肌肉分化：生肌调节因子网络的更多复杂性。

Muscle differentiation: more complexity to the network of myogenic regulators.

作者信息

Arnold H H, Winter B

机构信息

Department of Cell and Molecular Biology, Institute of Biochemistry andBiotechnology, University of Braunschweig, Spielmannstrasse 7, 38106, Braunschweig, Germany.

出版信息

Curr Opin Genet Dev. 1998 Oct;8(5):539-44. doi: 10.1016/s0959-437x(98)80008-7.

DOI:10.1016/s0959-437x(98)80008-7

PMID:9794824

Abstract

Recent genetic and biochemical approaches have advanced our understanding of control mechanisms underlying myogenesis in vertebrate organisms. In particular, systematic combinations of targeted gene disruptions in mice have revealed unique and overlapping functions of members of the MyoD family of transcription factors within the regulatory network that establishes skeletal muscle cell lineages. Moreover, Pax3 has been identified as a key regulator of myogenesis which seems to act genetically upstream of MyoD. In addition, novel genes have been discovered that modulate myogenesis and the activity of myogenic basic helix-loop-helix (bHLH) proteins in positive or negative ways. The molecular mechanisms of these interactions and cooperativity are being elucidated, most notably between the myogenic bHLH factors and MEF2 transcription factors.

摘要

最近的遗传学和生物化学方法增进了我们对脊椎动物机体中肌发生潜在调控机制的理解。特别是，小鼠中靶向基因破坏的系统组合揭示了在建立骨骼肌细胞谱系的调控网络中，肌分化决定因子（MyoD）家族转录因子成员的独特及重叠功能。此外，配对盒基因3（Pax3）已被确定为肌发生的关键调节因子，它似乎在基因层面上作用于MyoD的上游。此外，还发现了一些新基因，它们以正向或负向方式调节肌发生以及肌源性碱性螺旋-环-螺旋（bHLH）蛋白的活性。这些相互作用和协同作用的分子机制正在被阐明，最显著的是在肌源性bHLH因子和肌细胞增强因子2（MEF2）转录因子之间。