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Congenital anomalies of the kidney and urinary tract (CAKUT), including hydroureter and hydronephrosis, have been reported in patients with MWS. However, the role of the\n                    <jats:italic>ZEB2<\/jats:italic>\n                    gene in urinary tract development and the cellular and molecular mechanisms underlying the CAKUT phenotypes in MWS remain unknown. In this study, we examined ZEB2 expression in the developing mouse ureter and generated\n                    <jats:italic>Zeb2<\/jats:italic>\n                    ureteral mesenchyme-specific conditional knockout mice (\n                    <jats:italic>Zeb2<\/jats:italic>\n                    cKO) by crossing\n                    <jats:italic>Zeb2<\/jats:italic>\n                    floxed mice with\n                    <jats:italic>Tbx18<\/jats:italic>\n                    Cre\n                    <jats:sup>+<\/jats:sup>\n                    mice. The urinary tract of\n                    <jats:italic>Zeb2<\/jats:italic>\n                    cKO mice and their wild-type littermates was analyzed for morphological and histological changes. Our results show that ZEB2 is expressed in TBX18\n                    <jats:sup>+<\/jats:sup>\n                    ureteral mesenchymal cells during mouse ureter development. Deleting\n                    <jats:italic>Zeb2<\/jats:italic>\n                    in these cells caused hydroureter and hydronephrosis, indicating obstructive uropathy. Cellular and molecular marker analysis revealed that the TAGLN\n                    <jats:sup>+<\/jats:sup>\n                    ACTA2\n                    <jats:sup>+<\/jats:sup>\n                    ureteral smooth muscle cell (SMC) layer was absent in\n                    <jats:italic>Zeb2<\/jats:italic>\n                    cKO mice. In contrast, the tunica adventitia cell layer was significantly expanded compared to controls. At the molecular level,\n                    <jats:italic>Zeb2<\/jats:italic>\n                    cKO mice had significantly decreased TBX18 expression but increased SOX9 expression in the developing ureter compared to wild-type controls. Our findings demonstrate that ZEB2 is crucial for normal ureteral SMC differentiation during ureter development. Additionally, our study suggests that MWS patients may have abnormal ureteral SMC development, which contributes to the abnormalities of the urinary tract.\n                  <\/jats:p>","DOI":"10.1371\/journal.pgen.1012028","type":"journal-article","created":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T18:52:08Z","timestamp":1769194328000},"page":"e1012028","update-policy":"https:\/\/doi.org\/10.1371\/journal.pgen.corrections_policy","source":"Crossref","is-referenced-by-count":1,"title":["Transcription factor ZEB2 is essential for ureteral smooth muscle cell differentiation"],"prefix":"10.1371","volume":"22","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1320-1306","authenticated-orcid":true,"given":"Sudhir","family":"Kumar","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xueping","family":"Fan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-8183-4582","authenticated-orcid":true,"given":"Harshita","family":"Pattam","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kun","family":"Yan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Easton 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