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Mehravar, M.

Publications and source records attributed to Mehravar, M..

3 recordsLinked to original sources

RNA m6A and 5hmC regulate monocyte and macrophage gene expression programs

BackgroundRNA modifications are essential for the establishment of cellular identity. Although increasing evidence indicates that RNA modifications regulate the innate immune response, their role in monocyte-to-macrophage differentiation and polarisation is unclear. To date, most studies have focused on m6A, while other RNA modifications, including 5hmC, remain poorly characterised. The interplay between different RNA modifications that may occur in specific cellular contexts remains similarly unexplored. ResultsWe profiled m6A and 5hmC epitranscriptomes, transcriptomes, translatomes and proteomes of monocytes and macrophages at rest and pro- and anti-inflammatory states. We observed that decreased expression of m6A and 5hmC writers, METTL3 and TET-enzymes respectively, facilitated monocyte-to-macrophage differentiation. Despite a global trend of m6A and 5hmC loss during macrophage differentiation, enrichment of m6A and/or 5hmC on specific categories of transcripts essential for macrophage differentiation positively correlated with their expression and translation. m6A and 5hmC mark and are associated with the expression of transcripts with critical functions in pro- and anti-inflammatory macrophages. Notably, we also discovered the coexistence of m6A and 5hmC marking alternatively-spliced isoforms and/or opposing ends of the untranslated regions (UTR) of transcripts with key roles in macrophage biology. In specific examples, RNA 5hmC controls the decay of transcripts independently of m6A. ConclusionsThis study: i) uncovers m6A, 5hmC and their writer enzymes as regulators of monocyte and macrophage gene expression programs and ii) provides a comprehensive dataset to interrogate the role of RNA modifications in a plastic system. Altogether, this work sheds light on the role of RNA modifications as central regulators of effector cells in innate immunity.

molecular biology↗

MOV10 facilitates messenger RNA decay in an N6-methyladenosine (m6A) dependent manner to maintain the mouse embryonic stem cells state

N6-methyladenosine (m6A) is the most predominant internal mRNA modification in eukaryotes, recognised by its reader proteins (so-called m6A-readers) for regulating subsequent mRNA fates -- splicing, export, localisation, decay, stability, and translation -- to control several biological processes. Although a few m6A-readers have been identified, yet the list is incomplete. Here, we identify a new m6A-reader protein, Moloney leukaemia virus 10 homologue (MOV10), in the m6A pathway. MOV10 recognises m6A-containing mRNAs with a conserved GGm6ACU motif. Mechanistic studies uncover that MOV10 facilitates mRNA decay of its bound m6A-containing mRNAs in an m6A-dependent manner within the cytoplasmic processing bodies (P-bodies). Furthermore, MOV10 decays the Gsk-3{beta} mRNA through m6A that stabilises the {beta}-CATENIN expression of a WNT/{beta}-CATENIN signalling pathway to regulate downstream NANOG expression for maintaining the mouse embryonic stem cells (mESCs) state. Thus, our findings reveal how a newly identified m6A-reader, MOV10 mediates mRNA decay via m6A that impact embryonic stem cell biology.

biochemistry↗

Histone demethylome map reveals combinatorial gene regulatory functions in embryonic stem cells

Epigenetic regulators and transcription factors establish distinct regulatory networks for gene regulation to maintain the embryonic stem cell (ESC) state. Although much has been learned regarding individual epigenetic regulators, their combinatorial functions remain elusive. Here, we report previously unknown combinatorial functions of histone demethylases (HDMs) in gene regulation of mouse ESCs. Generation of a histone demethylome (HDMome) map of 20 well-characterized HDMs based on their genome-wide binding revealed co-occupancy of HDMs in different combinations: KDM1A-KDM4B-KDM6A and JARID2-KDM2B-KDM4A-KDM4C-KDM5B largely co-occupy at enhancers and promoters, respectively. Mechanistic studies uncover that KDM1A-KDM6A combinatorially modulates P300/H3K27ac, H3K4me2 deposition and OCT4 recruitment that directs the OCT4/CORE regulatory network for target gene expression; while co-operative actions of JARID2-KDM2B-KDM4A-KDM4C-KDM5B control H2AK119ub1 and bivalent marks of polycomb-repressive complexes that facilitate the PRC regulatory network for target gene repression. Thus, combinatorial functions of HDMs differentially impact gene expression programs in mESCs.

genomics↗