Abstract

Beckwith‐Wiedemann syndrome is a human congenital disorder characterized by a wide variety of growth abnormalities, including developmental defects and predisposition to certain tumors. Genetic evidence has suggested a role for p57KIP2, a member of a family of cell cycle inhibitory genes, in Beckwith‐Wiedemann syndrome. Two independent groups(1,2) have reported the generation and characterization of mice lacking functional p57KIP2, These mice demonstrate a number of abnormal phenotypes which overlap with, although do not completely recapitulate, Beckwith‐Wiedemann syndrome. These findings advance the molecular characterization of a human disorder, and provide insight into the interplay between regulation of cell division and development.