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51. TFG binds LC3C to regulate ULK1 localization and autophagosome formation

Author

Carinci, Marianna, primary, Testa, Beatrice, additional, Bordi, Matteo, additional, Milletti, Giacomo, additional, Bonora, Massimo, additional, Antonucci, Laura, additional, Ferraina, Caterina, additional, Carro, Marta, additional, Kumar, Mukesh, additional, Ceglie, Donatella, additional, Eck, Franziska, additional, Nardacci, Roberta, additional, le Guerroué, Francois, additional, Petrini, Stefania, additional, Soriano, Maria E, additional, Caruana, Ignazio, additional, Doria, Valentina, additional, Manifava, Maria, additional, Peron, Camille, additional, Lambrughi, Matteo, additional, Tiranti, Valeria, additional, Behrends, Christian, additional, Papaleo, Elena, additional, Pinton, Paolo, additional, Giorgi, Carlotta, additional, Ktistakis, Nicholas T, additional, Locatelli, Franco, additional, Nazio, Francesca, additional, and Cecconi, Francesco, additional

Published
2021
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52. TFG binds LC3C to regulate ULK1 localization and autophagosome formation

Author

Carinci, Marianna, Testa, Beatrice, Bordi, Matteo, Milletti, Giacomo, Bonora, Massimo, Antonucci, Laura, Ferraina, Caterina, Carro, Marta, Kumar, Mukesh, Ceglie, Donatella, Eck, Franziska, Nardacci, Roberta, le Guerroué, Francois, Petrini, Stefania, Soriano, Maria E., Caruana, Ignazio, Doria, Valentina, Manifava, Maria, Peron, Camille, Lambrughi, Matteo, Tiranti, Valeria, Behrends, Christian, Papaleo, Elena, Pinton, Paolo, Giorgi, Carlotta, Ktistakis, Nicholas T., Locatelli, Franco, Nazio, Francesca, Cecconi, Francesco, Carinci, Marianna, Testa, Beatrice, Bordi, Matteo, Milletti, Giacomo, Bonora, Massimo, Antonucci, Laura, Ferraina, Caterina, Carro, Marta, Kumar, Mukesh, Ceglie, Donatella, Eck, Franziska, Nardacci, Roberta, le Guerroué, Francois, Petrini, Stefania, Soriano, Maria E., Caruana, Ignazio, Doria, Valentina, Manifava, Maria, Peron, Camille, Lambrughi, Matteo, Tiranti, Valeria, Behrends, Christian, Papaleo, Elena, Pinton, Paolo, Giorgi, Carlotta, Ktistakis, Nicholas T., Locatelli, Franco, Nazio, Francesca, and Cecconi, Francesco

Abstract

The early secretory pathway and autophagy are two essential and evolutionarily conserved endomembrane processes that are finely interlinked. Although growing evidence suggests that intracellular trafficking is important for autophagosome biogenesis, the molecular regulatory network involved is still not fully defined. In this study, we demonstrate a crucial effect of the COPII vesicle-related protein TFG (Trk-fused gene) on ULK1 puncta number and localization during autophagy induction. This, in turn, affects formation of the isolation membrane, as well as the correct dynamics of association between LC3B and early ATG proteins, leading to the proper formation of both omegasomes and autophagosomes. Consistently, fibroblasts derived from a hereditary spastic paraparesis (HSP) patient carrying mutated TFG (R106C) show defects in both autophagy and ULK1 puncta accumulation. In addition, we demonstrate that TFG activity in autophagy depends on its interaction with the ATG8 protein LC3C through a canonical LIR motif, thereby favouring LC3C-ULK1 binding. Altogether, our results uncover a link between TFG and autophagy and identify TFG as a molecular scaffold linking the early secretion pathway to autophagy.

