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575 results on '"Muñoz-Cánoves, Pura"'

1. Network-community analysis of cellular senescence

Author

Sabalic, Alda, Moiseeva, Victoria, Cisneros, Andres, Deryagin, Oleg, Perdiguero, Eusebio, Muñoz-Canoves, Pura, and Garcia-Ojalvo, Jordi

Subjects
Quantitative Biology - Quantitative Methods
Abstract

Most cellular phenotypes are genetically complex. Identifying the set of genes that are most closely associated with a specific cellular state is still an open question in many cases. Here we study the transcriptional profile of cellular senescence using a combination of network-based approaches, which include eigenvector centrality feature selection and community detection. We apply our method to cell-type-resolved RNA sequencing data obtained from injured muscle tissue in mice. The analysis identifies some genetic markers consistent with previous findings, and other previously unidentified ones, which are validated with previously published single-cell RNA sequencing data in a different type of tissue. The key identified genes, both those previously known and the newly identified ones, are transcriptional targets of factors known to be associated with established hallmarks of senescence, and can thus be interpreted as molecular correlates of such hallmarks. The method proposed here could be applied to any complex cellular phenotype even when only bulk RNA sequencing is available, provided the data is resolved by cell type., Comment: 20 pages, 11 figures

Published
2024

3. The G4 resolvase Dhx36 modulates cardiomyocyte differentiation and ventricular conduction system development

Author

Gómez-del Arco, Pablo, Isern, Joan, Jimenez-Carretero, Daniel, López-Maderuelo, Dolores, Piñeiro-Sabarís, Rebeca, El Abdellaoui-Soussi, Fadoua, Torroja, Carlos, Vera-Pedrosa, María Linarejos, Grima-Terrén, Mercedes, Benguria, Alberto, Simón-Chica, Ana, Queiro-Palou, Antonio, Dopazo, Ana, Sánchez-Cabo, Fátima, Jalife, José, de la Pompa, José Luis, Filgueiras-Rama, David, Muñoz-Cánoves, Pura, and Redondo, Juan Miguel

Published
2024
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4. Liver and muscle circadian clocks cooperate to support glucose tolerance in mice

Author

Smith, Jacob G, Koronowski, Kevin B, Mortimer, Thomas, Sato, Tomoki, Greco, Carolina M, Petrus, Paul, Verlande, Amandine, Chen, Siwei, Samad, Muntaha, Deyneka, Ekaterina, Mathur, Lavina, Blazev, Ronnie, Molendijk, Jeffrey, Kumar, Arun, Deryagin, Oleg, Vaca-Dempere, Mireia, Sica, Valentina, Liu, Peng, Orlando, Valerio, Parker, Benjamin L, Baldi, Pierre, Welz, Patrick-Simon, Jang, Cholsoon, Masri, Selma, Benitah, Salvador Aznar, Muñoz-Cánoves, Pura, and Sassone-Corsi, Paolo

Subjects
Biochemistry and Cell Biology, Biological Sciences, Digestive Diseases, Liver Disease, Sleep Research, Nutrition, Diabetes, 1.1 Normal biological development and functioning, Metabolic and endocrine, Mice, Animals, Circadian Clocks, Circadian Rhythm, Liver, Muscle, Skeletal, Glucose, Bmal1, CP: Metabolism, autonomy, circadian rhythms, endocrinology, glucose, inter-organ crosstalk, liver, metabolism, muscle, systems biology, Medical Physiology, Biological sciences
Abstract

Physiology is regulated by interconnected cell and tissue circadian clocks. Disruption of the rhythms generated by the concerted activity of these clocks is associated with metabolic disease. Here we tested the interactions between clocks in two critical components of organismal metabolism, liver and skeletal muscle, by rescuing clock function either in each organ separately or in both organs simultaneously in otherwise clock-less mice. Experiments showed that individual clocks are partially sufficient for tissue glucose metabolism, yet the connections between both tissue clocks coupled to daily feeding rhythms support systemic glucose tolerance. This synergy relies in part on local transcriptional control of the glucose machinery, feeding-responsive signals such as insulin, and metabolic cycles that connect the muscle and liver. We posit that spatiotemporal mechanisms of muscle and liver play an essential role in the maintenance of systemic glucose homeostasis and that disrupting this diurnal coordination can contribute to metabolic disease.

