chem⁵ homozygotes (as well as chem¹/chem⁵) are embryonic/larval lethal, the animals that die as embryos show severe cuticular defects (including no cuticle, dorsal open or head involution defective phenotypes) and disruption of the lateral epithelium architecture, chem⁵ epithelial cells are also significantly shorter compared to wild-type. When cultured separately from their balancer-containing heterozygous siblings some of the surviving homozygous larvae manage to pupariate and yield adults, these however die shortly after eclosion.

Embryos both maternally and zygotically mutant for chem⁵ (coming from mothers with chem⁵ germline clones generated by the OvoD method) display severe cuticular defects - stronger than in zygotic only mutants - with majority forming no cuticle at all, heteroallelic embryos coming from either chem¹ or chem³ mutant mothers and chem⁵ fathers show similarly severe cuticular defects. These embryonic phenotypes are significantly improved by paternal rescue.