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The signaling pathways downstream of PC1 in ADPKD are still not fully understood. Here, we provide genetic evidence for the necessity of G\u03b112 (encoded by Gna12, hereafter G\u03b112) for renal cystogenesis induced by Pkd1 knockout. There was no phenotype in mice with deletion of G\u03b112 (G\u03b112\u2212\/\u2212). Polyinosine-polycytosine (pI:pC)-induced deletion of Pkd1 (Mx1Cre+Pkd1f\/fG\u03b112+\/+) in 1-week-old mice resulted in multiple kidney cysts by 9\u2005weeks, but the mice with double knockout of Pkd1 and G\u03b112 (Mx1Cre+Pkd1f\/fG\u03b112\u2212\/\u2212) had no structural and functional abnormalities in the kidneys. These mice could survive more than one year without kidney abnormalities except multiple hepatic cysts in some mice, which indicates that the effect of G\u03b112 on cystogenesis is kidney specific. Furthermore, Pkd1 knockout promoted G\u03b112 activation, which subsequently decreased cell\u2013matrix and cell\u2013cell adhesion by affecting the function of focal adhesion and E-cadherin, respectively. Our results demonstrate that G\u03b112 is required for the development of kidney cysts induced by Pkd1 mutation in mouse ADPKD.<\/jats:p>","DOI":"10.1242\/jcs.190496","type":"journal-article","created":{"date-parts":[[2016,8,6]],"date-time":"2016-08-06T01:10:17Z","timestamp":1470445817000},"page":"3675-3684","source":"Crossref","is-referenced-by-count":25,"title":["G\u03b112 is required for renal cystogenesis induced by <i>Pkd1<\/i> inactivation"],"prefix":"10.1242","volume":"129","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6770-1328","authenticated-orcid":false,"given":"Yong","family":"Wu","sequence":"first","affiliation":[{"name":"Brigham and Women's Hospital, Harvard Medical School 1 Renal Division , , Boston, MA 02115 , USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4908-9459","authenticated-orcid":false,"given":"Jen X.","family":"Xu","sequence":"additional","affiliation":[{"name":"Brigham and Women's Hospital, Harvard 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