Genomic imprinting has been extensively studied as an epigenetic mechanism that controls embryonic growth and placental function through parent-of-origin-specific gene expression. Emerging evidence, including our own, suggests a broader role, with imprinted genes regulating maternal physiology and postnatal development during the critical transition from pregnancy to lactation.

Our recent work identifies the imprinting regulator ZFP57 as a key determinant of mammary gland function. Beyond its established role in maintaining genomic imprints during embryogenesis, ZFP57 regulates mammary epithelial differentiation, milk composition and offspring growth through a postnatal mechanism that is largely independent of canonical imprinting. These findings reveal a previously unrecognised genetic programme governing lactation and provide a direct mechanistic link between early postnatal nutritional resource control and the developmental origins of health and disease.

Viewed in an evolutionary context, our findings support a broader model in which genomic imprinting extends beyond fetal development to coordinate maternal investment across generations. By regulating the quantity and quality of nutrients delivered through milk, imprinted genes influence offspring growth and developmental trajectories during a critical window of physiological plasticity. This work reframes genomic imprinting as a regulator of postnatal physiology and maternal-offspring interactions, with implications for understanding the biology of lactation, developmental programming and the origins of metabolic disease.