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Widespread shortening of 3' untranslated regions and increased exon inclusion characterize the human macrophage response to infection

ABSTRACT: Widespread shortening of 3' untranslated regions and increased exon inclusion characterize the human macrophage response to infection

PROVIDER: PRJNA297863 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2529530.fastq.gz	Fastqsanger.gz
	SRR2529540.fastq.gz	Fastqsanger.gz
	SRR2529550.fastq.gz	Fastqsanger.gz
	SRR2529560.fastq.gz	Fastqsanger.gz
	SRR2529570.fastq.gz	Fastqsanger.gz

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Widespread shortening of 3' untranslated regions and increased exon inclusion characterize the human macrophage response to infection

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Widespread shortening of 3' untranslated regions and increased exon inclusion characterize the human macrophage response to infection

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Widespread shortening of 3’ untranslated regions and increased exon inclusion characterize the human macrophage response to infection [mRNA]

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Widespread Shortening of 3' Untranslated Regions and Increased Exon Inclusion Are Evolutionarily Conserved Features of Innate Immune Responses to Infection.

Project description:The contribution of pre-mRNA processing mechanisms to the regulation of immune responses remains poorly studied despite emerging examples of their role as regulators of immune defenses. We sought to investigate the role of mRNA processing in the cellular responses of human macrophages to live bacterial infections. Here, we used mRNA sequencing to quantify gene expression and isoform abundances in primary macrophages from 60 individuals, before and after infection with Listeria monocytogenes and Salmonella typhimurium. In response to both bacteria we identified thousands of genes that significantly change isoform usage in response to infection, characterized by an overall increase in isoform diversity after infection. In response to both bacteria, we found global shifts towards (i) the inclusion of cassette exons and (ii) shorter 3' UTRs, with near-universal shifts towards usage of more upstream polyadenylation sites. Using complementary data collected in non-human primates, we show that these features are evolutionarily conserved among primates. Following infection, we identify candidate RNA processing factors whose expression is associated with individual-specific variation in isoform abundance. Finally, by profiling microRNA levels, we show that 3' UTRs with reduced abundance after infection are significantly enriched for target sites for particular miRNAs. These results suggest that the pervasive usage of shorter 3' UTRs is a mechanism for particular genes to evade repression by immune-activated miRNAs. Collectively, our results suggest that dynamic changes in RNA processing may play key roles in the regulation of innate immune responses.

| S-EPMC5045211 | biostudies-literature

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Project description:Widespread shortening of 3’ untranslated regions and increased exon inclusion characterize the human macrophage response to infection [mRNA]

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Project description:Widespread shortening of 3’ untranslated regions and increased exon inclusion characterize the human macrophage response to infection [miRNA]

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Exon inclusion signatures enable accurate estimation of splicing factor activity

Project description:Splicing factors control exon inclusion in messenger RNA, shaping transcriptome and proteome diversity. Their catalytic activity is regulated by multiple layers, making single-omic measurements on their own fall short in identifying which splicing factors underlie a phenotype. Here, we propose that splicing factor activity can be estimated by interpreting changes in exon inclusion. To see if this is the case we benchmarked methods to construct splicing factor→exon networks and calculate splicing factor activity. Combining RNA-seq perturbation-based networks with VIPER (virtual inference of protein activity by enriched regulon analysis) accurately captures splicing factor activation modulated by different regulatory layers. This approach consolidates splicing factor regulation into a single score derived solely from exon inclusion signatures, allowing functional interpretation of heterogeneous conditions. As a proof of concept, we identify recurrent cancer splicing programs, revealing oncogenic- and tumor suppressor-like splicing factors missed by conventional methods. These programs correlate with patient survival and key cancer hallmarks: initiation, proliferation, and immune evasion. Altogether, we show splicing factor activity can be accurately estimated from exon inclusion changes, enabling comprehensive analyses of splicing regulation with minimal data requirements. In this dataset, we share our results from analyzing the BJ fibroblast-based model for carcinogenesis through proteomics and phosphoproteomics.

2025-07-27 | PXD066623 | Pride

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