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2. Obesity induces PD-1 on macrophages to suppress anti-tumour immunity

Author

Bader, Jackie E., Wolf, Melissa M., Lupica-Tondo, Gian Luca, Madden, Matthew Z., Reinfeld, Bradley I., Arner, Emily N., Hathaway, Emma S., Steiner, KayLee K., Needle, Gabriel A., Hatem, Zaid, Landis, Madelyn D., Faneuff, Eden E., Blackman, Amondrea, Wolf, Elysa M., Cottam, Matthew A., Ye, Xiang, Bates, Madison E., Smart, Kyra, Wang, Wenjun, Pinheiro, Laura V., Christofides, Anthos, Smith, DuPreez, Boussiotis, Vassiliki A., Haake, Scott M., Beckermann, Kathryn E., Wellen, Kathryn E., Reinhart-King, Cynthia A., Serezani, C. Henrique, Lee, Cheng-Han, Aubrey, Christa, Chen, Heidi, Rathmell, W. Kimryn, Hasty, Alyssa H., and Rathmell, Jeffrey C.

Published
2024
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3. Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism via the ACSS2–SP1–SAT1 axis

Author

Murthy, Divya, Attri, Kuldeep S., Shukla, Surendra K., Thakur, Ravi, Chaika, Nina V., He, Chunbo, Wang, Dezhen, Jha, Kanupriya, Dasgupta, Aneesha, King, Ryan J., Mulder, Scott E., Souchek, Joshua, Gebregiworgis, Teklab, Rai, Vikant, Patel, Rohit, Hu, Tuo, Rana, Sandeep, Kollala, Sai Sundeep, Pacheco, Camila, Grandgenett, Paul M., Yu, Fang, Kumar, Vikas, Lazenby, Audrey J., Black, Adrian R., Ulhannan, Susanna, Jain, Ajay, Edil, Barish H., Klinkebiel, David L., Powers, Robert, Natarajan, Amarnath, Hollingsworth, Michael A., Mehla, Kamiya, Ly, Quan, Chaudhary, Sarika, Hwang, Rosa F., Wellen, Kathryn E., and Singh, Pankaj K.

Published
2024
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4. Author Correction: Obesity induces PD-1 on macrophages to suppress anti-tumour immunity

Author

Bader, Jackie E., Wolf, Melissa M., Lupica-Tondo, Gian Luca, Madden, Matthew Z., Reinfeld, Bradley I., Arner, Emily N., Hathaway, Emma S., Steiner, KayLee K., Needle, Gabriel A., Hatem, Zaid, Landis, Madelyn D., Faneuff, Eden E., Blackman, Amondrea, Wolf, Elysa M., Cottam, Matthew A., Ye, Xiang, Bates, Madison E., Smart, Kyra, Wang, Wenjun, Pinheiro, Laura V., Christofides, Anthos, Smith, DuPreez, Boussiotis, Vassiliki A., Haake, Scott M., Beckermann, Kathryn E., Wellen, Kathryn E., Reinhart-King, Cynthia A., Serezani, C. Henrique, Lee, Cheng-Han, Aubrey, Christa, Chen, Heidi, Rathmell, W. Kimryn, Hasty, Alyssa H., and Rathmell, Jeffrey C.

Published
2024
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5. Acetate acts as a metabolic immunomodulator by bolstering T-cell effector function and potentiating antitumor immunity in breast cancer

Author

Miller, Katelyn D., O’Connor, Seamus, Pniewski, Katherine A., Kannan, Toshitha, Acosta, Reyes, Mirji, Gauri, Papp, Sara, Hulse, Michael, Mukha, Dzmitry, Hlavaty, Sabina I., Salcido, Kelsey N., Bertolazzi, Fabrizio, Srikanth, Yellamelli V. V., Zhao, Steven, Wellen, Kathryn E., Shinde, Rahul S., Claiborne, Daniel T., Kossenkov, Andrew, Salvino, Joseph M., and Schug, Zachary T.

