crm << bk1 << w << su(faswb) << bk2 << N
Deletes 5' half of the transcription unit immediately upstream of N (Kidd, Kelley and Young, 1986, Mol. Cell Biol. 6: 3094-3108)
Mutants embryos show a lack of myoblast fusion. Gaps are seen in the visceral mesoderm. At stage 14 the gaps within the visceral band contain undifferentiated myoblasts. During further embryogenesis the midgut is surrounded by numerous unfused globular cells that cannot be assigned to either somatic or visceral myoblasts.
There is a complete block in myoblast attraction and fusion in the large dorsal muscle DA1 of Df(1)w67k30 mutant embryos. Mononucleate muscle founder cells (FCs) form mini muscles surrounded by several unfused fusion competent myoblasts (FCMs) with randomly oriented filopodia.
Hemizygous embryonic garland cells lack diaphragms and lacunae.
Approximately 30% of garland cell nephrocytes (GCNs) remain mononucleate at early stage 16 in Df(1)w67k30 mutant embryos (in contrast to wild-type embryos where 99.6% of the GCNs are binucleate at this stage). The GCNs of stage 16 Df(1)w67k30 embryos are disorganised, misshapen and more loosely associated than in wild-type embryos.
Founder myoblasts fail to attract fusion-competent myoblasts and myoblast fusion stalls altogether - the average number of eve-positive nuclei within a DA1 muscle at stage 15 is approximately 1 compared to approximately 10 in wild type embryos.
The palisade of circular visceral muscle founder cells is distinctly separated from the adjacent population of fusion-competent cells in stage 13 mutant embryos, in contrast to wild type where they are closely apposed.
Mutants are embryonic lethal and show no myoblast fusion.
Embryos show a complete lack of fusion in the somatic mesoderm and gaps in the visceral mesoderm, whereas other mesodermal derivatives, such as fat body, gonads and heart develop normally. Myoblast fusion fails completely in Df(1)w67k30 embryos. Founder cells and fusion-competent myoblasts remain at different levels in the mesoderm, with the founders in close contact with the ectoderm, whereas the rest of the myoblasts are more internal. The myoblasts do extend filopodia, but they are randomly oriented and show no sign of being attracted preferentially toward the founders. At later stages, founder cells elongate to form mononucleate muscles that span the territory that they would have occupied as syncytia in wild-type embryos. A normal pattern of innervation by motorneurons is seen. Fusion competent myoblasts die and are eliminated by macrophages. Df(1)w67k30 embryos show an early defect in visceral mesoderm formation; instead of two bands of tightly packed visceral muscles, several gaps are seen. These gaps are not due to a reduction in the precursors, instead they might be a consequence of improper alignment or adhesion of the visceral muscles.
Heterozygous females exhibit slightly reduced viability and fertility.
homozygous lethal Homozygous germline clones produce viable cells.
Individuals are mutant in eye colour and texture and show the vertical bristle syndrome. Homozygous males are lethal.
Suppresses faswb Cell viable male lethal