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  1. 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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  2. 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 ... ...

    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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Mlg1, a yeast acyltransferase located in ER membranes associated with mitochondria (MAMs), is involved in de novo synthesis and remodelling of phospholipids.

    Laquel, Patricia / Ayciriex, Sophie / Doignon, François / Camougrand, Nadine / Fougère, Louise / Rocher, Christophe / Wattelet-Boyer, Valérie / Bessoule, Jean-Jacques / Testet, Eric

    The FEBS journal

    2024  

    Abstract: In cells, phospholipids contain acyl chains of variable lengths and saturation, features that affect their functions. Their de novo synthesis in the endoplasmic reticulum takes place via the cytidine diphosphate diacylglycerol (CDP-DAG) and Kennedy ... ...

    Abstract In cells, phospholipids contain acyl chains of variable lengths and saturation, features that affect their functions. Their de novo synthesis in the endoplasmic reticulum takes place via the cytidine diphosphate diacylglycerol (CDP-DAG) and Kennedy pathways, which are conserved in eukaryotes. PA is a key intermediate for all phospholipids (PI, PIPs, PS, PE, PC, PG and CL). The de novo synthesis of PA occurs by acylation of glycerophosphate leading to the synthesis of 1-acyl lysoPA and subsequent acylation of 1-acyl lysoPA at the sn-2 position. Using membranes from Escherichia coli overexpressing MLG1, we showed that the yeast gene MLG1 encodes an acyltransferase, leading specifically to the synthesis of PA from 1-acyl lysoPA. Moreover, after their de novo synthesis, phospholipids can be remodelled by acyl exchange with one and/or two acyl chains exchanged at the sn-1 and/or sn-2 position. Based on shotgun lipidomics of the reference and mlg1Δ strains, as well as biochemical assays for acyltransferase activities, we identified an additional remodelling activity for Mlg1p, namely, incorporation of palmitic acid into the sn-1 position of PS and PE. By using confocal microscopy and subcellular fractionation, we also found that this acyltransferase is located in ER membranes associated with mitochondria, a finding that highlights the importance of these organelles in the global cellular metabolism of lipids.
    Language English
    Publishing date 2024-01-31
    Publishing country England
    Document type Journal Article
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.17068
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Mitophagie et contrôle qualité des mitochondries.

    Vigié, Pierre / Camougrand, Nadine

    Medecine sciences : M/S

    2017  Volume 33, Issue 3, Page(s) 231–237

    Abstract: Mitochondria are highly dynamic organelles that provide essential metabolic functions and represent the major bioenergetic hub of eukaryotic cells. Mitochondrial dysfunctions are implicated in numerous diseases. Therefore, maintenance of a healthy pool ... ...

    Title translation Role of mitophagy in the mitochondrial quality control.
    Abstract Mitochondria are highly dynamic organelles that provide essential metabolic functions and represent the major bioenergetic hub of eukaryotic cells. Mitochondrial dysfunctions are implicated in numerous diseases. Therefore, maintenance of a healthy pool of mitochondria is required for cellular function and survival. Mitochondrial quality control is achieved through several mechanisms that act at different levels: proteases and chaperones, the Ubiquitin-Proteasome-System (UPS) and mitophagy. Multiple mitophagy-involved programs operate independently or undergo crosstalk, and require modulated receptor activities at the outer membranes of mitochondria. In mammals, different mitophagy effectors have been characterized such as the receptors NIX, BNIP3, FUNDC1, BCL2L13, cardiolipin and the PINK1/Parkin pathway. Here we discuss the different molecular mechanisms of these mitophagy involved pathways.
    MeSH term(s) Animals ; Cell Physiological Phenomena ; Eukaryotic Cells/physiology ; Eukaryotic Cells/ultrastructure ; Humans ; Mitochondria/physiology ; Mitochondrial Degradation/physiology ; Quality Control ; Ubiquitin-Protein Ligases/physiology
    Chemical Substances Ubiquitin-Protein Ligases (EC 2.3.2.27) ; parkin protein (EC 2.3.2.27)
    Language French
    Publishing date 2017-03
    Publishing country France
    Document type Journal Article ; Review
    ZDB-ID 632733-3
    ISSN 1958-5381 ; 0767-0974
    ISSN (online) 1958-5381
    ISSN 0767-0974
    DOI 10.1051/medsci/20173303008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: The SEACIT complex is involved in the maintenance of vacuole-mitochondria contact sites and controls mitophagy.

