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<p>Heterogeneous nuclear ribonucleoprotein A1 (<i>HNRNPA1</i>) is a highly abundant RNA binding protein alternatively spliced in two main isoforms named, hnRNP A1 and hnRNP A1B. While being ubiquitously expressed, both isoforms have different cellular localizations and are differentially expressed in tissues during development and aging. To improve our understanding of the cellular function of each isoform, we performed RNA sequencing in cells exclusively expressing hnRNP A1 or hnRNP A1B. As expected, some genes were commonly regulated, however &gt; 300 genes were differentially regulated by the two isoforms. Functional annotation indicated an enrichment for genes implicated in cellular defense, especially for innate immunity and dsRNA response. Here, we demonstrate that in basal conditions, hnRNP A1, but not hnRNP A1B, represses interferon stimulated genes including the family of dsRNA sensors oligoadenylate synthases (OASs). Thus, the dsRNA-mediated interferon antiviral response can be potentiated by the loss of hnRNP A1-mediated repression.</p>

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The differential impact of HNRNPA1 isoforms on gene expression and their relevance to dsRNA-mediated innate immune response

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月1日

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  • Jade-Emmanuelle Deshaies,
  • Valérie Triassi,
  • Andréanne Lacombe,
  • Myriam Gagné,
  • Karen Ling,
  • Asmita Ghosh,
  • Marjorie Labrecque,
  • Frank Rigo,
  • Paymaan Jafar-nejad,
  • Martine Tétreault,
  • Christine Vande Velde

摘要

Heterogeneous nuclear ribonucleoprotein A1 (HNRNPA1) is a highly abundant RNA binding protein alternatively spliced in two main isoforms named, hnRNP A1 and hnRNP A1B. While being ubiquitously expressed, both isoforms have different cellular localizations and are differentially expressed in tissues during development and aging. To improve our understanding of the cellular function of each isoform, we performed RNA sequencing in cells exclusively expressing hnRNP A1 or hnRNP A1B. As expected, some genes were commonly regulated, however > 300 genes were differentially regulated by the two isoforms. Functional annotation indicated an enrichment for genes implicated in cellular defense, especially for innate immunity and dsRNA response. Here, we demonstrate that in basal conditions, hnRNP A1, but not hnRNP A1B, represses interferon stimulated genes including the family of dsRNA sensors oligoadenylate synthases (OASs). Thus, the dsRNA-mediated interferon antiviral response can be potentiated by the loss of hnRNP A1-mediated repression.