A Key Role of the EMC Complex for Mitochondrial Respiration and Quiescence in Fission Yeasts

In eukaryotes, oxygen consumption is mainly driven by the respiratory activity of mitochondria, which generates most of the cellular energy that sustains life. This parameter provides direct information about mitochondrial activity of all aerobic biological systems. Using the Seahorse analyzer instr...

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Detalles Bibliográficos
Autores: Berraquero, Modesto, Álvarez Tallada, Víctor, Jiménez, Juan
Tipo de recurso: artículo
Fecha de publicación:2025
País:España
Institución:Universidad Pablo de Olavide (UPO)
Repositorio:RIO. Repositorio Institucional Olavide
Idioma:inglés
OAI Identifier:oai:dnet:rio_________::af52043c547850217329c3e80656d9aa
Acceso en línea:https://hdl.handle.net/10433/26633
Access Level:acceso abierto
Palabra clave:EMC complex
Ergosterol
Fission yeast
Mitochondria
Oxygen consumption
Quiescence
Descripción
Sumario:In eukaryotes, oxygen consumption is mainly driven by the respiratory activity of mitochondria, which generates most of the cellular energy that sustains life. This parameter provides direct information about mitochondrial activity of all aerobic biological systems. Using the Seahorse analyzer instrument, we show here that deletion of the oca3/emc2 gene (oca3Δ) encoding the Emc2 subunit of the ER membrane complex (EMC), a conserved chaperone/insertase that aids membrane protein biogenesis in the ER, severely affects oxygen consumption rates and quiescence survival in Schizosaccharomyces pombe yeast cells. Remarkably, the respiratory defect of the oca3Δ mutation (EMC dysfunction) is rescued synergistically by disruption of ergosterol biosynthesis (erg5Δ) and the action of the membrane fluidizing agent tween 20, suggesting a direct role of membrane fluidity and sterol composition in mitochondrial respiration in the fission yeast.