    Ma, Yinxing / Moors, Alexis / Camougrand, Nadine / Dokudovskaya, Svetlana

    Cellular and molecular life sciences : CMLS

    2019  Volume 76, Issue 8, Page(s) 1623–1640

    Abstract: The major signaling pathway that regulates cell growth and metabolism is under the control of the target of rapamycin complex 1 (TORC1). In Saccharomyces cerevisiae the SEA complex is one of the TORC1 upstream regulators involved in amino acid sensing ... ...

    Abstract The major signaling pathway that regulates cell growth and metabolism is under the control of the target of rapamycin complex 1 (TORC1). In Saccharomyces cerevisiae the SEA complex is one of the TORC1 upstream regulators involved in amino acid sensing and autophagy. Here, we performed analysis of the expression, interactions and localization of SEA complex proteins under different conditions, varying parameters such as sugar source, nitrogen availability and growth phase. Our results show that the SEA complex promotes mitochondria degradation either by mitophagy or by general autophagy. In addition, the SEACIT subcomplex is involved in the maintenance of the vacuole-mitochondria contact sites. Thus, the SEA complex appears to be an important link between the TORC1 pathway and regulation of mitochondria quality control.
    MeSH term(s) Autophagy/physiology ; Gene Deletion ; Glucose/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mitochondria/metabolism ; Mitochondrial Degradation/physiology ; Nitrogen/metabolism ; Oxygen/metabolism ; Reactive Oxygen Species/metabolism ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/growth & development ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Vacuoles/metabolism
    Chemical Substances Membrane Proteins ; Reactive Oxygen Species ; Saccharomyces cerevisiae Proteins ; TORC1 protein complex, S cerevisiae ; Transcription Factors ; Glucose (IY9XDZ35W2) ; Nitrogen (N762921K75) ; Oxygen (S88TT14065)
    Language English
    Publishing date 2019-01-23
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-019-03015-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: The SEACIT complex is involved in the maintenance of vacuole–mitochondria contact sites and controls mitophagy

    Ma, Yinxing / Moors, Alexis / Camougrand, Nadine / Dokudovskaya, Svetlana

    Cellular and molecular life sciences. 2019 Apr., v. 76, no. 8

    2019  

    Abstract: The major signaling pathway that regulates cell growth and metabolism is under the control of the target of rapamycin complex 1 (TORC1). In Saccharomyces cerevisiae the SEA complex is one of the TORC1 upstream regulators involved in amino acid sensing ... ...

    Abstract The major signaling pathway that regulates cell growth and metabolism is under the control of the target of rapamycin complex 1 (TORC1). In Saccharomyces cerevisiae the SEA complex is one of the TORC1 upstream regulators involved in amino acid sensing and autophagy. Here, we performed analysis of the expression, interactions and localization of SEA complex proteins under different conditions, varying parameters such as sugar source, nitrogen availability and growth phase. Our results show that the SEA complex promotes mitochondria degradation either by mitophagy or by general autophagy. In addition, the SEACIT subcomplex is involved in the maintenance of the vacuole–mitochondria contact sites. Thus, the SEA complex appears to be an important link between the TORC1 pathway and regulation of mitochondria quality control.
    Keywords Saccharomyces cerevisiae ; amino acids ; cell growth ; developmental stages ; metabolism ; mitochondria ; mitophagy ; nitrogen ; proteins ; rapamycin ; signal transduction ; sugars
    Language English
    Dates of publication 2019-04
    Size p. 1623-1640.
    Publishing place Springer International Publishing
    Document type Article
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-019-03015-6
    Database NAL-Catalogue (AGRICOLA)

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  7. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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