Bidirectional histone monoaminylation dynamics regulate neural rhythmicity

Zheng, Qingfei; Weekley, Benjamin H.; Vinson, David A.; Zhao, Shuai; Bastle, Ryan M.; Thompson, Robert E.; Stransky, Stephanie; Ramakrishnan, Aarthi; Cunningham, Ashley M.; Dutta, Sohini; Chan, Jennifer C; Salvo, G.; Chen, Min; Zhang, Nan; Wu, Jinghua; Fulton, Sasha L.; Kong, Lingchun; Wang, Haifeng; Zhang, Baichao; Vostal, Lauren E.; Upad, Akhil; Dierdorff, Lauren; Shen, Li; Molina, Henrik; Sidoli, Simone; Muir, Tom W.; Li, Haitao; David, Yael; Maze, Ian

doi:10.1038/s41586-024-08371-3

articleNatureJan 8, 2025HYBRID OA

Bidirectional histone monoaminylation dynamics regulate neural rhythmicity

QZQingfei Zheng BHBenjamin H. Weekley DADavid A. Vinson SZShuai Zhao RMRyan M. Bastle

Purdue University West Lafayette · The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · +16 more institutions

PubMed

Indexed incrossrefpubmed

Abstract

Abstract Histone H3 monoaminylations at Gln5 represent an important family of epigenetic marks in brain that have critical roles in permissive gene expression 1–3 . We previously demonstrated that serotonylation 4–10 and dopaminylation 9,11–13 of Gln5 of histone H3 (H3Q5ser and H3Q5dop, respectively) are catalysed by transglutaminase 2 (TG2), and alter both local and global chromatin states. Here we found that TG2 additionally functions as an eraser and exchanger of H3 monoaminylations, including H3Q5 histaminylation (H3Q5his), which displays diurnally rhythmic expression in brain and contributes to circadian gene expression and behaviour. We found that H3Q5his, in contrast to H3Q5ser, inhibits the binding of…

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Topics & keywords

Topics

Keywords

Histone H3
Chromatin
Epigenetics
Histone
Histone methyltransferase
Biology
Cell biology
Regulation of gene expression

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