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Article ; Online: Mitophagy in Yeast

Bhatia-Kissova Ingrid / Camougrand Nadine

Cells, Vol 10, Iss 3541, p

Decades of Research

2021 Volume 3541

Abstract: Mitophagy, the selective degradation of mitochondria by autophagy, is one of the most important mechanisms of mitochondrial quality control, and its proper functioning is essential for cellular homeostasis. In this review, we describe the most important ... ...

Abstract	Mitophagy, the selective degradation of mitochondria by autophagy, is one of the most important mechanisms of mitochondrial quality control, and its proper functioning is essential for cellular homeostasis. In this review, we describe the most important milestones achieved during almost 2 decades of research on yeasts, which shed light on the molecular mechanisms, regulation, and role of the Atg32 receptor in this process. We analyze the role of ROS in mitophagy and discuss the physiological roles of mitophagy in unicellular organisms, such as yeast; these roles are very different from those in mammals. Additionally, we discuss some of the different tools available for studying mitophagy.
Keywords	yeast ; mitochondria ; quality control ; mitophagy ; Atg32 protein ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-12-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Mitophagy in Yeast: Decades of Research.

Bhatia-Kissova, Ingrid / Camougrand, Nadine

Cells

2021 Volume 10, Issue 12

Abstract	Mitophagy, the selective degradation of mitochondria by autophagy, is one of the most important mechanisms of mitochondrial quality control, and its proper functioning is essential for cellular homeostasis. In this review, we describe the most important milestones achieved during almost 2 decades of research on yeasts, which shed light on the molecular mechanisms, regulation, and role of the Atg32 receptor in this process. We analyze the role of ROS in mitophagy and discuss the physiological roles of mitophagy in unicellular organisms, such as yeast; these roles are very different from those in mammals. Additionally, we discuss some of the different tools available for studying mitophagy.
MeSH term(s)	Humans ; Mitochondria/metabolism ; Mitophagy ; Models, Biological ; Reactive Oxygen Species/metabolism ; Research ; Saccharomyces cerevisiae/metabolism
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2021-12-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10123541
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Article ; Online: The Dep1 protein: A new regulator of mitophagy in yeast.

Camougrand, Nadine / Vigié, Pierre / Dompierre, Jim / Massoni-Laporte, Aurélie / Lasserre, Jean Paul / Bhatia-Kiššová, Ingrid

Biochemical and biophysical research communications

2022 Volume 635, Page(s) 218–226

Abstract: Mitochondria play a crucial role in most eukaryotic cells. Mitophagy is a process that controls their quality and quantity within the cells. The outer mitochondrial membrane protein, Atg32, serves as the mitophagic receptor. It interacts with the Atg11 ... ...

Abstract	Mitochondria play a crucial role in most eukaryotic cells. Mitophagy is a process that controls their quality and quantity within the cells. The outer mitochondrial membrane protein, Atg32, serves as the mitophagic receptor. It interacts with the Atg11 protein to initiate mitophagy and with the Atg8 protein to ensure the engulfment of mitochondria into the autophagosomes for elimination. The Atg32 protein is regulated at the transcriptional level but also by posttranslational modifications. In this study, we described a new regulator of mitophagy, the protein Dep1, identified as a part of the Rpd3L histone deacetylase complex. We showed that the Dep1 protein is localized in the nucleus and associated with mitochondria. This protein is needed for mitophagy and to regulate the transcription and expression of the Atg32 protein. The absence of this protein affects the mitophagy process induced by either starvation for nitrogen or the stationary phase of growth.
MeSH term(s)	Autophagy ; Autophagy-Related Proteins/genetics ; Autophagy-Related Proteins/metabolism ; Mitophagy ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Cytoplasmic and Nuclear/metabolism ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism
Chemical Substances	Atg32 protein, S cerevisiae ; Autophagy-Related Proteins ; Receptors, Cytoplasmic and Nuclear ; Saccharomyces cerevisiae Proteins ; Dep1 protein, S cerevisiae
Language	English
Publishing date	2022-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2022.10.052
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Article ; Online: The yeast mitophagy receptor Atg32 is ubiquitinated and degraded by the proteasome.

Camougrand, Nadine / Vigié, Pierre / Gonzalez, Cécile / Manon, Stéphen / Bhatia-Kiššová, Ingrid

PloS one

2020 Volume 15, Issue 12, Page(s) e0241576

Abstract: Mitophagy, the process that degrades mitochondria selectively through autophagy, is involved in the quality control of mitochondria in cells grown under respiratory conditions. In yeast, the presence of the Atg32 protein on the outer mitochondrial ... ...

