Ubp2 modulates DJ-1-mediated redox-dependent mitochondrial dynamics in Saccharomyces cerevisiae.

Publication date: Jul 03, 2025

Mitochondrial integrity is a crucial determinant of overall cellular health. Mitochondrial dysfunction and impediments in regulating organellar homeostasis contribute majorly to the pathophysiological manifestation of several neurological disorders. Mutations in human DJ-1 (PARK7) have been implicated in the deregulation of mitochondrial homeostasis, a critical cellular etiology observed in Parkinson’s disease progression. DJ-1 is a multifunctional protein belonging to the DJ-1/ThiJ/PfpI superfamily, conserved across the phylogeny. Although the pathophysiological significance of DJ-1 has been well-established, the underlying molecular mechanism(s) by which DJ-1 paralogs modulate mitochondrial maintenance and other cellular processes remains elusive. Using Saccharomyces cerevisiae as the model organism, we unravel the intricate mechanism by which yeast DJ-1 paralogs (collectively called Hsp31 paralogs) modulate mitochondrial homeostasis. Our study establishes a genetic synthetic interaction between Ubp2, a cysteine-dependent deubiquitinase, and DJ-1 paralogs. In the absence of DJ-1 paralogs, mitochondria adapt to a highly tubular network due to enhanced expression of Fzo1. Intriguingly, the loss of Ubp2 restores the mitochondrial integrity in the DJ-1 deletion background by modulating the ubiquitination status of Fzo1. Besides, the loss of Ubp2 in the absence of DJ-1 restores mitochondrial respiration and functionality by regulating the mitophagic flux. Further, Ubp2 deletion makes cells resistant to oxidative stress without DJ-1 paralogs. For the first time, our study deciphers functional crosstalk between Ubp2 and DJ-1 in regulating mitochondrial homeostasis and cellular health.

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Concepts Keywords
Dj Absence
Genetic Cellular
Mitophagic Cerevisiae
Park7 Dependent
Yeast Dj
Health
Homeostasis
Integrity
Mitochondrial
Modulate
Paralogs
Pathophysiological
Regulating
Saccharomyces
Ubp2

Semantics

Type Source Name
disease MESH Mitochondrial dysfunction
disease MESH neurological disorders
disease MESH etiology
disease MESH disease progression
drug DRUGBANK L-Cysteine
disease MESH oxidative stress
disease MESH neurodegenerative disorders
pathway REACTOME Metabolism
pathway REACTOME Reproduction
drug DRUGBANK Dihydrostreptomycin
pathway REACTOME SUMOylation
pathway REACTOME Deubiquitination
drug DRUGBANK Isoxaflutole
disease MESH defects
drug DRUGBANK Glycerin
drug DRUGBANK Dextrose unspecified form
drug DRUGBANK Coenzyme M
drug DRUGBANK Activated charcoal
drug DRUGBANK Pentaerythritol tetranitrate
drug DRUGBANK L-Leucine

Original Article

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