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在果蝇胚胎发育过程中,盾片的致死需要无女儿基因的过表达来引发异位神经元发育。

Lethal of scute requires overexpression of daughterless to elicit ectopic neuronal development during embryogenesis in Drosophila.

作者信息

Giebel B, Stüttem I, Hinz U, Campos-Ortega J A

机构信息

Institut für Entwicklungsbiologie, Universität zu Köln, Germany.

出版信息

Mech Dev. 1997 Apr;63(1):75-87. doi: 10.1016/s0925-4773(97)00029-4.

Abstract

Classical genetics indicates that the achaete-scute gene complex (AS-C) of Drosophila promotes development of neural progenitor cells. To further analyze the function of proneural genes, we have studied the effects of Gal4-mediated expression of lethal of scute, a member of the AS-C, during embryogenesis. Expression of lethal of scute forces progenitor cells of larval internal sensory organs, which are normally committed to this fate independently of the activity of the AS-C, to take on features of external sensory organs. Supernumerary neural cells can be induced ectopically only if daughterless is overexpressed, either alone or together with lethal of scute: cells of the amnioserosa and the hindgut then express neuronal markers. Furthermore, cells of the proctodeal anlage, which normally lack neural competence, acquire the ability to develop as neuroblasts following transplantation into the neuroectoderm. We show here that activated Notch prevents the cells of the neuroectoderm from forming extra neural tissue when they express an excess of proneural proteins. Under the present conditions, lateral inhibition is thus dominant over the activity of proneural genes.

摘要

经典遗传学表明,果蝇的无刚毛-毛缘基因复合体(AS-C)促进神经祖细胞的发育。为了进一步分析原神经基因的功能,我们研究了在胚胎发育过程中,由Gal4介导的AS-C成员之一scute致死基因的表达所产生的影响。scute致死基因的表达使幼虫内部感觉器官的祖细胞呈现外部感觉器官的特征,而这些祖细胞通常独立于AS-C的活性而决定其命运。只有当无女儿基因单独或与scute致死基因一起过表达时,才能异位诱导出多余的神经细胞:羊膜和后肠的细胞随后会表达神经元标记。此外,通常缺乏神经能力的原肛原基细胞,在移植到神经外胚层后,获得了发育成神经母细胞的能力。我们在此表明,激活的Notch可防止神经外胚层细胞在表达过量原神经蛋白时形成额外的神经组织。因此,在当前条件下,侧向抑制作用强于原神经基因的活性。

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