Fig. 2.
The MCH phenotype in embryos lacking both CHES-1-like and jumu functions is not caused by defects in mesoderm migration. (A-C) Mef2 antibody staining of the mesoderm, illustrating the presence or absence of mesoderm migration defects in ventral views of representative Stage 9 embryos that are (A) wild type, (B) homozygous for the stumpsYY202 mutation and (C) lack both Fkh genes. Note that the dorsolateral margin of the mesoderm in the stumps mutant (B) is ragged and exhibits discontinuities (arrows) characteristic of migration defects. By contrast, the migrating mesoderm of both wild-type embryos (A) and embryos lacking both CHES-1-like and jumu (C) exhibit smooth dorsolateral margins (arrowheads). Scale bar: 50 μm. (D-F) Mef2 antibody staining (red) of the migrating mesoderm in representative transverse views of the ventral halves of Stage 10 embryos that are (D) wild type, (E) lack stumps function, and (F) lack both Fkh genes. Note that the mesoderm migrates dorsolaterally as a monolayer in both the wild-type embryo and the CHES-1-like; jumu double homozygote, but remains aggregated ventrally and unable to reach the dorsalmost positions in the stumps mutant. Scale bar: 25 μm.