Yue Feng

Porcine reproductive and respiratory syndrome virus is a major pathogen that causes massive economic losses in the global swine industry. Lysine propionylation and malonylation are metabolism-sensitive post-translational modifications, yet their coordinated regulatory roles during PRRSV pulmonary infection remain unknown. This study combined quantitative proteomics, propionylome and malonylome to characterize host molecular alterations between healthy and PRRSV-infected porcine lung tissues (three piglets per group). Quantitative proteomics identified 1467 significantly downregulated proteins and only 129 upregulated proteins, indicating a profound host protein shutoff during PRRSV pulmonary infection. The two acyl modifications displayed opposite regulatory patterns independent of global protein expression changes: 51 propionylation sites (24 proteins) were upregulated with only 1 downregulated, while 37 malonylation sites (30 proteins) were downregulated and only 5 upregulated. Functional enrichment and PPI network analysis revealed clear functional divergence: hyper-propionylated hub proteins were exclusively enriched in mitochondrial energy metabolism pathways, whereas hypo-malonylated core proteins were mainly involved in lipid metabolism and cell fate regulation. Integrated multi-omics analysis confirmed that protein expression and lysine acylation constitute two coordinated but independent regulatory layers, with histone H4 identified as a candidate target of competitive propionylation/malonylation. This work reports the comprehensive landscape of lysine propionylation and malonylation upon PRRSV infection, reveals a dual-PTM remodeling strategy for viral hijacking of host homeostasis, and provides candidate targets for future functional investigation and antiviral development.

Ubiquitous environmental endocrine-disrupting chemicals (EDCs), including bisphenols, phthalates, and heavy metals, pose a severe and persistent threat to mammalian reproductive health worldwide. Oxidative stress acts as the pivotal mediator which drives epigenetic dysregulation in germ cells upon EDC exposure, including aberrant DNA methylation, abnormal histone post-translational modifications and dysregulated non-coding RNA networks. EDC-induced oxidative stress damages endogenous antioxidant defense systems and inactivates key epigenetic regulators, forming a self-reinforcing cycle of redox imbalance and epigenetic dysregulation, which ultimately leads to impaired gametogenesis, reduced fertility, and transgenerational reproductive abnormalities. This review summarizes current evidence indicating that multiple antioxidants, including melatonin, vitamin C, resveratrol, and epigallocatechin gallate, alleviate EDC-induced reproductive toxicity by targeting epigenetic dysregulation. Their protective effects encompass scavenging excessive reactive oxygen species, activating endogenous antioxidant signaling cascades, restoring activity of epigenetic enzymes, and rectifying aberrant histone modification profiles, contributing to the maintenance of epigenetic homeostasis in germ cells. This review clarifies the intrinsic mechanistic link among EDC exposure, oxidative stress, epigenetic dysregulation and reproductive toxicity, which provides a theoretical basis for formulating reproductive health protection strategies against EDC exposure and guides the exploration of clinical epigenetic biomarkers.

Semen quality is the most crucial indicator for evaluating the reproductive capacity of boars. Semen traits, including semen volume, sperm density, motility and abnormality rate, exhibit low to moderate heritability, making genetic improvement through conventional breeding challenging. Advances in genome sequencing have enabled GWAS to identify genetic markers for economically important traits. In this study, 172 Large White boars with 56,427 phenotypic records across seven semen quality traits were subjected to 15× whole‐genome resequencing. GWAS was performed using the FarmCPU model, identifying 2824 significant SNPs and annotating 573 candidate genes associated with seven semen traits. After linkage disequilibrium (LD)‐based clumping (r ² < 0.1, 1 Mb window), 916 independent genomic loci were identified as significantly associated with the seven semen quality traits. Functional analysis revealed key biological processes, including growth regulation, extrinsic apoptotic signalling pathway and the TOR signalling pathway. In an expanded population, six SNPs associated with semen quality traits were identified in the SOX6, CACNA1H, FOXP4, EFNA3 and ITGA9 genes. Significant associations were found between SOX6 gene and sperm abnormality rate, CACNA1H gene and semen volume, sperm density, motility, and abnormality rate, FOXP4 gene and sperm density, EFNA3 gene and semen volume, sperm density, ITGA9 gene and semen volume, sperm density, motility, and abnormality rate. These findings enhance understanding of the genetic architecture of boar semen quality and provide molecular markers for genetic selection, facilitating improved breeding strategies.

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.

Post-translational modifications (PTMs) of proteins, as the core mechanism for dynamically regulating follicular development, affect the maintenance of mammalian fertility by precisely coordinating granulosa cell–oocyte interaction, metabolic reprogramming, and epigenetic remodeling. Dysregulation of these modifications directly contributes to major reproductive diseases, including polycystic ovary syndrome (PCOS) and premature ovarian insufficiency (POI). Post-translational modifications regulate follicular development through intricate mechanisms. Thus, this review systematically synthesizes recent advances in PTMs, encompassing traditional ones such as phosphorylation, ubiquitination, and acetylation, alongside emerging modifications including lactylation, SUMOylation, and ISGylation, thereby constructing a more comprehensive PTM landscape of follicular development. Furthermore, this study dissects the molecular interaction networks of these PTMs during follicular activation, maturation, and ovulation, and uncovers the common mechanisms through which PTM dysregulation contributes to pathological conditions, including hyperandrogenism in PCOS and follicular depletion in POI. Finally, this review ultimately provides a theoretical basis for improving livestock reproductive efficiency and precise intervention in clinical ovarian diseases.