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Single-cell RNAseq Reveals Developmental Origins and Ontogenetic Stability of Neurexin Alternative Splicing Profiles

ABSTRACT: Single-cell RNAseq Reveals Developmental Origins and Ontogenetic Stability of Neurexin Alternative Splicing Profiles

PROVIDER: PRJNA498023 | ENA |

REPOSITORIES: ENA

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Single-cell RNAseq Reveals Developmental Origins and Ontogenetic Stability of Neurexin Alternative Splicing Profiles

Project description:Neurexins are key synaptic organizers which exist in thousands of alternatively spliced isoforms. Because trans-synaptic neurexin interactions with different post-synaptic molecules are largely isoform dependent, a cell type-level census of different neurexin isoforms could predict molecular interactions relating to synapse identity and function. Using single-cell transcriptomics to study the origin of neurexin diversity in multiple murine hippocampal and cortical cell types, we have discovered shared expression patterns in developmentally-related cell types. By comparing neurexin profiles in immature embryonic neurons, we show that neurexin profiles are specified during early development and remain unchanged throughout neuronal maturation. In contrast to this, we find that expression of other cell-adhesion molecules is modulated throughout circuit maturation. Thus, our findings reveal that ontogenetic stability of neurexin expression is unique among the broader landscape of cell-adhesion molecules, whose coordinated expression progressively governs the emergence of cell type identity.

2019-06-23 | GSE121653 | GEO

Epitranscriptomic addition of m6A regulates HIV-1 RNA stability and alternative splicing

Project description:Epitranscriptomic addition of m6A regulates HIV-1 RNA stability and alternative splicing

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Epitranscriptomic addition of m6A regulates HIV-1 RNA stability and alternative splicing

Project description:Epitranscriptomic addition of m6A regulates HIV-1 RNA stability and alternative splicing

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Modulation of Yorkie activity by alternative splicing is required for developmental stability.

Project description: Not available

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Phosphorylated SIRT1 associates with replication origins to prevent excess replication initiation and preserve genomic stability

Project description:Chromatin structure affects DNA replication patterns, but the role of specific chromatin modifiers in regulating the replication process is yet unclear. We report that phosphorylation of the human SIRT1 deacetylase on Threonine 530 (T530-pSIRT1) modulates DNA synthesis. T530-pSIRT1 associates with replication origins and inhibits replication from a group of ÒdormantÓ potential replication origins, which initiate replication only when cells are subject to replication stress. Although both active and dormant origins bind T530-pSIRT1, active origins are distinguished from dormant origins by their unique association with an open chromatin mark, histone H3 methylated on lysine 4. SIRT1 phosphorylation also facilitates leading and lagging strand coordination. SIRT1 T530 phosphorylation is essential to prevent DNA breakage upon replication stress and cells harboring SIRT1 that cannot be phosphorylated exhibit a high prevalence of extrachromosomal elements, hallmarks of perturbed replication. These observations suggest that SIRT1 phosphorylation modulates the distribution of replication initiation events to insure genomic stability.

2017-06-02 | GSE94403 | GEO

Epitranscriptomic addition of m6A regulates HIV-1 RNA stability and alternative splicing

Project description:Several prior reports have demonstrated that the epitranscriptomic addition of m6A to viral transcripts promotes the replication and pathogenicity of a wide range of viruses yet the underlying mechanism(s) causing this positive effect has remained unclear. It is known that m6A function is largely mediated by cellular m6A binding proteins or readers, however, how these m6A reader proteins contribute to the regulation of HIV-1 gene expression has remained controversial. Here, we confirm that m6A indeed enhances HIV-1 gene expression. We demonstrate that this effect is collectively mediated by the cytoplasmic reader YTHDF2, which increases HIV-1 transcript stability, and the nuclear m6A reader YTHDC1, which binds HIV-1 RNA at 7 distinct m6A methylated sites, regulating viral transcript alternative splicing.

2021-06-21 | GSE165473 | GEO

Epitranscriptomic addition of m6A regulates HIV-1 RNA stability and alternative splicing

2021-02-06 | GSE166237 | GEO

Alternative polyadenylation isoform abundance and stability of HEK293T cells

Project description:Alternative polyadenylation isoform abundance and stability of HEK293T cells

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INO80C chromatin remodeler prevents promiscuous transcription at replication origins

Project description:INO80C chromatin remodeler colocalizes to yeast replication origins together with the transcription factors Mot1 and NC2. INO80C maintains genome stability by preventing noncoding transcription around origins both in yeast and mammals.

2020-09-07 | GSE144072 | GEO

Alternative splicing is a developmental switch for hTERT expression

Project description:Telomere length control is critical for cellular lifespan and tumor suppression. Telomerase is activated in the inner cell mass of the developing blastocyst to reset telomere reserves and its subsequent silencing in differentiated cells leads to gradual telomere shortening. Here, we report that transcriptional control through cis-regulatory elements minimally impact telomerase regulation as a function of pluripotency. Instead, developmental control of telomerase is largely driven by an alternative splicing event, centered around hTERT exon-2. Skipping of exon-2 triggers hTERT mRNA decay in differentiated cells. Conversely, its retention in pluripotent cells promotes telomerase accumulation. Our study also identifies SON as a regulator of exon-2 alternative splicing and we report a patient with insufficient telomerase and short telomeres and harboring a SON mutation. In summary, our study highlights a critical role for hTERT alternative splicing in the developmental regulation of telomerase and implicates defective splicing in telomere biology disorders.

2021-03-04 | GSE168193 | GEO

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