Teuliere Jerome, Garriga Gian
Department of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, CA, USA.
Results Probl Cell Differ. 2017;61:141-163. doi: 10.1007/978-3-319-53150-2_6.
Apoptosis is a form of programmed cell death used by metazoans to eliminate abnormal cells, control cell number, and shape the development of organs. The use of the nematode Caenorhabditis elegans as a model for the study of apoptosis has led to important insights into how cells die and how their corpses are removed. Eighty percent of these apoptotic cell deaths occur during nervous system development and in daughters of neuroblasts that divide asymmetrically. Pioneering work defined a conserved apoptosis pathway that is initiated in C. elegans by the BH3-only protein EGL-1 and that leads to the activation of the caspase CED-3. While the execution of the apoptotic fate is well understood, much less is known about the mechanisms that specify the apoptotic fate of particular cells. In some cells fated to die, this regulation occurs at the level of the egl-1 gene transcription, and investigators have identified several lineage-specific transcription factors that both positively and negatively regulate egl-1. In this review, we focus on a second set of molecules that appear to influence apoptosis by controlling the position of the cleavage plane in divisions that produce apoptotic cells.
细胞凋亡是后生动物用于清除异常细胞、控制细胞数量并塑造器官发育的一种程序性细胞死亡形式。利用线虫秀丽隐杆线虫作为细胞凋亡研究模型,使人们对细胞如何死亡以及其尸体如何被清除有了重要的认识。这些凋亡性细胞死亡的80%发生在神经系统发育过程中以及不对称分裂的神经母细胞的子代细胞中。开创性的工作确定了一条保守的细胞凋亡途径,该途径在秀丽隐杆线虫中由仅含BH3结构域的蛋白EGL-1启动,并导致半胱天冬酶CED-3的激活。虽然凋亡命运的执行已得到很好的理解,但对于指定特定细胞凋亡命运的机制却知之甚少。在一些注定要死亡的细胞中,这种调节发生在egl-1基因转录水平,研究人员已经鉴定出几种对egl-1起正向和负向调节作用的谱系特异性转录因子。在这篇综述中,我们关注另一组分子,它们似乎通过控制产生凋亡细胞的分裂中切割平面的位置来影响细胞凋亡。