Skeletal muscle is the most abundant tissue in teleost and represents the primary edible component in aquaculture species such as Atlantic salmon (Salmo salar). In recent years, a pathological condition characterized by discoloured lesions in the muscle, referred to as melanised focal changes (MFCs), has emerged as a significant quality concern in farmed salmonids. Although MFCs were first documented in 2005 and have been studied extensively in the Norwegian salmon industry, their increasing occurrence in Chilean aquaculture has raised serious concerns. These lesions lead to substantial economic losses due to the downgrading of affected products, while their underlying causes remain under active investigation. In this study, we employed an integrative approach combining transcriptomic profiling, oxidative stress analysis and apoptosis assessments to elucidate the pathways involved in MFC development. Skeletal muscle was obtained from the thoracic region with and without focal melanosis (MFC) from Atlantic Salmon (Salmo salar) from a processing plant in Puerto Montt, Chile. Total RNA was extracted from the skeletal muscle samples using the “Direct-zol RNAMiniprep Plus” kit, for construction of cDNA libraries using the Truseq RNA Library prep kit V2, subsequently sequencing using the Illumina Novaseq6000 platform (150bp PE). RNA-seq analysis revealed 2,084 transcripts upregulated in the MFC group, primarily enriched in pathways related to cytokine–cytokine receptor interaction, C-type lectin receptor signaling, and NOD-like receptor signaling. Conversely, 337 transcripts were downregulated, predominantly associated with autophagy, insulin signaling, and mTOR signaling pathways. RT-qPCR validation of selected differentially expressed genes, alongside oxidative damage measurements and western blot analysis of caspase-cleaved proteins, confirmed elevated oxidative stress, inflammation, and apoptosis in MFC-affected muscle. Our results propose a model wherein MFCs originate from unresolved oxidative damage and sustained inflammation, with pigment production potentially functioning as an adaptive redox-buffering mechanism. This study advances our understanding of the immunometabolic basis of muscle melanisation and identifies potential molecular targets for mitigation strategies in salmonid aquaculture.
Funding: FONDECYT POSTDOCTORAL 3230212; FONDECYT 1230794; FONDAP 1522A0004; FONDAP1523A0007.