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M6A-mediated epi-transcriptomic dysregulation underlies synaptic dysfunction in fragile X syndrome [MeRIP-seq]

ABSTRACT: m6A-mediated epi-transcriptomic dysregulation underlies synaptic dysfunction in fragile X syndrome [MeRIP-seq]

PROVIDER: PRJNA1168478 | ENA |

REPOSITORIES: ENA

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m6A-mediated epi-transcriptomic dysregulation underlies synaptic dysfunction in fragile X syndrome [MeRIP-seq]

Project description:N6-methyladenosine (m6A) is a prevalent mRNA modification essential for post-transcriptional regulation. Fragile X syndrome (FXS), the leading genetic cause of intellectual disability, arises from FMR1 gene silencing and loss of FMRP, which has been shown to antagonize m6A readers. However, the impact of FMRP loss on transcriptome-wide m6A modifications in human FXS remains unknown. Using cortical neurons derived from healthy subjects and FXS patient-induced pluripotent stem cells, we found that FXS neurons exhibited synaptic and neuronal network defects, mirroring clinical EEG data from the same FXS patients. FMRP deficiency led to increased translation of m6A writers, resulting in transcriptome-wide hypermethylation, primarily affecting synapse-associated transcripts and increasing mRNA decay. Treatment with an m6A writer inhibitor rescued synaptic defects in FXS neurons, highlighting its therapeutic potential. Our findings uncover an epi-transcriptomic mechanism by which FMRP deficiency disrupts m6A modifications in FXS, contributing to FXS pathogenesis, and suggest a promising avenue for m6A-targeted therapies.

2025-02-26 | GSE278698 | GEO

m6A-mediated epi-transcriptomic dysregulation underlies synaptic dysfunction in fragile X syndrome [RNA-seq]

Project description:m6A-mediated epi-transcriptomic dysregulation underlies synaptic dysfunction in fragile X syndrome [RNA-seq]

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m6A-mediated epi-transcriptomic dysregulation underlies synaptic dysfunction in fragile X syndrome [RNA-seq]

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MeRIP-sequencing for dynamic epi-transcriptomic landscape mapping with disease progression in ER-positive breast cancer

Project description:Advanced breast cancer is characterised by enhanced tumour adaptability to therapeutic pressure and the metastatic microenvironment. Targeting epi-transcriptomic modulators may reverse cellular adaptability, offering new therapeutic strategies to treat metastatic disease. This study looks into the dynamic adaptations that occur in cancer cells in response to therapeutic pressure and metastatic evolution by profiling mRNA epi-transcriptomic modifications in models of disease progression. ER positive (ER+) cell models were used to represent progressive breast cancer, MCF7 (endocrine sensitive), LY2 (endocrine resistant) and T347 (derived from an ER-positive, treatment resistant brain metastatic patient tumour) cells. MeRIP sequencing was undertaken to determine genome-wide RNA methylated regions.

2023-05-16 | GSE176533 | GEO

Spatially coordinated heterochromatinization of long synaptic genes in fragile X syndrome

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