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New strategies for the identification of intronic variants related to splicing events in pancreas cancer [iCELL8]

ABSTRACT: New strategies for the identification of intronic variants related to splicing events in pancreas cancer [iCELL8]

PROVIDER: PRJNA952549 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24078633.fastq.gz	Fastqsanger.gz
	SRR24078634.fastq.gz	Fastqsanger.gz
	SRR24078635.fastq.gz	Fastqsanger.gz
	SRR24078636.fastq.gz	Fastqsanger.gz
	SRR24078637.fastq.gz	Fastqsanger.gz

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New strategies for the identification of intronic variants related to splicing events in pancreas cancer [iCELL8]

Project description:Most clinical diagnostic settings and genomic research focus almost exclusively on coding regions and essential splice sites, mostly ignoring non-coding variants. Indeed, the investigation of intronic mis-splicing variants interpreting mechanisms to disease-associated splicing events requires both genomic and transcriptomic data. Unfortunately, there are not many datasets where both are available, leading to the understanding of intronic variants in diseases full of gaps. In this study, we present for the first time a full-length single nuclei RNA-sequencing (snRNA-Seq) approach improving the proper investigation of pathogenic mis-splicing intronic variants in pancreatic cancer showing its contribution to abnormal splicing changes and their transcriptional effects. Finally, we discuss the demands of further machine learning-based methods to process the growing number of single cell data and to enhance the precision and recall.

2024-05-10 | GSE229006 | GEO

New strategies for the identification of intronic variants related to splicing events in pancreas cancer

Project description:New strategies for the identification of intronic variants related to splicing events in pancreas cancer

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New strategies for the identification of intronic variants related to splicing events in pancreas cancer

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Continuous clonal labeling reveals uniform progenitor potential in the adult exocrine pancreas

Project description:The tissue dynamics that govern maintenance and regeneration of the pancreas remain largely unknown. In particular, the presence and nature of a cellular hierarchy remains a topic of debate. Previous lineage tracing strategies in the pancreas relied on specific marker genes for clonal labeling, which left other populations untested and failed to account for potential widespread phenotypical plasticity. Here we employed a tracing system that depends on replication-induced clonal marks. We found that in homeostasis, steady acinar replacement events characterize tissue dynamics, to which all acinar cells have an equal ability to contribute. Similarly, regeneration following pancreatitis was best characterized by an acinar self-replication model, as no evidence for a cellular hierarchy was detected. In particular, rapid regeneration in the pancreas was found to be driven by an accelerated rate of acinar fission-like events. Together these results provide a comprehensive and quantitative model of cell dynamics in the exocrine pancreas.

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Spliceosome-Mediated-Decay (SMD) regulates expression of non-intronic genes in budding yeast

Project description:Purpose: The goals of this study were to determine whether the spliceosome interacts with non-intronic mRNAs Methods: RNAseq was performed on RNA that immunoprecipitated with the yeast SMD1 protein. Tandem-affinity-purified RNAs were extracted and RNAseq libraries were generated using the EpiCentre ScriptSeq kit (v1). We also performed RNAseq experiments on rRNA depleted total RNA extracted from an exosome mutant (rrp6M-NM-^T), a temperature-sensitive splicing mutant (prp40-1) and a parental strain (BY4741). The rRNA was depleted using the Invitrogen RiboMinus kit, according to manufactureres procedures. The depleted RNA was subsequently treated with Turbo DNAse I (Ambion) and RNAseq libraries were generated using the EpiCentre ScriptSeq kit (v1). Results: The SM RNAseq data identified a number of non-intronic mRNAs that appeard to be bound by the spliceosome. Among these was the BDF2 mRNA, which enocdes for a bromo-domain protein. BDF2 was highly enriched in both SM-IP datasets and was therefore analyzed in more detail. To determine if other non-intronic mRNAs could be regulated by the spliceosome, we analysed the transcriptome in the rrp6M-NM-^T, the prp40-1 and a parental strain. Bioinformatic analysis of these data sets revealed that roughly 1% of the non-intronic mRNAs in yeast could be targeted by the spliceosome. TopHat revealed cannonical splice junctions in roughly 30 non-intronic mRNAs, indicating that these messages are spliced. Conclusions: We demonstrate, for the first time, that the spliceosome can regulate expression of non-intronic mRNAs via one and/or two RNA cleavage events. We refer to this process as Spliceosome Mediated Decay (SMD). We report RNAseq data for two SM immunoprecipitation experiments and RNAseq datasets for the parental strain (BY4741), the prp40-1 mutant, and the rrp6M-NM-^T strain.

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Histone variant H3F3A promotes lung cancer cell migration through intronic regulation.

Project description:Although several somatic single nucleotide variations in histone H3.3 have been investigated as cancer drivers, other types of aberrations have not been well studied. Here, we demonstrate that overexpression of H3F3A, encoding H3.3, is associated with lung cancer progression and promotes lung cancer cell migration by activating metastasis-related genes. H3.3 globally activates gene expression through the occupation of intronic regions in lung cancer cells. Moreover, H3.3 binding regions show characteristics of regulatory DNA elements. We show that H3.3 is deposited at a specific intronic region of GPR87, where it modifies the chromatin status and directly activates GPR87 transcription. The expression levels of H3F3A and GPR87, either alone or in combination, are robust prognostic markers for early stage lung cancer, and may indicate potential for the development of treatments involving GPR87 antagonists. Our results demonstrate that intronic regulation by H3F3A may be a target for the development of novel therapeutic strategies. We performed microarray-based global gene expression analysis of H3F3A-overexpressing and H3F3A knockdown A549 cells.

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