The Mitochondrial Fission Protein hFis1 Requires the Endoplasmic Reticulum Gateway to Induce Apoptosis

Alirol, Emilie; James, Dominic I.; Huber, Denise; Marchetto, Andrea; Vergani, Lodovica; Martinou, Jean‐Claude; Scorrano, Luca

doi:10.1091/mbc.e06-05-0377

Cited by 120 publications

(107 citation statements)

References 53 publications

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“…In this work, it was demonstrated that expression of fission dead Fis1 could still induce cell death. When the apoptotic dead mutant of Fis1 was expressed, mitochondria could still undergo fission but there is no induction of cell death [73]. Overall, these results show that although fission is required for cell death, fission in itself was not sufficient for cell death induction.…”

Section: What Is the Role Of Mitochondrial Fission In Cell Death?mentioning

confidence: 83%

Mitochondrial dynamics in the regulation of neuronal cell death

2007

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Mitochondria undergo continuous fission and fusion events in physiological situations. Fragmentation of mitochondria during cell death has been shown to play a key role in cell death progression, including release of the mitochondrial apoptotic proteins. Ultrastructural changes in mitochondria, such as cristae remodeling, is also involved in cell death initiation. Here, we emphasize the important role of mitochondrial fission/fusion machinery in neuronal cell death. Unlike many other cell types such as immortalized cell lines, neurons are distinct morphologically and functionally. We will discuss how this uniqueness presents special challenges in the cellular response to neurotoxic stresses, and how this affects the mitochondrial dynamics in the regulation of cell death in neurons.

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Section: What Is the Role Of Mitochondrial Fission In Cell Death?mentioning

confidence: 83%

Mitochondrial dynamics in the regulation of neuronal cell death

2007

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“…Overexpression of the mitochondrial fission protein Fis-1 induces apoptosis in some cell types, which suggests that mitochondrial fission may be a driver of apoptosis (Alirol et al, 2006;James et al, 2003;Yu et al, 2005).…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

Mitochondrial fission/fusion dynamics and apoptosis

2010

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Mitochondria play an important role in the progression of apoptosis through the release of pro-apoptotic factors, such as cytochrome c, from the mitochondrial intermembrane space.During this process, mitochondrial networks are dramatically reorganised from long filamentous interconnected tubules into small punctate spheres. Whether remodelling of mitochondrial networks is necessary for apoptosis-associated cytochrome c release, or merely an accompanying process, has been a subject of debate. Here we discuss evidence for and against the role of mitochondrial fragmentation in the progression of apoptosis and highlight recent advances which indicate that mitochondrial fission is not a critical requirement for apoptosis-associated cytochrome c release. We also discuss an emerging role for Bcl-2 family members as regulators of mitochondrial fission and fusion dynamics, independent of the role of this family in the regulation of apoptosis.

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“…Concomitantly, Drp1 and hFis1 levels are elevated in early apoptosis in cultured cardiomyocytes (Parra et al, 2008;Ong et al, 2010) and in heart failure model as well (Chen et al, 2009). Drp1 (Frank et al, 2001;Lee et al, 2004) and hFis1 (Lee et al, 2004;Alirol et al, 2006) participate in the process of cell death. During cardiac myocytes apoptosis, Drp1 translocates to mitochondria from cytosol (Wang et al, 2011a).…”

Section: Mitochondria Mediate Apoptosis In Heartmentioning

confidence: 99%

Mitochondrial network in the heart

Zhou

Gao

et al. 2012

Protein Cell

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Mitochondria are subcellular organelles that provide energy for the cell. They form a dynamic tubular network and play an important role in maintaining the cell function and integrity. Heart is a powerful organ that supplies the motivation for circulation, thereby requiring large amounts of energy. Thus, the healthiness of cardiomyocytes and mitochondria is necessary for the normal cardiac function. Mitochondria not only lie in the center of the cell apoptotic pathway, but also are the major source of reactive oxygen species (ROS) generation. Mitochondrial morphological change includes fission and fusion that are regulated by a large number of proteins. In this review we discuss the regulators of mitochondrial fission/fusion and their association with cell apoptosis, autophagy and ROS production in the heart.

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The Mitochondrial Fission Protein hFis1 Requires the Endoplasmic Reticulum Gateway to Induce Apoptosis

Cited by 120 publications

References 53 publications

Mitochondrial dynamics in the regulation of neuronal cell death

Mitochondrial dynamics in the regulation of neuronal cell death

Mitochondrial fission/fusion dynamics and apoptosis

Mitochondrial network in the heart

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