Language

English

Publication Date

7-1-2025

Journal

Disease Models & Mechanisms

DOI

10.1242/dmm.052303

PMID

40421838

PMCID

PMC12208401

PubMedCentral® Posted Date

6-20-2025

PubMedCentral® Full Text Version

Post-print

Abstract

Carbamoyl phosphate synthetase 1 (CPS1) deficiency is a rare metabolic disorder that, in neonatal onset, is typically characterized by severe life-threatening and neurologically injuring hyperammonemic episodes with high unmet patient need. Patients that retain limited enzyme activity may present later in life with less severe hyperammonemia. CPS1 drives the first step in the urea cycle, the pathway terrestrial mammals utilize to metabolize nitrogen. In order to probe the effect of hyperammonemia on the developing nervous system and explore new therapies, a murine Cps1 exon 3-4 mutant was previously generated. However, these mice die within 24 h of birth, limiting study capabilities. Herein, we developed a novel Cps1 hypomorphic murine model with residual enzyme activity that maintains survival, but with dysfunction of Cps1 that could be detected biochemically. Characterization, based on the orthologous human variant Asn674Ile, revealed that the variant is reproducible, 100% penetrant and biochemically phenocopies the human disorder. The hypomorph presents with elevated ammonia and glutamate, and reduced citrulline, and with an impaired rate of ureagenesis, providing a novel platform to study and develop therapies for CPS1 deficiency.

Keywords

Animals, Hyperammonemia, Disease Models, Animal, Carbamoyl-Phosphate Synthase (Ammonia), Nervous System, Humans, Mice, Carbamoyl-Phosphate Synthase I Deficiency Disease, Ammonia, Citrulline, Phenotype, Glutamic Acid, Mutation, Carbamoyl phosphate synthetase 1 deficiency, Human mutation, Enzyme activity, Hyperammonemia, Glutamine

Published Open-Access

yes

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