Published
2023
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6. A subpopulation of lipogenic brown adipocytes drives thermogenic memory

Author

Lundgren, Patrick, Sharma, Prateek V., Dohnalová, Lenka, Coleman, Kyle, Uhr, Giulia T., Kircher, Susanna, Litichevskiy, Lev, Bahnsen, Klaas, Descamps, Hélène C., Demetriadou, Christina, Chan, Jacqueline, Chellappa, Karthikeyani, Cox, Timothy O., Heyman, Yael, Pather, Sarshan R., Shoffler, Clarissa, Petucci, Christopher, Shalem, Ophir, Raj, Arjun, Baur, Joseph A., Snyder, Nathaniel W., Wellen, Kathryn E., Levy, Maayan, Seale, Patrick, Li, Mingyao, and Thaiss, Christoph A.

Published
2023
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8. Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism via the ACSS2–SP1–SAT1 axis

Author

Murthy, Divya, Attri, Kuldeep S., Shukla, Surendra K., Thakur, Ravi, Chaika, Nina V., He, Chunbo, Wang, Dezhen, Jha, Kanupriya, Dasgupta, Aneesha, King, Ryan J., Mulder, Scott E., Souchek, Joshua, Gebregiworgis, Teklab, Rai, Vikant, Patel, Rohit, Hu, Tuo, Rana, Sandeep, Kollala, Sai Sundeep, Pacheco, Camila, Grandgenett, Paul M., Yu, Fang, Kumar, Vikas, Lazenby, Audrey J., Black, Adrian R., Ulhannan, Susanna, Jain, Ajay, Edil, Barish H., Klinkebiel, David L., Powers, Robert, Natarajan, Amarnath, Hollingsworth, Michael A., Mehla, Kamiya, Ly, Quan, Chaudhary, Sarika, Hwang, Rosa F., Wellen, Kathryn E., and Singh, Pankaj K.

Published
2024
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10. The interaction between the gut microbiota and dietary carbohydrates in nonalcoholic fatty liver disease.

Author

Park, Grace, Jung, Sunhee, Wellen, Kathryn E, and Jang, Cholsoon

Subjects
Biochemistry & Molecular Biology, Medicinal and Biomolecular Chemistry
Abstract

Imbalance between fat production and consumption causes various metabolic disorders. Nonalcoholic fatty liver disease (NAFLD), one such pathology, is characterized by abnormally increased fat synthesis and subsequent fat accumulation in hepatocytes1,2. While often comorbid with obesity and insulin resistance, this disease can also be found in lean individuals, suggesting specific metabolic dysfunction2. NAFLD has become one of the most prevalent liver diseases in adults worldwide, but its incidence in both children and adolescents has also markedly increased in developed nations3,4. Progression of this disease into nonalcoholic steatohepatitis (NASH), cirrhosis, liver failure, and hepatocellular carcinoma in combination with its widespread incidence thus makes NAFLD and its related pathologies a significant public health concern. Here, we review our understanding of the roles of dietary carbohydrates (glucose, fructose, and fibers) and the gut microbiota, which provides essential carbon sources for hepatic fat synthesis during the development of NAFLD.

Published
2021

11. ACSS2 gene variants determine kidney disease risk by controlling de novo lipogenesis in kidney tubules

Author

Mukhi, Dhanunjay, Li, Lingzhi, Liu, Hongbo, Doke, Tomohito, Kolligundla, Lakshmi P., Ha, Eunji, Kloetzer, Konstantin, Abedini, Amin, Mukherjee, Sarmistha, Wu, Junnan, Dhillon, Poonam, Hu, Hailong, Guan, Dongyin, Funai, Katsuhiko, Uehara, Kahealani, Titchenell, Paul M., Baur, Joseph A., Wellen, Kathryn E., and Susztak, Katalin

Subjects
Infection control, Medical research, Medicine, Experimental, Chromatin -- Genetic aspects, Gene expression -- Genetic aspects, Genetic research -- Genetic aspects, Genes -- Genetic aspects, Fatty acids -- Synthesis -- Genetic aspects, Kidney diseases -- Genetic aspects -- Risk factors -- Prevention, Health care industry
Abstract

