Amino acid replacement: Q292term.
Nucleotide substitution: C?T.
C6991704T
C?T
Q292term | bin-PA
Q292term
In binR22 stage 17 embryos, the testes often exhibit dispersed aggregates of germline niche cells, unlike the single anterior niche position in controls; most PS 11 niche cells remain in their original, more central positions rather than migrating to the anterior and are less frequently associated with PS 10 niche cells; germline stem cells are less frequently quiescent and frequently exhibit both centrosomes displaced from the interface with the nearby niche cells.
In embryos homozygous mutant for binR22 longitudinal visceral muscle (LVM) founder cell migration initiates similarly to the wild type, but the tracks become progressively irregular during germ band retraction at stage 12. By the end of germ band retraction none of the cells have reached the anterior of the trunk visceral mesoderm (TVM).
binR22 mutants show a salivary gland phenotype. At stage 14, mutant salivary glands remain associated with the inner circular muscle layer, while in wild type, these structures become separate. After stage 15, cells from the distal tips of the binR22 salivary glands spread into the region of the undifferentiated midgut that forms the gastric caecae in the wild-type embryos. The mutant glands become mispositioned and/or elongated and maintain contact with the area of the midgut immediately adjacent to the proventriculus.
The salivary glands in mutant embryos have no defects in turning or posterior migration.
The presumptive trunk visceral mesoderm primordia segregate towards the interior and coalesce into a band as in mutant embryos (as in wild type), but there are irregularities in their arrangement, which become much more pronounced after stage 11. At stage 13, these cells fail to become columnar, are not tightly attached to the endoderm and become clustered segmentally (in wild type they remain a continuous band). During stages 14-17 the cells are mostly scattered in areas within or underneath the somatic mesoderm. Midgut constrictions are not formed. Cells which originate from trunk visceral mesoderm primordia fuse into syncytia of somatic muscles.
binR22 has abnormal cell migration | embryonic stage 12 phenotype, suppressible | partially by Scer\GAL4tey-5053A/BacA\p35UAS.cHa
binR22 has longitudinal visceral muscle primordium | embryonic stage 12 phenotype, suppressible | partially by Scer\GAL4tey-5053A/BacA\p35UAS.cHa
Expression of BacA\p35Scer\UAS.cHa under the control of Scer\GAL4tey-5053A partially suppresses the longitudinal visceral muscle (LVM) founder cell migration defects seen in homozygous binR22 embryos. LVM founder cells regain much of the ability to migrate, however their tracks are less regular. The migrating cell occupy a broader lateral area without being subdivided into a dorsal and a ventral stream and fewer cells reach the very anterior end of the trunk visceral mesoderm (TVM) compared to wild type.
binR22/binI1 is partially rescued by Scer\GAL4bap.3/binUAS.cZa