Okamura Y, Ono F, Okagaki R, Chong J A, Mandel G
Department of Neurobiology, Faculty of Medicine, University of Tokyo, Japan.
Neuron. 1994 Oct;13(4):937-48. doi: 10.1016/0896-6273(94)90259-3.
In the protochordate Halocynthia roretzi, voltage-activated sodium current undergoes a change in kinetics within 48 hr of fertilization. Molecular cloning and microinjection of antisense DNA into single cells suggest that the kinetic changes are due to the increased expression of a putative neural-specific sodium channel gene, TuNa I. TuNa I gene transcription is first induced in late stage gastrulae, preceding the appearance of the rapidly inactivating sodium current unique to neural cells. In cleavage-arrested and intact embryos, cell interactions between specific animal and vegetal blastomeres are required for induction of TuNa I gene expression. Our results implicate cell contact, prior to neurulation, as a mechanism for selectively activating the TuNa I gene expressed in cells of the neural lineage.
在原索动物柄海鞘中,电压激活的钠电流在受精后48小时内动力学发生变化。分子克隆以及将反义DNA显微注射到单细胞中表明,动力学变化是由于一种假定的神经特异性钠通道基因TuNa I表达增加所致。TuNa I基因转录首先在原肠胚后期被诱导,早于神经细胞特有的快速失活钠电流的出现。在卵裂阻滞和完整的胚胎中,特定动物和植物卵裂球之间的细胞相互作用是诱导TuNa I基因表达所必需的。我们的结果表明,在神经胚形成之前的细胞接触是一种选择性激活神经谱系细胞中表达的TuNa I基因的机制。