Worldwide, over 800 million people are affected by kidney disease, yet its pathogenesis remains elusive, hindering the development of novel therapeutics. In this study, we used kidney-specific expression of quantitative traits and single-nucleus open chromatin analysis to show that genetic variants linked to kidney dysfunction on chromosome 20 target the acyl-CoA synthetase short-chain family 2 (ACSS2). By generating ACSS2-KO mice, we demonstrated their protection from kidney fibrosis in multiple disease models. Our analysis of primary tubular cells revealed that ACSS2 regulated de novo lipogenesis (DNL), causing NADPH depletion and increasing ROS levels, ultimately leading to NLRP3-dependent pyroptosis. Additionally, we discovered that pharmacological inhibition or genetic ablation of fatty acid synthase safeguarded kidney cells against profibrotic gene expression and prevented kidney disease in mice. Lipid accumulation and the expression of genes related to DNL were elevated in the kidneys of patients with fibrosis. Our findings pinpoint ACSS2 as a critical kidney disease gene and reveal the role of DNL in kidney disease., Introduction Over 800 million people in the world have chronic kidney disease (CKD) (1). CKD is a major cause of cardiovascular death and if left untreated leads to end-stage kidney [...]

Published
2024
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12. Serotonin reduction in post-acute sequelae of viral infection

Author

Wong, Andrea C., Devason, Ashwarya S., Umana, Iboro C., Cox, Timothy O., Dohnalová, Lenka, Litichevskiy, Lev, Perla, Jonathan, Lundgren, Patrick, Etwebi, Zienab, Izzo, Luke T., Kim, Jihee, Tetlak, Monika, Descamps, Hélène C., Park, Simone L., Wisser, Stephen, McKnight, Aaron D., Pardy, Ryan D., Kim, Junwon, Blank, Niklas, Patel, Shaan, Thum, Katharina, Mason, Sydney, Beltra, Jean-Christophe, Michieletto, Michaël F., Ngiow, Shin Foong, Miller, Brittany M., Liou, Megan J., Madhu, Bhoomi, Dmitrieva-Posocco, Oxana, Huber, Alex S., Hewins, Peter, Petucci, Christopher, Chu, Candice P., Baraniecki-Zwil, Gwen, Giron, Leila B., Baxter, Amy E., Greenplate, Allison R., Kearns, Charlotte, Montone, Kathleen, Litzky, Leslie A., Feldman, Michael, Henao-Mejia, Jorge, Striepen, Boris, Ramage, Holly, Jurado, Kellie A., Wellen, Kathryn E., O’Doherty, Una, Abdel-Mohsen, Mohamed, Landay, Alan L., Keshavarzian, Ali, Henrich, Timothy J., Deeks, Steven G., Peluso, Michael J., Meyer, Nuala J., Wherry, E. John, Abramoff, Benjamin A., Cherry, Sara, Thaiss, Christoph A., and Levy, Maayan

Published
2023
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14. Dietary fructose feeds hepatic lipogenesis via microbiota-derived acetate.

Author

Zhao, Steven, Jang, Cholsoon, Liu, Joyce, Uehara, Kahealani, Gilbert, Michael, Izzo, Luke, Zeng, Xianfeng, Trefely, Sophie, Fernandez, Sully, Carrer, Alessandro, Miller, Katelyn D, Schug, Zachary T, Snyder, Nathaniel W, Gade, Terence P, Titchenell, Paul M, Rabinowitz, Joshua D, and Wellen, Kathryn E

Subjects
Liver, Hepatocytes, Animals, Mice, Acetates, Citric Acid, Acetyl Coenzyme A, Acetate-CoA Ligase, ATP Citrate (pro-S)-Lyase, Fructose, Fatty Acids, Isotope Labeling, Gene Expression Regulation, Substrate Specificity, Male, Lipogenesis, Gastrointestinal Microbiome, Dietary Sugars, Digestive Diseases, Liver Disease, Nutrition, Obesity, Oral and gastrointestinal, General Science & Technology
Abstract

