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Epithelial CFTR expression is highest in rare cells called ionocytes. We studied CFTR regulation in control and ionocyte-enriched cultures by transducing bronchial basal cells with adenoviruses that encode only eGFP or FOXI1 (forkhead box I1)\u2009+\u2009eGFP as separate polypeptides. FOXI1 dramatically increased the number of transcripts for ionocyte markers ASCL3 (Achaete-Scute Family BHLH Transcription Factor 3), BSND, ATP6V1G3, ATP6V0D2, KCNMA1, and CFTR without altering those for secretory (SCGB1A1), basal (KRT5, KRT6, TP63), goblet (MUC5AC), or ciliated (FOXJ1) cells. The number of cells displaying strong FOXI1 expression was increased 7-fold, and there was no evidence for a broad increase in background immunofluorescence. Total CFTR mRNA and protein levels increased 10-fold and 2.5-fold, respectively. Ionocyte-enriched cultures displayed elevated basal current, increased adenylyl cyclase 5 expression, and tonic suppression of CFTR activity by the phosphodiesterase PDE1C, which has not been shown previously to regulate CFTR activity. The results indicate that CFTR regulation depends on cell type and identifies PDE1C as a potential target for therapeutics that aim to increase CFTR function specifically in ionocytes.<\/jats:p>","DOI":"10.1165\/rcmb.2022-0241oc","type":"journal-article","created":{"date-parts":[[2023,3,23]],"date-time":"2023-03-23T16:58:45Z","timestamp":1679590725000},"page":"281-294","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":19,"title":["Ionocyte-Specific Regulation of Cystic Fibrosis Transmembrane Conductance Regulator"],"prefix":"10.1093","volume":"69","author":[{"given":"Yukiko","family":"Sato","sequence":"first","affiliation":[{"name":"Department of Physiology"},{"name":"Cystic Fibrosis Translational Research Center"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dusik","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Physiology"},{"name":"Cystic Fibrosis Translational Research 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