Language

English

Publication Date

1-1-2025

Journal

Cellular and Molecular Gastroenterology and Hepatology

DOI

10.1016/j.jcmgh.2025.101496

PMID

40081569

PMCID

PMC12198032

PubMedCentral® Posted Date

3-11-2025

PubMedCentral® Full Text Version

Post-print

Abstract

Background & aims: Although it is well-known that ribosomes are critical for cell function, and their synthesis (known as ribosome biogenesis [RiBi]) is energy-intensive, surprisingly little is known about RiBi in vivo in adult tissue.

Methods: Using a mouse model with conditional deletion of Nat10, an essential gene for RiBi and subsequent translation of mRNA, we investigated the effects of RiBi blockade in vivo, with a focus on pancreatic acinar cells during homeostasis and tumorigenesis.

Results: We observed an unexpected latency of several weeks between Nat10 deletion and onset of structural and functional abnormalities and p53-dependent acinar cell death. Although deletion of Trp53 rescued acinar cells from apoptotic cell death, Nat10Δ/Δ; Trp53Δ/Δ acinar cells remained morphologically and functionally abnormal. Deletion of Nat10 in acinar cells blocked Kras-oncogene-driven pancreatic ductal adenocarcinoma, regardless of Trp53 mutation status.

Conclusions: Together, our results provide initial insights into how differentiated cells respond to defects in RiBi and translation in vivo in various physiological contexts.

Keywords

Animals, Tumor Suppressor Protein p53, Ribosomes, Mice, Pancreatic Neoplasms, Acinar Cells, Apoptosis, Carcinoma, Pancreatic Ductal, Proto-Oncogene Proteins p21(ras), Mice, Knockout, Organelle Biogenesis, N-Acetyltransferase 10, Nucleolus, Paligenosis, Ribosome, p53

Published Open-Access

yes

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