Published
2023

5. Multimodal cell atlas of the ageing human skeletal muscle

Author

Lai, Yiwei, Ramírez-Pardo, Ignacio, Isern, Joan, An, Juan, Perdiguero, Eusebio, Serrano, Antonio L., Li, Jinxiu, García-Domínguez, Esther, Segalés, Jessica, Guo, Pengcheng, Lukesova, Vera, Andrés, Eva, Zuo, Jing, Yuan, Yue, Liu, Chuanyu, Viña, José, Doménech-Fernández, Julio, Gómez-Cabrera, Mari Carmen, Song, Yancheng, Liu, Longqi, Xu, Xun, Muñoz-Cánoves, Pura, and Esteban, Miguel A.

Published
2024
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7. The central clock suffices to drive the majority of circulatory metabolic rhythms

Author

Petrus, Paul, Smith, Jacob G, Koronowski, Kevin B, Chen, Siwei, Sato, Tomoki, Greco, Carolina M, Mortimer, Thomas, Welz, Patrick-Simon, Zinna, Valentina M, Shimaji, Kohei, Cervantes, Marlene, Punzo, Daniela, Baldi, Pierre, Muñoz-Cánoves, Pura, Sassone-Corsi, Paolo, and Benitah, Salvador Aznar

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Sleep Research, Neurosciences, Nutrition
Abstract

Life on Earth anticipates recurring 24-hour environmental cycles via genetically encoded molecular clocks active in all mammalian organs. Communication between these clocks controls circadian homeostasis. Intertissue communication is mediated, in part, by temporal coordination of metabolism. Here, we characterize the extent to which clocks in different organs control systemic metabolic rhythms, an area that remains largely unexplored. We analyzed the metabolome of serum from mice with tissue-specific expression of the clock gene Bmal1. Having functional hepatic and muscle clocks can only drive a minority (13%) of systemic metabolic rhythms. Conversely, limiting Bmal1 expression to the central pacemaker in the brain restores rhythms to 57% of circulatory metabolites. Rhythmic feeding imposed on clockless mice resulted in a similar rescue, indicating that the central clock mainly regulates metabolic rhythms via behavior. These findings explicate the circadian communication between tissues and highlight the importance of the central clock in governing those signals.

Published
2022

8. The epidermal circadian clock integrates and subverts brain signals to guarantee skin homeostasis

Author

Mortimer, Thomas, Zinna, Valentina M., Atalay, Muge, Laudanna, Carmelo, Deryagin, Oleg, Posas, Guillem, Smith, Jacob G., García-Lara, Elisa, Vaca-Dempere, Mireia, Monteiro de Assis, Leonardo Vinícius, Heyde, Isabel, Koronowski, Kevin B., Petrus, Paul, Greco, Carolina M., Forrow, Stephen, Oster, Henrik, Sassone-Corsi, Paolo, Welz, Patrick-Simon, Muñoz-Cánoves, Pura, and Benitah, Salvador Aznar

Published
2024
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9. Integration of feeding behavior by the liver circadian clock reveals network dependency of metabolic rhythms

Author

Greco, Carolina M, Koronowski, Kevin B, Smith, Jacob G, Shi, Jiejun, Kunderfranco, Paolo, Carriero, Roberta, Chen, Siwei, Samad, Muntaha, Welz, Patrick-Simon, Zinna, Valentina M, Mortimer, Thomas, Chun, Sung Kook, Shimaji, Kohei, Sato, Tomoki, Petrus, Paul, Kumar, Arun, Vaca-Dempere, Mireia, Deryagin, Oleg, Van, Cassandra, Kuhn, José Manuel Monroy, Lutter, Dominik, Seldin, Marcus M, Masri, Selma, Li, Wei, Baldi, Pierre, Dyar, Kenneth A, Muñoz-Cánoves, Pura, Benitah, Salvador Aznar, and Sassone-Corsi, Paolo

Subjects
Biochemistry and Cell Biology, Biological Sciences, Sleep Research, Digestive Diseases, Nutrition, Obesity, Genetics, Liver Disease, 1.1 Normal biological development and functioning
Abstract