Published
2021

53. ATP synthesis and storage

Author

Bonora, Massimo, Patergnani, Simone, Rimessi, Alessandro, De Marchi, Elena, Suski, Jan M., Bononi, Angela, Giorgi, Carlotta, Marchi, Saverio, Missiroli, Sonia, Poletti, Federica, Wieckowski, Mariusz R., and Pinton, Paolo

Published
2012
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56. A naturally occurring mutation in ATP synthase subunit c is associated with increased damage following hypoxia/reoxygenation in STEMI patients

Author

Morciano, Giampaolo, primary, Pedriali, Gaia, additional, Bonora, Massimo, additional, Pavasini, Rita, additional, Mikus, Elisa, additional, Calvi, Simone, additional, Bovolenta, Matteo, additional, Lebiedzinska-Arciszewska, Magdalena, additional, Pinotti, Mirko, additional, Albertini, Alberto, additional, Wieckowski, Mariusz R., additional, Giorgi, Carlotta, additional, Ferrari, Roberto, additional, Galluzzi, Lorenzo, additional, Campo, Gianluca, additional, and Pinton, Paolo, additional

Published
2021
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60. Mitochondrial P2X7 Receptor Localization Modulates Energy Metabolism Enhancing Physical Performance

Author

Sarti, Alba Clara, primary, Vultaggio-Poma, Valentina, additional, Falzoni, Simonetta, additional, Missiroli, Sonia, additional, Giuliani, Anna Lisa, additional, Boldrini, Paola, additional, Bonora, Massimo, additional, Faita, Francesco, additional, Di Lascio, Nicole, additional, Kusmic, Claudia, additional, Solini, Anna, additional, Novello, Salvatore, additional, Morari, Michele, additional, Rossato, Marco, additional, Wieckowski, Mariusz R, additional, Giorgi, Carlotta, additional, Pinton, Paolo, additional, and Di Virgilio, Francesco, additional

Published
2021
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63. Rehabilitation Improves Mitochondrial Energetics in Progressive Multiple Sclerosis: The Significant Role of Robot-Assisted Gait Training and of the Personalized Intensity

Author

Manfredini, Fabio, primary, Straudi, Sofia, additional, Lamberti, Nicola, additional, Patergnani, Simone, additional, Tisato, Veronica, additional, Secchiero, Paola, additional, Bernardi, Francesco, additional, Ziliotto, Nicole, additional, Marchetti, Giovanna, additional, Basaglia, Nino, additional, Bonora, Massimo, additional, and Pinton, Paolo, additional

Published
2020
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64. The P2X7 receptor localizes to the mitochondria, modulates mitochondrial energy metabolism and enhances physical performance

Author

Sarti, Alba Clara, primary, Vultaggio-Poma, Valentina, additional, Falzoni, Simonetta, additional, Missiroli, Sonia, additional, Giuliani, Anna Lisa, additional, Boldrini, Paola, additional, Bonora, Massimo, additional, Faita, Francesco, additional, Di Lascio, Nicole, additional, Kusmic, Claudia, additional, Solini, Anna, additional, Novello, Salvatore, additional, Morari, Michele, additional, Rossato, Marco, additional, Wieckowski, Mariusz R, additional, Giorgi, Carlotta, additional, Pinton, Paolo, additional, and Di Virgilio, Francesco, additional

Published
2020
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67. Mitophagy in Cardiovascular Diseases

Author

Morciano, Giampaolo, primary, Patergnani, Simone, additional, Bonora, Massimo, additional, Pedriali, Gaia, additional, Tarocco, Anna, additional, Bouhamida, Esmaa, additional, Marchi, Saverio, additional, Ancora, Gina, additional, Anania, Gabriele, additional, Wieckowski, Mariusz R., additional, Giorgi, Carlotta, additional, and Pinton, Paolo, additional

Published
2020
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68. New Evidence on the Pathological Role of Permeability Transition Pore in Patients with STEMI

Author

Morciano, Giampaolo, primary, Pedriali, Gaia, additional, Bonora, Massimo, additional, Pavasini, Rita, additional, Mikus, Elisa, additional, Calvi, Simone, additional, Bovolenta, Matteo, additional, Pinotti, Mirko, additional, Albertini, Alberto, additional, Wieckowski, Mariusz, additional, Giorgi, Carlotta, additional, Ferrari, Roberto, additional, Galluzzi, Lorenzo, additional, Campo, Gianluca, additional, and Pinton, Paolo, additional

Published
2020
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69. Autophagy and mitophagy biomarkers are reduced in sera of patients with Alzheimer’s disease and mild cognitive impairment

