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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Abnormal development of the renal collecting system contributes to congenital anomalies of the kidney and urinary tract (CAKUT), a major cause of pediatric end-stage renal disease. ATP-citrate lyase (ACLY) is an enzyme that transfers acetyl-CoA from the mitochondria to the nucleus, where it serves as an essential substrate for histone acetylation. Given its abundant expression in renal collecting duct cells, we hypothesized that ACLY plays a critical role in the epigenetic regulation of collecting duct morphogenesis.
To explore the role of ACLY in renal development, we generated Acly knockout mice and examined renal morphology and function. We further performed single-cell RNA sequencing (scRNA-seq) and CUT&Tag-seq analyses on collecting duct cells to characterize transcriptional and epigenetic alterations associated with ACLY deficiency.
Six-week-old Acly knockout mice displayed reduced kidney weight, nephron number, and structural abnormalities in the collecting system. Immunostaining showed decreased expression of aquaporin-2 (AQP2) and several ion channels, suggesting impaired collecting duct differentiation. Single-cell transcriptomic analysis revealed a significant downregulation of ribosomal protein genes in Acly-deficient collecting duct cells, while CUT&Tag-seq demonstrated reduced histone acetylation at ribosomal gene promoters. These findings indicate that ACLY is essential for maintaining ribosomal gene transcription and epigenetic homeostasis in collecting duct cells.
ACLY-mediated acetyl-CoA transport supports histone acetylation and ribosomal gene expression required for proper collecting duct development. Loss of ACLY disrupts ribosomal biogenesis and ion channel synthesis, leading to structural and functional defects that may underlie CAKUT. Our study identifies an epigenetic mechanism by which cellular metabolism regulates renal morphogenesis.
