A protein known as heat-shock factor-1 (HSF1) is a major transactivator of stress-inducible genes in response to environmental changes, but it is also implicated in extra-embryonic development and female fertility in mice1,2. Here we show that mouse embryos whose mothers lack this protein are unable to develop properly beyond the zygotic stage, although oocytes were ovulated and fertilized normally. Wild-type spermatozoa do not save zygotes from lethality, indicating that the reproductive failure of females deficient in this factor is caused by a 'maternal effect' mutation3, and that HSF1 from the mother normally controls early post-fertilization development.