61bp deletion, resulting in the deletion of amino acids 114-134 and a subsequent frameshift producing three new amino acids (TRR) and a stop codon.
61bp are deleted causing the removal of amino acid residues 114-133 and part of codon 134 of the 1059aa Pvr isoform. This leads to a frameshift that causes premature translation termination after the addition of 3 novel amino acids (TRR). Position of mutation on reference sequence inferred by FlyBase curator.
Pvr5363 mutants show hemocyte distribution defects: in contrast to wild-type, hemocytes are completely absent from the germband and ventral midline of stage 12 embryos, posterior hemocytes are also missing in stage 13 embryos while abnormal aggregations of hemocytes appear in the head.
Pvr5363 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 Pvr5363 clones are comprised entirely of Dl-positive clones.
Infection of Pvr5363 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.
Pvr5363 homozygous clones in the dorsal air sac primordium grow normally and populate the tip of the air sac primordium to the same degree as wild-type clones.
The longitudinal tracts are closer together than in the wild type in mutant embryos, giving the axon scaffold a rounded appearance in each segment. In stage 16 mutant embryos, repo-positive glia accumulate at the midline and there are fewer repo-positive glia in the longitudinal tract region than in wild-type embryos. No inappropriate axon crossing of the midline is detected.
Pvr5363 is partially rescued by Scer\GAL4crq.PO/PvrCA.UAS
Expression of PvrCA.Scer\UAS under the control of Scer\GAL4crq.PO in the Pvr5363 homozygous mutant background restores the impaired posterior migration of ventral hemocytes and partially rescues the failed transition of hemocytes across the ventral nerve cord in the anterior (but not posterior) of the mutant embryos. It however does not restore the invasion of hemocytes into the extended germband.
