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The stability of m6A-marked transcripts is linked to cell identity in planarians [EJC KD]

ABSTRACT: Using Nanopore dRNA-Seq, we called m6A sites (minimal methylation rate of 15% in at least two replicates) across the planarian transcriptome to detect influences on m6A deposition upon depletion of the exon junction complex (EJC). We observed m6A placement according to the EJC exclusion model, albeit with an exclusion zone shifted downstream of the splice junction and dependent on exon length.

ORGANISM(S): Schmidtea mediterranea

PROVIDER: GSE325808 | GEO | 2026/08/18

REPOSITORIES: GEO

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The Cellular EJC Interactome Reveals Higher-Order mRNP Structure and an EJC-SR Protein Nexus

Project description:To uncover exon junction complex (EJC) deposition sites on cellular mRNAs, RNA footprints of EJC immuo-purified from HEK293 cells were deep sequenced. The analysis of these data revealed that major “canonical” EJC occupancy site in vivo lies 24 nucleotides upstream of exon junctions (-24 position) and that the majority of exon junctions carry an EJC. Unexpectedly, we find that many sites further upstream of -24 position are also enriched in these EJC footprints. These "non-canonical" sites are binding sites of EJC-interacting proteins with a subset being occupied by SR proteins. Thus, an EJC-SR protein nexus exists within spliced mRNPs and is revealed here.

2012-10-18 | GSE41154 | GEO

The Cellular EJC Interactome Reveals Higher-Order mRNP Structure and an EJC-SR Protein Nexus

2012-10-18 | E-GEOD-41154 | biostudies-arrayexpress

Exon Architecture Controls mRNA m6A Suppression and Gene Expression

Project description:N6–methyladenosine (m6A) is the most abundant mRNA modification and plays crucial roles in diverse physiological processes. Utilizing a Massively Parallel Assay for m6A (MPm6A), we discover that m6A specificity is globally regulated by “suppressors” that prevent m6A deposition in unmethylated transcriptome regions. We identify Exon Junction Complexes (EJCs) as m6A suppressors that protect exon junction-proximal RNA within coding sequences from methylation and regulate mRNA stability through m6A suppression. EJC suppression of m6A underlies multiple global characteristics of mRNA m6A specificity, with the local range of EJC protection sufficient to suppress m6A deposition in average-length internal exons, but not in long internal and terminal exons. EJC-suppressed methylation sites co-localize with EJC-suppressed splice sites, suggesting that exon architecture broadly determines local mRNA accessibility to regulatory complexes.

2023-02-01 | GSE162199 | GEO

Magoh, Y14, eIF4AIII interactomes by TurboID proximity labelling provide no evidence for a canonical EJC in (almost) intron-less trypanosomatids

Project description:In metazoans, mRNA quality is tightly monitored from transcription to translation. A key role lies with the exon junction complex (EJC) that is placed upstream of the exon-exon junction after splicing. The EJC inner core is composed of Magoh, Y14, eIF4AIII and BTZ and the outer core of proteins involved in mRNA splicing (CWC22), export (Yra1), translation (PYM) and non-sense mediated decay (NMD, UPF1/2/3). The protozoan parasite Trypanosoma brucei encodes only two genes with introns, but all mRNAs are processed by trans-splicing. The presence of the three core EJC proteins and a potential BTZ homologue (Rbp25) in trypanosomes has been suggested as an adaptation of the EJC function to mark trans-spliced mRNAs. Here we explore the interactome of Magoh, Y14, eIF4AIII in T. brucei by TurboID proximity labelling.

2024-03-25 | PXD050946 | Pride

Transcriptional profiling of EJC depletion by RNA-Seq using the SOLiD platform (Applied Biosystems)

Project description:Signaling pathways are controlled by a vast array of post-translational mechanisms. By contrast, little is known regarding the mechanisms that regulate the expression of their core components. We conducted an RNAi screen in Drosophila for factors modulating RAS/MAPK signaling and identified the Exon Junction Complex (EJC) as a novel key element of this pathway. The EJC binds the exon-exon junctions of mRNAs, and thus far, has been linked exclusively to post-splicing events. Here, we report that the EJC is required for proper splicing of mapk transcripts by a mechanism that apparently controls exon definition. Moreover, whole transcriptome and RT-PCR analyses of EJC-depleted cells revealed that the splicing of long intron-containing genes, which includes mapk, is sensitive to EJC activity. These results identify a role for the EJC in the splicing of a subset of transcripts and suggest that RAS/MAPK signaling depends on the regulation of MAPK levels by the EJC.

