Effects of KD USF2 on gene expressions in C2C12
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ABSTRACT:
PROVIDER: PRJNA1021546 | ENA |
REPOSITORIES: ENA
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Project description:USF2 has emerged as a key player in various cellular processes, including cell cycle regulation， apoptosi, metabolism, and response to cellular stress. In the context of muscle biology, the role of USF2 is not clear. To elucidate the functional significance of USF2, we conducted knockdown (KD) experiments targeting USF2 in C2C12 myoblast cells. The KD of USF2 resulted in the differential expression of a set of genes, and functional enrichment analysis of genes affected by KD of USF2 were performed.
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Project description:Intricate regulation of lysosome and autophagy processes is essential for maintaining cellular homeostasis and basal metabolism. While the consequences of disrupting or attenuating lysosome and autophagy systems have been extensively studied, little is known about the impact of hyper-activation of lysosomal and autophagy genes on homeostasis. Our research uncovers previously unknown transcriptional repression mechanism by upstream stimulatory factor 2 (USF2), which inhibits lysosomal and autophagy genes in nutrient-rich conditions. USF2 binds to the CLEAR motif within lysosomal genes along with HDAC1, which diminishes H3K27 acetylation levels, restrains chromatin accessibility, and lowers lysosomal gene expression. Under starvation, USF2 competes with TFEB, a master transcriptional activator of lysosomal and autophagy genes, to bind target gene promoters in phosphorylation-dependent manner. Phosphorylation of the S155 site by GSK3b plays a pivotal role in controlling USF2's DNA binding activity for the repression of lysosomal genes while GSK3b-mediated phosphorylation of TFEB enhances its cytoplasmic retention. Applying these discoveries has potential for treating diseases associated with protein aggregation, including alpha-1 antitrypsin deficiency. These findings demonstrate that the USF2 repression mechanism could be a potent therapeutic strategy for various lysosome and autophagy-related diseases.
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Project description:Effects of melatonin derivatives on gene expressions in human normal keratincytes
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