RNautophagic regulation of DNMT3a-dependent DNA methylation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA874430 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21283840_1.fastq.gz | Fastqsanger.gz | |||
| SRR21283840_2.fastq.gz | Fastqsanger.gz | |||
| SRR21283841_1.fastq.gz | Fastqsanger.gz | |||
| SRR21283841_2.fastq.gz | Fastqsanger.gz | |||
| SRR21283842_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 18 |
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Project description:RNautophagic regulation of DNMT3a-dependent DNA methylation
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Project description:Calorie restriction has long been known to extend lifespans and inhibit carcinogenesis in multiple species by slowing age-related epigenetic changes while the underlying mechanisms remain largely unknown. Herein, we found that starvation activated autophagy to remodel DNA methylation profile by inhibiting DNMT3a expression. Autophagy is impaired in chemoresistance which was associated with differential DNA methylation and could be reversed by DNMT3a inhibition. Autophagy activation decreases the expression of DNMT3a mRNA, accompanied with the downregulation of chemoresistance-related Linc00942. Knockdown of Linc00942 reduces DNMT3a expression and genome-wide DNA methylation while Linc00942 overexpression increased DNMT3a expression and correlated hypermethylation in cancer cells and primary tumor tissues. As a result, inhibition of autophagy increases Linc00942 expression to promote chemoresistance and autophagy activation or hypomethylating agent decitabine restores chemosensitivity by reducing global DNA methylation.
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Project description:Calorie restriction has long been known to extend lifespans and inhibit carcinogenesis in multiple species by slowing age-related epigenetic changes while the underlying mechanisms remain largely unknown. Herein, we found that starvation activated autophagy to remodel DNA methylation profile by inhibiting DNMT3a expression. Autophagy is impaired in chemoresistance which was associated with differential DNA methylation and could be reversed by DNMT3a inhibition. Autophagy activation decreases the expression of DNMT3a mRNA, accompanied with the downregulation of chemoresistance-related Linc00942. Knockdown of Linc00942 reduces DNMT3a expression and genome-wide DNA methylation while Linc00942 overexpression increased DNMT3a expression and correlated hypermethylation in cancer cells and primary tumor tissues. As a result, inhibition of autophagy increases Linc00942 expression to promote chemoresistance and autophagy activation or hypomethylating agent decitabine restores chemosensitivity by reducing global DNA methylation. Taken together, our study identifies a novel methylation cascade linking impaired RNautophagy to global hypermethylation in chemoresistance, and provides a rationale for repurposing decitabine to overcome chemoresistance in cancer treatment.
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Project description:DNA methylation plays a fundamental role in regulating transcription during development, cell differentiation, and maintenance of cellular identity. However, the functional role of DNA methylation in the regulation of endothelial cell (EC) transcription during state transition, meaning the switch from an angiogenic to a quiescent cell state, has not been determined. Here, we conducted a DNA methylome analysis over a longitudinal postnatal timeline of EC in the murine pulmonary vasculature, revealing two significant observations. First, prominent alterations in DNA methylation patterns occurred during the transition from angiogenic to quiescent EC. Second, once a quiescent state is established, DNA methylation marks remain stable throughout further EC aging. These longitudinal differentially methylated regions correlated with endothelial gene expression and provided evidence for the recruitment of de novo DNA methyltransferase 3a (DNMT3A). Comprehensive loss-of-function studies in mice revealed that the absence of DNMT3A-dependent DNA methylation led to the loss of active enhancers, resulting in mild transcriptional changes, likely due to loss of active enhancer integrity. These results underline the importance of DNA methylation as a key epigenetic mechanism of EC function during state transition. Furthermore, we showed that DNMT3A-dependent DNA methylation appears to be involved in establishing the proper histone landscape required for accurate transcriptome regulation.
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Project description:DNA methylation plays a fundamental role in regulating transcription during development, cell differentiation, and maintenance of cellular identity. However, the functional role of DNA methylation in the regulation of endothelial cell (EC) transcription during state transition, meaning the switch from an angiogenic to a quiescent cell state, has not been determined. Here, we conducted a DNA methylome analysis over a longitudinal postnatal timeline of EC in the murine pulmonary vasculature, revealing two significant observations. First, prominent alterations in DNA methylation patterns occurred during the transition from angiogenic to quiescent EC. Second, once a quiescent state is established, DNA methylation marks remain stable throughout further EC aging. These longitudinal differentially methylated regions correlated with endothelial gene expression and provided evidence for the recruitment of de novo DNA methyltransferase 3a (DNMT3A). Comprehensive loss-of-function studies in mice revealed that the absence of DNMT3A-dependent DNA methylation led to the loss of active enhancers, resulting in mild transcriptional changes, likely due to loss of active enhancer integrity. These results underline the importance of DNA methylation as a key epigenetic mechanism of EC function during state transition. Furthermore, we showed that DNMT3A-dependent DNA methylation appears to be involved in establishing the proper histone landscape required for accurate transcriptome regulation.
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Project description:DNA methylation plays a fundamental role in regulating transcription during development, cell differentiation, and maintenance of cellular identity. However, the functional role of DNA methylation in the regulation of endothelial cell (EC) transcription during state transition, meaning the switch from an angiogenic to a quiescent cell state, has not been determined. Here, we conducted a DNA methylome analysis over a longitudinal postnatal timeline of EC in the murine pulmonary vasculature, revealing two significant observations. First, prominent alterations in DNA methylation patterns occurred during the transition from angiogenic to quiescent EC. Second, once a quiescent state is established, DNA methylation marks remain stable throughout further EC aging. These longitudinal differentially methylated regions correlated with endothelial gene expression and provided evidence for the recruitment of de novo DNA methyltransferase 3a (DNMT3A). Comprehensive loss-of-function studies in mice revealed that the absence of DNMT3A-dependent DNA methylation led to the loss of active enhancers, resulting in mild transcriptional changes, likely due to loss of active enhancer integrity. These results underline the importance of DNA methylation as a key epigenetic mechanism of EC function during state transition. Furthermore, we showed that DNMT3A-dependent DNA methylation appears to be involved in establishing the proper histone landscape required for accurate transcriptome regulation.
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Project description:DNA methylation plays a fundamental role in regulating transcription during development, cell differentiation, and maintenance of cellular identity. However, the functional role of DNA methylation in the regulation of endothelial cell (EC) transcription during state transition, meaning the switch from an angiogenic to a quiescent cell state, has not been determined. Here, we conducted a DNA methylome analysis over a longitudinal postnatal timeline of EC in the murine pulmonary vasculature, revealing two significant observations. First, prominent alterations in DNA methylation patterns occurred during the transition from angiogenic to quiescent EC. Second, once a quiescent state is established, DNA methylation marks remain stable throughout further EC aging. These longitudinal differentially methylated regions correlated with endothelial gene expression and provided evidence for the recruitment of de novo DNA methyltransferase 3a (DNMT3A). Comprehensive loss-of-function studies in mice revealed that the absence of DNMT3A-dependent DNA methylation led to the loss of active enhancers, resulting in mild transcriptional changes, likely due to loss of active enhancer integrity. These results underline the importance of DNA methylation as a key epigenetic mechanism of EC function during state transition. Furthermore, we showed that DNMT3A-dependent DNA methylation appears to be involved in establishing the proper histone landscape required for accurate transcriptome regulation.
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