Consumption of fructose has risen markedly in recent decades owing to the use of sucrose and high-fructose corn syrup in beverages and processed foods1, and this has contributed to increasing rates of obesity and non-alcoholic fatty liver disease2-4. Fructose intake triggers de novo lipogenesis in the liver4-6, in which carbon precursors of acetyl-CoA are converted into fatty acids. The ATP citrate lyase (ACLY) enzyme cleaves cytosolic citrate to generate acetyl-CoA, and is upregulated after consumption of carbohydrates7. Clinical trials are currently pursuing the inhibition of ACLY as a treatment for metabolic diseases8. However, the route from dietary fructose to hepatic acetyl-CoA and lipids remains unknown. Here, using in vivo isotope tracing, we show that liver-specific deletion of Acly in mice is unable to suppress fructose-induced lipogenesis. Dietary fructose is converted to acetate by the gut microbiota9, and this supplies lipogenic acetyl-CoA independently of ACLY10. Depletion of the microbiota or silencing of hepatic ACSS2, which generates acetyl-CoA from acetate, potently suppresses the conversion of bolus fructose into hepatic acetyl-CoA and fatty acids. When fructose is consumed more gradually to facilitate its absorption in the small intestine, both citrate cleavage in hepatocytes and microorganism-derived acetate contribute to lipogenesis. By contrast, the lipogenic transcriptional program is activated in response to fructose in a manner that is independent of acetyl-CoA metabolism. These data reveal a two-pronged mechanism that regulates hepatic lipogenesis, in which fructolysis within hepatocytes provides a signal to promote the expression of lipogenic genes, and the generation of microbial acetate feeds lipogenic pools of acetyl-CoA.

Published
2020

17. O-GlcNAc transferase regulates glioblastoma acetate metabolism via regulation of CDK5-dependent ACSS2 phosphorylation

Author

Ciraku, Lorela, Bacigalupa, Zachary A., Ju, Jing, Moeller, Rebecca A., Le Minh, Giang, Lee, Rusia H., Smith, Michael D., Ferrer, Christina M., Trefely, Sophie, Izzo, Luke T., Doan, Mary T., Gocal, Wiktoria A., D’Agostino, Luca, Shi, Wenyin, Jackson, Joshua G., Katsetos, Christos D., Wellen, Kathryn E., Snyder, Nathaniel W., and Reginato, Mauricio J.

Published
2022
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19. Blood-based gene expression signature associated with metastatic castrate-resistant prostate cancer patient response to abiraterone plus prednisone or enzalutamide

Author

Haas, Naomi B., LaRiviere, Michael J., Buckingham, Thomas H., Cherkas, Yauheniya, Calara-Nielsen, Karl, Foulk, Brad, Patel, Jaymala, Gross, Steven, Smirnov, Denis, Vaughn, David J., Amaravadi, Ravi, Wellen, Kathryn E., Savitch, Samantha L., Majmundar, Krishna J., Black, Taylor A., Yee, Stephanie S., He, Miaoling, Min, Eun Jeong, Long, Qi, Jones, Jeremy O., Pal, Sumanta K., and Carpenter, Erica L.

Published
2021
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21. ACSS2 gene variants determine kidney disease risk by controlling de novo lipogenesis in kidney tubules

Author

Mukhi, Dhanunjay, primary, Li, Lingzhi, additional, Liu, Hongbo, additional, Doke, Tomohito, additional, Kolligundla, Lakshmi P., additional, Ha, Eunji, additional, Kloetzer, Konstantin, additional, Abedini, Amin, additional, Mukherjee, Sarmistha, additional, Wu, Junnan, additional, Dhillon, Poonam, additional, Hu, Hailong, additional, Guan, Dongyin, additional, Funai, Katsuhiko, additional, Uehara, Kahealani, additional, Titchenell, Paul M., additional, Baur, Joseph A., additional, Wellen, Kathryn E., additional, and Susztak, Katalin, additional

Published
2023
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22. Regulation of nuclear epigenome by mitochondrial DNA heteroplasmy

Author

Kopinski, Piotr K., Janssen, Kevin A., Schaefer, Patrick M., Trefely, Sophie, Perry, Caroline E., Potluri, Prasanth, Tintos-Hernandez, Jesus A., Singh, Larry N., Karch, Kelly R., Campbell, Sydney L., Doan, Mary T., Jiang, Helen, Nissim, Itzhak, Nakamaru-Ogiso, Eiko, Wellen, Kathryn E., Snyder, Nathaniel W., Garcia, Benjamin A., and Wallace, Douglas C.