Author

Castellazzi, Massimiliano, primary, Patergnani, Simone, additional, Donadio, Mariapina, additional, Giorgi, Carlotta, additional, Bonora, Massimo, additional, Bosi, Cristina, additional, Brombo, Gloria, additional, Pugliatti, Maura, additional, Seripa, Davide, additional, Zuliani, Giovanni, additional, and Pinton, Paolo, additional

Published
2019
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72. Dysregulation of FLVCR1a-dependent mitochondrial calcium handling in neural progenitors causes congenital hydrocephalus

Author

Bertino, Francesca, Mukherjee, Dibyanti, Bonora, Massimo, Bagowski, Christoph, Nardelli, Jeannette, Metani, Livia, Zanin Venturini, Diletta Isabella, Chianese, Diego, Santander, Nicolas, Salaroglio, Iris Chiara, Hentschel, Andreas, Quarta, Elisa, Genova, Tullio, McKinney, Arpana Arjun, Allocco, Anna Lucia, Fiorito, Veronica, Petrillo, Sara, Ammirata, Giorgia, De Giorgio, Francesco, Dennis, Evan, Allington, Garrett, Maier, Felicitas, Shoukier, Moneef, Gloning, Karl-Philipp, Munaron, Luca, Mussano, Federico, Salsano, Ettore, Pareyson, Davide, di Rocco, Maja, Altruda, Fiorella, Panagiotakos, Georgia, Kahle, Kristopher T., Gressens, Pierre, Riganti, Chiara, Pinton, Paolo P., Roos, Andreas, Arnold, Thomas, Tolosano, Emanuela, and Chiabrando, Deborah

Abstract

Congenital hydrocephalus (CH), occurring in approximately 1/1,000 live births, represents an important clinical challenge due to the limited knowledge of underlying molecular mechanisms. The discovery of novel CH genes is thus essential to shed light on the intricate processes responsible for ventricular dilatation in CH. Here, we identify FLVCR1(feline leukemia virus subgroup C receptor 1) as a gene responsible for a severe form of CH in humans and mice. Mechanistically, our data reveal that the full-length isoform encoded by the FLVCR1gene, FLVCR1a, interacts with the IP3R3-VDAC complex located on mitochondria-associated membranes (MAMs) that controls mitochondrial calcium handling. Loss of Flvcr1ain mouse neural progenitor cells (NPCs) affects mitochondrial calcium levels and energy metabolism, leading to defective cortical neurogenesis and brain ventricle enlargement. These data point to defective NPCs calcium handling and metabolic activity as one of the pathogenetic mechanisms driving CH.

Published
2024
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73. TFEB-mediated increase in peripheral lysosomes regulates store-operated calcium entry

Author

Sbano, Luigi, Bonora, Massimo, Marchi, Saverio, Baldassari, Federica, Medina, Diego L., Giorgi, Carlotta, Pinton, Paolo, MEDINA SANABRIA, Diego Luis, BALLABIO, ANDREA, Sbano, Luigi, Bonora, Massimo, Marchi, Saverio, Baldassari, Federica, Medina, Diego L., Ballabio, Andrea, Giorgi, Carlotta, Pinton, Paolo, and MEDINA SANABRIA, Diego Luis

Subjects
0301 basic medicine, molecular mechanisms, chemistry.chemical_element, Gene Expression, Calcium, plasma membrane, Endoplasmic Reticulum, Exocytosis, Article, NO, Ca2+ regulated exocytosis, 03 medical and health sciences, Ca2+ release, Aequorin, L-phenylalanine 2-naphthylamide, endoplasmic reticulum, Ca2+ release, Ca2+ regulated exocytosis, molecular mechanisms, cellular clearance, plasma membrane, MDCK cells, homeostasis, biogenesis, homeostasis, Humans, L-phenylalanine 2-naphthylamide, Calcium Signaling, Multidisciplinary, Chemistry, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Endoplasmic reticulum, MDCK cells, Cell Membrane, Biological Transport, cellular clearance, biogenesis, Store-operated calcium entry, Cell biology, Cytosol, 030104 developmental biology, Gene Expression Regulation, Gene Knockdown Techniques, TFEB, Lysosomes, Intracellular, Homeostasis, HeLa Cells, Signal Transduction
Abstract

