Dataset Information

Genome-wide circadian regulation: A unique system for computational biology.

ABSTRACT: Circadian rhythms are 24-hour oscillations affecting an organism at multiple levels from gene expression all the way to tissues and organs. They have been observed in organisms across the kingdom of life, spanning from cyanobacteria to humans. In mammals, the master circadian pacemaker is located in the hypothalamic suprachiasmatic nuclei (SCN) in the brain where it synchronizes the peripheral oscillators that exist in other tissues. This system regulates the circadian activity of a large part of the transcriptome and recent findings indicate that almost every cell in the body has this clock at the molecular level. In this review, we briefly summarize the different factors that can influence the circadian transcriptome, including light, temperature, and food intake. We then summarize recently identified general principles governing genome-scale circadian regulation, as well as future lines of research. Genome-scale circadian activity represents a fascinating study model for computational biology. For this purpose, systems biology methods are promising exploratory tools to decode the global regulatory principles of circadian regulation.

SUBMITTER: Sun L

PROVIDER: S-EPMC7385043 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Genome-wide circadian regulation: A unique system for computational biology.

Sun Lingying L Ma Junjie J Turck Christoph W CW Xu Pin P Wang Guang-Zhong GZ

Computational and structural biotechnology journal 20200710

Circadian rhythms are 24-hour oscillations affecting an organism at multiple levels from gene expression all the way to tissues and organs. They have been observed in organisms across the kingdom of life, spanning from cyanobacteria to humans. In mammals, the master circadian pacemaker is located in the hypothalamic suprachiasmatic nuclei (SCN) in the brain where it synchronizes the peripheral oscillators that exist in other tissues. This system regulates the circadian activity of a large part o ...[more]

PMID: 32774786

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Project description:Numerous studies suggest genetic influences on sleepiness and circadian rhythms. The Sleep Heart Health Study collected questionnaire data on sleep habits and sleepiness from 2848 Framingham Heart Study Offspring Cohort participants. More than 700 participants were genotyped using the Affymetrix 100K SNP GeneChip, providing a unique opportunity to assess genetic linkage and association of these traits.Sleepiness (defined as the Epworth Sleepiness Scale score), usual bedtime and usual sleep duration were assessed by self-completion questionnaire. Standardized residual measures adjusted for age, sex and BMI were analyzed. Multipoint variance components linkage analysis was performed. Association of SNPs to sleep phenotypes was analyzed with both population-based and family-based association tests, with analysis limited to 70,987 autosomal SNPs with minor allele frequency > or =10%, call rate > or =80%, and no significant deviation from Hardy-Weinberg equilibrium (p > or = 0.001).Heritability of sleepiness was 0.29, bedtime 0.22, and sleep duration 0.17. Both genotype and sleep phenotype data were available for 749 subjects. Linkage analysis revealed five linkage peaks of LOD >2: four to usual bedtime, one to sleep duration. These peaks include several candidate sleep-related genes, including CSNK2A2, encoding a known component of the circadian molecular clock, and PROK2, encoding a putative transmitter of the behavioral circadian rhythm from the suprachiasmatic nucleus. Association tests identified an association of usual bedtime with a non-synonymous coding SNP in NPSR1 that has been shown to encode a gain of function mutation of the neuropeptide S receptor, whose endogenous ligand is a potent promoter of wakefulness. Each copy of the minor allele of this SNP was associated with a 15 minute later mean bedtime. The lowest p value was for association of sleepiness with a SNP located in an intron of PDE4D, which encodes a cAMP-specific phosphodiesterase widely expressed in human brain. Full association results are posted at http://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?id=phs000007 webcite.This analysis confirms prior reports of significant heritability of sleepiness, usual bedtime, and usual sleep duration. Several genetic loci with suggestive linkage to these traits are identified, including linkage peaks containing circadian clock-related genes. Association tests identify NPSR1 and PDE4D as possible mediators of bedtime and sleepiness.

Dataset Information

Genome-wide circadian regulation: A unique system for computational biology.

Publications

Genome-wide circadian regulation: A unique system for computational biology.

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