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Pexophagy: A Model for Selective Autophagy
 
 
Communication

The Peroxisomal PTS1-Import Defect of PEX1- Deficient Cells Is Independent of Pexophagy in Saccharomyces cerevisiae

Biochemie Intrazellulärer Transportprozesse, Ruhr-Universität Bochum, Universitätsstr. 150, 44801 Bochum, Germany
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Int. J. Mol. Sci. 2020, 21(3), 867; https://doi.org/10.3390/ijms21030867
Received: 10 January 2020 / Revised: 25 January 2020 / Accepted: 27 January 2020 / Published: 29 January 2020
(This article belongs to the Special Issue Peroxisomes under the Spotlight: Collaboration is the Way to Go)
The important physiologic role of peroxisomes is shown by the occurrence of peroxisomal biogenesis disorders (PBDs) in humans. This spectrum of autosomal recessive metabolic disorders is characterized by defective peroxisome assembly and impaired peroxisomal functions. PBDs are caused by mutations in the peroxisomal biogenesis factors, which are required for the correct compartmentalization of peroxisomal matrix enzymes. Recent work from patient cells that contain the Pex1(G843D) point mutant suggested that the inhibition of the lysosome, and therefore the block of pexophagy, was beneficial for peroxisomal function. The resulting working model proposed that Pex1 may not be essential for matrix protein import at all, but rather for the prevention of pexophagy. Thus, the observed matrix protein import defect would not be caused by a lack of Pex1 activity, but rather by enhanced removal of peroxisomal membranes via pexophagy. In the present study, we can show that the specific block of PEX1 deletion-induced pexophagy does not restore peroxisomal matrix protein import or the peroxisomal function in beta-oxidation in yeast. Therefore, we conclude that Pex1 is directly and essentially involved in peroxisomal matrix protein import, and that the PEX1 deletion-induced pexophagy is not responsible for the defect in peroxisomal function. In order to point out the conserved mechanism, we discuss our findings in the context of the working models of peroxisomal biogenesis and pexophagy in yeasts and mammals. View Full-Text
Keywords: Atg36; Pex1; pexophagy; peroxisomal protein import Atg36; Pex1; pexophagy; peroxisomal protein import
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MDPI and ACS Style

Mastalski, T.; Brinkmeier, R.; Platta, H.W. The Peroxisomal PTS1-Import Defect of PEX1- Deficient Cells Is Independent of Pexophagy in Saccharomyces cerevisiae. Int. J. Mol. Sci. 2020, 21, 867. https://doi.org/10.3390/ijms21030867

AMA Style

Mastalski T, Brinkmeier R, Platta HW. The Peroxisomal PTS1-Import Defect of PEX1- Deficient Cells Is Independent of Pexophagy in Saccharomyces cerevisiae. International Journal of Molecular Sciences. 2020; 21(3):867. https://doi.org/10.3390/ijms21030867

Chicago/Turabian Style

Mastalski, Thomas, Rebecca Brinkmeier, and Harald W. Platta. 2020. "The Peroxisomal PTS1-Import Defect of PEX1- Deficient Cells Is Independent of Pexophagy in Saccharomyces cerevisiae" International Journal of Molecular Sciences 21, no. 3: 867. https://doi.org/10.3390/ijms21030867

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