Lysosomes are membrane-bound organelles mainly involved in catabolic processes. In addition, lysosomes can expel their contents outside of the cell via lysosomal exocytosis. Some of the key steps involved in these important cellular processes, such as vesicular fusion and trafficking, require calcium (Ca2+) signaling. Recent data show that lysosomal functions are transcriptionally regulated by transcription factor EB (TFEB) through the induction of genes involved in lysosomal biogenesis and exocytosis. Given these observations, we investigated the roles of TFEB and lysosomes in intracellular Ca2+ homeostasis. We studied the effect of transient modulation of TFEB expression in HeLa cells by measuring the cytosolic Ca2+ response after capacitative Ca2+ entry activation and Ca2+ dynamics in the endoplasmic reticulum (ER) and directly in lysosomes. Our observations show that transient TFEB overexpression significantly reduces cytosolic Ca2+ levels under a capacitative influx model and ER re-uptake of calcium, increasing the lysosomal Ca2+ buffering capacity. Moreover, lysosomal destruction or damage abolishes these TFEB-dependent effects in both the cytosol and ER. These results suggest a possible Ca2+ buffering role for lysosomes and shed new light on lysosomal functions during intracellular Ca2+ homeostasis.

Published
2017

76. Calcium signaling around Mitochondria Associated Membranes (MAMs)

Author

Rimessi Alessandro, Poletti Federica, Missiroli Sonia, Marchi Saverio, Giorgi Carlotta, De Marchi Elena, Bonora Massimo, Bononi Angela, Agnoletto Chiara, Suski Jan M, Patergnani Simone, Duszynski Jerzy, Wieckowski Mariusz R, and Pinton Paolo

Subjects
Medicine, Cytology, QH573-671
Abstract

Abstract Calcium (Ca2+) homeostasis is fundamental for cell metabolism, proliferation, differentiation, and cell death. Elevation in intracellular Ca2+ concentration is dependent either on Ca2+ influx from the extracellular space through the plasma membrane, or on Ca2+ release from intracellular Ca2+ stores, such as the endoplasmic/sarcoplasmic reticulum (ER/SR). Mitochondria are also major components of calcium signalling, capable of modulating both the amplitude and the spatio-temporal patterns of Ca2+ signals. Recent studies revealed zones of close contact between the ER and mitochondria called MAMs (Mitochondria Associated Membranes) crucial for a correct communication between the two organelles, including the selective transmission of physiological and pathological Ca2+ signals from the ER to mitochondria. In this review, we summarize the most up-to-date findings on the modulation of intracellular Ca2+ release and Ca2+ uptake mechanisms. We also explore the tight interplay between ER- and mitochondria-mediated Ca2+ signalling, covering the structural and molecular properties of the zones of close contact between these two networks.

Published
2011
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77. Additional file 1: of The effectiveness of Robot-Assisted Gait Training versus conventional therapy on mobility in severely disabled progressIve MultiplE sclerosis patients (RAGTIME): study protocol for a randomized controlled trial

Author

Straudi, Sofia, Manfredini, Fabio, Lamberti, Nicola, Zamboni, Paolo, Bernardi, Francesco, Marchetti, Giovanna, Pinton, Paolo, Bonora, Massimo, Secchiero, Paola, Tisato, Veronica, Volpato, Stefano, and Basaglia, Nino

Abstract

SPIRIT filled checklist. (DOC 124Â kb)

Published
2017
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78. A mitochondrial NADPH-cholesterol axis regulates extracellular vesicle biogenesis to support hematopoietic stem cell fate

Author

Bonora, Massimo, Morganti, Claudia, van Gastel, Nick, Ito, Kyoko, Calura, Enrica, Zanolla, Ilaria, Ferroni, Letizia, Zhang, Yang, Jung, Yookyung, Sales, Gabriele, Martini, Paolo, Nakamura, Takahisa, Lasorsa, Francesco Massimo, Finkel, Toren, Lin, Charles P., Zavan, Barbara, Pinton, Paolo, Georgakoudi, Irene, Romualdi, Chiara, Scadden, David T., and Ito, Keisuke

