Programmed cell death in Leishmania: biochemical evidence and role in parasite infectivity.
Programmed cell death in Leishmania: biochemical evidence and role in parasite infectivity.
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DOI：
10.3389/fcimb.2012.00095
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发表时间：
2012
影响因子：
5.7
通讯作者：
Debrabant A
中科院分区：
文献类型：
--
作者：
Gannavaram S;Debrabant A
原生动物寄生虫程序性细胞死亡（PCD）途径的研究引起了分子寄生虫学领域的广泛关注和争论。在利什曼原虫中发现了几种典型的哺乳动物细胞凋亡标记，这表明在这些生物中存在类似细胞凋亡的死亡。然而，阐明与磷脂酰丝氨酸暴露、线粒体膜电位丧失、细胞色素c释放和发生这种细胞死亡的细胞中caspase样活性相关的下游事件的研究仍然是一个持续的挑战。基因组测序和化学生物学的最新进展应该有助于解决其中的一些挑战。利什曼原虫基因突变体缺乏PCD途径的调节因子/效应物，这不仅有助于证明PCD的机制，而且还为更好地理解该途径在种群控制和建立成功的宿主感染中的假定作用提供了工具。
Demonstration of features of a programmed cell death (PCD) pathway in protozoan parasites initiated a great deal of interest and debate in the field of molecular parasitology. Several of the markers typical of mammalian apoptosis have been shown in Leishmania which suggested the existence of an apoptosis like death in these organisms. However, studies to elucidate the downstream events associated with phosphotidyl serine exposure, loss of mitochondrial membrane potential, cytochrome c release, and caspase-like activities in cells undergoing such cell death remain an ongoing challenge. Recent advances in genome sequencing, chemical biology should help to solve some of these challenges. Leishmania genetic mutants that lack putative regulators/effectors of PCD pathway should not only help to demonstrate the mechanisms of PCD but also provide tools to better understand the putative role for this pathway in population control and in the establishment of a successful infection of the host.
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