BMP signaling inhibits intestinal stem cell self-renewal by suppressing Wnt-β-catenin signaling. Mutations in BMPR1A, SMAD4, and PTEN are associated with juvenile polyposis, juvenile intestinal polyposis, and Cowden disease, respectively. The study shows that conditional inactivation of Bmpr1a in mice leads to intestinal polyposis resembling human juvenile polyposis. BMP signaling suppresses Wnt signaling to maintain a balance in stem cell self-renewal. PTEN, through PI3K-Akt, mediates the convergence of BMP and Wnt pathways on β-catenin control. BMP signaling may control intestinal stem cell duplication, preventing crypt fission and increased crypt number. Wnt signaling through β-catenin promotes cell proliferation and leads to adenomatous polyposis. The BMP pathway is crucial during gastrointestinal development and maintains tissue homeostasis. BMP2 and BMP4 function by binding to their type II receptor and recruiting type I receptors. BMP signaling is regulated by its antagonist, Noggin. PTEN, a tumor suppressor, inhibits Akt activity and downstream signals. Intestinal stem cells (ISCs) are located at the fourth or fifth cell position from the base of each crypt. BMP4 is expressed in mesenchymal cells adjacent to ISCs. Bmpr1a is expressed in epithelial cells along the crypt-villus axis and in ISCs. Noggin is expressed in the submucosal region adjacent to the crypt bottom. Active BMP signaling is reflected by the presence of P-Smad1, P-Smad5, and P-Smad8 in villi and ISCs. Bmpr1a mutant mice develop multiple polyps, with increased crypt number and fused villi. The polyps develop into structures with cystically dilated glands. BMP signaling restricts crypt cell fate. Wnt signaling favors crypt cell fate over villus differentiation. Increased crypt number suggests Wnt signaling may be affected in Bmpr1a mutant mice. Wnt signaling was active in normal and polyp crypts. β-catenin transcriptional activity was detected primarily in ISCs. PTEN inactivation activates Akt and nuclear accumulation of β-catenin. P-PTEN is present specifically in ISCs. P-Akt is detected in BrdU-retaining ISCs. β-catenin is associated with the membrane in quiescent ISCs but is found in the nucleus of P-PTEN+ ISCs. Nuclear localization of β-catenin correlates with activation of Top-d2GFP reporter plasmid in P-PTEN+ ISCs. β-catenin is also found in dividing ISCs. BMP signaling regulates PTEN-Akt pathway in ISCs. Inactivation of Bmpr1a leads to increased ISC number and crypt number. BMP signaling inhibits β-catenin activity, balancing the role of WntBMP signaling inhibits intestinal stem cell self-renewal by suppressing Wnt-β-catenin signaling. Mutations in BMPR1A, SMAD4, and PTEN are associated with juvenile polyposis, juvenile intestinal polyposis, and Cowden disease, respectively. The study shows that conditional inactivation of Bmpr1a in mice leads to intestinal polyposis resembling human juvenile polyposis. BMP signaling suppresses Wnt signaling to maintain a balance in stem cell self-renewal. PTEN, through PI3K-Akt, mediates the convergence of BMP and Wnt pathways on β-catenin control. BMP signaling may control intestinal stem cell duplication, preventing crypt fission and increased crypt number. Wnt signaling through β-catenin promotes cell proliferation and leads to adenomatous polyposis. The BMP pathway is crucial during gastrointestinal development and maintains tissue homeostasis. BMP2 and BMP4 function by binding to their type II receptor and recruiting type I receptors. BMP signaling is regulated by its antagonist, Noggin. PTEN, a tumor suppressor, inhibits Akt activity and downstream signals. Intestinal stem cells (ISCs) are located at the fourth or fifth cell position from the base of each crypt. BMP4 is expressed in mesenchymal cells adjacent to ISCs. Bmpr1a is expressed in epithelial cells along the crypt-villus axis and in ISCs. Noggin is expressed in the submucosal region adjacent to the crypt bottom. Active BMP signaling is reflected by the presence of P-Smad1, P-Smad5, and P-Smad8 in villi and ISCs. Bmpr1a mutant mice develop multiple polyps, with increased crypt number and fused villi. The polyps develop into structures with cystically dilated glands. BMP signaling restricts crypt cell fate. Wnt signaling favors crypt cell fate over villus differentiation. Increased crypt number suggests Wnt signaling may be affected in Bmpr1a mutant mice. Wnt signaling was active in normal and polyp crypts. β-catenin transcriptional activity was detected primarily in ISCs. PTEN inactivation activates Akt and nuclear accumulation of β-catenin. P-PTEN is present specifically in ISCs. P-Akt is detected in BrdU-retaining ISCs. β-catenin is associated with the membrane in quiescent ISCs but is found in the nucleus of P-PTEN+ ISCs. Nuclear localization of β-catenin correlates with activation of Top-d2GFP reporter plasmid in P-PTEN+ ISCs. β-catenin is also found in dividing ISCs. BMP signaling regulates PTEN-Akt pathway in ISCs. Inactivation of Bmpr1a leads to increased ISC number and crypt number. BMP signaling inhibits β-catenin activity, balancing the role of Wnt