Mitochondrial phosphatidylserine decarboxylase 1 (Psd1) is involved in nitrogen starvation-induced mitophagy in yeast

Vigié, Pierre; Cougouilles, Elodie; Bhatia‐Kiššová, Ingrid; Salin, Bénédicte; Blancard, Corinne; Camougrand, Nadine

doi:10.1242/jcs.221655

Cited by 12 publications

(10 citation statements)

References 47 publications

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“…This hypothesis is supported by our anti-Psd1 immunoblots, suggesting decreased proteolytic activation of Psd1 ( Figure S4b,c ) in por1 ∆. Another recent study investigated the involvement of Psd1 during mitophagy in yeast [ 77 ]. Interestingly, the study reports that Psd1 is predominantly involved in nitrogen-starvation-induced mitophagy, whereas Psd2 is required for mitophagy induction in the stationary phase.…”

Section: Discussionsupporting

confidence: 83%

“…PSD1 overexpression has been shown to increase the autophagic capacity [ 17 ], whereas knockout of PSD1 and PSD2 resulted in reduced autophagy [ 76 ]. PSD1 and PSD2 single mutants have been studied regarding their role in mitophagy, as discussed later [ 77 ]. Since Psd1 accounts for 70–80% of total PSD activity in yeast [ 22 ], it can be assumed to be of predominant importance for autophagy.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Porin 1 Modulates Autophagy in Yeast

Broeskamp

Edrich

Knittelfelder

et al. 2021

Cells

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Autophagy is a cellular recycling program which efficiently reduces the cellular burden of ageing. Autophagy is characterised by nucleation of isolation membranes, which grow in size and further expand to form autophagosomes, engulfing cellular material to be degraded by fusion with lysosomes (vacuole in yeast). Autophagosomal membranes do not bud from a single cell organelle, but are generated de novo. Several lipid sources for autophagosomal membranes have been identified, but the whole process of their generation is complex and not entirely understood. In this study, we investigated how the mitochondrial outer membrane protein porin 1 (Por1), the yeast orthologue of mammalian voltage-dependent anion channel (VDAC), affects autophagy in yeast. We show that POR1 deficiency reduces the autophagic capacity and leads to changes in vacuole and lipid homeostasis. We further investigated whether limited phosphatidylethanolamine (PE) availability in por1∆ was causative for reduced autophagy by overexpression of the PE-generating phosphatidylserine decarboxylase 1 (Psd1). Altogether, our results show that POR1 deficiency is associated with reduced autophagy, which can be circumvented by additional PSD1 overexpression. This suggests a role for Por1 in Psd1-mediated autophagy regulation.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

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Porin 1 Modulates Autophagy in Yeast

Broeskamp

Edrich

Knittelfelder

et al. 2021

Cells

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“…Are these modifications dependent on mitophagy induction conditions (e.g., nutrient starvation, stationary phase of growth, or rapamycin treatment)? Previously, we showed that depending on the condition of induction, mitophagy may exploit various signaling pathways [36]. The need of cells to employ various pathways could reflect different purposes of self-eating mitochondria in cell physiology at certain moments, the bioenergetic state/deficit of cells, a cell's capacity to carry a burden of damaged components, and so on.…”

Section: Why Is Atg32 Regulated By Multiple Posttranslational Modificmentioning

confidence: 99%

The yeast mitophagy receptor Atg32 is ubiquitinated and degraded by the proteasome

et al. 2020

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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.

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“…Multiple studies establish that perturbation of phospholipid homeostasis in mitochondria or the ER could affect mitophagy. Psd1 and Psd2, two phosphatidylserine decarboxylases that synthesize PE from PS (phosphatidylserine), are required for efficient mitophagy [44]. Intriguingly, Psd1 is only required for nitrogen starvation-induced mitophagy, while Psd2 is more critical for prolonged respiration-induced mitophagy but also partially for nitrogen starvation-induced mitophagy.…”

Section: Relevance Of Phospholipids In Mitophagymentioning

confidence: 99%

Mitochondrial clearance: mechanisms and roles in cellular fitness

Onishi

Okamoto

2021

FEBS Letters

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Edited by Agnieszka ChacinskaMitophagy is one of the selective autophagy pathways that catabolizes dysfunctional or superfluous mitochondria. Under mitophagy-inducing conditions, mitochondria are labeled with specific molecular landmarks that recruit the autophagy machinery to the surface of mitochondria, enclosed into autophagosomes, and delivered to lysosomes (vacuoles in yeast) for degradation. As damaged mitochondria are the major sources of reactive oxygen species, mitophagy is critical for mitochondrial quality control and cellular health. Moreover, appropriate control of mitochondrial quantity via mitophagy is vital for the energy supply-demand balance in cells and whole organisms, cell differentiation, and developmental programs. Thus, it seems conceivable that defects in mitophagy could elicit pleiotropic pathologies such as excess inflammation, tissue injury, neurodegeneration, and aging. In this review, we will focus on the molecular basis and physiological relevance of mitophagy, and potential of mitophagy as a therapeutic target to overcome such disorders.

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Mitochondrial phosphatidylserine decarboxylase 1 (Psd1) is involved in nitrogen starvation-induced mitophagy in yeast

Cited by 12 publications

References 47 publications

Porin 1 Modulates Autophagy in Yeast

Porin 1 Modulates Autophagy in Yeast

The yeast mitophagy receptor Atg32 is ubiquitinated and degraded by the proteasome

Mitochondrial clearance: mechanisms and roles in cellular fitness

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