Abstract	Mitophagy, the process that degrades mitochondria selectively through autophagy, is involved in the quality control of mitochondria in cells grown under respiratory conditions. In yeast, the presence of the Atg32 protein on the outer mitochondrial membrane allows for the recognition and targeting of superfluous or damaged mitochondria for degradation. Post-translational modifications such as phosphorylation are crucial for the execution of mitophagy. In our study we monitor the stability of Atg32 protein in the yeast S. cerevisiae and show that Atg32 is degraded under normal growth conditions, upon starvation or rapamycin treatment. The Atg32 turnover can be prevented by inhibition of the proteasome activity, suggesting that Atg32 is also ubiquitinated. Mass spectrometry analysis of purified Atg32 protein revealed that at least lysine residue in position 282 is ubiquitinated. Interestingly, the replacement of lysine 282 with alanine impaired Atg32 degradation only partially in the course of cell growth, suggesting that additional lysine residues on Atg32 might also be ubiquitinated. Our results provide the foundation to further elucidate the physiological significance of Atg32 turnover and the interplay between mitophagy and the proteasome.
MeSH term(s)	Alanine/genetics ; Alanine/metabolism ; Autophagy-Related Proteins/genetics ; Autophagy-Related Proteins/isolation & purification ; Autophagy-Related Proteins/metabolism ; Lysine/genetics ; Lysine/metabolism ; Mitochondria/metabolism ; Mitochondrial Membranes/metabolism ; Mitophagy ; Mutagenesis, Site-Directed ; Proteasome Endopeptidase Complex/metabolism ; Protein Stability ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Cytoplasmic and Nuclear/isolation & purification ; Receptors, Cytoplasmic and Nuclear/metabolism ; Saccharomyces cerevisiae/physiology ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/isolation & purification ; Saccharomyces cerevisiae Proteins/metabolism ; Ubiquitination/physiology
Chemical Substances	Atg32 protein, S cerevisiae ; Autophagy-Related Proteins ; Receptors, Cytoplasmic and Nuclear ; Saccharomyces cerevisiae Proteins ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Lysine (K3Z4F929H6) ; Alanine (OF5P57N2ZX)
Language	English
Publishing date	2020-12-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0241576
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Article ; Online: Mitophagy: a process that adapts to the cell physiology.

Bhatia-Kiššová, Ingrid / Camougrand, Nadine

The international journal of biochemistry & cell biology

2013 Volume 45, Issue 1, Page(s) 30–33

Abstract: This focus makes a case that mitophagy is not a straightforward process obeying simple rules. It is a complex process through which the cell gets rid of both damaged and healthy untainted mitochondria to adjust their amount, and in accordance with ... ...

Abstract	This focus makes a case that mitophagy is not a straightforward process obeying simple rules. It is a complex process through which the cell gets rid of both damaged and healthy untainted mitochondria to adjust their amount, and in accordance with cellular energy requirements. Several aspects of mitophagy have been described in both yeast and mammalian cells. They have revealed a number of discrepancies in the regulation of this process in the two eukaryotic models. Data have shown that mitophagy is a function of cell physiology. This article is part of a Directed Issue entitled: Bioenergetic dysfunction, adaptation and therapy.
MeSH term(s)	Animals ; Cell Physiological Phenomena ; Eukaryotic Cells/physiology ; Humans ; Mitochondria/physiology ; Mitochondrial Degradation/physiology
Language	English
Publishing date	2013-01
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2012.07.006
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Article ; Online: Mitophagy is not induced by mitochondrial damage but plays a role in the regulation of cellular autophagic activity.

Bhatia-Kiššová, Ingrid / Camougrand, Nadine

Autophagy

2013 Volume 9, Issue 11, Page(s) 1897–1899

Abstract: It was postulated that mitophagy removes damaged mitochondria, which is critical for proper cellular homeostasis; dysfunctional mitochondria can generate excess reactive oxygen species (ROS) that can further damage the organelle as well as other cellular ...

