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Widespread exon-skipping triggers degradation by nuclear RNA surveillance in fission yeast

ABSTRACT: Interrogation of the S. pombe transcriptome using strand specific RNA sequencing (polyA enriched,ribosomal depleted total RNA). A total of 116 transcriptomes were interrogated in the study with the aim to identify exon-skipping events. Expression level summaries were not computed. Only exon-exon junction and exon-skipping diagnostic reads were used throughout. The vast majority (110/116) of transcriptomes are published and available elsewhere, while only 6 transcriptomes were sequenced here: two biological repeats of dhp1-ts and prp2-ts, a single wild-type strain and a single transcription compromised strain - nmt1-rpb4. Note that growth and library construction protocols varied across the samples.

PROVIDER: PRJEB7379 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR637354.fastq.gz	Fastqsanger.gz
	ERR637355.fastq.gz	Fastqsanger.gz
	ERR637356.fastq.gz	Fastqsanger.gz
	ERR637357.fastq.gz	Fastqsanger.gz
	ERR637358.fastq.gz	Fastqsanger.gz

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Cellular senescence induced by down-regulation of PTBP1 correlates with exon skipping of mitochondrial related gene NDUFV3

Project description:As the most prevalent type of alternative splicing in animal cells, exon skipping plays an important role in expanding the diversity of transcriptome and proteome, thereby participating the regulation of diverse physiological and pathological processes such as development, aging and cancer. Cellular senescence serves as an anti-cancer mechanism could also contribute to individual aging. Although the dynamic changes of exon skipping during cellular senescence were revealed, its biological consequence and upstream regulator remain poorly understood. Here, by using human foreskin fibroblasts (HFF) replicative senescence as a model, we discovered that splicing factor PTBP1 was an important contributor for global exon skipping events during senescence. Down-regulated expression of PTBP1 induced senescence-associated phenotypes and related mitochondrial functional changes. Mechanistically, PTBP1 binds to the third exon of mitochondrial complex I subunit coding gene NDUFV3 and protects the exon from skipping. We further confirmed that exon skipping of NDUFV3 correlates with and partially contributes to cellular senescence and related mitochondrial functional changes upon PTBP1 knockdown. Together, we revealed for the first time that mitochondrial related gene NDUFV3 is a new downstream target for PTBP1-regulated exon skipping to mediate cellular senescence and mitochondrial functional changes.

2024-05-18 | GSE266081 | GEO

Inherited epigenetic repression of the Celf2a splicing factor mediates the amelioration of a Duchenne phenotype

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SPLICER: A Highly Efficient Base Editing Toolbox That Enables in vivo Exon Skipping For Targeting Alzheimer’s Disease [RNA-seq]

Project description:Exon skipping technologies enable exclusion of targeted exons from mature mRNA transcripts, which has broad applications in molecular and cellular biology, medicine and biotechnology. Existing exon skipping techniques include antisense oligonucleotides, targetable nucleases and base editors, which, while effective for specific applications at some target exons, remain hindered by shortcomings preventing their broader implementation including transient effects in the case of oligonucleotides or limiting PAM motifs, sequence context preferences for deaminases, and undesirable cryptic splicing in the case of gene editing tools. To overcome these limitations, we created SPLICER, a toolbox of next-generation base editors consisting of near-PAMless Cas9 nickase variants fused with different deaminases for simultaneous editing of splice acceptor (SA) and splice donor (SD) sequences. Synchronized SA and SD editing not only improves exon skipping rates but also reduces aberrant outcomes such as cryptic splicing and intron retention. SPLICER enables editing of exon splice sites with high efficiency, including many exons refractory to splicing reprogramming by the native SpCas9 BEs. To demonstrate the therapeutic potential of SPLICER, we targeted APP exon 17, which contains the amino acid residues responsible for the formation of Aβ plaques in Alzheimer’s disease. SPLICER enabled precise and highly efficient exon skipping, which reduced the formation of Aβ42 peptides in vitro while inducing DNA editing and exon skipping in vivo within a humanized mouse model of Alzheimer’s disease. Overall, SPLICER is a widely applicable and highly efficient toolbox for exon skipping with broad therapeutic applications.

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An Alternative Splicing Event Amplifies Evolutionary Differences Between Vertebrates

Project description:Alternative splicing (AS) generates extensive transcriptomic and proteomic complexity. However, the functions of species- and lineage-specific splice variants are largely unknown. Here, we show that mammalian-specific skipping of exon 9 of PTBP1 alters its splicing regulatory activities and affects the inclusion levels of numerous exons. During neurogenesis, skipping of exon 9 reduces PTBP1 repressive activity so as to facilitate activation of a brain-specific AS program. Engineered skipping of the orthologous exon in chicken cells induces a large number of mammalian-like AS changes in PTBP1 target exons. These results thus reveal that a single exon skipping event in an RNA binding regulator directs numerous AS changes between species. The results further suggest that these changes contributed to evolutionary differences in the formation of vertebrate nervous systems. This study contains two sets of samples: (Set 1) mRNA profiling of human 293 cells subjected to four different conditions in two biological replicates: non-targetting control siRNA, PTBP1 and PTBP2 siRNA, PTBP1 and PTBP2 siRNA with overexpression of full-length human PTBP1, PTBP1 and PTBP2 siRNA with overexpression of exon-excluded human PTBP1. (Set 2) mRNA profiling of chicken DT40 cells with 3 genotypes in two bioligcal replicates: wildtype cells, cells with PTBP1 exon 8 (orthologous to human PTBP1 exon 9) deleted in one allele, and cells with PTBP1 exon 8 deleted in both alleles.

2015-09-01 | E-GEOD-69656 | biostudies-arrayexpress

An Alternative Splicing Event Amplifies Evolutionary Differences Between Vertebrates

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CRISPR induced exon skipping of beta-catenin reveals unexpected tumorigenic mutants driving distinct subtypes of liver cancer

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