Key result
Actin treadmilling inhibitors reveal actin remodeling consumes <5% of oyster cellular energy budgets.
Why the study?
Experimental quantifications of the energy expenditures incurred by actin treadmilling reorganization, especially in ectotherms, remain scarce.
Actin remodeling contributes minimally to the cellular energy budget in oyster cells, but specific disruption by cytochalasin D increases mitochondrial proton leak, highlighting a link between actin dynamics and mitochondrial metabolism.
Answers are grounded in this paper and cite their sources.
Leaves open actin-mitochondria links in mammals; hypothesis-generating for cardiovascular bioenergetics research.
Actin, the most abundant cellular protein, is essential for maintaining structural organization, mechanical stability and cellular motility. The actin cytoskeleton undergoes continuous ATP-dependent reorganization, incurring significant energy costs through treadmilling. However, experimental quantifications of these energy expenditures, especially in ectotherms, remain scarce. In this study, we assessed the energy costs of actin remodeling in the Pacific oyster Crassostrea [also Magallana] gigas, a marine bivalve, by measuring oxygen consumption in the presence of inhibitors of actin treadmilling (latrunculin B, jasplakinolide and cytochalasin D). Our results indicate that under normal physiological conditions, actin remodeling contributes less than 5% to the cellular energy budget in gill and mantle cells of oysters. Unexpectedly, cytochalasin D induced a marked increase in mitochondrial proton leak, observed both in intact cells and isolated mitochondria, suggesting a connection between actin disorganization and increased mitochondrial maintenance costs. Notably, jasplakinolide and latrunculin B, which inhibit actin treadmilling through different mechanisms from those of cytochalasin D, had no effect on mitochondrial respiration. This suggests that different mechanisms of actin cytoskeleton disruption can lead to distinct cellular outcomes. Given the significant role of proton leak in cellular respiration, these findings suggest that actin dynamics may play a crucial role in regulating mitochondrial metabolism, with broad implications for cellular energy costs. Further studies are needed to elucidate the underlying mechanisms of actin-mitochondria interactions and their broader relevance to the regulation of cellular metabolism in ectothermic species.
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Sokolov et al. (2025) studied Cellular energy metabolism. Actin treadmilling inhibitors (latrunculin B, jasplakinolide, cytochalasin D) vs. Normal physiological conditions was evaluated on Oxygen consumption and cellular energy budget. Actin treadmilling inhibitors revealed that actin remodeling contributes <5% to the cellular energy budget in oyster cells, though cytochalasin D unexpectedly increased mitochondrial proton leak.
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