Both maternal and zygotic expression of many essential genes are required for normal development. For some of these genes, absence of maternal function yields striking embryonic defects. The experiments reported here examine two questions about such genes: (1) Are embryonic effects of maternal deficits a common property of maternally-and-zygotically active genes? and (2) Is use of the maternal products of these genes restricted to early embryogenesis? A comparison of times of lethality of mutant sons of normal and mutant-heterozygous mothers has been made for six mutations in the zeste-white region of the Drosophila X chromosome. Four of the mutations are defective in single cistrons and two are deficiencies that between them remove thirteen essential loci. All of these mutations had previously been shown to have both maternal and zygotic effects, and all of them had been tested, using homozygous germ-line clones, for the effects of complete maternal defects. For several of them, homozygous germ-line clones cause embryonic defects. Of the six, only one, Df(l)K95, shows a shift from larval to embryonic lethality when the mothers are heterozygous, and even in that case lethality occurs at the very end of embryogenesis. These results have two implications: (1) maternally-derived transcripts do not always serve a solely embryonic role; and (2) an embryonic effect of a complete maternal deficit does not by itself demonstrate an embryo-restricted function for the maternal transcript.