Homozygous jeb-c1 mutant longitudinal visceral muscle (LVM) founder cells in stage 12 embryos migrate normally towards the trunk visceral mesoderm (TVM) and very few dying cells are seen. At stage 13 the front migrating cells reach the anterior end of the trunk visceral mesoderm as in wild type. However during late stage 13 the migration becomes disordered and progressive founder cell death is seen.
jeb-c1 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 jeb-c1 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.
Marker analysis indicates that no visceral muscle founders are specified in jeb-c1 mutant embryos. Myoblasts do form in the visceral mesoderm of these embryos, but these cells fuse with somatic muscle founders (i.e.- they are still fusion competent). The resulting animals exhibit loss of visceral musculature, but have normal somatic muscle patterning.
Differentiated visceral mesoderm is not seen in mutant embryos, although other mesodermal tissues (somatic muscles, heart, fat body and hemocytes) develop normally. Visceral mesoderm precursor cells are specified but fail to migrate normally. There is an increase in the number of nuclei in positions consistent with an increase in somatic muscle precursors, but there is no major disruption of somatic muscle patterning. The midgut endoderm is specified normally and migrates to form two longitudinal bands. Subsequent dorsal and ventral endoderm migration is abnormal (probably because this migration depends on the visceral mesoderm).