biostudies-literatureHesselson DNIDDK NIH HHS712-7https://www.ebi.ac.uk/biostudies/studies/S-EPMC3081919biostudies-literatureUnknown21(8)Pluripotent embryonic cells become progressively lineage restricted during development in a process that culminates in the differentiation of stable organ-specific cell types that perform specialized functions. Terminally differentiated pancreatic acinar cells do not have the innate capacity to contribute to the endocrine β cell lineage, which is destroyed in individuals with autoimmune diabetes. Some cell types can be reprogrammed using a single factor, whereas other cell types require continuous activity of transcriptional regulators to repress alternate cell fates. Thus, we hypothesized that a transcriptional network continuously maintains the pancreatic acinar cell fate. We found that postembryonic antagonism of Ptf1a, a master regulator of pancreatic development and acinar cell fate sCurrent biology : CBSuppression of Ptf1a activity induces acinar-to-endocrine conversion.PMC3081919DK075032R01 DK075032-04R01 DK075032-05R01 DK075032R01 DK075032-04S1Stainier DYHesselson DAnderson RMfalseSuppression of Ptf1a activity induces acinar-to-endocrine conversion.Pluripotent embryonic cells become progressively lineage restricted during development in a process that culminates in the differentiation of stable organ-specific cell types that perform specialized functions. Terminally differentiated pancreatic acinar cells do not have the innate capacity to contribute to the endocrine β cell lineage, which is destroyed in individuals with autoimmune diabetes. Some cell types can be reprogrammed using a single factor, whereas other cell types require continuous activity of transcriptional regulators to repress alternate cell fates. Thus, we hypothesized that a transcriptional network continuously maintains the pancreatic acinar cell fate. We found that postembryonic antagonism of Ptf1a, a master regulator of pancreatic development and acinar cell fate s2011-01-01T00:00:00Z2011 Apr2025-04-25T21:49:56.04Z2019-03-27T00:40:55ZS-EPMC30819192149709210.1016/j.cub.2011.03.041