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Yet, disease expression is highly variable and includes very early-onset PKD presentations in utero or infancy. In animal models, the RNA-binding molecule Bicc1 has been shown to play a crucial role in the pathogenesis of PKD. To study the interaction between BICC1, PKD1, and PKD2, we combined biochemical approaches, knockout studies in mice and\n                    <jats:italic>Xenopus,<\/jats:italic>\n                    genetic engineered human kidney cells carrying\n                    <jats:italic>BICC1<\/jats:italic>\n                    variants, as well as genetic studies in a large ADPKD cohort. We first demonstrated that BICC1 physically binds to the proteins Polycystin-1 and -2 encoded by\n                    <jats:italic>PKD1<\/jats:italic>\n                    and\n                    <jats:italic>PKD2<\/jats:italic>\n                    via distinct protein domains. Furthermore, PKD was aggravated in loss-of-function studies in\n                    <jats:italic>Xenopus<\/jats:italic>\n                    and mouse models, resulting in more severe disease when\n                    <jats:italic>Bicc1<\/jats:italic>\n                    was depleted in conjunction with\n                    <jats:italic>Pkd1 or Pkd2<\/jats:italic>\n                    . Finally, in a large human patient cohort, we identified a sibling pair with a homozygous\n                    <jats:italic>BICC1<\/jats:italic>\n                    variant and patients with very early onset PKD (VEO-PKD) that exhibited compound heterozygosity of\n                    <jats:italic>BICC1<\/jats:italic>\n                    in conjunction with\n                    <jats:italic>PKD1 and PKD2<\/jats:italic>\n                    variants. Genome editing demonstrated that these\n                    <jats:italic>BICC1<\/jats:italic>\n                    variants were hypomorphic in nature and impacted disease-relevant signaling pathways. These findings support the hypothesis that BICC1 cooperates functionally with PKD1 and PKD2, and that\n                    <jats:italic>BICC1<\/jats:italic>\n                    variants may aggravate PKD severity, highlighting RNA metabolism as an important new concept for disease modification in ADPKD.\n                  <\/jats:p>","DOI":"10.7554\/elife.106342","type":"journal-article","created":{"date-parts":[[2025,6,11]],"date-time":"2025-06-11T10:30:25Z","timestamp":1749637825000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.106342","source":"Crossref","is-referenced-by-count":0,"title":["BICC1 interacts with PKD1 and PKD2 to drive cystogenesis in ADPKD"],"prefix":"10.7554","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6498-9765","authenticated-orcid":true,"given":"Uyen","family":"Tran","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03xjacd83","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Heart, Blood & Kidney 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