The role of mitochondria in apoptosis induction in Caenorhabditis elegans: more than just innocent bystanders?

Conradt, Barbara

doi:10.1038/sj.cdd.4401980

Cited by 16 publications

(11 citation statements)

References 24 publications

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“…So far, no irrefutable evidence of the release of Cyt C from the intermembrane space has been found. Also, the involvement of Cyt C in the apoptosome formation in Drosophila is controversial, and some evidence suggests that Cyt C is not necessary (Rolland & Conradt, 2006). The current evidence indicates that the whole process of apoptosis -including the involved proteins and the regulation mechanisms-in crustaceans is far more diverse than has been assumed from the studies with model organisms.…”

Section: The Role Of Mitochondria In Invertebrate Programmed Cell Deamentioning

confidence: 53%

“…In mammals, the active role of mitochondria in apoptosis induction has been wellestablished. In invertebrate models of apoptosis, such as the fly Drosophila melanogaster and the worm C. elegans, the role that mitochondria play during apoptosis and, in particular, during apoptosis initiation is less clear (Rolland & Conradt, 2006). While key regulators of apoptosis in Drosophila and C. elegans have been found in association with mitochondria, the significance of these associations has not been rigorously tested.…”

Section: The Role Of Mitochondria In Invertebrate Programmed Cell Deamentioning

confidence: 99%

See 1 more Smart Citation

Invertebrates Mitochondrial Function and Energetic Challenges

Martínez‐Cruz¹,

Sánchez‐Paz²,

García‐Carreño³

et al. 2012

Bioenergetics

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Section: The Role Of Mitochondria In Invertebrate Programmed Cell Deamentioning

confidence: 53%

Section: The Role Of Mitochondria In Invertebrate Programmed Cell Deamentioning

confidence: 99%

Invertebrates Mitochondrial Function and Energetic Challenges

Martínez‐Cruz¹,

Sánchez‐Paz²,

García‐Carreño³

et al. 2012

Bioenergetics

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“…The mitochondrial contribution to the death program in C. elegans is only recently becoming appreciated (Rolland and Conradt, 2006). In response to a death stimulus, the pro-apoptotic Bcl-2 family protein EGL-1 interacts with CED-9, which is a mitochondria-bound, anti-apoptotic homolog of mammalian Bcl-2 (Fig.1A).…”

Section: Mitochondrial Involvement In Cell Death and Comparison Of Pamentioning

confidence: 99%

Mitochondria in energy-limited states: mechanisms that blunt the signaling of cell death

Hand

Menze

2008

Journal of Experimental Biology

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SUMMARY Cellular conditions experienced during energy-limited states –elevated calcium, shifts in cellular adenylate status, compromised mitochondrial membrane potential – are precisely those that trigger, at least in mammals, the mitochondrion to initiate opening of the permeability transition pore, to assemble additional protein release channels, and to release pro-apoptotic factors. These pro-apototic factors in turn activate initiator and executer caspases. How is activation of mitochondria-based pathways for the signaling of apoptotic and necrotic cell death avoided under conditions of hypoxia, anoxia, diapause, estivation and anhydrobiosis?Functional trade-offs in environmental tolerance may have occurred in parallel with the evolution of diversified pathways for the signaling of cell death in eukaryotic organisms. Embryos of the brine shrimp, Artemia franciscana, survive extended periods of anoxia and diapause, and evidence indicates that opening of the mitochondrial permeability transition pore and release of cytochrome c (cyt-c) do not occur. Further, caspase activation in this crustacean is not dependent on cyt-c. Its caspases display regulation by nucleotides that is consistent with `applying the brakes' to cell death during energy limitation. Unraveling the mechanisms by which organisms in extreme environments avoid cell death may suggest possible interventions during disease states and biostabilization of mammalian cells.

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“…In addition to this ‘direct’ pathway of apoptosis induction, several lines of evidence suggest the existence of an ‘indirect’ pathway involving additional pro-apoptotic factors [30]. First, the inhibition of cell death seen in a weak ced-3 loss-of-function mutation, is enhanced by the loss of ced-9 function [31].…”

Section: Cell Death Pathways In Non-mammalian Models: Mitochondrimentioning

confidence: 99%

Mitochondrial involvement in cell death of non-mammalian eukaryotes

Abdelwahid

Rolland

Teng

et al. 2011

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Although mitochondria are essential organelles for long-term survival of eukaryotic cells, recent discoveries in biochemistry and genetics have advanced our understanding of the requirements for mitochondria in cell death. Much of what we understand about cell death is based on the identification of conserved cell death genes in Drosophila melanogaster and Caenorhabditis elegans. However, the role of mitochondria in cell death in these models has been much less clear. Considering the active role that mitochondria play in apoptosis in mammalian cells, the mitochondrial contribution to cell death in non-mammalian systems has been an area of active investigation. In this article, we review the current research on this topic in three non-mammalian models, C. elegans, Drosophila and Saccharomyces cerevisiae. In addition, we discuss how non-mammalian models have provided important insight into the mechanisms of human disease as they relate to the mitochondrial pathway of cell death. The unique perspective derived from each of these model systems provides a more complete understanding of mitochondria in programmed cell death.

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The role of mitochondria in apoptosis induction in Caenorhabditis elegans: more than just innocent bystanders?

Cited by 16 publications

References 24 publications

Invertebrates Mitochondrial Function and Energetic Challenges

Invertebrates Mitochondrial Function and Energetic Challenges

Mitochondria in energy-limited states: mechanisms that blunt the signaling of cell death

Mitochondrial involvement in cell death of non-mammalian eukaryotes

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