Clock-dependent chromatin topology modulates circadian transcription and behavior

Mar 25, 2018Genes & development

Daily biological clock changes in DNA structure influence daily gene activity and behavior

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Abstract

Oscillatory promoter-enhancer interactions were discovered along the 24-h cycle in mouse liver and kidney tissues.

Daily active enhancers may modulate rhythmic gene transcription in mammalian tissues.
Rhythms in chromatin interactions were abolished in arrhythmic knockout mice.
Deleting a specific intronic enhancer element compromised rhythmic chromatin contacts in tissues.
The deletion also reduced the daily dynamics of transcriptional burst frequency.
Remarkably, it shortened the circadian period of locomotor activity rhythms.

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The circadian clock in animals orchestrates widespread oscillatory gene expression programs, which underlie 24-h rhythms in behavior and physiology. Several studies have shown the possible roles of transcription factors and chromatin marks in controlling cyclic gene expression. However, how daily active enhancers modulate rhythmic gene transcription in mammalian tissues is not known. Using circular chromosome conformation capture (4C) combined with sequencing (4C-seq), we discovered oscillatory promoter-enhancer interactions along the 24-h cycle in the mouse liver and kidney. Rhythms in chromatin interactions were abolished in arrhythmicknockout mice. Deleting a contacted intronic enhancer element in the() gene was sufficient to compromise the rhythmic chromatin contacts in tissues. Moreover, the deletion reduced the daily dynamics oftranscriptional burst frequency and, remarkably, shortened the circadian period of locomotor activity rhythms. Our results establish oscillating and clock-controlled promoter-enhancer looping as a regulatory layer underlying circadian transcription and behavior. Bmal1Cryptochrome 1Cry1Cry1

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Clock-dependent chromatin topology modulates circadian transcription and behavior

Abstract

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