Mutation at a splice donor site. This disrupts the splicing of the third intron, and the incompletely spliced transcript gains a premature stop codon, resulting in a short peptide being produced.
Nucleotide substitution: G9321A.
G7902139A
G9321A
G to A mutation in the splice donor site of the third intron of pbl.
Approximately 20% of homozygous stage 13 embryos show no left-right asymmetry in their hindgut, which normally curves to the right at this stage. A small fraction of the embryos showing inverse left-right asymmetry. The number of cells in the epithelium of the hindgut at stage 13 is significantly reduced compared to wild type. However, there is no significant correlation between the number of cells and the left-right asymmetry phenotype of homozygotes.
pbl2/pblfortune and pblfortune/Df(3L)BSC388 stage 13 embryos show defects in the left-right asymmetry in their hindgut, with some embryos show no asymmetry, and others showing inverse asymmetry.
Females carrying homozygous germline clones are sterile.
pblfortune is rescued by Scer\GAL4arm.PS/pblUAS.cPa
pblfortune is rescued by Scer\GAL4byn-Gal4/pblUAS.cPa
pblfortune is rescued by Scer\GAL4NP2432/pblUAS.cPa
pblfortune is partially rescued by pblUAS.cPa
pblScer\UAS.cPa reduces the frequency of defects in the left-right asymmetry of the hindgut by half in homozygous pblfortune embryos, even in the absence of a Scer\GAL4 driver. When expression is driven by Scer\GAL4arm.PS, Scer\GAL4byn-Gal4 or Scer\GAL4NP2432 the left-right asymmetry are rescued. Expression driven by either Scer\GAL4how-24B, Scer\GAL4elav.PU or Scer\GAL448Y does not increase level of rescue above that seen without a Scer\GAL4 driver.
Expression of pblScer\UAS.cPa under the control of Scer\GAL4byn-Gal4 rescues the reduced number of cells in the epithelium of stage 13 pblfortune homozygous embryos.