The mammalian circadian clock, expressed throughout the brain and body, controls daily metabolic homeostasis. Clock function in peripheral tissues is required, but not sufficient, for this task. Because of the lack of specialized animal models, it is unclear how tissue clocks interact with extrinsic signals to drive molecular oscillations. Here, we isolated the interaction between feeding and the liver clock by reconstituting Bmal1 exclusively in hepatocytes (Liver-RE), in otherwise clock-less mice, and controlling timing of food intake. We found that the cooperative action of BMAL1 and the transcription factor CEBPB regulates daily liver metabolic transcriptional programs. Functionally, the liver clock and feeding rhythm are sufficient to drive temporal carbohydrate homeostasis. By contrast, liver rhythms tied to redox and lipid metabolism required communication with the skeletal muscle clock, demonstrating peripheral clock cross-talk. Our results highlight how the inner workings of the clock system rely on communicating signals to maintain daily metabolism.

Published
2021

11. Senescence atlas reveals an aged-like inflamed niche that blunts muscle regeneration

Author

Moiseeva, Victoria, Cisneros, Andrés, Sica, Valentina, Deryagin, Oleg, Lai, Yiwei, Jung, Sascha, Andrés, Eva, An, Juan, Segalés, Jessica, Ortet, Laura, Lukesova, Vera, Volpe, Giacomo, Benguria, Alberto, Dopazo, Ana, Aznar-Benitah, Salvador, Urano, Yasuteru, del Sol, Antonio, Esteban, Miguel A., Ohkawa, Yasuyuki, Serrano, Antonio L., Perdiguero, Eusebio, and Muñoz-Cánoves, Pura

Published
2023
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12. Polycomb Ezh1 maintains murine muscle stem cell quiescence through non-canonical regulation of Notch signaling

Author

Feng, Xuesong, Wang, A. Hongjun, Juan, Aster H., Ko, Kyung Dae, Jiang, Kan, Riparini, Giulia, Ciuffoli, Veronica, Kaba, Aissah, Lopez, Christopher, Naz, Faiza, Jarnik, Michal, Aliberti, Elizabeth, Hu, Shenyuan, Segalés, Jessica, Khateb, Mamduh, Acevedo-Luna, Natalia, Randazzo, Davide, Cheung, Tom H., Muñoz-Cánoves, Pura, Dell’Orso, Stefania, and Sartorelli, Vittorio

Published
2023
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13. 3-Deazaadenosine alleviates senescence to promote cellular fitness and cell therapy efficiency in mice

Author

Guerrero, Ana, Innes, Andrew J., Roux, Pierre-François, Buisman, Sonja C., Jung, Johannes, Ortet, Laura, Moiseeva, Victoria, Wagner, Verena, Robinson, Lucas, Ausema, Albertina, Potapova, Anna, Perdiguero, Eusebio, Weersing, Ellen, Aarts, Marieke, Martin, Nadine, Wuestefeld, Torsten, Muñoz-Cánoves, Pura, de Haan, Gerald, Bischof, Oliver, and Gil, Jesús

Published
2022
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14. Stem Cells and Aging

Author

Perdiguero, Eusebio, primary, García-Prat, Laura, additional, Sousa-Victor, Pedro, additional, and Muñoz-Cánoves, Pura, additional

Published
2023
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15. Sestrin prevents atrophy of disused and aging muscles by integrating anabolic and catabolic signals.

Author

Segalés, Jessica, Perdiguero, Eusebio, Serrano, Antonio L, Sousa-Victor, Pedro, Ortet, Laura, Jardí, Mercè, Budanov, Andrei V, Garcia-Prat, Laura, Sandri, Marco, Thomson, David M, Karin, Michael, Hee Lee, Jun, and Muñoz-Cánoves, Pura

Subjects
Muscle, Skeletal, Animals, Mice, Inbred C57BL, Mice, Transgenic, Humans, Mice, Muscular Atrophy, Disease Models, Animal, Muscle Proteins, Heat-Shock Proteins, Nuclear Proteins, Signal Transduction, Gene Expression, Aging, Autophagy, Male, Sarcopenia, Forkhead Box Protein O1, Forkhead Box Protein O3, Mechanistic Target of Rapamycin Complex 1, Disease Models, Animal, Inbred C57BL, Transgenic, Muscle, Skeletal
Abstract

