Drosophila melanogaster embryos undergo a dramatic genomic transformation in the hour preceding gastrulation, as thousands of promoters and regulatory regions become biochemically distinct before they become active.

In fruit flies, maternally deposited RNA-binding proteins are removed during the maternal-to-zygotic transition via a mechanism of translational upregulation of Kondo, the key E2 enzyme, at egg activation.

ME31B is a general repressor of gene expression in the Drosophila early embryo, repressing translation before the maternal-to-zygotic transition and stimulating mRNA decay after activation of the zygotic genome.

Epigenetic reprogramming by LSD1/KDM1A acts at fertilization in mice to enable embryogenesis and prevent behavioural abnormalities.

Soon after fertilisation, a critical portion of the embryonic genome is switched on through the actions of maternally inherited Stella, in part through controlling the activation of transposable elements.

Following fertilization, the pioneering transcription factors GAGA factor (GAF) and Zelda are independently required to reprogram the zygotic genome of Drosophila and activate the first wave of gene expression.

The gene Odd-paired is a late-acting regulator of zygotic gene expression, functioning coordinately with Zelda to influence chromatin accessibility and affecting genes expressed along both axes of Drosophila embryos.

Early development involves both maternal and zygotic genetic effects. This dual genetic basis shapes the evolution of developmental mode in a marine annelid.

The maternally provided histone demethylase LSD1/KDM1A has an instrumental role at the beginning of life, shaping the histone methylation landscape and the transcriptional repertoire of the early mouse embryo.

Mechanisms for shaping the chromatin accessibility landscape operate during development to regulate how embryonic patterning information is interpreted at the level of gene regulatory networks.