{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T12:24:02Z","timestamp":1787747042067,"version":"build-2784847793"},"reference-count":57,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","license":[{"start":{"date-parts":[[2025,12,16]],"date-time":"2025-12-16T00:00:00Z","timestamp":1765843200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"crossref","award":["DK120911"],"award-info":[{"award-number":["DK120911"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"crossref","award":["DK100592"],"award-info":[{"award-number":["DK100592"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"crossref","award":["DK120534"],"award-info":[{"award-number":["DK120534"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Amy P. Goldman Foundation","award":["grant"],"award-info":[{"award-number":["grant"]}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["JASN"],"published-print":{"date-parts":[[2026,7]]},"abstract":"\n Key Points<\/jats:title>\n \n \n \n Dual inactivation of Glis3 and Pkd1 exacerbated polycystic kidney disease compared with Pkd1 inactivation alone in mouse models of autosomal dominant polycystic kidney disease.<\/jats:p>\n <\/jats:list-item>\n \n RNA-Seq and ATAC-Seq suggested Glis3 inactivation resulted in dysregulated fatty acid metabolism and alteration of circadian regulation.<\/jats:p>\n <\/jats:list-item>\n \n Glis3 was involved in a transcriptional network consisting of the transcription factors HNF1 homeobox B, hepatic nuclear factor 4, alpha, and D site albumin promoter binding protein.<\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>\n \n Background<\/jats:title>\n \n Autosomal dominant polycystic kidney disease is caused by mutations affecting polycystin-1 or polycystin-2. The existence of a cilia-dependent cyst activation pathway has been identified by showing that structurally intact primary cilia are crucial for rapid cyst growth following loss of polycystins. We previously used translating ribosome affinity purification RNA-Seq on precystic mouse kidneys to determine a translatome that meets the criteria for cilia-dependent cyst activation. From this, we identified\n Glis2<\/jats:italic>\n as an early effector of polycystin signaling and a potential target for therapy. Here, we investigate the role of\n Glis3<\/jats:italic>\n which, while not transcriptionally altered in autosomal dominant polycystic kidney disease models, encodes a cilia-localized transcription factor belonging to the same gene family as\n Glis2<\/jats:italic>\n .\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n We used live cell imaging along with gene and protein expression studies to determine the relationships between Glis3, Glis2, and polycystin-1 expression. We used\n Glis3<\/jats:italic>\n conditional knockout mice to investigate the\n in vivo<\/jats:italic>\n genetic interaction between\n Glis3<\/jats:italic>\n and\n Pkd1<\/jats:italic>\n . We used gene expression and chromatin accessibility analyses by RNA-Seq and ATAC-Seq, respectively, on an allelic series of\n Glis3<\/jats:italic>\n and\n Pkd1<\/jats:italic>\n inactivation models to explore the genetic relationships between the two genes.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n The ciliary localization of Glis3 was not affected by\n Pkd1<\/jats:italic>\n mutation status. Kidney selective inactivation of\n Glis3<\/jats:italic>\n by itself did not affect kidney structure or function, but dual inactivation of\n Glis3<\/jats:italic>\n and\n Pkd1<\/jats:italic>\n significantly worsened polycystic kidney disease. Integration of transcriptomic profiling and chromatin accessibility assays suggested that kidney tubule-specific\n Glis3<\/jats:italic>\n inactivation resulted in dysregulated fatty acid metabolism and alteration of circadian regulation.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Glis3 is a primary cilium localized transcription factor that genetically interacts with\n Pkd1<\/jats:italic>\n and modifies kidney epithelial cell metabolism and circadian function.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1681\/asn.0000000980","type":"journal-article","created":{"date-parts":[[2025,12,16]],"date-time":"2025-12-16T17:01:44Z","timestamp":1765904504000},"page":"1423-1437","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":3,"title":["Glis3 Is a Modifier of Cyst Progression in Autosomal Dominant Polycystic Kidney Disease"],"prefix":"10.1681","volume":"37","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4865-3866","authenticated-orcid":false,"given":"Zemeng","family":"Wei","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut"},{"name":"Department of Genetics, Yale School of Medicine, New Haven, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9337-5017","authenticated-orcid":false,"given":"Jianlei","family":"Gu","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, Yale University School of Public Health, New Haven, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0003-1616-9097","authenticated-orcid":false,"given":"Xin","family":"Tian","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-0451-3077","authenticated-orcid":false,"given":"Chao","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1195-9607","authenticated-orcid":false,"given":"Hongyu","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Genetics, Yale School of Medicine, New Haven, Connecticut"},{"name":"Department of Biostatistics, Yale University School of Public Health, New Haven, Connecticut"},{"name":"Computational Biology and Bioinformatics Program, Yale University, New Haven, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5062-4629","authenticated-orcid":false,"given":"Stefan","family":"Somlo","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut"},{"name":"Department of Genetics, Yale School of Medicine, New Haven, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2025,12,16]]},"reference":[{"issue":"6","key":"B1-20260826","doi-asserted-by":"crossref","first-page":"881","DOI":"10.1016\/0092-8674(94)90137-6","article-title":"The polycystic kidney disease 1 gene encodes a 14 kb transcript and lies within a duplicated region on chromosome 16","volume":"77","year":"1994","journal-title":"Cell."},{"issue":"2","key":"B2-20260826","doi-asserted-by":"crossref","first-page":"289","DOI":"10.1016\/0092-8674(95)90339-9","article-title":"Polycystic kidney disease - the complete structure of the PKD1 gene and its protein","volume":"81","year":"1995","journal-title":"Cell."},{"issue":"5266","key":"B3-20260826","doi-asserted-by":"crossref","first-page":"1339","DOI":"10.1126\/science.272.5266.1339","article-title":"PKD2, a gene for polycystic kidney disease that encodes an integral membrane protein","volume":"272","author":"Mochizuki","year":"1996","journal-title":"Science."},{"issue":"1","key":"B4-20260826","doi-asserted-by":"crossref","first-page":"50","DOI":"10.1038\/s41572-018-0047-y","article-title":"Polycystic kidney disease","volume":"4","author":"Bergmann","year":"2018","journal-title":"Nat Rev Dis Primers."},{"issue":"6","key":"B5-20260826","doi-asserted-by":"crossref","first-page":"2315","DOI":"10.1172\/JCI72272","article-title":"Genetic mechanisms and signaling pathways in autosomal dominant polycystic kidney disease","volume":"124","author":"Harris","year":"2014","journal-title":"J Clin 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