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A cohort of mRNAs undergo high-stoichiometry NSUN6-mediated site-specific m5C modification

ABSTRACT: A cohort of mRNAs undergo high-stoichiometry NSUN6-mediated site-specific m5C modification

PROVIDER: PRJNA1176035 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31072232_1.fastq.gz	Fastqsanger.gz
	SRR31072232_2.fastq.gz	Fastqsanger.gz
	SRR31072233_1.fastq.gz	Fastqsanger.gz
	SRR31072233_2.fastq.gz	Fastqsanger.gz
	SRR31072234_1.fastq.gz	Fastqsanger.gz

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A cohort of mRNAs undergo high-stoichiometry NSUN6-mediated site-specific m5C modification

Project description:mRNA modifications are vital in regulating cellular processes. Beyond N6-methyladenosine (m6A), most other internal mRNA modifications lack dedicated catalytic machinery and are typically introduced by tRNA-modifying enzymes. The distribution and stoichiometry of these modifications on mRNAs remain debated and require further validation. Furthermore, their precise function remains controversial due to the challenges of excluding the intricate combinational effects of tRNA modifications. Here, we biochemically validate that NSUN6, a tRNA structure-dependent methyltransferase, independently catalyzes 5-methylcytidine (m5C) formation with robust activity on mRNA by recognizing the CUCCA motif in a certain stem-loop structure. NSUN6 employs different strategies to recognize tRNA and mRNA substrates. By introducing mutations, we further separate its catalytic capabilities toward mRNA and tRNA revealing that NSUN6 promotes breast cancer cell migration depending on mRNA m5C modification. Mechanistically, a cohort of mRNAs involved in cell migration carries high levels of NSUN6-mediated site-specific m5C modification, thus being stabilized by the preferential binding of m5C readers YBX1 and YBX3. Moreover, introducing a single-site high-level m5C can significantly increase the stability of therapeutic mRNAs in cells. Our findings underscore the pivotal role of m5C-modified mRNAs in promoting breast cancer metastasis and their potential for therapeutic applications.

2025-05-05 | GSE280051 | GEO

A cohort of mRNAs undergo high-stoichiometry NSUN6-mediated site-specific m5C modification to promote breast cancer metastasis

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A cohort of mRNAs undergo high-stoichiometry NSUN6-mediated site-specific m5C modification to promote breast cancer metastasis

Project description:A cohort of mRNAs undergo high-stoichiometry NSUN6-mediated site-specific m5C modification to promote breast cancer metastasis

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Effects of NSUN6 deficiency by systematic transcriptomes and m5C profiles in mice across tissue [RNA-Seq]

Project description:we constructed Nsun6-KO mouse, and observed that the wight and appearance of KO mice didn’t show abnormality. Through Bisulfite sequencing (BS-seq) in wild-type (WT) as well as KO mice and mRNA-seq, we identified high confident Nsun6-dependent m5C sites and performed the transcriptome analysis across five tissues.

2022-06-16 | GSE200952 | GEO

Effects of NSUN6 deficiency by systematic transcriptomes and m5C profiles in mice across tissue [BS-Seq]

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Sequence- and structure-specific cytosine-5 methylation in mRNAs by NSUN6

Project description:Methylation is the most common internal modification in mRNA. While the highly abundant N6-methyladonsine (m6A) modification affects most aspects of mRNA function, the precise functions of the rarer 5-methylcytosine (m5C) remains largely unknown. Here, we map m5C in the human transcriptome using methylation-dependent individual-nucleotide resolution cross-linking and immunoprecipitation (miCLIP) combined with RNA bisulfite sequencing. We identify NSUN6 as a methyltransferase with strong substrate specificity towards mRNA. NSUN6 primarily targeted three prime untranslated regions (3’UTR) at the consensus sequence motif CTCCA. Knockout and rescue experiments revealed that only mRNA methylation sites containing the consensus motif depended on the presence of NSUN6. Furthermore, ribosome profiling demonstrated that NSUN6-specific consensus motifs marked translation termination. However, even though NSUN6-methylated mRNAs were reduced in NSUN6 knockout cells, NSUN6 was dispensable for mouse embryonic development. Thus, our study identifies NSUN6 as methyltransferase targeting mRNA in a sequence- and structure-specific manner.

