Calcium and reactive oxygen species in regulation of the mitochondrial permeability transition and of programmed cell death in yeast.
Calcium and reactive oxygen species in regulation of the mitochondrial permeability transition and of programmed cell death in yeast.
复制标题
DOI：
10.1016/j.ceca.2016.03.005
复制
发表时间：
2016-08
期刊：
影响因子：
4
通讯作者：
Bernardi P
中科院分区：
文献类型：
--
作者：
Carraro M;Bernardi P
酵母线粒体依赖性程序性细胞死亡(PCD)与哺乳动物固有的细胞凋亡途径有许多相似之处。在多种刺激下，胞浆内[Ca~(2+)]和ROS的生成增加是导致线粒体通透性和促凋亡因子释放的触发信号，从而启动酵母PCD。在哺乳动物中，通透性转换孔(PTP)是一种由基质钙离子和氧化应激激活的高电导内膜通道，被认为是这种信号级联反应的一部分，但在酵母中是否存在类似的过程仍存在争议。PTP在酵母PCD中的潜在作用通常被忽视，因为酵母线粒体缺乏钙单一转运体，在哺乳动物中，这种单一转运体允许细胞内钙与基质快速平衡。在这篇简短的综述中，我们讨论了酵母通透性转换的本质，并重新评估了它在由钙离子和氧化应激触发的酵母PCD效应阶段的潜在作用。
Mitochondria-dependent programmed cell death (PCD) in yeast shares many features with the intrinsic apoptotic pathway of mammals. With many stimuli, increased cytosolic [Ca2+] and ROS generation are the triggering signals that lead to mitochondrial permeabilization and release of proapoptotic factors, which initiates yeast PCD. While in mammals the permeability transition pore (PTP), a high-conductance inner membrane channel activated by increased matrix Ca2+ and oxidative stress, is recognized as part of this signaling cascade, whether a similar process occurs in yeast is still debated. The potential role of the PTP in yeast PCD has generally been overlooked because yeast mitochondria lack the Ca2+ uniporter, which in mammals allows rapid equilibration of cytosolic Ca2+ with the matrix. In this short review we discuss the nature of the yeast permeability transition and reevaluate its potential role in the effector phase of yeast PCD triggered by Ca2+ and oxidative stress.