Antioxidants (Basel, Switzerland)Aug 27, 2026

Calcium Entry into Mitochondria May Cause Energy Defects in Muscle Lacking PDR-1/Parkin in C. elegans

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Abstract

Silencing of pdr-1 in Caenorhabditis elegans resulted in elevated mitochondrial reactive oxygen species (mtROS) levels and locomotor impairments.

PDR-1/Parkin deficiency is linked to mitochondrial dysfunction and muscle cell damage.
Age-related mitochondrial fragmentation was reduced by silencing pdr-1, but this led to later locomotor activity impairments.
Elevated mtROS levels were observed in muscle cells lacking PDR-1 by day 2 of adulthood.
In PDR-1-deficient muscle cells, mitochondrial membrane potential was reduced alongside increased mtROS.
Mitochondrial calcium levels were higher in muscle cells deficient in PDR-1.
The mtROS increase related to PDR-1 deficiency was decreased in mcu-1 mutants, suggesting a role for mitochondrial calcium in oxidative stress.

Simplified

Parkinson's disease (PD) is widely regarded as a disorder of dopaminergic neurons that involves mitochondrial dysfunction, impaired mitophagy, and oxidative stress. However, the nature and significance of skeletal muscle pathology remain unclear. In this study, we used Caenorhabditis elegans, which lack muscle stem cells in adulthood, to examine the effects of PDR-1/Parkin deficiency on mitochondrial homeostasis and motor function under conditions where muscle regeneration does not occur. Silencing of pdr-1 attenuated age-related mitochondrial fragmentation in body-wall muscle cells but was associated with later impairments in locomotor activity and loss of nuclear GFP signals, suggesting progressive muscle cell damage. By day 2 of adulthood, mitochondrial reactive oxygen species (mtROS) levels were elevated in muscle cells subjected to pdr-1 RNAi, and in the pdr-1(gk448) mutant this mtROS elevation was accompanied by a reduction in mitochondrial membrane potential (ΔΨm). In vivo imaging further revealed elevated mitochondrial Ca²⁺ levels ([Ca²⁺]_mito) in PDR-1-deficient muscle cells. Moreover, the mtROS increase associated with PDR-1 deficiency was suppressed in mcu-1 mutants. These findings support a model in which MCU-1-dependent elevation of [Ca²⁺]_mito contributes to oxidative mitochondrial defects in PDR-1/Parkin-deficient muscle.

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Calcium Entry into Mitochondria May Cause Energy Defects in Muscle Lacking PDR-1/Parkin in C. elegans

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