Published
2019

24. Macrophage ATP citrate lyase deficiency stabilizes atherosclerotic plaques

Author

Baardman, Jeroen, Verberk, Sanne G. S., van der Velden, Saskia, Gijbels, Marion J. J., van Roomen, Cindy P. P. A., Sluimer, Judith C., Broos, Jelle Y., Griffith, Guillermo R., Prange, Koen H. M., van Weeghel, Michel, Lakbir, Soufyan, Molenaar, Douwe, Meinster, Elisa, Neele, Annette E., Kooij, Gijs, de Vries, Helga E., Lutgens, Esther, Wellen, Kathryn E., de Winther, Menno P. J., and Van den Bossche, Jan

Published
2020
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27. Acetylcarnitine shuttling links mitochondrial metabolism to histone acetylation and lipogenesis

Author

Izzo, Luke T., primary, Trefely, Sophie, additional, Demetriadou, Christina, additional, Drummond, Jack M., additional, Mizukami, Takuya, additional, Kuprasertkul, Nina, additional, Farria, Aimee T., additional, Nguyen, Phuong T. T., additional, Murali, Nivitha, additional, Reich, Lauren, additional, Kantner, Daniel S., additional, Shaffer, Joshua, additional, Affronti, Hayley, additional, Carrer, Alessandro, additional, Andrews, Andrew, additional, Capell, Brian C., additional, Snyder, Nathaniel W., additional, and Wellen, Kathryn E., additional

Published
2023
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30. Data from Acetyl-CoA Metabolism Supports Multistep Pancreatic Tumorigenesis

Author

Carrer, Alessandro, primary, Trefely, Sophie, primary, Zhao, Steven, primary, Campbell, Sydney L., primary, Norgard, Robert J., primary, Schultz, Kollin C., primary, Sidoli, Simone, primary, Parris, Joshua L.D., primary, Affronti, Hayley C., primary, Sivanand, Sharanya, primary, Egolf, Shaun, primary, Sela, Yogev, primary, Trizzino, Marco, primary, Gardini, Alessandro, primary, Garcia, Benjamin A., primary, Snyder, Nathaniel W., primary, Stanger, Ben Z., primary, and Wellen, Kathryn E., primary

Published
2023
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31. Supplementary Data from Acetyl-CoA Metabolism Supports Multistep Pancreatic Tumorigenesis

Author

Carrer, Alessandro, primary, Trefely, Sophie, primary, Zhao, Steven, primary, Campbell, Sydney L., primary, Norgard, Robert J., primary, Schultz, Kollin C., primary, Sidoli, Simone, primary, Parris, Joshua L.D., primary, Affronti, Hayley C., primary, Sivanand, Sharanya, primary, Egolf, Shaun, primary, Sela, Yogev, primary, Trizzino, Marco, primary, Gardini, Alessandro, primary, Garcia, Benjamin A., primary, Snyder, Nathaniel W., primary, Stanger, Ben Z., primary, and Wellen, Kathryn E., primary

Published
2023
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34. Therapeutic targeting of ACLY in T-ALLin vivo

Author

Silva-Diz, Victoria da, primary, Singh, Amartya, additional, Lancho, Olga, additional, Aleksandrova, Maya, additional, Mandleywala, Komal, additional, Nunes, Patricia Renck, additional, Khatun, Jesminara, additional, Kim, Oekyung, additional, Chiles, Eric, additional, Su, Xiaoyang, additional, Khiabanian, Hossein, additional, Wellen, Kathryn E., additional, and Herranz, Daniel, additional

Published
2023
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35. The mitochondrial Ca2+channel MCU is critical for tumor growth by supporting cell cycle progression and proliferation

Author

García, Emily Fernández, Paudel, Usha, Noji, Michael C., Bowman, Caitlyn E., Pitarresi, Jason R., Rustgi, Anil K., Wellen, Kathryn E., Arany, Zolt, Weissenrieder, Jillian S., and Foskett, J. Kevin

