Browsing by Subject "Respiration"

Now showing 1 - 4 of 4
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    cAMP-Protein Kinase A and Stress-Activated MAP Kinase 1 signaling mediate transcriptional control of autophagy in fission yeast during glucose limitation or starvation.
    (Taylor and Francis Group, 2022-09-26) Pérez Díaz, Armando Jesús; Vázquez Marín, Beatriz; Vicente Soler, Jero; Prieto Ruiz, Francisco; Soto, Teresa; Franco, Alejandro; Cansado Vizoso, José; Madrid, Marisa; Genética y Microbiología
    Macroautophagy/autophagy is an essential adaptive physiological response in eukaryotes induced during nutrient starvation, including glucose, the primary immediate carbon and energy source for most cells. Although the molecular mechanisms that induce autophagy during glucose starvation have been extensively explored in the budding yeast Saccharomyces cerevisiae, little is known about how this coping response is regulated in the evolutionary distant fission yeast Schizosaccharomyces pombe. Here, we show that S. pombe autophagy in response to glucose limitation relies on mitochondrial respiration and the electron transport chain (ETC), but, in contrast to S. cerevisiae, the AMP-activated protein kinase (AMPK) and DNA damage response pathway components do not modulate fission yeast autophagic flux under these conditions. In the presence of glucose, the cAMP-protein kinase A (PKA) signaling pathway constitutively represses S. pombe autophagy by downregulating the transcription factor Rst2, which promotes the expression of respiratory genes required for autophagy induction under limited glucose availability. Furthermore, the stress-activated protein kinase (SAPK) signaling pathway, and its central mitogen-activated protein kinase (MAPK) Sty1, positively modulate autophagy upon glucose limitation at the transcriptional level through its downstream effector Atf1 and by direct in vivo phosphorylation of Rst2 at S292. Thus, our data indicate that the signaling pathways that govern autophagy during glucose shortage or starvation have evolved differently in S. pombe and uncover the existence of sophisticated and multifaceted mechanisms that control this self-preservation and survival response.
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    CORM-3 mitigates hypoxia/reoxygenation-induced injury in neonatal rat cardiomyocytes by regulating mitochondrial-mediated apoptosis and complex IV activity
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Qingsheng Niu; Xiaojuan Yang; Junwei Zheng; Xiaohong Wang; Fang Du; Biología Celular e Histología
    Background. Myocardial ischemia-reperfusion injury (MIRI) is a major contributor to myocardial infarction and leads to significant myocardial dysfunction. Mitochondria, crucial for cellular energy production, are particularly susceptible to damage during ischemia/reperfusion (I/R) events. Carbon monoxide-releasing molecule-3 (CORM-3), a water-soluble compound that releases carbon monoxide (CO), has demonstrated multiple protective effects against I/R injury. Mitochondria are recognized as selective targets for CO’s protective actions in cells. Purpose. This study aimed to explore whether CORM-3 mitigates cardiomyocyte injury during hypoxia/reoxygenation (H/R) by regulating the mitochondrial-mediated apoptosis pathway and mitochondrial respiration. Methods. Neonatal rat cardiomyocytes were cultured and randomly assigned into four groups: control group, H/R group (hypoxia for three hours followed by reoxygenation for six hours), CORM-3 group, and inactivated CORM-3 (iCORM-3) group. CORM-3 and iCORM-3 (12.5 μmol/L) were administered at the onset of hypoxia. Mitochondrial ultrastructure was assessed using transmission electron microscopy. The protein levels of caspase-3, caspase-9, mitochondrial cytochrome c, and cytosolic cytochrome c were analyzed via western blot. Mitochondrial membrane potential and intracellular reactive oxygen species (ROS) were measured by flow cytometry. ATP levels were quantified using an ATP Assay Kit, and mitochondrial respiratory chain complex IV activity was determined using a cytochrome oxidase activity colorimetric assay kit. Results. CORM-3 effectively reduced myocardial mitochondrial structural damage induced by H/R and downregulated the expression of caspase-3, caspase-9, and cytosolic cytochrome c. Moreover, CORM-3 inhibited cytochrome c release from mitochondria and enhanced mitochondrial membrane potential. Additionally, CORM-3 diminished ROS production and increased the activity of mitochondrial respiratory complex IV in cardiomyocytes. CORM-3 also alleviated the decline in ATP levels following H/R. The protective effects were lost when using inactivated CORM-3 (iCORM-3), suggesting that CO is the active mediator. Conclusion. The results indicate that CORM-3 effectively alleviates myocardial injury during H/R by inhibiting mitochondria-mediated apoptosis and enhancing mitochondrial respiratory function
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    Modelling of photosynthesis, respiration and nutrients yield coefficients in Scenedemus almeriensis culture as a function of nitrogen and phosphorus.