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The stability of m6A-marked transcripts is linked to cell identity in planarians [MTC KD]

Project description:Using Nanopore dRNA-Seq, we generated a high-confidence atlas of ~72,200 m6A sites (minimal methylation rate of 15% in at least two replicates) across the planarian transcriptome. We identified planarian m6A sites to be installed in a DRAYW context and to be highly enriched near stop codons. Upon depletion of METTL14 – a core component of the methyltransferase complex – we observed a significant reduction of m6A levels by 73.2%, as well as significant gene expression changes in 1059 genes. Loss of m6A resulted in up- as well as downregulation of genes, but cell type markers were found to be specifically represented in both gene classes.

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PYM1 controls non-canonical EJC occupancy and maintains homeostatic expression of membrance targeted transcripts

Project description:During pre-mRNA splicing in the nucleus, the spliceosome deposits the Exon Junction Complex (EJC) ~24 nucleotides upstream of exon-exon junctions. The EJC core thus deposited comprises of EIF4A3, RBM8A and MAGOH and remains stably bound to RNA to modulate mRNA fate at multiple post-transcriptional steps until its disassembly during translation. Such EJC disassembly is proposed to be mediated by PYM1, a factor that can bind both the ribosome and the RBM8A/MAGOH heterodimer of the EJC core. Here, we investigated the role of PYM1 in regulating EJC binding in human embryonic kidney 293 (HEK293) cells using a MAGOH mutant that assembles into EJC but is impaired in PYM1 interaction. We find that EJCs lacking PYM1 interaction show no defect in translation dependent disassembly. Surprisingly, PYM1 interaction deficient EJCs are enriched on sites away from the canonical EJC binding position including on transcripts without introns or fewer and longer exons. Additionally, acute reduction and elevation of PYM1 levels in HEK293 cells result in a modest NMD inhibition and stabilization of mRNAs that localize to endoplasmic reticulum associated TIS-granules and are characterized by fewer and longer exons. These gene expression changes are mirrored in flavivirus infected cells, suggesting a potential role for PYM1 in host-pathogen interactions, as flaviviruses are known to target this protein.

2025-07-31 | GSE289360 | GEO

ChIP of PolII in S2R+ cells depleted for EJC components or RnpS1 [Promoter-proximal pausing mediated by the exon junction complex regulates splicing]

Project description:Promoter-proximal pausing of RNA polymerase II (Pol II) is a widespread transcriptional regulatory step across metazoans. Here we find that the nuclear exon junction complex (pre-EJC) is a critical and conserved regulator of this process. Depletion of pre-EJC subunits leads to a global decrease in Pol II pausing and to premature entry into elongation. This effect occurs, at least in part, via non-canonical recruitment of pre-EJC components at promoters. Failure to recruit the pre-EJC at promoters results in increased binding of the positive transcription elongation complex (P-TEFb) and in enhanced Pol II release. Notably, restoring pausing is sufficient to rescue exon skipping and the photoreceptor differentiation defect associated with depletion of pre-EJC components in vivo. We propose that the pre-EJC serves as an early transcriptional checkpoint to prevent premature entry into elongation, ensuring proper recruitment of RNA processing components that are necessary for exon definition.

2019-01-22 | GSE106907 | GEO

Exclusion of m6A from splice-site-proximal regions by the exon-junction complex dictates m6A topologies and mRNA stability

Project description:N6-methyladenosine (m6A), a widespread destabilizing mark on mRNA, is non-uniformly distributed across the transcriptome, yet the basis for its selective deposition is unknown. Here, we uncover that m6A deposition is not selective. Instead, m6A distribution is exclusion-based: m6A-consensus harboring sites are methylated by default, unless they are within a window of up to ~200 nt from an exon-intron junction. A simple model which we extensively validate, relying exclusively on presence of m6A motifs and exon-intron architecture allows high accuracy recapitulation of experimentally-measured m6A profiles and of the vast majority of m6A hallmarks. Finally, we provide strong evidence that this exclusion is mediated by the exon-junction complex. Our findings establish a mechanism by which the memory of nuclear RNA splicing is covalently etched on an mRNA in the form of m6A, and determines its cytoplasmic stability, with broad implications on the regulation, function, and evolution of the exon-junction complex and m6A.

2023-01-02 | GSE204980 | GEO

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