Subjects
Cell Biology, Article, Developmental Biology
Abstract

The mitochondrial uniporter (MCU) Ca2+ion channel represents the primary means for Ca2+uptake into mitochondria. Here we employedin vitroandin vivomodels with MCU genetically eliminated to understand how MCU contributes to tumor formation and progression. Transformation of primary fibroblastsin vitrowas associated with increased MCU expression, enhanced mitochondrial Ca2+uptake, suppression of inactivating-phosphorylation of pyruvate dehydrogenase, a modest increase of basal mitochondrial respiration and a significant increase of acute Ca2+-dependent stimulation of mitochondrial respiration. Inhibition of mitochondrial Ca2+uptake by genetic deletion of MCU markedly inhibited growth of HEK293T cells and of transformed fibroblasts in mouse xenograft models. Reduced tumor growth was primarily a result of substantially reduced proliferation and fewer mitotic cellsin vivo, and slower cell proliferationin vitroassociated with delayed progression through S-phase of the cell cycle. MCU deletion inhibited cancer stem cell-like spheroid formation and cell invasionin vitro, both predictors of metastatic potential. Surprisingly, mitochondrial matrix Ca2+concentration, membrane potential, global dehydrogenase activity, respiration and ROS production were unchanged by genetic deletion of MCU in transformed cells. In contrast, MCU deletion elevated glycolysis and glutaminolysis, strongly sensitized cell proliferation to glucose and glutamine limitation, and altered agonist-induced cytoplasmic Ca2+signals. Our results reveal a dependence of tumorigenesis on MCU, mediated by a reliance on mitochondrial Ca2+uptake for cell metabolism and Ca2+dynamics necessary for cell-cycle progression and cell proliferation.

Published
2023

38. Acly Deficiency Enhances Myelopoiesis through Acetyl Coenzyme A and Metabolic–Epigenetic Cross-Talk

Author

Greenwood, Dalton L., primary, Ramsey, Haley E., additional, Nguyen, Phuong T. T., additional, Patterson, Andrew R., additional, Voss, Kelsey, additional, Bader, Jackie E., additional, Sugiura, Ayaka, additional, Bacigalupa, Zachary A., additional, Schaefer, Samuel, additional, Ye, Xiang, additional, Dahunsi, Debolanle O., additional, Madden, Matthew Z., additional, Wellen, Kathryn E., additional, Savona, Michael R., additional, Ferrell, P. Brent, additional, and Rathmell, Jeffrey C., additional

Published
2022
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39. The carnitine shuttle links mitochondrial metabolism to histone acetylation and lipogenesis

Author

Izzo, Luke, primary, Trefely, Sophie, additional, Demetriadou, Christina, additional, Drummond, Jack, additional, Mizukami, Takuya, additional, Kuprasertkul, Nina, additional, Farria, Aimee, additional, Nguyen, Phuong, additional, Reich, Lauren, additional, Shaffer, Joshua, additional, Affronti, Hayley, additional, Carrer, Alessandro, additional, Andrews, Andrew, additional, Capell, Brian C., additional, Snyder, Nathaniel W., additional, and Wellen, Kathryn E., additional

Published
2022
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40. Akt-Dependent Metabolic Reprogramming Regulates Tumor Cell Histone Acetylation

Author

Lee, Joyce V., Carrer, Alessandro, Shah, Supriya, Snyder, Nathaniel W., Wei, Shuanzeng, Venneti, Sriram, Worth, Andrew J., Yuan, Zuo-Fei, Lim, Hee-Woong, Liu, Shichong, Jackson, Ellen, Aiello, Nicole M., Haas, Naomi B., Rebbeck, Timothy R., Judkins, Alexander, Won, Kyoung-Jae, Chodosh, Lewis A., Garcia, Benjamin A., Stanger, Ben Z., Feldman, Michael D., Blair, Ian A., and Wellen, Kathryn E.

Published
2014
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44. Quantitative subcellular acyl-CoA analysis reveals distinct nuclear metabolism and isoleucine-dependent histone propionylation

Author

Trefely, Sophie, primary, Huber, Katharina, additional, Liu, Joyce, additional, Noji, Michael, additional, Stransky, Stephanie, additional, Singh, Jay, additional, Doan, Mary T., additional, Lovell, Claudia D., additional, von Krusenstiern, Eliana, additional, Jiang, Helen, additional, Bostwick, Anna, additional, Pepper, Hannah L., additional, Izzo, Luke, additional, Zhao, Steven, additional, Xu, Jimmy P., additional, Bedi, Kenneth C., additional, Rame, J. Eduardo, additional, Bogner-Strauss, Juliane G., additional, Mesaros, Clementina, additional, Sidoli, Simone, additional, Wellen, Kathryn E., additional, and Snyder, Nathaniel W., additional

Published
2022
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45. Glutamine deprivation triggers NAGK-dependent hexosamine salvage

