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Keywords = Pexophage

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18 pages, 7007 KiB  
Article
Autophagy-Related Proteins (ATGs) Are Differentially Required for Development and Virulence of Sclerotinia sclerotiorum
by Thilini Weerasinghe, Josh Li, Xuanye Chen, Jiayang Gao, Lei Tian, Yan Xu, Yihan Gong, Weijie Huang, Yuelin Zhang, Liwen Jiang and Xin Li
J. Fungi 2025, 11(5), 391; https://doi.org/10.3390/jof11050391 - 19 May 2025
Viewed by 698
Abstract
Sclerotinia sclerotiorum is a devastating fungal pathogen that can colonize numerous crops. Despite its economic importance, the regulation of its development and pathogenicity remains poorly understood. From a forward genetic screen in S. sclerotiorum, six UV mutants were identified with loss-of-function mutations [...] Read more.
Sclerotinia sclerotiorum is a devastating fungal pathogen that can colonize numerous crops. Despite its economic importance, the regulation of its development and pathogenicity remains poorly understood. From a forward genetic screen in S. sclerotiorum, six UV mutants were identified with loss-of-function mutations in SsATG1, SsATG2, SsATG4, SsATG5, SsATG9, and SsATG26. Functional validation through gene knockouts revealed that each ATG is essential for sclerotia formation, although the morphology of appressoria was not significantly altered in the mutants. Different levels of virulence attenuation were observed among these mutants. Autophagy, monitored using GFP-ATG8, showed dynamic activities during sclerotia development. These findings suggest that macroautophagy and pexophagy contribute to sclerotia maturation and virulence processes. Future work will reveal how autophagy controls target organelle or protein turnover to regulate these processes. Full article
(This article belongs to the Special Issue Current Research in Soil Borne Plant Pathogens)
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12 pages, 1976 KiB  
Article
Knockdown of PEX16 Induces Autophagic Degradation of Peroxisomes
by Xiaofan Wei, Yunash Maharjan, Debra Dorotea, Raghbendra-Kumar Dutta, Donghyun Kim, Hyunsoo Kim, Yizhu Mu, Channy Park and Raekil Park
Int. J. Mol. Sci. 2021, 22(15), 7989; https://doi.org/10.3390/ijms22157989 - 26 Jul 2021
Cited by 6 | Viewed by 3646
Abstract
Peroxisome abundance is regulated by homeostasis between the peroxisomal biogenesis and degradation processes. Peroxin 16 (PEX16) is a peroxisomal protein involved in trafficking membrane proteins for de novo peroxisome biogenesis. The present study demonstrates that PEX16 also modulates peroxisome abundance through pexophagic degradation. [...] Read more.
Peroxisome abundance is regulated by homeostasis between the peroxisomal biogenesis and degradation processes. Peroxin 16 (PEX16) is a peroxisomal protein involved in trafficking membrane proteins for de novo peroxisome biogenesis. The present study demonstrates that PEX16 also modulates peroxisome abundance through pexophagic degradation. PEX16 knockdown in human retinal pigment epithelial-1 cells decreased peroxisome abundance and function, represented by reductions in the expression of peroxisome membrane protein ABCD3 and the levels of cholesterol and plasmalogens, respectively. The activation of pexophagy under PEX16 knockdown was shown by (i) abrogated peroxisome loss under PEX16 knockdown in autophagy-deficient ATG5 knockout cell lines, and (ii) increased autophagy flux and co-localization of p62—an autophagy adaptor protein—with ABCD3 in the presence of the autophagy inhibitor chloroquine. However, the levels of cholesterol and plasmalogens did not recover despite the restoration of peroxisome abundance following chloroquine treatment. Thus, PEX16 is indispensable for maintaining peroxisome homeostasis by regulating not only the commonly known biogenesis pathway but also the autophagic degradation of peroxisomes. Full article
(This article belongs to the Special Issue Molecular Regulatory Mechanisms of Membrane Trafficking)
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