased compared to controls. The mutant hemocytes are unable to invade and pass through the epithelial junctions of the germband (although the posterior migration of dorsally located hemocytes is intact) which results in a marked deficit in posterior hemocytes in stage 13 embryos.

Df(2L)PvfΔ2-3 is homozygous lethal.

Df(2L)PvfΔ2-3 mutant MARCM clones appear significantly smaller than their wild-type counterparts. The intestinal stem cell developmental programme in these mutants appears to be completely disrupted as no large polyploid epithelial enteroblasts are found within the clones. All Df(2L)PvfΔ2-3 clones are comprised entirely of Dl-positive clones.

Infection of Df(2L)PvfΔ2-3 mutant MARCM clones with P. entomophila results in the wild-type response of an increase in size and cellular architecture in intestinal stem cells, indicating a normal innate immunity response.