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LncRNA-splicing factor condensates regulate hypoxia-responsive pre-mRNA processing near nuclear speckles.

You Jin Song1, Min Kyung Shinn2, Sushant Bangru3

  • 1Department of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, Urbana, IL, USA; Cancer Center at Illinois, University of Illinois at Urbana-Champaign, Urbana, IL, USA.

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Summary
This summary is machine-generated.

The long noncoding RNA MALAT1 organizes splicing factors near nuclear speckles, promoting alternative splicing (AS) in response to hypoxia. This mechanism is crucial for regulating gene expression in tumors.

Keywords:
RNA splicingRNA-binding proteinbreast cancergene regulationnuclear domainsnuclear organizationphase separation

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Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Gene Regulation

Background:

  • Alternative splicing (AS) is vital for cellular processes, and its dysregulation contributes to cancer.
  • Hypoxia, prevalent in tumors, induces AS in numerous genes, but the underlying mechanisms are poorly understood.

Purpose of the Study:

  • To elucidate the mechanisms governing hypoxia-induced alternative splicing.
  • To investigate the role of the lncRNA MALAT1 in hypoxia-responsive AS.

Main Methods:

  • Analysis of hypoxia-responsive spliced exons and their genomic locations.
  • Investigating the association of MALAT1 with hypoxia-responsive genes.
  • Assessing MALAT1's effect on SRSF1-pre-mRNA interactions and SRSF1 condensation.
  • Evaluating the role of RNAPII in recruiting splicing factors.

Main Results:

  • Hypoxia-induced spliced exons are inefficiently spliced and located near nuclear speckles.
  • The speckle-enriched lncRNA MALAT1 is upregulated by hypoxia and associates with target genes.
  • MALAT1 promotes AS by enhancing SRSF1 condensation, facilitating RNAPII-mediated recruitment of splicing factors to pre-mRNAs.

Conclusions:

  • MALAT1 plays a critical role in orchestrating hypoxia-induced alternative splicing.
  • MALAT1 organizes splicing factor condensates near nuclear speckles, enhancing splicing efficiency during hypoxia.
  • This mechanism highlights a novel regulatory pathway for gene expression in the tumor microenvironment.