A unique property of skeletal muscle is its ability to adapt its mass to changes in activity. Inactivity, as in disuse or aging, causes atrophy, the loss of muscle mass and strength, leading to physical incapacity and poor quality of life. Here, through a combination of transcriptomics and transgenesis, we identify sestrins, a family of stress-inducible metabolic regulators, as protective factors against muscle wasting. Sestrin expression decreases during inactivity and its genetic deficiency exacerbates muscle wasting; conversely, sestrin overexpression suffices to prevent atrophy. This protection occurs through mTORC1 inhibition, which upregulates autophagy, and AKT activation, which in turn inhibits FoxO-regulated ubiquitin-proteasome-mediated proteolysis. This study reveals sestrin as a central integrator of anabolic and degradative pathways preventing muscle wasting. Since sestrin also protected muscles against aging-induced atrophy, our findings have implications for sarcopenia.

Published
2020

17. Mitochondrial dynamics maintain muscle stem cell regenerative competence throughout adult life by regulating metabolism and mitophagy

Author

Hong, Xiaotong, Isern, Joan, Campanario, Silvia, Perdiguero, Eusebio, Ramírez-Pardo, Ignacio, Segalés, Jessica, Hernansanz-Agustín, Pablo, Curtabbi, Andrea, Deryagin, Oleg, Pollán, Angela, González-Reyes, José A., Villalba, José M., Sandri, Marco, Serrano, Antonio L., Enríquez, José A., and Muñoz-Cánoves, Pura

Published
2022
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18. Spatiotemporal transcriptomic atlas of mouse organogenesis using DNA nanoball-patterned arrays

Author

Chen, Ao, Liao, Sha, Cheng, Mengnan, Ma, Kailong, Wu, Liang, Lai, Yiwei, Qiu, Xiaojie, Yang, Jin, Xu, Jiangshan, Hao, Shijie, Wang, Xin, Lu, Huifang, Chen, Xi, Liu, Xing, Huang, Xin, Li, Zhao, Hong, Yan, Jiang, Yujia, Peng, Jian, Liu, Shuai, Shen, Mengzhe, Liu, Chuanyu, Li, Quanshui, Yuan, Yue, Wei, Xiaoyu, Zheng, Huiwen, Feng, Weimin, Wang, Zhifeng, Liu, Yang, Wang, Zhaohui, Yang, Yunzhi, Xiang, Haitao, Han, Lei, Qin, Baoming, Guo, Pengcheng, Lai, Guangyao, Muñoz-Cánoves, Pura, Maxwell, Patrick H., Thiery, Jean Paul, Wu, Qing-Feng, Zhao, Fuxiang, Chen, Bichao, Li, Mei, Dai, Xi, Wang, Shuai, Kuang, Haoyan, Hui, Junhou, Wang, Liqun, Fei, Ji-Feng, Wang, Ou, Wei, Xiaofeng, Lu, Haorong, Wang, Bo, Liu, Shiping, Gu, Ying, Ni, Ming, Zhang, Wenwei, Mu, Feng, Yin, Ye, Yang, Huanming, Lisby, Michael, Cornall, Richard J., Mulder, Jan, Uhlén, Mathias, Esteban, Miguel A., Li, Yuxiang, Liu, Longqi, Xu, Xun, and Wang, Jian

Published
2022
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20. Cell transcriptomic atlas of the non-human primate Macaca fascicularis

