| Summary: | 碩士 === 國立嘉義大學 === 生物農業科技學系研究所 === 104 === Mstn gene is a transforming growth factor-β family member, and acts as a negative regulator of skeletal muscle mass. Over-expression of Mstn gene significantly decreases the skeletal muscle cell growth and differentiation, while the lack of Mstn expression increases skeletal muscle. For example, the famous Belgian Blue cattle strains with doubling muscle mass is exactly due to the mutation of Mstn gene. Contrarily, Four and a half LIM domain 1 (Fhl1) gene promotes cell fusion and tube formation, while the lack of Fhl1 expression reduces muscle tube in skeletal muscle. For example, FHL1 gene mutation shave been reported in human clinical myopathy, reducing body myopathy, X-linked dominant scapuloperoneal myopathy (SPM) and hypertrophic cardiomyopathy (HCM). These mutations have been further verified in cell or animal models those can cause muscle atrophy and dysfunction, and eventually lead to diseases. Because Mstn and Fhl1 are functional oppositely, in this study we attempted to investigate the relationship between Mstn and Fhl1 in muscle cell development. Basically, I modulated the green expression of Mstn and Fhl1, either over-expression or down-expression of each of them, or overexpressed both genes in C2C12 cells. Their differentiation statues were compared by the marker gene expression, such as MyoD, Myogenin (MyoG) and Myosin heavy chain (MyHC), examined by real time RT-PCR, as well as by immunohistochemistry and Western blot. Interestingly, it seemed that a clever mechanism of regulated exists between Mstn and Fhl1 because when cell differentiation is stimulated by overexpressed Fhl1, the expression of Mstn is also increased. On the other hand, once the cell differentiation is inhibited by overexpressed Mstn, the expression of Fhl1 is also increased as well. However, when cells are co-overexpressed by Mstn and Fhl1, cell differentiation is similar to the control, implying that Mstn and Fhl1 regulated the expression of each other, in turn to make the cell differentiation in balance.
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