FlyBase curator comment: this entry is used to capture phenotypic information when the particular allele (or allele combination) used by the author could not be determined but the context of the experiment suggests that the phenotype being described is some kind of loss of function.
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. 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.
Many germ cells remain associated with the basal surface of the gut, instead of moving into lateral mesoderm. Those germ cells that do leave the PMG often appear disorganised within the mesoderm and do not correctly navigate toward the somatic gonadal precursors (SGPs). There is always a small number of germ cells in each mutant that are able to associate correctly with SGPs. The number of gonadal mesodermal cells is reduced in stage 14 embryos, the cells present are irregularly shaped.
4 mutants are isolated.