The mammary gland undergoes significant postnatal development that is temporally regulated by hormonal signalling. During pregnancy, side branches form from the mammary ductal tree and alveoli develop at their tips; both are lost in progesterone receptor (Pgr)-null mice. To investigate how hormonal and β-catenin signalling (which also acts in pregnancy-induced mammary differentiation) intersect during postnatal mammary development,Hiremath et al. tested whether a non-degradable form of β-catenin(MMTV-ΔN89β-catenin) could rescue the phenotype of Pgr-null mice (see ). They found that although stabilized β-catenin rescues alveogenesis at ductal tips, it cannot stimulate alveolar development along the lateral borders of mammary ducts. This, the authors propose, is due to the existence of two β-catenin-responsive cell populations: one at ductal tips that is intrinsically β-catenin responsive; the other, a progenitor population, at the lateral ductal borders of virgin glands that requires Pgr signalling to become primed for alveogenesis in response to β-catenin. These findings advance mammary development research, not least by identifying this novel progenitor population.
