Hedgehog signalling is required for maintenance of myf5 and myoD expression and timely terminal differentiation in zebrafish adaxial myogenesis
Hedgehog signalling is required for maintenance of myf5 and myoD expression and timely terminal differentiation in zebrafish adaxial myogenesis
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DOI：
10.1006/dbio.2001.0193
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发表时间：
2001-08-01
影响因子：
2.7
通讯作者：
Hughes, SM
中科院分区：
文献类型：
--
作者：
Coutelle, O;Blagden, CS;Hughes, SM
Hedgehog蛋白参与了脊椎动物体节中肌细胞发生的调控。在小鼠中，生肌转录因子基因myf 5的正常轴上表达依赖于Sonic hedgehog。在这里，我们研究在斑马鱼的刺猬信号，myoD家族基因的表达，包括新克隆的斑马鱼myf 5，和缓慢的肌肉发生之间的相互作用。我们发现，Sonic hedgehog是必要的myf 5和myoD在近轴慢肌前体的正常表达，但不是在侧旁轴中胚层。这两个基因的表达通常在缺少所有Sonic hedgehog的Sonic you突变体的吻端前体中胚层中启动。在尾芽生长过程中，当形成尾体节的细胞产生时，类似的起始继续进行。然而，近轴细胞在声波你胚胎的终末分化延迟和尾部近轴细胞不能维持生肌调节因子的表达。尽管有这些缺陷，其他信号能够维持，或重新启动，一些缓慢的肌肉发育在音速你突变体。在剑水蚤突变体中，没有地板衍生的Tiggywinkle刺猬和Sonic刺猬对缓慢的近轴肌发生没有明显的影响。类似地，缺乏脊索衍生的Sonic hedgehog和Echidna hedgehog的突变体缺乏脊索延迟，但不阻止，近轴缓慢肌肉发育。相比之下，从独眼巨人的胚胎中线去除声波刺猬和地板信号，可能是Tiggywinkle刺猬;声波你双突变体基本上废除了缓慢的肌发生。我们的结论是，几个中线信号，可能是各种刺猬，合作，以维持近轴缓慢的肌肉发生在斑马鱼胚胎。此外，数据表明，在缺乏这种所需的Hedgehog信号传导的情况下，myf 5和myoD的表达不足以使细胞进行近轴肌发生。(C)北京：科学出版社.
Hedgehog proteins have been implicated in the control of myogenesis in the medial vertebrate somite. In the mouse, normal epaxial expression of the myogenic transcription factor gene myf5 is dependent on Sonic hedgehog. Here we examine in zebrafish the interaction between Hedgehog signals, the expression of myoD family genes, including the newly cloned zebrafish myf5, and slow myogenesis. We show that Sonic hedgehog is necessary for normal expression of both myf5 and myoD in adaxial slow muscle precursors, but not in lateral paraxial mesoderm. Expression of both genes is initiated normally in rostral presomitic mesoderm in sonic you mutants, which lack all Sonic hedgehog. Similar initiation continues during tailbud outgrowth when the cells forming caudal somites are generated. However, adaxial cells in sonic you embryos are delayed in terminal differentiation and caudal adaxial cells fail to maintain myogenic regulatory factor expression. Despite these defects, other signals are able to maintain, or reinitiate, some slow muscle development in sonic you mutants. In the cyclops mutant, the absence of floorplate-derived Tiggywinkle hedgehog and Sonic hedgehog has no discernible effect on slow adaxial myogenesis. Similarly, the absence of notochord-derived Sonic hedgehog and Echidna hedgehog in mutants lacking notochord delays, but does not prevent, adaxial slow muscle development. In contrast, removal of both Sonic hedgehog and a floorplate signal, probably Tiggywinkle hedgehog, from the embryonic midline in cyclops;sonic you double mutants essentially abolishes slow myogenesis. We conclude that several midline signals, likely to be various Hedgehogs, collaborate to maintain adaxial slow myogenesis in the zebrafish embryo. Moreover, the data demonstrate that, in the absence of this required Hedgehog signalling, expression of myf5 and myoD is insufficient to commit cells to adaxial myogenesis. (C) 2001 Academic Press.