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首页> 外文期刊>Mechanisms of Development >ventral veins lacking is required for specification of the tritocerebrum in embryonic brain development of Drosophila
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ventral veins lacking is required for specification of the tritocerebrum in embryonic brain development of Drosophila

机译:果蝇胚胎脑发育中三脑的规格要求缺少腹静脉

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摘要

The homeotic or Hox genes encode a network of conserved transcription factors which provide axial positional information and control segment morphology in development and evolution. During embryonic brain development of Drosophila, the Hox gene labial (lab) is essential for tritocerebral neuromere specification; lab loss of function results in tritocerebral cells that fail to adopt a neuronal identity, causing axonal pathfinding defects. Here we present evidence that the POU-homeodomain DNA-binding protein ventral veins lacking (vvl) acts genetically downstream of lab in the specification of the tritocerebral neuromere. In the embryonic brain, vvl expression is seen in all brain neuromeres, including the tritocerebral lab domain. Lab mutant analysis shows that vvl expression in the tritocerebrum is dependent on lab activity. Loss-of-function analysis focussed on the tritocerebrum reveals that inactivation of vvl results in patterning defects which are comparable to the brain phenotype caused by null mutation of lab. In the absence of vvl, mutant tritocerebral cells are generated and positioned correctly, but these cells fail to express neuronal markers indicating defects in neuronal differentiation. Moreover, longitudinal axon pathways in the tritocerebrum are severely reduced or absent and the tritocerebral commissure is missing in the vvl mutant brain. Genetic rescue experiments show that vvl is able to partially replace lab in the specification of the tritocerebral neuromere. Our results indicate that vvl acts downstream of the Hox gene lab and regulates specific aspects of neuronal differentiation within the tritocerebral neuromere during embryonic brain development of Drosophila.
机译:同源或Hox基因编码一个保守的转录因子网络,可在发育和进化过程中提供轴向位置信息并控制片段的形态。在果蝇的胚胎脑发育期间,Hox基因唇(实验室)对于三脑神经的规格至关重要。实验室功能丧失导致三脑细胞无法采用神经元身份,从而导致轴突寻路缺陷。在这里,我们提供的证据表明,缺乏(vvl)的POU-同源域DNA结合蛋白腹侧静脉在三脑神经绒的规范中在实验室的下游起作用。在胚胎脑中,在所有脑神经绒毛中都可以看到vvl表达,包括三脑实验室区域。实验室突变体分析显示,三脑中vvl的表达取决于实验室活动。针对三脑的功能丧失分析表明,vvl的失活导致图案缺陷,可与实验室无效突变引起的脑表型相媲美。在不存在vvl的情况下,会生成突变的三脑细胞并正确定位,但是这些细胞无法表达表明神经元分化缺陷的神经元标记。此外,在vvl突变型大脑中,三角脑中的纵向轴突途径被严重减少或不存在,并且三角脑连合缺失。遗传挽救实验表明,vvl能够部分替代三脑神经绒毛规范中的lab。我们的结果表明,vvl在果蝇胚胎脑发育过程中在Hox基因实验室的下游起作用,并调节三脑神经绒毛内神经元分化的特定方面。

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