Journal
COMMUNICATIONS BIOLOGY
Volume 3, Issue 1, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s42003-020-0942-0
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Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan [26116713, 17H06401, 26870283, 15H01843, 18H04015]
- Japan Science and Technology Agency [CREST/JPMJCR14W3]
- Kato Memorial Bioscience Foundation
- Senri Life Science Foundation [S-26003]
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Kyoto University internal grant ISHIZUE
- USA NIH/NIGMS [GM067152, GM107434]
- Royal Society [UF160685, RGF\EA\180192]
- National Research Agency (ANPCyT) [PICT-2015-0572]
- National University of Quilmes
- Wellcome TrustUniversity of Edinburgh Institutional Strategic Support Fund
- Deutsche Forschungsgemeinschaft [STA421/7-1]
- Grants-in-Aid for Scientific Research [18H04015, 15H01843, 26870283, 17H06401, 26116713] Funding Source: KAKEN
- UKRI [MR/S031812/1] Funding Source: UKRI
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Fustin et al. reveal the evolutionarily conserved link between methyl metabolism and biological clocks. This study suggests the possibility of translating fundamental understanding of methylation deficiencies to clinical applications. The methyl cycle is a universal metabolic pathway providing methyl groups for the methylation of nuclei acids and proteins, regulating all aspects of cellular physiology. We have previously shown that methyl cycle inhibition in mammals strongly affects circadian rhythms. Since the methyl cycle and circadian clocks have evolved early during evolution and operate in organisms across the tree of life, we sought to determine whether the link between the two is also conserved. Here, we show that methyl cycle inhibition affects biological rhythms in species ranging from unicellular algae to humans, separated by more than 1 billion years of evolution. In contrast, the cyanobacterial clock is resistant to methyl cycle inhibition, although we demonstrate that methylations themselves regulate circadian rhythms in this organism. Mammalian cells with a rewired bacteria-like methyl cycle are protected, like cyanobacteria, from methyl cycle inhibition, providing interesting new possibilities for the treatment of methylation deficiencies.
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