Affiliations: 1 Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada.
Keywords:
endonuclease G, viral attenuation, mitochondria, yeast, gametogenesis, programmed cell death
Corresponding Author(s):
Marc D. Meneghini, Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada; marc.meneghini@utoronto.ca
Conflict of interest statement:
The authors declare no conflict of interest.
Please cite this article as:
Jie Gao, Sabrina Chau and Marc D. Meneghini (2019). Viral attenuation by Endonuclease G during yeast gametogenesis: insights into ancestral roles of programmed cell death? Microbial Cell 7(2): 32-35. doi: 10.15698/mic2020.02.705
© 2019 Gao et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduc-tion in any medium, provided the original author and source are acknowledged.
Viral attenuation by Endonuclease G during yeast gametogenesis: insights into ancestral roles of programmed cell death?
Authors:Jie Gao1, Sabrina Chau1 and Marc D. Meneghini1
doi: 10.15698/mic2020.02.705
Volume 7, pp. 32 to 35, published 17/12/2019.
1 Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada.
Keywords:
endonuclease G, viral attenuation, mitochondria, yeast, gametogenesis, programmed cell death
Corresponding Author(s):
Conflict of interest statement:
The authors declare no conflict of interest.
Please cite this article as:
Jie Gao, Sabrina Chau and Marc D. Meneghini (2019). Viral attenuation by Endonuclease G during yeast gametogenesis: insights into ancestral roles of programmed cell death? Microbial Cell 7(2): 32-35. doi: 10.15698/mic2020.02.705
© 2019 Gao et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduc-tion in any medium, provided the original author and source are acknowledged.
Abstract:
Viruses and other genetic parasites are present in virtually all forms of life. This chronic condition has led to diverse host cell adaptations such as CRISPR and RNAi, whose functions attenuate these parasites. It is hypothesized that programmed cell death (PCD) is an additional adaptation whose origins reside in viral defense. A core event of apoptotic PCD is the regulated release of mitochondrial inter-membrane space proteins into the cytosol, following which these apoptogenic proteins bring about the demise of the cell. The most well studied example of this is found in animals, where the release of mitochondrial cytochrome C nucleates the formation of the apoptosome, which then activates caspase mediated cell death. The release of mitochondrial proteins contributes to PCD in diverse organisms lacking the apoptosome, indicating that regulated mitochondrial release predates the evolution of canonical apoptosis. Using the budding yeast Saccharomyces cerevisiae, we recently confirmed an early study showing that Nuc1, a homolog of the mitochondrial apoptotic driver protein Endonuclease G, attenuates cytosolic double stranded RNA (dsRNA) viruses, which are endemic to yeast and many other organisms. Viral attenuation by Nuc1 occurs most prominently during meiosis and in association with its developmentally programmed relocation from the mitochondria to the cytosol. Intriguingly, meiotic viral attenuation by Nuc1 occurs within the context of meiotic PCD of the superfluous mother cell that we have also discovered. These findings are discussed here.