Angptl8 mediates food-driven resetting of hepatic circadian clock in mice
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ABSTRACT:
PROVIDER: PRJNA551214 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9602530_1.fastq.gz | Fastqsanger.gz | |||
| SRR9602530_2.fastq.gz | Fastqsanger.gz | |||
| SRR9602522_1.fastq.gz | Fastqsanger.gz | |||
| SRR9602522_2.fastq.gz | Fastqsanger.gz | |||
| SRR9602523_1.fastq.gz | Fastqsanger.gz |
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Project description:Mammalian circadian clocks precisely control the rhythms of behavior and physiology, and can be reset by various environmental signals. While the light-dark (LD) cycle resets the master clock, timed food intake is a potent synchronizer of peripheral clocks. As the largest metabolic organ, the liver sensitively responds to the food signals and secrets hepatokines, leading to the robust regulation of metabolic and clock processes. However, it remains unknown which hepatokine mediates the food-driven resetting of the liver clock independent of the master clock. In our current study, we clustered high-throughput RNA sequencing results to screen out candidate genes that mediate the food-driven resetting of the liver clock
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Project description:Diurnal light-dark cycle resets the master clock, while timed food intake is another potent synchronizer of peripheral clocks in mammals. As the largest metabolic organ, the liver sensitively responds to the food signals and secretes hepatokines, leading to the robust regulation of metabolic and clock processes. However, it remains unknown which hepatokine mediates the food-driven resetting of the liver clock independent of the master clock. Here, we identify Angptl8 as a hepatokine that resets diurnal rhythms of hepatic clock and metabolic genes in mice. Mechanistically, the resetting function of Angptl8 is dependent on the signal relay of the membrane receptor PirB, phosphorylation of kinases and transcriptional factors, and consequently transient activation of the central clock gene Per1. Importantly, inhibition of Angptl8 signaling partially blocks food-entrained resetting of liver clock in mice. We have thus identified Angptl8 as a key regulator of the liver clock in response to food.
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Project description:Circadian clocks generate endogenous rhythms in most organisms from cyanobacteria to humans and facilitate entrainment to environmental diurnal cycles, thus conferring a fitness advantage. Both transcriptional and posttranslational mechanisms are prominent in the basic network architecture of circadian systems. Posttranscriptional regulation, including mRNA processing, is emerging as a critical step for the clock function. However, little is known about the molecular mechanisms linking RNA metabolism to the circadian clock network. Here we report that a conserved SNW/SKIP domain protein, SKIP, a splicing factor and component of the spliceosome, is involved in the posttranscriptional regulation of circadian clock genes in Arabidopsis. Mutation in SKIP lengthens the circadian period in a temperature sensitive manner, affects light input and the sensitivity of light resetting to the clock. SKIP physically interacts with the spliceosomal splicing factor SR45 and associates with the pre-mRNA of clock genes, such as PRR7 and PRR9, and is necessary for the regulation of their alternative splicing and mRNA maturation. Genome-wide investigations reveal that SKIP functions in regulating alternative splicing of many genes, presumably through modulating recognition or cleavage of 5' and 3' splicing site. Our study addresses a fundamental question on how the mRNA splicing machinery contributes to circadian clock functions at a posttranscriptional level. Our findings revealed that AtSKIP is a splicing factor and a component of spliceosome. To further investigate effects of mutation in SKIP on the genome-wide changes of alternative splicing, we performed ultra-highthroughput RNA sequencing, using 10-day old seedlings. Two biological replicates for both wild type (Col-0) and skip-2 were designed.
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Project description:Circadian clocks generate endogenous rhythms in most organisms from cyanobacteria to humans and facilitate entrainment to environmental diurnal cycles, thus conferring a fitness advantage. Both transcriptional and posttranslational mechanisms are prominent in the basic network architecture of circadian systems. Posttranscriptional regulation, including mRNA processing, is emerging as a critical step for the clock function. However, little is known about the molecular mechanisms linking RNA metabolism to the circadian clock network. Here we report that a conserved SNW/SKIP domain protein, SKIP, a splicing factor and component of the spliceosome, is involved in the posttranscriptional regulation of circadian clock genes in Arabidopsis. Mutation in SKIP lengthens the circadian period in a temperature sensitive manner, affects light input and the sensitivity of light resetting to the clock. SKIP physically interacts with the spliceosomal splicing factor SR45 and associates with the pre-mRNA of clock genes, such as PRR7 and PRR9, and is necessary for the regulation of their alternative splicing and mRNA maturation. Genome-wide investigations reveal that SKIP functions in regulating alternative splicing of many genes, presumably through modulating recognition or cleavage of 5' and 3' splicing site. Our study addresses a fundamental question on how the mRNA splicing machinery contributes to circadian clock functions at a posttranscriptional level.
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Analysis of differential protein expression in the hemolymph from flies reared on a high protein diet. Comparison of flies with and without a functional circadian clock within their photoreceptors.
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