A set of ~50 targeted deficiencies created by exploiting hybrid element insertion (HEI) and resolution; designed to fill gaps in deletion coverage.
48B7-48C1;48C2-48C4
In Df(2R)BSC25/Df(2R)BSC259 (FGF8 null) mutant embryos the longitudinal gut musculature fails to form. A reduced number of LVM founder cells is seen in stage 11 embryos, and by stage 12 almost all of the founders lose contact with the trunk visceral mesoderm (TVM) rather than spreading out across it. By stage 13 the vast majority of these cells undergo cell death. The few cells that do survive are capable of producing a small number of LVM fibres.
Infiltration of astrocyte processes into the neuropil is severely impaired in mutant embryos, and the ventral-most astrocyte cell in each hemisegment does not migrate to its normal position.
Homozygous embryos show defects in mesoderm migration following gastrulation; in 28% of cases mesoderm spreading occurs but formation of a monolayer of cells is defective, while in 72% of cases neither spreading nor monolayer formation occurs.
Homozygous embryos show delayed mesoderm spreading; the mesoderm cells remain clumped in the mutant embryos at a stage at which wild-type cells have already begun to migrate. The mutant mesoderm cells do eventually migrate to contact dpp-expressing ectodermal cells almost as fully as wild-type cells do. The expanded mesoderm fors a single layer of cells in wild-type embryos, but is multilayered in the mutant embryos. Mutant embryos that have undergone germ-band retraction show loss of dorsal mesoderm derivatives, such as the heart and dorsal somatic muscles. There is also a severe loss of the ventral oblique muscles.
Breakpoints differ from the sites of the progenitor insertions.