ArticleFish physiology and biochemistry2025
Functional Analysis of the mstn1 Gene and Its Transcriptional Regulation by Mef2 Factors in Yellowfin Seabream, Acanthopagrus latus (Hottuyn, 1782).
Article in Fish physiology and biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Myocyte Enhancer Factor 2 (Mef2) is a transcription factor that exert crucial functions in muscle cells, neurons and other cell types. These Mef2 family members modulate the expression of target genes to participate in a broad spectrum of biological processes, such as, but not restricted to, muscle differentiation and heart development. Myostatin (mstn), a protein from the Transforming Growth Factor-β (TGF-β) superfamily, is of great significance in muscle growth and development. Its principal function lies in suppressing the proliferation and differentiation of skeletal muscle cells, thus controlling muscle mass. In this study, we obtained the genomic sequence of mstn1 from Acanthopagrus latus, which is 2,198 bp in length and encodes 384 amino acids. It consists of three distinct domains: a TGF-β domain, a TGF-β propeptide domain and a signal peptide. Through phylogenetic analysis, it was found that mstn1 and mstn2 from A. latus are closely grouped with those from Sparus aurata, which implies a high level of similarity between the two species. Additionally, mstn1 was mainly expressed in the brain, white muscle, and skin. To further investigate the regulatory mechanisms underlying mstn1 in muscle growth, we analyzed the transcriptional levels of mstn1 in white muscle under conditions of starvation and refeeding. The results indicated that during the 56-day experimental period, the expression of the mstn1 gene decreased notably as the starvation period extended. Truncation experiments revealed that the region from - 645 to + 112 bp constitutes the core promoter region responsive to Mef2a and Mef2b. The point mutation analysis verified that the transcriptional activity of mstn1 is contingent upon the mutation of binding site 3 (M3) regulated by Mef2a and Mef2b. Moreover, siRNA-mediated knockdown experiments demonstrated that downregulation of mef2a or mef2b significantly decreased the transcription of mstn1. These findings provide novel insights into how Mef2 transcription factors regulate mstn1 expression, enhancing our understanding of the molecular mechanisms underlying muscle development in teleost fish.
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