A surprising substitution

Jun and JunB are components of a transcription factor (AP-1) involved in cell development and apoptosis, but their functional equivalence in vivo is unknown. In 2 January online Nature Genetics, Emmanuelle Passegué and colleagues from Research Institute of Molecular Pathology, Vienna, Austria, show that JunB — although transcriptionally less active than Jun — has the potential to substitute functionally for Jun.

Passegué et al. used a knock-in mouse model, and observed that JunB restores the expression of genes regulated by Jun/Fos, but not those regulated by Jun/ATF. The JunB substitution rescued the Jun-dependent liver and cardiac defects in vivo as well as the defects observed in primary fibroblasts and fetal hepatoblasts in vitro (Nature Genet 2002, DOI: 10.1038/ng790).

This study suggests, "that the spatial and temporal regulation of AP-1 expression is more important than the coding sequence of its components", said the authors.