GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE337nnn/GSE337067/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE337067GEOGSEfalseKidney-specific deletion of the BicC family RNA binding protein 1 triggers an ADPKD-like cystogenic programAutosomal dominant polycystic kidney disease (ADPKD) arises from mutations in polycystin-1/PKD1 or polycystin-2/PKD2 that induce injury-repair pathways and dysregulate cAMP and YAP/TAZ signaling to promote cyst growth. Cystic kidneys with elevated cAMP levels also develop in mouse embryos lacking the BicC family RNA-binding protein 1 (Bicc1). To prevent embryonic lethality, we flanked Bicc1 exon 4 with loxP sites for conditional knockout (cKO) in renal tubules using inducible Pax8rtTA-driven Cre in adults, or distal segment-specific deletion in utero using Ksp-Cre. Whereas Bicc1-deficient adult kidneys formed relatively few cysts within six months, distal nephron-specific deletion induced aggressive PKD-like disease. Automated Renal Tubule Cyst Quantification (ARTCyQ), a novel machine-learning pipeline to analyze immunofluorescent stainings, revealed increasing ambiguity in nephron segment identity and activation of ADPKD-related pathways, including YAP signaling. Accordingly, transcriptional profiling revealed overlap with PKD and injury-repair signatures, supporting a role for Bicc1 in polycystin signaling.2026/06/30GSE337067GSM9847676GSM9847677GSM9847674GSM9847675GSM9847669GSM9847678GSM9847679GSM9847680GSM9847672GSM9847683GSM9847673GSM9847684GSM9847670GSM9847681GSM9847682GSM984767124247337067Mus musculus