Abstract	It was postulated that mitophagy removes damaged mitochondria, which is critical for proper cellular homeostasis; dysfunctional mitochondria can generate excess reactive oxygen species (ROS) that can further damage the organelle as well as other cellular components. Although proper cell physiology requires the maintenance of a healthy pool of mitochondria, little is known about the mechanism underlying the recognition and selection of damaged organelles. We investigated the cellular fate of mitochondria damaged by the action of oxidative phosphorylation inhibitors (antimycin A, myxothiazol, KCN, oligomycin, CCCP). Only antimycin A and KCN effectively induce nonspecific autophagy, but not mitophagy, in a wild-type strain; however, low or no autophagic activity was measured in strains deficient in genes, including ATG32, ATG11 and BCK1, encoding proteins that are involved in mitophagy. These results provide evidence for a major role of specific mitophagy factors in the control of a general autophagic cellular response induced by mitochondrial alteration. Moreover, significant reduction of cytochrome b, one of the components of the respiratory chain, could be the first signal of this induction pathway.
MeSH term(s)	Autophagy/physiology ; Cytochromes b/metabolism ; Mitochondria/physiology ; Mitochondrial Degradation/physiology
Chemical Substances	Cytochromes b (9035-37-4)
Language	English
Publishing date	2013-11-01
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.4161/auto.23979
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Article ; Online: The mitochondrial phosphatidylserine decarboxylase Psd1 is involved in nitrogen starvation-induced mitophagy in yeast.

Vigié, Pierre / Cougouilles, Elodie / Bhatia-Kiššová, Ingrid / Salin, Bénédicte / Blancard, Corinne / Camougrand, Nadine

Journal of cell science

2019 Volume 132, Issue 1

Abstract: Mitophagy, the selective degradation of mitochondria by autophagy, is a central process that is essential for the maintenance of cell homeostasis. It is implicated in the clearance of superfluous or damaged mitochondria and requires specific proteins and ...

Abstract	Mitophagy, the selective degradation of mitochondria by autophagy, is a central process that is essential for the maintenance of cell homeostasis. It is implicated in the clearance of superfluous or damaged mitochondria and requires specific proteins and regulators to perform. In yeast, Atg32, an outer mitochondrial membrane protein, interacts with the ubiquitin-like Atg8 protein, promoting the recruitment of mitochondria to the phagophore and their sequestration within autophagosomes. Atg8 is anchored to the phagophore and autophagosome membranes thanks to a phosphatidylethanolamine tail. In
MeSH term(s)	Autophagy ; Autophagy-Related Protein 8 Family/genetics ; Autophagy-Related Protein 8 Family/metabolism ; Autophagy-Related Proteins/genetics ; Autophagy-Related Proteins/metabolism ; Carboxy-Lyases/genetics ; Carboxy-Lyases/metabolism ; Mitochondria/metabolism ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Mitophagy ; Nitrogen/deficiency ; Phosphatidylethanolamines/metabolism ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Cytoplasmic and Nuclear/metabolism ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/growth & development ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Starvation ; Vacuoles/metabolism
Chemical Substances	ATG8 protein, S cerevisiae ; Atg32 protein, S cerevisiae ; Autophagy-Related Protein 8 Family ; Autophagy-Related Proteins ; Mitochondrial Proteins ; Phosphatidylethanolamines ; Receptors, Cytoplasmic and Nuclear ; Saccharomyces cerevisiae Proteins ; phosphatidylethanolamine (39382-08-6) ; Carboxy-Lyases (EC 4.1.1.-) ; Psd1 protein, S cerevisiae (EC 4.1.1.-) ; Nitrogen (N762921K75)
Language	English
Publishing date	2019-01-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.221655
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Article ; Online: Mitophagy in yeast: actors and physiological roles.

Bhatia-Kiššová, Ingrid / Camougrand, Nadine

FEMS yeast research

2010 Volume 10, Issue 8, Page(s) 1023–1034

Abstract: Mitochondria are essential for oxidative energy production in aerobic eukaryotic cells, where they are also required for multiple biosynthetic pathways to take place. Mitochondria also monitor and evaluate complex information from the environment and ... ...

