Borycki A G, Strunk K E, Savary R, Emerson C P
Department of Cell and Developmental Biology, University of Pennsylvania School of Medicine, Philadelphia 19104-6058, USA.
Dev Biol. 1997 May 15;185(2):185-200. doi: 10.1006/dbio.1997.8555.
Pax1 and QmyoD are early sclerotome and myotome-specific genes that are activated in epithelial somites of quail embryos in response to axial notochord/neural tube signals. In situ hybridization experiments reveal that the developmental kinetics of activation of pax1 and QmyoD differ greatly, suggesting that myotome and sclerotome specification are controlled by distinct developmental mechanisms. pax1 activation always occurs in somite IV throughout development, indicating that pax1 regulation is tightly coordinated with early steps in somite maturation. In contrast, QmyoD is delayed and does not occur until embryos have 12-14 somites. At this time, QmyoD is the first of the myogenic regulatory factor (MRF) genes to be activated in preexisting somites in a rapid, anterior to posterior progression until the 22 somite stage, after which time QmyoD is activated in somite I immediately following somite formation. Experiments involving transplantation of newly formed somites to ectopic sites along the anterior to posterior embryonic axis were performed to distinguish the contributions of axial signals and somite response pathways to the developmental regulation of pax1 and QmyoD. These studies show that pax1 activation is regulated by somite formation and maturation, not by the availability of axial signals, which are expressed prior to somite formation. In contrast, the delayed activation of QmyoD is controlled by developmental regulation of the production of axial signals as well as by the competence of somites to respond to these signals. These somite transplantation studies, therefore, provide a basis for understanding the different developmental kinetics of activation of pax1 and QmyoD during sclerotome and myotome specification, and suggest specific molecular models for the developmental regulation of myotome and sclerotome formation in somites through distinct signal/response pathways.
Pax1和QmyoD是早期体节和生肌节特异性基因，在鹌鹑胚胎的上皮体节中，它们会响应轴向脊索/神经管信号而被激活。原位杂交实验表明，pax1和QmyoD的激活发育动力学差异很大，这表明生肌节和体节的特化是由不同的发育机制控制的。在整个发育过程中，pax1的激活总是发生在第四体节，这表明pax1的调控与体节成熟的早期步骤紧密协调。相比之下，QmyoD的激活则延迟，直到胚胎有12 - 14个体节时才会发生。此时，QmyoD是第一个在已有的体节中被激活的生肌调节因子（MRF）基因，它以快速的从前向后的顺序激活，直到22体节阶段，此后QmyoD在体节形成后立即在第一体节中被激活。为了区分轴向信号和体节反应途径对pax1和QmyoD发育调控的贡献，进行了将新形成的体节移植到胚胎前后轴异位部位的实验。这些研究表明，pax1的激活受体节形成和成熟的调控，而不是受在体节形成之前就已表达的轴向信号可用性的调控。相比之下，QmyoD的延迟激活受轴向信号产生的发育调控以及体节对这些信号作出反应的能力的控制。因此，这些体节移植研究为理解在体节和生肌节特化过程中pax1和QmyoD激活的不同发育动力学提供了基础，并提出了通过不同信号/反应途径对体节中生肌节和体节形成进行发育调控的具体分子模型。
