# MCEE Promotes Intramuscular Fat Deposition in Pigs Through Regulating Mitochondrial Function

## TL;DR

This study shows that the MCEE gene affects fat deposition in pigs by regulating mitochondrial function, which could help improve pork quality.

## Contribution

The novel finding is that MCEE regulates intramuscular fat deposition in pigs through mitochondrial function modulation.

## Key findings

- MCEE overexpression increases proliferation and adipogenic differentiation of porcine preadipocytes.
- MCEE influences mitochondrial function, including reactive oxygen species levels and membrane potential.
- Transcriptomic analysis links MCEE to oxidative phosphorylation and mitochondrial dysfunction pathways.

## Abstract

Intramuscular fat (IMF) content is one of the key factors influencing pork quality. Previous whole-genome resequencing and genome-wide association study (GWAS) analyses identified methylmalonyl-CoA epimerase enzyme (MCEE) as a candidate gene associated with porcine IMF. Experimental validation revealed that MCEE overexpression in porcine preadipocytes promotes cell proliferation and adipogenic differentiation, whereas its suppression exerts the opposite effect. Transcriptome profiling of MCEE-overexpressing and knockdown cells demonstrated that differentially expressed genes (DEGs) were primarily enriched in pathways related to oxidative phosphorylation and mitochondrial dysfunction-related disorders. Further experiments indicated that MCEE overexpression enhances mitochondrial function, while its inhibition impairs it. These findings suggest that MCEE regulates IMF deposition by modulating mitochondrial function, providing a potential target for improving livestock meat quality, especially pork meat quality.

IMF is a key determinant of meat quality, influencing tenderness, juiciness and flavor, yet the mechanisms underlying its formation remain poorly understood. Previous studies performed whole-genome resequencing and GWAS on pigs with divergent IMF content, identifying MCEE as a candidate gene associated with IMF deposition. Subsequently, gain- and loss-of-function approaches were employed to investigate the role of MCEE in porcine intramuscular preadipocytes. Here, we isolated primary preadipocytes and subjected them to adipogenic induction. The overexpression of MCEE enhanced the proliferation and adipogenic differentiation of porcine intramuscular preadipocytes, whereas its knockdown exerted the opposite effect. Transcriptomic analysis revealed that DEGs were primarily enriched in pathways related to oxidative phosphorylation, mitochondrial dysfunction-associated disorders and others. Subcellular localization prediction indicated mitochondrial targeting of MCEE, and its expression level influenced mitochondrial function, including reactive oxygen species levels, mitochondrial membrane potential and permeability transition pore opening. Collectively, MCEE regulates IMF deposition by modulating mitochondrial function, and these findings provide a potential molecular target for improving meat quality.