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EC Number
General Information
Commentary
Reference
evolution
both the nucleotide position and percent methylation of tRNAs and rRNAs m5C sites are conserved across all species analysed
evolution
both the nucleotide position and percent methylation of tRNAs and rRNAs m5C sites are conserved across all species analysed, overview
evolution
both the nucleotide position and percent methylation of tRNAs and rRNAs m5C sites were conserved across all species analysed
evolution
Identification of m5C sites in nuclear, chloroplast and mitochondrial tRNAs. 39 cytosine 5-methylation sites are identified at 5 structural positions and are located in tRNA secondary structure at positions C38, C48, C49, C50 and C72, pattern of methylation in individual tRNA isodecoders, overview. Identification of single-nucleotide resolution of cytosine 5-methylation sites in non-coding ribosomal RNAs and transfer RNAs of all three subcellular transcriptomes across six diverse species. Both the nucleotide position and percent methylation of tRNAs and rRNAs cytosine 5-methylation sites are conserved across all species analysed, overview
evolution
the enzyme belongs to the RsmF/YebU/NSUN2 family of cytosine 5-methylation-RNA methyltransferases utilizing two cysteines in their catalytic pocket
malfunction
autosomal-recessive loss of the NSUN2 gene is a causative link to intellectual disability disorders in humans. Loss of cytosine-5 methylation in vault RNAs causes aberrant processing into Argonaute-associated small RNA fragments that can function as microRNAs. Impaired processing of vault ncRNA may contribute to the etiology of NSun2-deficiency human disorders
malfunction
disruption of the ORF YBL024w leads to the complete absence of m5C in total yeast tRNA. No tRNA:m5C-methyltransferase activity towards all potential m5C methylation sites is detected in the extract of the disrupted yeast strain. The protein product of a single gene is responsible for complete m5C methylation of yeast tRNA
malfunction
in trm4a defective mutants, the cytosine 5-methylation profile is the same as wild-type, showing that TRM4A is not required for methylation of any of the detected tRNAs. In contrast for trm4b-1 and trm4b-2 mutants, a total of 18 sites have no detectable methylation and 7 sites have reduced methylation when compared to wild-type, the sites are corresponding to structural positions C48, C49, and C50. trdmt1/trm4b double mutants are hypersensitive to the antibiotic hygromycin B
malfunction
NSUN2 is associated with Myc-induced proliferation of cancer cells, mitotic spindle stability, infertility in male mice, and the balance of selfrenewal and differentiation in skin stem cells. In humans NSUN2 mutations cause an autosomal recessive syndrome characterized by intellectual disability and mental retardation
malfunction
yeast strains depleted of tRNAHis guanylyltransferase accumulate uncharged tRNAHis lacking the G-1 residue and subsequently accumulate additional 5-methylcytidine (m5C) at residues C48 and C50 of tRNAHis, due to the activity of the m5Cmethyltransferase Trm4. The increase in tRNAHis m5C levels does not require loss of Thg1, loss of G-1 of tRNAHis, or cell death but is associated with growth arrest following different stress conditions. Substantially increased tRNAHis m5C levels occur after temperature-sensitive strains are grown at nonpermissive temperature, and after wild-type strains are grown to stationary phase, starved for required amino acids, or treated with rapamycin. More modest accumulations of m5C in tRNAHis occur after starvation for glucose and after starvation for uracil. In virtually all cases examined, the additional m5C on tRNAHis occurs while cells are fully viable, and the increase is neither due to the GCN4 pathway, nor to increased Trm4 levels, phenotypes, overview. The increased amount of m5C is specific to tRNAHis. tRNAVal(AAC), which also normally has unmodified C48 and C50 residues adjacent to m5C49, has only marginally increased levels of m5C 7 h after temperature shift in the fcp1-1ts mutant
Results 1 - 10 of 18 > >>