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by claude@2026-07, 2026-07-06
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The paper investigates how EGF stimulation remodels mitochondrial behavior in human A431 carcinoma cells, focusing on the regulation of mitochondrial fission, transport, and localization during filopodia formation. It finds that EGF-induced cytosolic calcium drives mitochondrial fission into smaller, more mobile mitochondria that move to filopodia tips, with a calcium-dependent switch from Kif5B-mediated transport to Myo19-mediated transport. Mitochondrial calcium uptake via the MCU channel is required for mitochondrial redistribution, shape changes, and filopodia extension, and disrupting fission or calcium buffering impairs mitochondrial motility and protrusion formation. The study is limited to A431 carcinoma cells and EGF signaling, so findings may not directly extend to other cell types or in vivo contexts. This paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.
Abstract
SUMMARY Mitochondria are highly adaptable organelles that change their shape, distribution, and movement to meet cellular needs. We investigate how EGF stimulation remodels mitochondrial behavior in human A431 carcinoma cells, where EGF suppresses proliferation but enhances calcium signaling and cell motility. EGF triggers mitochondrial fission, resulting in smaller, more mobile mitochondria that relocate to the tips of newly formed filopodia. Mitochondrial transport involves Kif5B (microtubule-based) and Myo19 (actin-based) motor proteins, which are regulated differently by calcium. EGF stimulation increases cytosolic calcium, weakening Kif5B-mediated transport and making Myo19 the primary transporter. Mitochondrial calcium uptake through the MCU channel is essential for redistribution, shape changes, and filopodia extension. Disrupting mitochondrial fission or calcium buffering impairs mitochondrial motility and the formation of filopodia. High-resolution imaging reveals the coordinated transport of mitochondria, involving fission, motor switching, and localized calcium signaling. We provide insights into how mitochondrial transport supports actin remodeling and protrusive activity, with implications for cell migration and therapies targeting mitochondrial-cytoskeletal interactions. HIGHLIGHTS EGF stimulation remodels the morphology of the mitochondrial network Kif5B and Myo19 are required for mitochondrial motility Mitochondria display two different velocities depending on the cell region Calcium homeostasis contributes to mitochondrial network remodeling eTOC BLURB Cell powerhouses called mitochondria can change shape and move within cells along tracks called the cytoskeleton. Stimulation of cells by stressors, such as growth factors, can generate signals that cause mitochondria to migrate to the cell edges using molecular motors. Importantly, this movement enables cells to form finger-like projections, providing the energy necessary for cell migration.
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SUMMARY
Mitochondria are highly adaptable organelles that change their shape, distribution, and movement to meet cellular needs. We investigate how EGF stimulation remodels mitochondrial behavior in human A431 carcinoma cells, where EGF suppresses proliferation but enhances calcium signaling and cell motility. EGF triggers mitochondrial fission, resulting in smaller, more mobile mitochondria that relocate to the tips of newly formed filopodia. Mitochondrial transport involves Kif5B (microtubule-based) and Myo19 (actin-based) motor proteins, which are regulated differently by calcium. EGF stimulation increases cytosolic calcium, weakening Kif5B-mediated transport and making Myo19 the primary transporter. Mitochondrial calcium uptake through the MCU channel is essential for redistribution, shape changes, and filopodia extension. Disrupting mitochondrial fission or calcium buffering impairs mitochondrial motility and the formation of filopodia. High-resolution imaging reveals the coordinated transport of mitochondria, involving fission, motor switching, and localized calcium signaling. We provide insights into how mitochondrial transport supports actin remodeling and protrusive activity, with implications for cell migration and therapies targeting mitochondrial-cytoskeletal interactions.
HIGHLIGHTS
EGF stimulation remodels the morphology of the mitochondrial network
Kif5B and Myo19 are required for mitochondrial motility
Mitochondria display two different velocities depending on the cell region
Calcium homeostasis contributes to mitochondrial network remodeling
eTOC BLURB Cell powerhouses called mitochondria can change shape and move within cells along tracks called the cytoskeleton. Stimulation of cells by stressors, such as growth factors, can generate signals that cause mitochondria to migrate to the cell edges using molecular motors. Importantly, this movement enables cells to form finger-like projections, providing the energy necessary for cell migration.
Competing Interest Statement
The authors have declared no competing interest.
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