Author

Han, Lei, Wei, Xiaoyu, Liu, Chuanyu, Volpe, Giacomo, Zhuang, Zhenkun, Zou, Xuanxuan, Wang, Zhifeng, Pan, Taotao, Yuan, Yue, Zhang, Xiao, Fan, Peng, Guo, Pengcheng, Lai, Yiwei, Lei, Ying, Liu, Xingyuan, Yu, Feng, Shangguan, Shuncheng, Lai, Guangyao, Deng, Qiuting, Liu, Ya, Wu, Liang, Shi, Quan, Yu, Hao, Huang, Yunting, Cheng, Mengnan, Xu, Jiangshan, Liu, Yang, Wang, Mingyue, Wang, Chunqing, Zhang, Yuanhang, Xie, Duo, Yang, Yunzhi, Yu, Yeya, Zheng, Huiwen, Wei, Yanrong, Huang, Fubaoqian, Lei, Junjie, Huang, Waidong, Zhu, Zhiyong, Lu, Haorong, Wang, Bo, Wei, Xiaofeng, Chen, Fengzhen, Yang, Tao, Du, Wensi, Chen, Jing, Xu, Shibo, An, Juan, Ward, Carl, Wang, Zongren, Pei, Zhong, Wong, Chi-Wai, Liu, Xiaolei, Zhang, Huafeng, Liu, Mingyuan, Qin, Baoming, Schambach, Axel, Isern, Joan, Feng, Liqiang, Liu, Yan, Guo, Xiangyu, Liu, Zhen, Sun, Qiang, Maxwell, Patrick H., Barker, Nick, Muñoz-Cánoves, Pura, Gu, Ying, Mulder, Jan, Uhlen, Mathias, Tan, Tao, Liu, Shiping, Yang, Huanming, Wang, Jian, Hou, Yong, Xu, Xun, Esteban, Miguel A., and Liu, Longqi

Published
2022
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23. A Network of Macrophages Supports Mitochondrial Homeostasis in the Heart

Author

Nicolás-Ávila, José A., Lechuga-Vieco, Ana V., Esteban-Martínez, Lorena, Sánchez-Díaz, María, Díaz-García, Elena, Santiago, Demetrio J., Rubio-Ponce, Andrea, Li, Jackson LiangYao, Balachander, Akhila, Quintana, Juan A., Martínez-de-Mena, Raquel, Castejón-Vega, Beatriz, Pun-García, Andrés, Través, Paqui G., Bonzón-Kulichenko, Elena, García-Marqués, Fernando, Cussó, Lorena, A-González, Noelia, González-Guerra, Andrés, Roche-Molina, Marta, Martin-Salamanca, Sandra, Crainiciuc, Georgiana, Guzmán, Gabriela, Larrazabal, Jagoba, Herrero-Galán, Elías, Alegre-Cebollada, Jorge, Lemke, Greg, Rothlin, Carla V., Jimenez-Borreguero, Luis Jesús, Reyes, Guillermo, Castrillo, Antonio, Desco, Manuel, Muñoz-Cánoves, Pura, Ibáñez, Borja, Torres, Miguel, Ng, Lai Guan, Priori, Silvia G., Bueno, Héctor, Vázquez, Jesús, Cordero, Mario D., Bernal, Juan A., Enríquez, José A., and Hidalgo, Andrés

Published
2020
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26. Author Correction: Senescence atlas reveals an aged-like inflamed niche that blunts muscle regeneration

Author

Moiseeva, Victoria, Cisneros, Andrés, Sica, Valentina, Deryagin, Oleg, Lai, Yiwei, Jung, Sascha, Andrés, Eva, An, Juan, Segalés, Jessica, Ortet, Laura, Lukesova, Vera, Volpe, Giacomo, Benguria, Alberto, Dopazo, Ana, Benitah, Salvador Aznar, Urano, Yasuteru, del Sol, Antonio, Esteban, Miguel A., Ohkawa, Yasuyuki, Serrano, Antonio L., Perdiguero, Eusebio, and Muñoz-Cánoves, Pura

Published
2023
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27. The ins and outs of muscle stem cell aging.

Author

Brack, Andrew S and Muñoz-Cánoves, Pura

Subjects
Muscle, Skeletal, Satellite Cells, Skeletal Muscle, Animals, Humans, Cell Aging, Signal Transduction, Cell Differentiation, Cell Proliferation, Phenotype, Stem Cell Niche, Cellular Senescence, Muscle, Skeletal, Satellite Cells, Skeletal Muscle
Abstract

