Feces
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA822715 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18644100_1.fastq.gz | Fastqsanger.gz | |||
| SRR18644100_2.fastq.gz | Fastqsanger.gz | |||
| SRR18644200_1.fastq.gz | Fastqsanger.gz | |||
| SRR18644200_2.fastq.gz | Fastqsanger.gz | |||
| SRR18644101_1.fastq.gz | Fastqsanger.gz |
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Project description:In mice and humans, sleep quantity of individuals are governed by genetic factors and exhibit age-dependent variations. However, the core molecular pathways and effector mechanisms that regulate sleep time in mammals remain unclear. Here, we characterize a major signaling pathway for transcriptional regulation of sleep quantity in mice by adeno-associated virus-mediated somatic genetics analysis. Adult brain chimeric-knockout of LKB1 kinase, an activator of AMPK-related protein kinase SIK3/SLEEPY, markedly reduces non-rapid eye movement sleep (NREMS) amount and delta power–a measure of sleep depth. Downstream of LKB1-SIK3 pathway, gain or loss-of-function of histone deacetylases HDAC4/5 in adult brain neurons causes bidirectional changes of NREMS amount and delta power. Phosphorylation of HDAC4/5 is regulated in relation to sleep need, and HDAC4 specifically regulates sleep amount in posterior hypothalamus. Genetic and transcriptomic studies reveal that HDAC4 cooperates with CREB in both transcriptional and sleep regulation. These findings introduce the concept of signaling pathways targeting transcription modulators to regulate daily sleep amount and demonstrate utility of somatic genetics in mouse sleep research.
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Project description:One of sleep’s putative functions is mediation of adaptation to waking experiences. Chronic stress is a common waking experience, however, which specific aspect of sleep is most responsive, and how sleep changes relate to behavioral disturbances and molecular correlates remain unknown. We quantified sleep, physical, endocrine, and behavioral variables, as well as the brain and blood transcriptome in mice exposed to 9 weeks of unpredictable chronic mild stress (UCMS). Comparing 46 phenotypical variables revealed that rapid-eye-movement sleep (REMS), corticosterone regulation, and coat state were most responsive to UCMS. REMS theta oscillations were enhanced, whereas delta oscillations in non-REMS were unaffected. Transcripts affected by UCMS in the prefrontal cortex, hippocampus, hypothalamus, and blood were associated with inflammatory and immune responses. A machine-learning approach controlling for unspecific UCMS effects identified transcriptomic predictor sets for REMS parameters that were enriched in 193 pathways, including some involved in stem cells, immune response, apoptosis, and survival. Only three pathways were enriched in predictor sets for non-REMS. Transcriptomic predictor sets for variation in REMS continuity and theta activity shared many pathways with corticosterone regulation, in particular pathways implicated in apoptosis and survival, including mitochondrial apoptotic machinery. Predictor sets for REMS, and anhedonia shared pathways involved in oxidative stress, cell proliferation, and apoptosis. These data identify REMS as a core and early element of the response to chronic stress, and identify apoptosis and survival pathways as a putative mechanism by which REMS may mediate the response to stressful waking experiences.
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