    (2021-09-14) Gómez serrano, Cintia; Acién Fernández, Francisco Gabriel; Fernández Sevilla, José María; Molina Grima, Emilio; Sánchez Zurano, Ana; Ingeniería Química
    Se aplicaron técnicas foto-respirométricas para evaluar la actividad fotosintética en organismos fototróficos. Estos métodos permiten analizar la respuesta fotosintética bajo diferentes condiciones. En este trabajo, se estudió la influencia de la disponibilidad de nutrientes (nitrato, amonio y fosfato) en la fotosíntesis y la respiración de Scenedesmus almeriensis mediante mediciones foto-respirométricas cortas. Tanto la fotosíntesis como la respiración aumentaron hasta un valor de saturación y posteriormente disminuyeron, mostrando inhibición a concentraciones altas. En cuanto a la influencia de la concentración de fósforo en las células de microalgas, se observó una tendencia hiperbólica similar, aunque no se detectó inhibición a concentraciones elevadas. A partir de estos datos experimentales, las tasas de respiración y fotosíntesis de S. almeriensis se modelaron utilizando la ecuación de Haldane para los datos de nitrato y amonio, y la ecuación de Monod para los datos de fosfato. Además, se realizaron experimentos para determinar los coeficientes de rendimiento de nitrógeno y fósforo en los cultivos de S. almeriensis. Los resultados mostraron que estos coeficientes no son constantes y se modifican según la concentración de nutrientes, evidenciando el fenómeno de absorción de lujo. Finalmente, los modelos propuestos se incorporaron en una herramienta de simulación para evaluar la actividad fotosintética y los coeficientes de rendimiento de nutrientes de S. almeriensis cuando se utilizan diferentes medios de cultivo y aguas residuales como fuente de nitrógeno y fósforo para su crecimiento.
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    Myosin II regulatory light chain phosphorylation and formin availability modulate cytokinesis upon changes in carbohydrate metabolism.
    (eLife Sciences Publications, 2023-03-10) Prieto Ruiz, Francisco; Gómez Gil, Elisa; Martín García, Rebeca; Pérez Díaz, Armando J.; Vicente Soler, Jero; Franco, Alejandro; Soto, Teresa; Pérez, Pilar; Madrid, Marisa; Cansado Vizoso, José; Genética y Microbiología
    Cytokinesis, which achieves the separation of daughter cells after mitosis completion, relies in animal cells on a contractile actomyosin ring (CAR), made of actin and class II myosins, whose activity is heavily influenced by regulatory light chain (RLC) phosphorylation. However, in simple eukaryotes such as fission yeast Schizosaccharomyces pombe, regulation of CAR dynamics by RLC phosphorylation seems dispensable. We found that redundant phosphorylation at Ser35 of the S. pombe RLC homolog Rlc1 by the p21-activated kinases Pak1 and Pak2, modulates Myosin II Myo2 activity and becomes essential for cytokinesis and cell growth during respiration. Previously, we showed that the Stress Activated Protein Kinase Pathway (SAPK) MAPK Sty1 controls fission yeast CAR integrity by downregulating formin For3 levels (Gomez-Gil et al.,2020). Here we report that reduced availability of formin For3-nucleated actin filaments for the CAR is the main reason for the required control of myosin II contractile activity by RLC phosphorylation during respiration-induced oxidative stress. Hence, recovery of For3 levels with antioxidants bypasses the control of Myosin II function regulated by RLC phosphorylation to allow cytokinesis and cell proliferation during respiration. Therefore, a fine-tuned interplay between Myosin II function by Rlc1 phosphorylation and environmentally controlled actin filament availability is critical for a successful cytokinesis in response to a switch to a respiratory carbohydrate metabolism.