Abstract

Mitochondrial fatty acid oxidation (FAO) is essential for hematopoietic stem cell (HSC) self-renewal; however, the mechanism by which mitochondrial metabolism controls HSC fate remains unknown. Here, we show that within the hematopoietic lineage, HSCs have the largest mitochondrial NADPH pools, which are required for proper HSC cell fate and homeostasis. Bioinformatic analysis of the HSC transcriptome, biochemical assays, and genetic inactivation of FAO all indicate that FAO-generated NADPH fuels cholesterol synthesis in HSCs. Interference with FAO disturbs the segregation of mitochondrial NADPH toward corresponding daughter cells upon single HSC division. Importantly, we have found that the FAO-NADPH-cholesterol axis drives extracellular vesicle (EV) biogenesis and release in HSCs, while inhibition of EV signaling impairs HSC self-renewal. These data reveal the existence of a mitochondrial NADPH-cholesterol axis for EV biogenesis that is required for hematopoietic homeostasis and highlight the non-stochastic nature of HSC fate determination.

Published
2024
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81. Discovery of Novel 1,3,8-Triazaspiro[4.5]decane Derivatives That Target the c Subunit of F1/FO-Adenosine Triphosphate (ATP) Synthase for the Treatment of Reperfusion Damage in Myocardial Infarction

Author

Morciano, Giampaolo, primary, Preti, Delia, additional, Pedriali, Gaia, additional, Aquila, Giorgio, additional, Missiroli, Sonia, additional, Fantinati, Anna, additional, Caroccia, Natascia, additional, Pacifico, Salvatore, additional, Bonora, Massimo, additional, Talarico, Anna, additional, Morganti, Claudia, additional, Rizzo, Paola, additional, Ferrari, Roberto, additional, Wieckowski, Mariusz R., additional, Campo, Gianluca, additional, Giorgi, Carlotta, additional, Trapella, Claudio, additional, and Pinton, Paolo, additional

Published
2018
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85. Mitochondrial permeability transition involves dissociation of F 1F O ATPsynthase dimers and C‐ring conformation

Author

Bonora, Massimo, primary, Morganti, Claudia, additional, Morciano, Giampaolo, additional, Pedriali, Gaia, additional, Lebiedzinska‐Arciszewska, Magdalena, additional, Aquila, Giorgio, additional, Giorgi, Carlotta, additional, Rizzo, Paola, additional, Campo, Gianluca, additional, Ferrari, Roberto, additional, Kroemer, Guido, additional, Wieckowski, Mariusz R, additional, Galluzzi, Lorenzo, additional, and Pinton, Paolo, additional

Published
2017
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88. The effectiveness of Robot-Assisted Gait Training versus conventional therapy on mobility in severely disabled progressIve MultiplE sclerosis patients (RAGTIME): study protocol for a randomized controlled trial

Author

Straudi, Sofia, primary, Manfredini, Fabio, additional, Lamberti, Nicola, additional, Zamboni, Paolo, additional, Bernardi, Francesco, additional, Marchetti, Giovanna, additional, Pinton, Paolo, additional, Bonora, Massimo, additional, Secchiero, Paola, additional, Tisato, Veronica, additional, Volpato, Stefano, additional, and Basaglia, Nino, additional

Published
2017
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90. PML at Mitochondria-Associated Membranes Is Critical for the Repression of Autophagy and Cancer Development

Author

Missiroli, Sonia, primary, Bonora, Massimo, additional, Patergnani, Simone, additional, Poletti, Federica, additional, Perrone, Mariasole, additional, Gafà, Roberta, additional, Magri, Eros, additional, Raimondi, Andrea, additional, Lanza, Giovanni, additional, Tacchetti, Carlo, additional, Kroemer, Guido, additional, Pandolfi, Pier Paolo, additional, Pinton, Paolo, additional, and Giorgi, Carlotta, additional

Published
2016
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91. Involvement of the P2X7-NLRP3 axis in leukemic cell proliferation and death

Author

Salaro, Erica, primary, Rambaldi, Alessia, additional, Falzoni, Simonetta, additional, Amoroso, Francesca Saveria, additional, Franceschini, Alessia, additional, Sarti, Alba Clara, additional, Bonora, Massimo, additional, Cavazzini, Francesco, additional, Rigolin, Gian Matteo, additional, Ciccone, Maria, additional, Audrito, Valentina, additional, Deaglio, Silvia, additional, Pelegrin, Pablo, additional, Pinton, Paolo, additional, Cuneo, Antonio, additional, and Di Virgilio, Francesco, additional