Author

Campbell, Sydney, primary, Mesaros, Clementina, additional, Izzo, Luke, additional, Affronti, Hayley, additional, Noji, Michael, additional, Schaffer, Bethany E, additional, Tsang, Tiffany, additional, Sun, Kathryn, additional, Trefely, Sophie, additional, Kruijning, Salisa, additional, Blenis, John, additional, Blair, Ian A, additional, and Wellen, Kathryn E, additional

Published
2021
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47. Lactate supports a metabolic-epigenetic link in macrophage polarization

Author

Noe, Jordan T., primary, Rendon, Beatriz E., additional, Geller, Anne E., additional, Conroy, Lindsey R., additional, Morrissey, Samantha M., additional, Young, Lyndsay E.A., additional, Bruntz, Ronald C., additional, Kim, Eun J., additional, Wise-Mitchell, Ashley, additional, Barbosa de Souza Rizzo, Mariana, additional, Relich, Eric R., additional, Baby, Becca V., additional, Johnson, Lance A., additional, Affronti, Hayley C., additional, McMasters, Kelly M., additional, Clem, Brian F., additional, Gentry, Matthew S., additional, Yan, Jun, additional, Wellen, Kathryn E., additional, Sun, Ramon C., additional, and Mitchell, Robert A., additional

Published
2021
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49. The carnitine shuttle links mitochondrial metabolism to histone acetylation and lipogenesis.

Author

Izzo, Luke, Trefely, Sophie, Demetriadou, Christina, Drummond, Jack, Takuya Mizukami, Kuprasertkul, Nina, Farria, Aimee, Phuong Nguyen, Reich, Lauren, Shaffe, Joshua, Affronti, Hayley, Carrer, Alessandro, Andrews, Andrew, Capell, Brian C., Snyder, Nathaniel W., and Wellen, Kathryn E.

Subjects
RODENTS, CARNITINE, ANIMAL experimentation, GENETIC disorders, CELL physiology, MITOCHONDRIA, TRANSFERASES, LIPID metabolism disorders, GLUCOSE, CELL lines, FATTY acids
Abstract

Acetyl-CoA is a central metabolite used for lipid synthesis in the cytosol and histone acetylation in the nucleus, among other pathways. The two major precursors to acetyl-CoA in the nuclear-cytoplasmic compartment are citrate and acetate, which are processed to acetyl-CoA by ATP-citrate lyase (ACLY) and acyl-CoA synthetase short-chain 2 (ACSS2), respectively. While some evidence has suggested the existence of additional routes to nuclear-cytosolic acetyl-CoA, such pathways remain poorly defined. To investigate this, we generated cancer cell lines lacking both ACLY and ACSS2. Unexpectedly, and in contrast to observations in fibroblasts, ACLY and ACSS2 double knockout (DKO) cancer cells remain viable and proliferate, maintain pools of cytosolic acetyl-CoA, and are competent to acetylate proteins in both cytosolic and nuclear compartments. Using stable isotope tracing, we show that both glucose and fatty acids feed acetyl-CoA pools and histone acetylation in DKO cells. Moreover, we provide evidence for the carnitine shuttle and carnitine acetyltransferase (CrAT) as a substantial pathway to transfer two-carbon units from mitochondria to cytosol independent of ACLY. Indeed, in the absence of ACLY, glucose can feed fatty acid synthesis in a carnitine responsive and CrAT-dependent manner. This work defines a carnitine-facilitated route to produce nuclear-cytosolic acetyl-CoA, shedding light on the intricate regulation and compartmentalization of acetyl-CoA metabolism [ABSTRACT FROM AUTHOR]

Published
2022
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50. Reciprocal regulation of p53 and malic enzymes modulates metabolism and senescence

Author

Jiang, Peng, Du, Wenjing, Mancuso, Anthony, Wellen, Kathryn E., and Yang, Xiaolu

Subjects
Cells -- Aging, Tumor suppressor genes -- Physiological aspects, Cell metabolism -- Research, Malate dehydrogenase -- Physiological aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Cellular senescence both protects multicellular organisms from cancer and contributes to their ageing (1). The pre-eminent tumour suppressor p53 has an important role in the induction and maintenance of senescence, [...]

Published
2013
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