Inhibitor of differentiation‐1 (Id‐1) has been shown to play an essential role in cell proliferation, invasion, migration, and anti‐apoptosis. However, the effect of Id‐1 in mammary gland development remains unknown. Here, we generated MMTV‐Id‐1 transgenic mice to study the role of Id‐1 in mammary gland development. In virgin mice, Id‐1 overexpression led to precocious development and delayed regression of terminal end buds (TEBs) compared with wild‐type mice. The number of BrdU‐positive cells and the expression of Wnt signaling molecules, β‐catenin and cyclin D1, which regulate ductal extension and TEB formation in virgin, were statistically higher in Id‐1 transgenic mice than in wild‐type mice. Id‐1 also had an effect on the formation and proliferation of lobuloalveolar structures during early and mid‐pregnancy. Id‐1 transgenic mice had more lobulated and prominent alveolar budding than wild‐type mice and had significantly greater counts of lobuloalveolar structures in early pregnancy. The expression of BrdU, β‐catenin, and cyclin D1 was also predominantly increased in Id‐1 transgenic mice. Moreover, Id‐1 transgenic mice showed delayed involution. Id‐1 regulated the expression levels of anti‐apoptotic Bcl‐2 and pro‐apoptotic Bax, and resulted in delay of apoptotic peak during postlactational involution. We also found that Id‐1 was able to modulate expression of the regulators of Wnt/β‐catenin signaling such as phospho‐Akt, BMP2, FGF3, and RAR‐β in tubuloalveolar development of mammary glands. Taken together, our results suggest that Id‐1 plays a pivotal role in mammary gland development through Wnt signaling‐mediated acceleration of precocity and alveologenesis and Bcl‐2 family members‐mediated delay of involution. J. Cell. Physiol. 226: 1340–1352, 2011. © 2010 Wiley‐Liss, Inc.