Abstract	Mitochondria are essential for oxidative energy production in aerobic eukaryotic cells, where they are also required for multiple biosynthetic pathways to take place. Mitochondria also monitor and evaluate complex information from the environment and intracellular milieu, including the presence or absence of growth factors, oxygen, reactive oxygen species, and DNA damage. It follows that disturbances of the integrity of mitochondrial function lead to the disruption of cell function, expressed as disease, aging, or cell death. It has been assumed that the degradation of damaged mitochondria by an autophagy-related pathway specific to mitochondria (mitophagy), recently found to be strictly regulated, is a fundamental process essential for cell homeostasis. Until now, the main role of mitophagy has been tentatively defined as a 'house-cleaning' pathway that allows to eliminate altered mitochondria, but mitophagy may also play a role in the adaptation of the number and quality of mitochondria to new environmental conditions. In yeast, recent data defined two categories of mitophagy actors: ones constitutively required for mitophagy and those with mitophagy-regulatory functions. Situations were also uncovered in normal physiology in which cells utilize mitophagy to eliminate damaged, dysfunctional, and superfluous mitochondria to adjust to changing physiological demands.
MeSH term(s)	Autophagy ; Homeostasis ; Mitochondria/metabolism ; Saccharomyces cerevisiae/physiology
Language	English
Publishing date	2010-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2036775-2
ISSN	1567-1364 ; 1567-1356
ISSN (online)	1567-1364
ISSN	1567-1356
DOI	10.1111/j.1567-1364.2010.00659.x
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Article: Mitophagy in yeast: actors and physiological roles

Bhatia‐Kiššová, Ingrid / Camougrand, Nadine

FEMS yeast research. 2010 Dec., v. 10, no. 8

2010

Abstract	Mitochondria are essential for oxidative energy production in aerobic eukaryotic cells, where they are also required for multiple biosynthetic pathways to take place. Mitochondria also monitor and evaluate complex information from the environment and intracellular milieu, including the presence or absence of growth factors, oxygen, reactive oxygen species, and DNA damage. It follows that disturbances of the integrity of mitochondrial function lead to the disruption of cell function, expressed as disease, aging, or cell death. It has been assumed that the degradation of damaged mitochondria by an autophagy‐related pathway specific to mitochondria (mitophagy), recently found to be strictly regulated, is a fundamental process essential for cell homeostasis. Until now, the main role of mitophagy has been tentatively defined as a ‘house‐cleaning' pathway that allows to eliminate altered mitochondria, but mitophagy may also play a role in the adaptation of the number and quality of mitochondria to new environmental conditions. In yeast, recent data defined two categories of mitophagy actors: ones constitutively required for mitophagy and those with mitophagy‐regulatory functions. Situations were also uncovered in normal physiology in which cells utilize mitophagy to eliminate damaged, dysfunctional, and superfluous mitochondria to adjust to changing physiological demands.
Language	English
Dates of publication	2010-12
Size	p. 1023-1034.
Publishing place	Blackwell Publishing Ltd
Document type	Article
ZDB-ID	2036775-2
ISSN	1567-1364 ; 1567-1356
ISSN (online)	1567-1364
ISSN	1567-1356
DOI	10.1111/j.1567-1364.2010.00659.x
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Insights into the relationship between the proteasome and autophagy in human and yeast cells.

Athané, Axel / Buisson, Anthony / Challier, Marion / Beaumatin, Florian / Manon, Stéphen / Bhatia-Kiššová, Ingrid / Camougrand, Nadine

The international journal of biochemistry & cell biology

2015 Volume 64, Page(s) 167–173

Abstract: In eukaryotes, the ubiquitin-proteasome system (UPS) and autophagy are two major intracellular protein degradation pathways. Several lines of evidence support the emerging concept of a coordinated and complementary relationship between these two ... ...

Abstract	In eukaryotes, the ubiquitin-proteasome system (UPS) and autophagy are two major intracellular protein degradation pathways. Several lines of evidence support the emerging concept of a coordinated and complementary relationship between these two processes, and a particularly interesting finding is that the inhibition of the proteasome induces autophagy. Yet, there is limited knowledge of the regulation of the UPS by autophagy. In this study, we show that the disruption of ATG5 and ATG32 genes in yeast cells under both nutrient-deficient conditions as well as stress that causes mitochondrial dysfunction leads to an activation of proteasome. The same scenario occurs after pharmacological inhibition of basal autophagy in cultured human cells. Our findings underline the view that the two processes are interconnected and tend to compensate, to some extent, for each other's functions.
MeSH term(s)	Autophagy ; Autophagy-Related Protein 5 ; Autophagy-Related Proteins ; Gene Expression ; HCT116 Cells ; HeLa Cells ; Humans ; Proteasome Endopeptidase Complex/physiology ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Cytoplasmic and Nuclear/metabolism ; Saccharomyces cerevisiae/cytology ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	ATG5 protein, S cerevisiae ; Atg32 protein, S cerevisiae ; Autophagy-Related Protein 5 ; Autophagy-Related Proteins ; Receptors, Cytoplasmic and Nuclear ; Saccharomyces cerevisiae Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2015-04-13
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2015.04.002
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