Skeletal muscle has a remarkable capacity to regenerate by virtue of its resident stem cells (satellite cells). This capacity declines with aging, although whether this is due to extrinsic changes in the environment and/or to cell-intrinsic mechanisms associated to aging has been a matter of intense debate. Furthermore, while some groups support that satellite cell aging is reversible by a youthful environment, others support cell-autonomous irreversible changes, even in the presence of youthful factors. Indeed, whereas the parabiosis paradigm has unveiled the environment as responsible for the satellite cell functional decline, satellite cell transplantation studies support cell-intrinsic deficits with aging. In this review, we try to shed light on the potential causes underlying these discrepancies. We propose that the experimental paradigm used to interrogate intrinsic and extrinsic regulation of stem cell function may be a part of the problem. The assays deployed are not equivalent and may overburden specific cellular regulatory processes and thus probe different aspects of satellite cell properties. Finally, distinct subsets of satellite cells may be under different modes of molecular control and mobilized preferentially in one paradigm than in the other. A better understanding of how satellite cells molecularly adapt during aging and their context-dependent deployment during injury and transplantation will lead to the development of efficacious compensating strategies that maintain stem cell fitness and tissue homeostasis throughout life.

Published
2016

28. FoxO maintains a genuine muscle stem-cell quiescent state until geriatric age

Author

García-Prat, Laura, Perdiguero, Eusebio, Alonso-Martín, Sonia, Dell’Orso, Stefania, Ravichandran, Srikanth, Brooks, Stephen R., Juan, Aster H., Campanario, Silvia, Jiang, Kan, Hong, Xiaotong, Ortet, Laura, Ruiz-Bonilla, Vanessa, Flández, Marta, Moiseeva, Victoria, Rebollo, Elena, Jardí, Mercè, Sun, Hong-Wei, Musarò, Antonio, Sandri, Marco, del Sol, Antonio, Sartorelli, Vittorio, and Muñoz-Cánoves, Pura

Published
2020
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29. The ins and outs of muscle stem cell aging

Author

Brack, Andrew S and Muñoz-Cánoves, Pura

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Regenerative Medicine, Transplantation, Stem Cell Research, Aging, Stem Cell Research - Nonembryonic - Non-Human, 1.1 Normal biological development and functioning, Underpinning research, Animals, Cell Differentiation, Cell Proliferation, Cellular Senescence, Humans, Muscle, Skeletal, Phenotype, Satellite Cells, Skeletal Muscle, Signal Transduction, Stem Cell Niche, Genetics, Medical physiology
Abstract

Skeletal muscle has a remarkable capacity to regenerate by virtue of its resident stem cells (satellite cells). This capacity declines with aging, although whether this is due to extrinsic changes in the environment and/or to cell-intrinsic mechanisms associated to aging has been a matter of intense debate. Furthermore, while some groups support that satellite cell aging is reversible by a youthful environment, others support cell-autonomous irreversible changes, even in the presence of youthful factors. Indeed, whereas the parabiosis paradigm has unveiled the environment as responsible for the satellite cell functional decline, satellite cell transplantation studies support cell-intrinsic deficits with aging. In this review, we try to shed light on the potential causes underlying these discrepancies. We propose that the experimental paradigm used to interrogate intrinsic and extrinsic regulation of stem cell function may be a part of the problem. The assays deployed are not equivalent and may overburden specific cellular regulatory processes and thus probe different aspects of satellite cell properties. Finally, distinct subsets of satellite cells may be under different modes of molecular control and mobilized preferentially in one paradigm than in the other. A better understanding of how satellite cells molecularly adapt during aging and their context-dependent deployment during injury and transplantation will lead to the development of efficacious compensating strategies that maintain stem cell fitness and tissue homeostasis throughout life.

Published
2015

30. Translational control by DHX36 binding to 5′UTR G-quadruplex is essential for muscle stem-cell regenerative functions

Author

Chen, Xiaona, Yuan, Jie, Xue, Guang, Campanario, Silvia, Wang, Di, Wang, Wen, Mou, Xi, Liew, Shiau Wei, Umar, Mubarak Ishaq, Isern, Joan, Zhao, Yu, He, Liangqiang, Li, Yuying, Mann, Christopher J., Yu, Xiaohua, Wang, Lei, Perdiguero, Eusebio, Chen, Wei, Xue, Yuanchao, Nagamine, Yoshikuni, Kwok, Chun Kit, Sun, Hao, Muñoz-Cánoves, Pura, and Wang, Huating

