#4181 THE AUTOSOMAL RECESSIVE POLYCYSTIC KIDNEY DISEASE PROTEIN, FPC, RELEASES MITOCHONDRIA LOCALISING FRAGMENTS INVOLVED IN PREVENTING CYSTOGENESIS

نویسندگان

چکیده

Abstract Background and Aims Autosomal recessive polycystic kidney disease is caused by mutations in PKHD1 encoding FPC, characterized severe renal cystogenesis neonates, yet mouse models do not fully recapitulate the human phenotype. Indeed, even Pkhd1 null allele does cause mouse. Several cleavage products of FPC are reported their function remains unknown. The aim this study was to determine effects on cyst development ARPKD. Method Three mutant lines cystic Pkd1V were crossed produce digenic mice with which cystogenesis. Biochemical analysis used investigate patterns using a panel new antibodies. Cell electron microscopy revealed underlying mitochondrial defects Knockout mice. Results mutation modifies Pkd1 uncleavable (Pkd1V), enhancing phenotype both pancreas. hypomorphic KO enhance phenotype, making distal tubule cysts more initiating proximal tubules. displays differential fragments unknown function. New antibodies generated interrogate products. small C terminal identified contain targeting sequence recruited mitochondria. Mitochondrial ultrastructural changes evident after deletion including fragmentation dilated cristae, suggesting disrupted Deletion just C-terminal fragment (ΔCT), portion that directly corresponds cleaves localises mitochondria, sufficient PC1 mutant. Unlike other mutants however, (ΔCT) result pancreatic when combined Pkd1V, terminus required prevent development. Conclusion Our results suggest C-terminus plays an important role preventing via newly discovered mitochondria specific work reveal some aspects FPC's function, particular previously unrecognised mediated through essential enhancement model.

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ژورنال

عنوان ژورنال: Nephrology Dialysis Transplantation

سال: 2023

ISSN: ['1460-2385', '0931-0509']

DOI: https://doi.org/10.1093/ndt/gfad063a_4181