Transcriptomic profiling of skeletal muscle reveals candidate genes influencing muscle growth and associated lipid composition in Portuguese local pig breeds

• Autor(a) principal: Albuquerque, A.
• Data de Publicação: 2021
• Outros Autores: Óvilo, C., Núñez, Y., Benítez, R., López-Garcia, A., Félix, M.R., Laranjo, M., Charneca, R., Martins, J.M.
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• Texto Completo: http://hdl.handle.net/10174/30201; https://doi.org/10.3390/ani11051423
• topic: Alentejano pig; Bísaro pig; transcriptome; skeletal muscle; meat quality; intramuscular fat; MYH3; MYH7; MAP3K14

Gene expression is one of the main factors to influence meat quality by modulating fatty acid metabolism, composition, and deposition rates in muscle tissue. This study aimed to explore the transcriptomics of the Longissimus lumborum muscle in two local pig breeds with distinct genetic background using next-generation sequencing technology and Real-Time qPCR. RNA-seq yielded 49 differentially expressed genes between breeds, 34 overexpressed in the Alentejano (AL) and 15 in the Bísaro (BI) breed. Specific slow type myosin heavy chain components were associated with AL (MYH7) and BI (MYH3) pigs, while an overexpression of MAP3K14 in AL may be associated with their lower loin proportion, induced insulin resistance, and increased inflammatory response via NFkB activation. Overexpression of RUFY1 in AL pigs may explain the higher intramuscular (IMF) content via higher GLUT4 recruitment and consequently higher glucose uptake that can be stored as fat. Several candidate genes for lipid metabolism, excluded in the RNA-seq analysis due to low counts, such as ACLY, ADIPOQ, ELOVL6, LEP and ME1 were identified by qPCR as main gene factors defining the processes that influence meat composition and quality. These results agree with the fatter profile of the AL pig breed and adiponectin resistance can be postulated as responsible for the overexpression of MAP3K140s coding product NIK, failing to restore insulin sensitivity.