Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA244979 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1257430.fastq.gz | Fastqsanger.gz | |||
| SRR1257440.fastq.gz | Fastqsanger.gz | |||
| SRR1257431.fastq.gz | Fastqsanger.gz | |||
| SRR1257441.fastq.gz | Fastqsanger.gz | |||
| SRR1257432.fastq.gz | Fastqsanger.gz |
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2014-11-17 | E-GEOD-56932 | biostudies-arrayexpress
Project description:Autophagy is the primary catabolic process triggered in response to starvation. Although autophagic regulation within the cytosolic compartment is well established, it is becoming clear that nuclear events also regulate the induction or repression of autophagy. Nevertheless, a thorough understanding of the mechanisms by which sequence-specific transcription factors modulate expression of genes required for autophagy is lacking. Here, we identify Foxk proteins (Foxk1 and Foxk2) as transcriptional repressors of autophagy in muscle cells and fibroblasts. Interestingly, Foxk1/2 serve to counter-balance another forkhead transcription factor, Foxo3, which induces an overlapping set of autophagic and atrophic targets in muscle. Foxk1/2 specifically recruits Sin3A-HDAC complexes to restrict acetylation of histone H4 and expression of critical autophagy genes. Remarkably, mTOR promotes the transcriptional activity of Foxk1 by facilitating nuclear entry to specifically limit basal levels of autophagy in nutrient-rich conditions. Our study highlights an ancient, conserved mechanism whereby nutritional status is interpreted by mTOR to restrict autophagy by repressing essential autophagy genes via Foxk-Sin3-mediated transcriptional control.
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Project description:Histone arginine methyltransferase CARM1 Is Crucial for Epigenetic Regulation of Starvation-induced Autophagy
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Project description:Autophagy is a highly conserved self-digestion process, essential to maintain homeostasis and viability in response to nutrient starvation. Although the components of autophagy in the cytoplasm have been well-studied, molecular basis for the epigenetic regulation of autophagy is poorly understood. Here, we identify histone arginine methyltransferase CARM1 as a critical component of autophagy. We found that nutrient starvation increased CARM1 protein level and subsequently histone H3R17 dimethylation. Genome-wide analyses reveal that CARM1 exerts transcriptional coactivator function on autophagy-related genes and lysosomal genes through TFEB. Our findings demonstrate a previously unrecognized role of CARM1-dependent histone arginine methylation as a critical nuclear event of autophagy.
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