Cell death in neural precursor cells and neurons before neurite formation prevents the emergence of abnormal neural structures in the Drosophila optic lobe.
Cell death in neural precursor cells and neurons before neurite formation prevents the emergence of abnormal neural structures in the Drosophila optic lobe.
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神经前体细胞和神经元在神经突形成之前的细胞死亡可以防止果蝇视叶中异常神经结构的出现。
DOI：
10.1016/j.ydbio.2018.02.004
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发表时间：
2018
影响因子：
2.7
通讯作者：
Hiromi Akagawa and Hidenobu Tsujimura
中科院分区：
文献类型：
--
作者：
Yusuke Hara;Tatsuya Sudo;Yu Togane;Hiromi Akagawa and Hidenobu Tsujimura
程序性细胞死亡是脊椎动物和无脊椎动物神经发育的保守策略，并且在从神经发生到成年的脑中的各个发育阶段被识别。为了理解中枢神经系统的发育，不仅要揭示分子机制，而且要揭示神经细胞死亡的作用（Pinto-Teixeira et al.，2016年）。为了了解细胞死亡在神经发育中的作用，我们研究了抑制细胞死亡对视叶发育的影响。我们的数据表明，在视叶ofDrosophila，细胞死亡发生在神经前体细胞和神经元轴突形成和功能，以防止各种发育异常之前。当神经元细胞死亡被效应半胱天冬酶抑制剂p35抑制时，在视叶发育过程中出现多种异常的神经元结构-例如，扩大或融合的神经末梢，错误的神经元和异常的神经突肿块。细胞死亡的抑制也诱导了板层和髓质发育中的形态发生缺陷-例如，板层和髓质皮质分离失败以及髓质旋转失败。这些缺陷在起始半胱天冬酶dronc的突变体中复制。如果细胞死亡是消除异常神经元结构的一种机制，我们也希望在有尸体清除缺陷的突变体中观察到它们。然而，在这些突变体中没有观察到它们。当用Apoliner观察死细胞膜时，仅在皮质中观察到，而在神经末梢中未观察到。这些结果表明，细胞死亡发生在成熟的神经突起形成之前。此外，我们发现，抑制细胞死亡诱导异位神经上皮细胞，神经母细胞和神经节母细胞在蛹后期阶段，在网站的外部和内部的增殖中心位于早期发育阶段。Caspase-3在增殖中心的神经上皮细胞和神经母细胞中被观察到活化。这些结果表明，细胞死亡是消除构成增殖中心的前体细胞所必需的。这项研究证实了早期神经细胞死亡对确保中枢神经系统正常发育的重要作用。
Programmed cell death is a conserved strategy for neural development both in vertebrates and invertebrates and is recognized at various developmental stages in the brain from neurogenesis to adulthood. To understand the development of the central nervous system, it is essential to reveal not only molecular mechanisms but also the role of neural cell death (Pinto-Teixeira et al., 2016). To understand the role of cell death in neural development, we investigated the effect of inhibition of cell death on optic lobe development. Our data demonstrate that, in the optic lobe ofDrosophila, cell death occurs in neural precursor cells and neurons before neurite formation and functions to prevent various developmental abnormalities. When neuronal cell death was inhibited by an effector caspase inhibitor,p35,multiple abnormal neuropil structures arose during optic lobe development—e.g., enlarged or fused neuropils, misrouted neurons and abnormal neurite lumps. Inhibition of cell death also induced morphogenetic defects in the lamina and medulla development—e.g., failures in the separation of the lamina and medulla cortices and the medulla rotation. These defects were reproduced in the mutant of an initiator caspase,dronc. If cell death was a mechanism for removing the abnormal neuropil structures, we would also expect to observe them in mutants defective for corpse clearance. However, they were not observed in these mutants. When dead cell-membranes were visualized with Apoliner, they were observed only in cortices and not in neuropils. These results suggest that the cell death occurs before mature neurite formation. Moreover, we found that inhibition of cell death induced ectopic neuroepithelial cells, neuroblasts and ganglion mother cells in late pupal stages, at sites where the outer and inner proliferation centers were located at earlier developmental stages. Caspase-3 activation was observed in the neuroepithelial cells and neuroblasts in the proliferation centers. These results indicate that cell death is required for elimination of the precursor cells composing the proliferation centers. This study substantiates an essential role of early neural cell death for ensuring normal development of the central nervous system.
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DOI：
10.1523/jneurosci.0864-16.2016
发表时间：
2016
期刊：
The Journal of Neuroscience
影响因子：
--
作者：
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作者：
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Tabata, Tetsuya
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DOI：
10.1242/dev.129.6.1467
发表时间：
2002
期刊：
Development (Cambridge, England)
影响因子：
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作者：
Peterson,Christian;Carney,GingerE;Taylor,BarbaraJ;White,Kristin
通讯作者：
White,Kristin
影响因子：
4.6
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通讯作者：
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