Peroxisome Degradation by Microautophagy in <i>Pichia pastoris</i>: Identification of Specific Steps and Morphological Intermediates

Sakai, Yasuyoshi; Koller, Antonius; Rangell, Linda; Keller, G A; Subramani, Suresh

doi:10.1083/jcb.141.3.625

Cited by 230 publications

(247 citation statements)

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“…9 Most of the mechanistic perception comes from genetic studies carried out in methylotrophic yeast Pichia pastoris, 10 in which metabolic adaptation is caused by changes in carbon source that drives pexophagy (degradation of peroxisomes) by either macro or microautophagy. 11 Morphologically, the hallmarks of microautophagy are indentations in the vacuolar or lysosomal boundary membrane that allow direct uptake of the cytosol and/or organelles.…”

Section: Introductionmentioning

confidence: 99%

Impairing the bioenergetic status and the biogenesis of mitochondria triggers mitophagy in yeast

et al. 2005

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Autophagy, a highly regulated programme found in almost all eukaryotes, is mainly viewed as a catabolic process that degrades nonessential cellular components into molecular building blocks, subsequently available for biosynthesis at a lesser expense than de novo synthesis. Autophagy is largely known to be regulated by nutritional conditions. Here we show that, in yeast cells grown under nonstarving conditions, autophagy can be induced by mitochondrial dysfunction. Electron micrographs and biochemical studies show that an autophagic activity can result from impairing the mitochondrial electrochemical transmembrane potential. Furthermore, mitochondrial damage-induced autophagy results in the preferential degradation of impaired mitochondria (mitophagy), before leading to cell death. Mitophagy appears to rely on classical macroautophagy machinery while being independent of cellular ATP collapse. These results suggest that in this case, autophagy can be envisioned either as a process of mitochondrial quality control, or as an ultimate cellular response triggered when cells are overwhelmed with damaged mitochondria.

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Section: Introductionmentioning

confidence: 99%

Impairing the bioenergetic status and the biogenesis of mitochondria triggers mitophagy in yeast

et al. 2005

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“…A second venue for selective peroxisome degradation occurs during glucose adaptation. Micropexophagy proceeds by a mechanism whereby the vacuolar membrane invaginates, resulting in protrusions that surround and engulf the entire cluster of peroxisomes (Tuttle et al, 1993;Sakai et al, 1998). Both pathways result in the degradation of peroxisomes within the vacuole by proteolytic enzymes.…”

Section: Introductionmentioning

confidence: 99%

PpATG9 Encodes a Novel Membrane Protein That Traffics to Vacuolar Membranes, Which Sequester Peroxisomes during Pexophagy inPichia pastoris

Chang

Schröder

Thomson

et al. 2005

MBoC

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When Pichia pastoris adapts from methanol to glucose growth, peroxisomes are rapidly sequestered and degraded within the vacuole by micropexophagy. During micropexophagy, sequestering membranes arise from the vacuole to engulf the peroxisomes. Fusion of the sequestering membranes and incorporation of the peroxisomes into the vacuole is mediated by the micropexophagy-specific membrane apparatus (MIPA). In this study, we show the P. pastoris ortholog of Atg9, a novel membrane protein is essential for the formation of the sequestering membranes and assembly of MIPA. During methanol growth, GFP-PpAtg9 localizes to multiple structures situated near the plasma membrane referred as the peripheral compartment (Atg9-PC). On glucose-induced micropexophagy, PpAtg9 traffics from the Atg9-PC to unique perivacuolar structures (PVS) that contain PpAtg11, but lack PpAtg2 and PpAtg8. Afterward, PpAtg9 distributes to the vacuole surface and sequestering membranes. Movement of the PpAtg9 from the Atg9-PC to the PVS requires PpAtg11 and PpVps15. PpAtg2 and PpAtg7 are essential for PpAtg9 trafficking from the PVS to the vacuole and sequestering membranes, whereas trafficking of PpAtg9 proceeds independent of PpAtg1, PpAtg18, and PpVac8. In summary, our data suggest that PpAtg9 transits from the Atg9-PC to the PVS and then to the sequestering membranes that engulf the peroxisomes for degradation.

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“…Glucoseinduced degradation, however, results in the uptake of clusters of peroxisomes in the central vacuole after engulfment by protrusions extending from this organelle. The latter process is analogous to the microautophagy described for mammalian cells (Tuttle and Dunn 1995;Sakai et al 1998).…”

Section: Introductionmentioning

confidence: 69%

“…The bar represents 0.5 mm activities as a byproduct of their vacuolar protein-sorting defects. However, this explanation is not likely since peroxisomes should then be observed to accumulate in vacuoles, as seen in mutants defective in vacuolar proteases (Tuttle and Dunn 1995;Chiang et al 1996;Sakai et al 1998). A more satisfactory explanation, and one that is consistent with their proposed roles in vacuolar protein sorting and endocytosis, is that Vps15p and Vps34p are involved in tagging the organelles by the phosphorylation of PtdIns molecules for delivery to the vacuole.…”

Section: Discussionmentioning

confidence: 99%

“…Numerous H. polymorpha and P. pastoris mutants a ected in the selective degradation of peroxisomes have been isolated in di erent laboratories (Titorenko et al 1995;Tuttle and Dunn 1995;Sakai et al 1998). We have isolated H. polymorpha mutants a ected in peroxisome degradation (pdd mutants) and used these to clone the genes involved in this process (PDD genes).…”

Section: Introductionmentioning

confidence: 99%

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A Pichia pastoris VPS15 homologue is required in selective peroxisome autophagy

Stasyk

Klei²,

Bellu

et al. 1999

Current Genetics

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A Pichia pastoris VPS15 homologue is required in selective peroxisome autophagy Stasyk, OV; van der Klei, Ida; Bellu, AR; Shen, SG; Kiel, Jan; Cregg, JM; Veenhuis, M; Stasyk, Oleh V.; Shen, Shigang; Cregg, James M. Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. Abstract Methylotrophic yeasts contain large peroxisomes during growth on methanol. Upon exposure to excess glucose or ethanol these organelles are selectively degraded by autophagy. Here we describe the cloning of a Pichia pastoris gene (PpVPS15) involved in peroxisome degradation, which is homologous to Saccharomyces cerevisiae VPS15. In methanol-grown cells of a P. pastoris VPS15 deletion strain, the levels of peroxisomal marker enzymes remained high after addition of excess glucose or ethanol. Electron microscopic studies revealed that the organelles were not taken up by vacuoles, suggesting that PpVPS15 is required at an early stage in peroxisome degradation.

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Peroxisome Degradation by Microautophagy in Pichia pastoris: Identification of Specific Steps and Morphological Intermediates

Cited by 230 publications

References 29 publications

Impairing the bioenergetic status and the biogenesis of mitochondria triggers mitophagy in yeast

Impairing the bioenergetic status and the biogenesis of mitochondria triggers mitophagy in yeast

PpATG9 Encodes a Novel Membrane Protein That Traffics to Vacuolar Membranes, Which Sequester Peroxisomes during Pexophagy inPichia pastoris

A Pichia pastoris VPS15 homologue is required in selective peroxisome autophagy

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