TY - JOUR
T1 - Methylation deficiency disrupts biological rhythms from bacteria to humans
AU - Fustin, Jean-Michel
AU - Ye, Shiqi
AU - Rakers, Christin
AU - Kaneko, Kensuke
AU - Fukumoto, Kazuki
AU - Yamano, Mayu
AU - Versteven, Marijke
AU - Grünewald, Ellen
AU - Cargill, Samantha J.
AU - Tamai, T. Katherine
AU - Xu, Yao
AU - Jabbur, Maria Luísa
AU - Kojima, Rika
AU - Lamberti, Melisa L.
AU - Yoshioka-Kobayashi, Kumiko
AU - Whitmore, David
AU - Tammam, Stephanie
AU - Howell, P. Lynne
AU - Kageyama, Ryoichiro
AU - Matsuo, Takuya
AU - Stanewsky, Ralf
AU - Golombek, Diego A.
AU - Johnson, Carl Hirschie
AU - Kakeya, Hideaki
AU - Ooijen, Gerben van
AU - Okamura, Hitoshi
N1 - Funding Information:
This work was supported in part by the Ministry of Education, Culture, Sports, Science and Technology of Japan: Grant-in-aid for Scientific Research on Innovative Areas (26116713, J.-M. F.; 17H06401, H.K.), for Young Scientists (26870283, J.-M. F.), for Scientific Research A (15H01843, H.O.; 18H04015, H.O.), a grant for Core Research for Evolutional Science and Technology, Japan Science and Technology Agency (CREST/ JPMJCR14W3, H.O.). J.-M.F. was also supported by grants from the Kato Memorial Bioscience Foundation, the Senri Life Science Foundation (S-26003), the Mochida Memorial Foundation for Medical and Pharmaceutical Research, and the Kyoto University internal grant ISHIZUE, and H.O. was also supported by the Kobayashi International Scholarship Foundation. C.H.J. is supported by grants from the USA NIH/ NIGMS: GM067152 and GM107434. G.vO. is supported by a Royal Society University Research Fellowship (UF160685) and research grant (RGF\EA\180192). D.A.G. is supported by grants from the National Research Agency (ANPCyT, PICT-2015-0572) and the National University of Quilmes. E.G. was supported by the Wellcome Trust-University of Edinburgh Institutional Strategic Support Fund. M.V. and R.S. are funded by a grant from the Deutsche Forschungsgemeinschaft (STA421/7-1). J.-M. F. is a UKRI Future Leaders Fellow (MR/S031812/1). We thank Adrienne K. Mehalow, Jay C. Dunlap, John O’Neill and Tokitaka Oyama for useful discussion and for kindly accepting to perform experiments. The authors thank G. Wolber, Freie Universität Berlin, Germany, for providing a LigandScout 4.2 license.
Publisher Copyright:
© 2020, The Author(s).
PY - 2020/5/6
Y1 - 2020/5/6
N2 - 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.
AB - 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.
KW - Animals
KW - Arabidopsis/physiology
KW - Caenorhabditis elegans/physiology
KW - Chlamydomonas reinhardtii/physiology
KW - Chlorophyta/physiology
KW - Circadian Rhythm
KW - Drosophila melanogaster/physiology
KW - Humans
KW - Methylation
KW - Mice/physiology
KW - Synechococcus/physiology
KW - Zebrafish/physiology
UR - http://www.scopus.com/inward/record.url?scp=85084406361&partnerID=8YFLogxK
U2 - 10.1038/s42003-020-0942-0
DO - 10.1038/s42003-020-0942-0
M3 - Article
C2 - 32376902
SN - 2399-3642
VL - 3
JO - Communications Biology
JF - Communications Biology
IS - 1
M1 - 211
ER -