Published
2021
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43. Biology of Stress Responses in Aging

Author

Maragkakis, Manolis, primary, Ferrucci, Luigi, primary, Gorospe, Myriam, primary, Malla, Sulochan, additional, Hatzoglou, Maria, additional, Trifunovic, Aleksandra, additional, Glick, Adam B., additional, Finkel, Toren, additional, Longo, Valter D., additional, Kaushik, Susmita, additional, Muñoz-Cánoves, Pura, additional, Lithgow, Gordon J., additional, Naidoo, Nirinjini, additional, Booth, Lauren N., additional, Payea, Matthew J., additional, Herman, Allison B., additional, de Cabo, Rafael, additional, and Wilson, David M., additional

Published
2023
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45. The Chromatin Remodeling Complex Chd4/NuRD Controls Striated Muscle Identity and Metabolic Homeostasis

Author

Gómez-del Arco, Pablo, Perdiguero, Eusebio, Yunes-Leites, Paula Sofia, Acín-Pérez, Rebeca, Zeini, Miriam, Garcia-Gomez, Antonio, Sreenivasan, Krishnamoorthy, Jiménez-Alcázar, Miguel, Segalés, Jessica, López-Maderuelo, Dolores, Ornés, Beatriz, Jiménez-Borreguero, Luis Jesús, D’Amato, Gaetano, Enshell-Seijffers, David, Morgan, Bruce, Georgopoulos, Katia, Islam, Abul B.M.M.K., Braun, Thomas, de la Pompa, José Luis, Kim, Johnny, Enriquez, José A., Ballestar, Esteban, Muñoz-Cánoves, Pura, and Redondo, Juan Miguel

Published
2016
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47. Liver and muscle circadian clocks cooperate to support glucose tolerance in mice.

Author

Smith, Jacob, Smith, Jacob, Koronowski, Kevin, Mortimer, Thomas, Sato, Tomoki, Greco, Carolina, Petrus, Paul, Verlande, Amandine, Chen, Siwei, Samad, Muntaha, Deyneka, Ekaterina, Mathur, Lavina, Blazev, Ronnie, Molendijk, Jeffrey, Kumar, Arun, Deryagin, Oleg, Vaca-Dempere, Mireia, Sica, Valentina, Liu, Peng, Orlando, Valerio, Parker, Benjamin, Masri, Selma, Benitah, Salvador, Muñoz-Cánoves, Pura, Sassone-Corsi, Paolo, Welz, Patrick-Simon, Baldi, Pierre, Jang, Cholsoon, Smith, Jacob, Smith, Jacob, Koronowski, Kevin, Mortimer, Thomas, Sato, Tomoki, Greco, Carolina, Petrus, Paul, Verlande, Amandine, Chen, Siwei, Samad, Muntaha, Deyneka, Ekaterina, Mathur, Lavina, Blazev, Ronnie, Molendijk, Jeffrey, Kumar, Arun, Deryagin, Oleg, Vaca-Dempere, Mireia, Sica, Valentina, Liu, Peng, Orlando, Valerio, Parker, Benjamin, Masri, Selma, Benitah, Salvador, Muñoz-Cánoves, Pura, Sassone-Corsi, Paolo, Welz, Patrick-Simon, Baldi, Pierre, and Jang, Cholsoon

Abstract

Physiology is regulated by interconnected cell and tissue circadian clocks. Disruption of the rhythms generated by the concerted activity of these clocks is associated with metabolic disease. Here we tested the interactions between clocks in two critical components of organismal metabolism, liver and skeletal muscle, by rescuing clock function either in each organ separately or in both organs simultaneously in otherwise clock-less mice. Experiments showed that individual clocks are partially sufficient for tissue glucose metabolism, yet the connections between both tissue clocks coupled to daily feeding rhythms support systemic glucose tolerance. This synergy relies in part on local transcriptional control of the glucose machinery, feeding-responsive signals such as insulin, and metabolic cycles that connect the muscle and liver. We posit that spatiotemporal mechanisms of muscle and liver play an essential role in the maintenance of systemic glucose homeostasis and that disrupting this diurnal coordination can contribute to metabolic disease.

Published
2023

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