Published
2016
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93. Mutations of C19orf12, coding for a transmembrane glycine zipper containing mitochondrial protein, cause mis-localization of the protein, inability to respond to oxidative stress and increased mitochondrial Ca2+

Author

Venco, Paola, Bonora, Massimo, Giorgi, Carlotta, Papaleo, Elena, Iuso, Arcangela, Prokisch, Holger, Pinton, Paolo, Tiranti, Valeria, Venco, Paola, Bonora, Massimo, Giorgi, Carlotta, Papaleo, Elena, Iuso, Arcangela, Prokisch, Holger, Pinton, Paolo, and Tiranti, Valeria

Abstract

Mutations in C19orf12 have been identified in patients affected by Neurodegeneration with Brain Iron Accumulation (NBIA), a clinical entity characterized by iron accumulation in the basal ganglia. By using western blot analysis with specific antibody and confocal studies, we showed that wild-type C19orf12 protein was not exclusively present in mitochondria, but also in the Endoplasmic Reticulum (ER) and MAM (Mitochondria Associated Membrane), while mutant C19orf12 variants presented a different localization. Moreover, after induction of oxidative stress, a GFP-tagged C19orf12 wild-type protein was able to relocate to the cytosol. On the contrary, mutant isoforms were not able to respond to oxidative stress. High mitochondrial calcium concentration and increased H2O2 induced apoptosis were found in fibroblasts derived from one patient as compared to controls. C19orf12 protein is a 17 kDa mitochondrial membrane-associated protein whose function is still unknown. Our in silico investigation suggests that, the glycine zipper motifs of C19orf12 form helical regions spanning the membrane. The N- and C-terminal regions with respect to the transmembrane portion, on the contrary, are predicted to rearrange in a structural domain, which is homologs to the N-terminal regulatory domain of the magnesium transporter MgtE, suggesting that C19orf12 may act as a regulatory protein for human MgtE transporters. The mutations here described affect respectively one glycine residue of the glycine zipper motifs, which are involved in dimerization of transmembrane helices and predicted to impair the correct localization of the protein into the membranes, and one residue present in the regulatory domain, which is important for protein-protein interaction.

Published
2015

94. Reversal of the glycolytic phenotype of primary effusion lymphoma cells by combined targeting of cellular metabolism and PI3K/Akt/ mTOR signaling

Author

Mediani, Laura, primary, Gibellini, Federica, additional, Bertacchini, Jessika, additional, Frasson, Chiara, additional, Bosco, Raffaella, additional, Accordi, Benedetta, additional, Basso, Giuseppe, additional, Bonora, Massimo, additional, Calabrò, Maria Luisa, additional, Mattiolo, Adriana, additional, Sgarbi, Gianluca, additional, Baracca, Alessandra, additional, Pinton, Paolo, additional, Riva, Giovanni, additional, Rampazzo, Enrico, additional, Petrizza, Luca, additional, Prodi, Luca, additional, Milani, Daniela, additional, Luppi, Mario, additional, Potenza, Leonardo, additional, De Pol, Anto, additional, Cocco, Lucio, additional, Capitani, Silvano, additional, and Marmiroli, Sandra, additional

Published
2015
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95. Discovery of Novel 1,3,8-Triazaspiro[4.5]decane Derivatives That Target the c Subunit of F1/FO‑Adenosine Triphosphate (ATP) Synthase for the Treatment of Reperfusion Damage in Myocardial Infarction.

Author

Morciano, Giampaolo, Preti, Delia, Pedriali, Gaia, Aquila, Giorgio, Missiroli, Sonia, Fantinati, Anna, Caroccia, Natascia, Pacifico, Salvatore, Bonora, Massimo, Talarico, Anna, Morganti, Claudia, Rizzo, Paola, Ferrari, Roberto, Wieckowski, Mariusz R., Campo, Gianluca, Giorgi, Carlotta, Trapella, Claudio, and Pinton, Paolo

Published
2018
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96. Mithocondrial physiology and calcium signalling partnership: from regulation of differentiation to oncosuppressor activity

