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Fig. 5. Kette and Blown fuse interact genetically. (A-D) Anti-ß3-Tubulin fluorescent staining of stage 15 embryos. (A) Homozygous ketteG1-37 hypomorphic mutant. (B) Homozygous blow2 null mutant. (C) Homozygous ketteG1-37 mutant with only one intact copy of blow (an enhancement of fusion defect takes place). (D) Double homozygous blow2 and ketteG1-37 mutant (further enhancement of fusion defects leads to a phenotype that resembles the original blow2 phenotype more than the ketteG1-37 phenotype). (E,F) Anti-ß3-Tubulin fluorescent staining (red); anti-ß-galactosidase staining (green) of rP298-lacZ enhancer trap. (E) Stage 16 blow2 mutant embryo (only minimuscles, presumably representing precursors, are formed, lareg gaps in the somatic mesoderm allow a direct view of the gut); ß3-Tubulin-positive cardioblasts are properly arranged. At this stage, unfused myoblasts have been engulfed by macrophages. (F) Mesodermal overexpression of UAS-hem with a twist-GAL4 driver line in blow2 mutant background rescues the blow phenotype, at least partially, at stage 16. The embryo forms clearly fused and attached muscles, although defects in muscle number, size and attachment occur.





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