Slow and fast fiber isoform gene expression is systematically altered in skeletal muscle of the Sox6 mutant, p100H
Slow and fast fiber isoform gene expression is systematically altered in skeletal muscle of the Sox6 mutant, p100H
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DOI：
10.1002/dvdy.20535
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发表时间：
2005-10-01
影响因子：
2.5
通讯作者：
Ly, A
中科院分区：
文献类型：
--
作者：
Hagiwara, N;Ma, B;Ly, A
我们之前已经证明，缺乏功能性Sox6基因的p(100h)突变小鼠在出生后不久就会出现骨骼和心肌退化，并出现心脏传导异常。为了了解Sox6在骨骼肌发育中的作用，我们鉴定了野生型和p(100h)突变的骨骼肌中差异表达的肌肉特异基因，并研究了它们在突变肌肉中的时间表达。我们发现，在突变的骨骼肌中，慢纤维和心脏亚型基因的表达水平显著高于野生型，而快纤维亚型基因的表达水平显著低于野生型。突变体中这种异常的纤维类型特异性基因表达的开始与小鼠胚胎第15-16天次级肌管形成的开始一致。结合我们早先的报告，证明了Sox6空-p(100h)突变体在出生后早期肌肉缺陷，目前的结果表明Sox6可能在肌肉发育中发挥重要作用。
We have previously demonstrated that p(100H) mutant mice, which lack a functional Sox6 gene, exhibit skeletal and cardiac muscle degeneration and develop cardiac conduction abnormalities soon after birth. To understand the role of Sox6 in skeletal muscle development, we identified muscle-specific genes differentially expressed between wild-type and p(100H) mutant skeletal muscles and investigated their temporal expression in the mutant muscle. We found that, in the mutant skeletal muscle, slow fiber and cardiac isoform genes are expressed at significantly higher levels, whereas fast fiber isoform genes are expressed at significantly lower levels than wild-type. Onset of this aberrant fiber type-specific gene expression in the mutant coincides with the beginning of the secondary myotube formation, at embryonic day 15-16 in mice. Together with our earlier report, demonstrating early postnatal muscle defects in the Sox6 null-p(100H) mutant, the present results suggest that Sox6 likely plays an important role in muscle development.