Rogulja-Ortmann Ana, Lüer Karin, Seibert Janina, Rickert Christof, Technau Gerhard M
Institute of Genetics, University of Mainz, Saarstrasse 21, D-55122 Mainz, Germany.
Development. 2007 Jan;134(1):105-16. doi: 10.1242/dev.02707.
Although programmed cell death (PCD) plays a crucial role throughout Drosophila CNS development, its pattern and incidence remain largely uninvestigated. We provide here a detailed analysis of the occurrence of PCD in the embryonic ventral nerve cord (VNC). We traced the spatio-temporal pattern of PCD and compared the appearance of, and total cell numbers in, thoracic and abdominal neuromeres of wild-type and PCD-deficient H99 mutant embryos. Furthermore, we have examined the clonal origin and fate of superfluous cells in H99 mutants by DiI labeling almost all neuroblasts, with special attention to segment-specific differences within the individually identified neuroblast lineages. Our data reveal that although PCD-deficient mutants appear morphologically well-structured, there is significant hyperplasia in the VNC. The majority of neuroblast lineages comprise superfluous cells, and a specific set of these lineages shows segment-specific characteristics. The superfluous cells can be specified as neurons with extended wild-type-like or abnormal axonal projections, but not as glia. The lineage data also provide indications towards the identities of neuroblasts that normally die in the late embryo and of those that become postembryonic and resume proliferation in the larva. Using cell-specific markers we were able to precisely identify some of the progeny cells, including the GW neuron, the U motoneurons and one of the RP motoneurons, all of which undergo segment-specific cell death. The data obtained in this analysis form the basis for further investigations into the mechanisms involved in the regulation of PCD and its role in segmental patterning in the embryonic CNS.
尽管程序性细胞死亡(PCD)在果蝇中枢神经系统发育过程中起着至关重要的作用,但其模式和发生率在很大程度上仍未得到研究。我们在此对胚胎腹神经索(VNC)中PCD的发生情况进行了详细分析。我们追踪了PCD的时空模式,并比较了野生型和PCD缺陷型H99突变胚胎的胸段和腹段神经节中PCD的出现情况及细胞总数。此外,我们通过用DiI标记几乎所有神经母细胞,研究了H99突变体中多余细胞的克隆起源和命运,特别关注了在个体识别的神经母细胞谱系内的节段特异性差异。我们的数据显示,尽管PCD缺陷型突变体在形态上结构良好,但VNC中存在明显的细胞增生。大多数神经母细胞谱系包含多余细胞,并且其中一组特定的谱系表现出节段特异性特征。多余细胞可被指定为具有类似野生型延长或异常轴突投射的神经元,但不是神经胶质细胞。谱系数据还为正常情况下在胚胎后期死亡的神经母细胞以及那些成为胚胎后并在幼虫中恢复增殖的神经母细胞的身份提供了线索。使用细胞特异性标记,我们能够精确识别一些子代细胞,包括GW神经元、U运动神经元和其中一个RP运动神经元,所有这些细胞都经历节段特异性细胞死亡。该分析中获得的数据为进一步研究PCD调控机制及其在胚胎中枢神经系统节段模式形成中的作用奠定了基础。