NDLI: Loss of the RNA polymerase III repressor MAF1 confers obesity resistance.

Please wait, while we are loading the content...

Loss of the RNA polymerase III repressor MAF1 confers obesity resistance.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Bonhoure, Nicolas Byrnes, Ashlee Moir, Robyn D. Hodroj, Wassim Preitner, Frédéric Praz, Viviane Marcelin, Genevieve Chua, Streamson C. Martinez-Lopez, Nuria Singh, Rajat Moullan, Norman Auwerx, Johan Willemin, Gilles Shah, Hardik Hartil, Kirsten Vaitheesvaran, Bhavapriya Kurland, Irwin Hernandez, Nouria Willis, Ian M.
Description	Author Affiliation: Bonhoure N ( Center for Integrative Genomics, Faculty of Biology and Medicine, University of Lausanne, 1015 Lausanne, Switzerland); Byrnes A ( Department of Biochemistry, Albert Einstein College of Medicine, Bronx, New York 10461, USA); Moir RD ( Department of Biochemistry, Albert Einstein College of Medicine, Bronx, New York 10461, USA); Hodroj W ( Center for Integrative Genomics, Faculty of Biology and Medicine, University of Lausanne, 1015 Lausanne, Switzerland); Preitner F ( Mouse Metabolic Evaluation Facility, Center for Integrative Genomics, University of Lausanne, 1015 Lausanne, Switzerland); Praz V ( Center for Integrative Genomics, Faculty of Biology and Medicine, University of Lausanne, 1015 Lausanne, Switzerland); Marcelin G ( Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA); Chua SC ( Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA); Martinez-Lopez N ( Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA); Singh R ( Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA); Moullan N ( Laboratory for Integrative and Systems Physiology, Ecole Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland.); Auwerx J ( Laboratory for Integrative and Systems Physiology, Ecole Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland.); Willemin G ( Center for Integrative Genomics, Faculty of Biology and Medicine, University of Lausanne, 1015 Lausanne, Switzerland); Shah H ( Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA); Hartil K ( Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA); Vaitheesvaran B ( Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA); Kurland I ( Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA); Hernandez N ( Center for Integrative Genomics, Faculty of Biology and Medicine, University of Lausanne, 1015 Lausanne, Switzerland); Willis IM ( Department of Biochemistry, Albert Einstein College of Medicine, Bronx, New York 10461, USA)
Abstract	MAF1 is a global repressor of RNA polymerase III transcription that regulates the expression of highly abundant noncoding RNAs in response to nutrient availability and cellular stress. Thus, MAF1 function is thought to be important for metabolic economy. Here we show that a whole-body knockout of Maf1 in mice confers resistance to diet-induced obesity and nonalcoholic fatty liver disease by reducing food intake and increasing metabolic inefficiency. Energy expenditure in Maf1(-/-) mice is increased by several mechanisms. Precursor tRNA synthesis was increased in multiple tissues without significant effects on mature tRNA levels, implying increased turnover in a futile tRNA cycle. Elevated futile cycling of hepatic lipids was also observed. Metabolite profiling of the liver and skeletal muscle revealed elevated levels of many amino acids and spermidine, which links the induction of autophagy in Maf1(-/-) mice with their extended life span. The increase in spermidine was accompanied by reduced levels of nicotinamide N-methyltransferase, which promotes polyamine synthesis, enables nicotinamide salvage to regenerate NAD(+), and is associated with obesity resistance. Consistent with this, NAD(+) levels were increased in muscle. The importance of MAF1 for metabolic economy reveals the potential for MAF1 modulators to protect against obesity and its harmful consequences.
File Format	HTM / HTML
ISSN	08909369
e-ISSN	15495477
DOI	10.1101/gad.258350.115
Journal	Genes & Development
Issue Number	9
Volume Number	29
Language	English
Publisher	Cold Spring Harbor Laboratory Press
Publisher Date	2015-05-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Molecular Discipline Biology__semicolon__developmental Discipline Biology__semicolon__genetics__semicolon__cell Discipline Biology Repressor Proteins Genetics Animals Autophagy Energy Metabolism Lipid Metabolism Longevity Mice, Inbred C57bl Mice, Knockout Non-alcoholic Fatty Liver Disease Obesity Rna, Transfer Metabolism Spermidine Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Genetics Developmental Biology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Loss of the RNA polymerase III repressor MAF1 confers obesity resistance

Fat chance for longevity.

Inhibition of microRNA-24 expression in liver prevents hepatic lipid accumulation and hyperlipidemia.

Cisd2 deficiency drives premature aging and causes mitochondria-mediated defects in mice.

JNK regulates FoxO-dependent autophagy in neurons.

Neuronal SIRT1 regulates endocrine and behavioral responses to calorie restriction.

Generation of Ski-knockdown mice by expressing a long double-strand RNA from an RNA polymerase II promoter.

Peroxisomes compensate hepatic lipid overflow in mice with fatty liver

Liver receptor homolog 1 is essential for ovulation.

Loss of the RNA polymerase III repressor MAF1 confers obesity resistance.

Similar Documents

Loss of the RNA polymerase III repressor MAF1 confers obesity resistance

Fat chance for longevity.

Inhibition of microRNA-24 expression in liver prevents hepatic lipid accumulation and hyperlipidemia.

Cisd2 deficiency drives premature aging and causes mitochondria-mediated defects in mice.

JNK regulates FoxO-dependent autophagy in neurons.

Neuronal SIRT1 regulates endocrine and behavioral responses to calorie restriction.

Generation of Ski-knockdown mice by expressing a long double-strand RNA from an RNA polymerase II promoter.

Peroxisomes compensate hepatic lipid overflow in mice with fatty liver

Liver receptor homolog 1 is essential for ovulation.

Loss of the RNA polymerase III repressor MAF1 confers obesity resistance.