Author

Bonora, Massimo

Subjects
inorganic chemicals, mitochondria, segnalazione cellulare, mitocondri, embryonic structures, differenziamento, BIO/11 Biologia molecolare, cancro, cancer, cell signalling, Settore BIO/11 - Biologia Molecolare, differentiation
Abstract

In recent years, mitochondria have gained much interest as organelles involved not only in the processes of obtaining energy, but also associated with novel roles in cell physiopathology. These roles range from mitochondria being the site for lipid synthesis, through constituting a buffering system for intracellular calcium, and from being a mediator of reactive oxygen species signalling to a regulator of different cell death types. This group of roles requires a highly regulated system of signalling mechanisms. One of these emerging mechanisms is the communication between the mitochondria and the endoplasmic reticulum. In fact, mitochondria and endoplasmic reticulum are tightly associated, in a region called mitochondria associated membranes, where several signalling events allow continuous communication between the two organelles. Among these signalling events, calcium signalling has been considered of great importance. Advanced techniques of molecular biology allow the development of tools for the investigation of these complex subcellular compartments. Particularly useful are those based on the green fluorescent protein and the calcium sensitive luminescent protein, aequorin. In this work, the aforementioned tools have been used to investigate mitochondrial physiology, especially its communications with the endoplasmic reticulum. Two different cellular events were studied: i) the regulation of apoptosis by a strategic oncosuppressor, p53 and ii) differentiation of oligodendrocytes progenitor cells into adult oligodendrocytes during stress condition generated by cytokines. Performed experiments allowed the describing of the endoplasmic reticulum as a new intracellular localization site of p53, where it increases the luminal calcium concentration, promoting the sensitivity to calcium dependent apoptotic stimuli. Simultaneously, it has been revealed how mitochondria are a target for TNFα in oligodendrocytes progenitors, where it promotes reactive oxygen species production and impairment of the respiratory chain activity, inhibiting cell differentiation without promoting cell death. In conclusion, these approaches reveal completely new relations between mitochondria, calcium signalling and cell physiology, shedding new light on the role for this fascinating organelle.

Published
2012

99. Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging

Author

Marchi, Saverio, Giorgi, Carlotta, Suski, Jan M., Agnoletto, Chiara, Bononi, Angela, Bonora, Massimo, De Marchi, Elena, Missiroli, Sonia, Patergnani, Simone, Poletti, Federica, Rimessi, Alessandro, Duszynski, Jerzy, Wieckowski, Mariusz R., and Pinton, Paolo

Subjects
Article Subject
Abstract

Reactive oxygen species (ROS) are highly reactive molecules, mainly generated inside mitochondria that can oxidize DNA, proteins, and lipids. At physiological levels, ROS function as “redox messengers” in intracellular signalling and regulation, whereas excess ROS induce cell death by promoting the intrinsic apoptotic pathway. Recent work has pointed to a further role of ROS in activation of autophagy and their importance in the regulation of aging. This review will focus on mitochondria as producers and targets of ROS and will summarize different proteins that modulate the redox state of the cell. Moreover, the involvement of ROS and mitochondria in different molecular pathways controlling lifespan will be reported, pointing out the role of ROS as a “balance of power,” directing the cell towards life or death.

Published
2012
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100. Protein Kinases and Phosphatases in the Control of Cell Fate

Author

Bononi, Angela, Agnoletto, Chiara, De Marchi, Elena, Marchi, Saverio, Patergnani, Simone, Bonora, Massimo, Giorgi, Carlotta, Missiroli, Sonia, Poletti, Federica, Rimessi, Alessandro, and Pinton, Paolo

Subjects
Article Subject
Abstract

Protein phosphorylation controls many aspects of cell fate and is often deregulated in pathological conditions. Several recent findings have provided an intriguing insight into the spatial regulation of protein phosphorylation across different subcellular compartments and how this can be finely orchestrated by specific kinases and phosphatases. In this review, the focus will be placed on (i) the phosphoinositide 3-kinase (PI3K) pathway, specifically on the kinases Akt and mTOR and on the phosphatases PP2a and PTEN, and on (ii) the PKC family of serine/threonine kinases. We will look at general aspects of cell physiology controlled by these kinases and phosphatases, highlighting the signalling pathways that drive cell division, proliferation, and apoptosis.

Published
2011
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