To further confirm this phenotype, and to exclude the possibility that the loss of zygotic setd2 (i.e., in the homozygous setd2 mutant) may also contribute to this developmental delay, we compared the setd2mNull embryos and the embryos produced by self-crossing of the heterozygous setd2 mutant; we also performed whole-mount in situ hybridization analysis of myod, which is specifically expressed in the somites and thus can be used to define developmental stages67. This evidence concerns the gene MYOD1 and Global developmental delay.