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Malignant transformed cells of bladder epithelium: control CdC12-V2 vs NSUN6-knockout Malignant transformed cells of bladder epithelium

Project description:m5C-specific methylated small RNA immunoprecipitation microarray analysis in CdC12-V2 vs NSUN6-knockout Malignant transformed cells of bladder epithelium

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Effects of NSUN6 deficiency by systematic transcriptomes and m5C profiles in mice across tissue

Project description:Effects of NSUN6 deficiency by systematic transcriptomes and m5C profiles in mice across tissue

| PRJNA827751 | ENA

Programmable RNA 5-methylcytosine (m5C) modification of cellular RNAs using dCasRx conjugated methyltransferase and demethylase

Project description:5-methylcytosine, an abundant RNA modification, plays a crucial role in regulating RNA fate and gene expression. While recent progress has been made in understanding the biological roles of m5C, the inability to introduce m5C at specific sites within transcripts has hindered efforts to elucidate direct links between specific m5C and phenotypic outcomes. Here we developed a CRISPR-Cas13d-based tool, named reengineered m5C modification systems (termed ‘RCMS’), for targeted m5C methylation and demethylation in specific transcripts. The RCMS editors consist of a nuclear-localised dCasRx conjugated to either to a methyltransferase, NSUN2/NSUN6 or a demethylase, the catalytic domain of mouse Tet2 (Tet2 CD), enabling the manipulation of methylation events at precise m5C sites. We demonstrate that the RCMS editors can direct site-specific m5C incorporation and demethylation. Furthermore, we confirm their effectiveness in modulating m5C levels within tRNAs and their ability to induce changes in transcript abundance and cell proliferation through m5C-mediated mechanisms. These findings collectively establish RCMS editors as a focused epitranscriptome engineering tool, facilitating the identification of individual m5C alterations and their consequential effects.

2025-01-19 | GSE253659 | GEO

RNA m5C Methylation in breast cancer using MeRIP-Seq

Project description:RNA m5C methylation profile of MCF10A and MDA486 by using MeRIP-Seq protocol Immunoprecipitation of Methylated mRNA at Cytosine (m5C) residues: Affinity purified of anti-methyl cytosine (m5C) polyclonal antibody 7ug (Zymo Research, Catalog#A3001-50) was conjugated with protein-A magnetic beads for 2 h at 4°C in end to end rotator. After that, conjugated beads were extensively washed with RNA immunoprecipitation (RIP) wash buffer to remove unbound antibody. Fragmented 25 ug polyA RNA (mRNA) was incubated with m5C conjugated beads for overnight at 4°C in in the rotating platform in RIP buffer. RIP was done using Megna RNA Immunoprecipitation kit (Millipore, Catalog#17-700). m5C mRNA-immune bead complex was treated with proteinase K buffer to release m5C mRNA from the conjugated antibody. To isolate m5C, mRNA was treated with phenol:chloroform:isoamyl and mixed with 400 ul of chloroform, which was centrifuged at 14000 rpm for 10 minutes to separate aqueous phase. The aqueous phase was ethanol precipitated at -80°C for overnight, to get m5C mRNA. This precipitated m5C mRNA pellet was washed twice with 70% ethanol and air dried. Finally, m5C mRNA pellet was dissolved in nuclease free Water. The m5C mRNA integrity and conentration was quantified by bioanalyzer (Agilent) and Qubit 2.0 flurometer (Invitrogen). The fragmented mRNA was used by following TruSeq RNA Sample Preparation Guide to develop RNA-Seq library for sequencing.

2014-02-20 | E-GEOD-53370 | biostudies-arrayexpress

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