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Mus musculus

ABSTRACT: Loss of cytosine-5 methylation in tRNA triggers stress responses in a disease model for Intellectual Disability

PROVIDER: PRJNA191532 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR771327.fastq.gz	Fastqsanger.gz
	SRR771328.fastq.gz	Fastqsanger.gz
	SRR771329.fastq.gz	Fastqsanger.gz
	SRR771330.fastq.gz	Fastqsanger.gz
	SRR771331.fastq.gz	Fastqsanger.gz

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Loss of cytosine-5 methylation in tRNA triggers stress responses in a disease model for Intellectual Disability

Project description:Mutations in the cytosine-5 RNA methyltransferase NSun2 can cause Intellectual Disability (ID) and symptoms commonly found in patients with Dubowitz syndrome. By analysing gene expression data with the global cytosine-5 RNA methylome in NSun2-deficient mice, we find that loss of cytosine-5 RNA methylation increases the fragmentation of transfer RNAs (tRNA) leading to an accumulation of 5M-bM-^@M-^Y halves. Cleavage of tRNAs by Angiogenin is a common cellular stress response to silence translational programmes, and we show that Angiogenin binds tRNAs lacking site-specific NSun2-methylation with higher affinity. Furthermore, cells lacking functional NSun2 up-regulate stress markers, and deletion of NSun2 compromises cellular survival in response stress stimuli including UV-light and oxidative stress. The decreased tolerance of NSun2 null cells towards oxidative stress can be rescued through inhibition of Angiogenin. In conclusion, cytosine-5 RNA methylation is an essential post-transcriptional mechanism during cellular stress responses and NSun2-mediated tRNA methylation protects from Angiogenin-dependent stress-induced RNA cleavage. RNA Methylation profiling by high throughput sequencing small non-coding RNA profiling by high throughput sequencing Pol III Chromatin-IP profiling by high throughput sequencing

2014-11-06 | E-GEOD-44746 | biostudies-arrayexpress

Homo sapiens

Project description:Loss of cytosine-5 methylation in tRNA triggers stress responses in a disease model for Intellectual Disabilities

| PRJNA209566 | ENA

Loss of cytosine-5 methylation in tRNA triggers stress responses in a disease model for Intellectual Disabilities

Project description:Loss of cytosine-5 methylation in tRNA triggers stress responses in a disease model for Intellectual Disabilities

| PRJNA209565 | ENA

Loss of cytosine-5 methylation in tRNA triggers stress responses in a disease model for Intellectual Disability

Project description:Mutations in the cytosine-5 RNA methyltransferase NSun2 can cause Intellectual Disability (ID) and symptoms commonly found in patients with Dubowitz syndrome. By analysing gene expression data with the global cytosine-5 RNA methylome in NSun2-deficient mice, we find that loss of cytosine-5 RNA methylation increases the fragmentation of transfer RNAs (tRNA) leading to an accumulation of 5’ halves. Cleavage of tRNAs by Angiogenin is a common cellular stress response to silence translational programmes, and we show that Angiogenin binds tRNAs lacking site-specific NSun2-methylation with higher affinity. Furthermore, cells lacking functional NSun2 up-regulate stress markers, and deletion of NSun2 compromises cellular survival in response stress stimuli including UV-light and oxidative stress. The decreased tolerance of NSun2 null cells towards oxidative stress can be rescued through inhibition of Angiogenin. In conclusion, cytosine-5 RNA methylation is an essential post-transcriptional mechanism during cellular stress responses and NSun2-mediated tRNA methylation protects from Angiogenin-dependent stress-induced RNA cleavage.

2014-11-06 | GSE44746 | GEO

NSun2-mediated cytosine-5 methylation in Vault non-coding RNA determines its processing into small RNAs [RNA-seq]

Project description:Autosomal-recessive loss of the NSUN2 gene has been recently identified as a causative link to intellectual disability disorders in humans. NSun2 is an RNA methyltransferase modifying cytosine-5 in transfer RNAs (tRNA). Whether NSun2 methylates additional RNA species is currently debated. Here, we adapted the individual-nucleotide resolution UV cross-linking and immunoprecipitation method (iCLIP) to identify NSun2-mediated methylation in RNA transcriptome. We confirm site-specific methylation in tRNA and identify messenger and non-coding RNAs as potential methylation targets for NSun2. Using RNA bisulfite sequencing we establish Vault non-coding RNAs as novel substrates for NSun2 and identified six cytosine-5 methylated sites. Furthermore, we show that loss of cytosine-5 methylation in Vault RNAs causes aberrant processing into argonaute-associating small RNA fragments (svRNA). Thus, impaired Vault non-coding RNA processing may be an important contributor to the etiology of NSUN2-deficieny human disorders. mRNA-seq in Embryonic kidney (HEK293) cells transfected with siRNA against Nsun2 vs control

2013-07-23 | E-GEOD-44384 | biostudies-arrayexpress

NSun2-mediated cytosine-5 methylation in Vault non-coding RNA determines its processing into small RNAs [iCLIP]

Project description:Autosomal-recessive loss of the NSUN2 gene has been recently identified as a causative link to intellectual disability disorders in humans. NSun2 is an RNA methyltransferase modifying cytosine-5 in transfer RNAs (tRNA). Whether NSun2 methylates additional RNA species is currently debated. Here, we adapted the individual-nucleotide resolution UV cross-linking and immunoprecipitation method (iCLIP) to identify NSun2-mediated methylation in RNA transcriptome. We confirm site-specific methylation in tRNA and identify messenger and non-coding RNAs as potential methylation targets for NSun2. Using RNA bisulfite sequencing we establish Vault non-coding RNAs as novel substrates for NSun2 and identified six cytosine-5 methylated sites. Furthermore, we show that loss of cytosine-5 methylation in Vault RNAs causes aberrant processing into argonaute-associating small RNA fragments (svRNA). Thus, impaired Vault non-coding RNA processing may be an important contributor to the etiology of NSUN2-deficieny human disorders. Identification of Nsun2 targets by miCLIP in Embryonic kidney (HEK293) cells

2013-07-23 | E-GEOD-44385 | biostudies-arrayexpress

NSun2-mediated cytosine-5 methylation in Vault non-coding RNA determines its processing into small RNAs [iCLIP]

2013-07-23 | GSE44385 | GEO

NSun2-mediated cytosine-5 methylation in Vault non-coding RNA determines its processing into small RNAs [RNA-seq]

2013-07-23 | GSE44384 | GEO

N7-methylguanosine methylation of tRNAs regulates survival to stress in cancer

Project description:Combining transcriptome-wide approaches to detect m7G RNA methylation, in vitro functional assays and Mettl1 knockout mouse models, we provide evidence that guanosine-7 tRNA methylation is required to protect tRNAs from cleavage in response to stress, leading to impaired regulation of protein synthesis. Loss of METTL1 and tRNA methylation sensitises cancer cells to stress, reducing tumour growth and increasing cytotoxic responses to convectional cancer treatments in vitro and in vivo. Our study uncovers the role of m7G methylation of tRNAs in stress responses and highlights the potential of targeting METTL1 to sensitise cancer cells to therapy.

2024-01-26 | PXD036009 | Pride

DNA methylation fingerprint of a KDM5C loss-of-function mutation in patients with intellectual disability

Project description:DNA methylation fingerprint of a KDM5C loss-of-function mutation in patients with intellectual disability

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