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Related Experiment Video

Updated: Feb 11, 2026

Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches
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Widespread intronic polyadenylation diversifies immune cell transcriptomes.

Irtisha Singh1,2, Shih-Han Lee3, Adam S Sperling4

  • 1Computational and Systems Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.

Nature Communications
|May 2, 2018
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Summary
This summary is machine-generated.

Intronic polyadenylation (IpA) generates shorter transcripts, impacting protein function and immune cell development. Multiple myeloma cells show a loss of IpA, correlating with poorer survival and treatment response.

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Area of Science:

  • Molecular Biology
  • Genomics
  • Immunology

Background:

  • Alternative cleavage and polyadenylation (ApA) primarily affects 3' untranslated region (3'UTR) length.
  • Intronic polyadenylation (IpA) can also lead to the loss of coding regions, generating transcript variants.
  • The functional consequences of IpA, particularly in immune cells and cancer, require further investigation.

Purpose of the Study:

  • To create an atlas of intronic polyadenylation (IpA) events in human tissues and immune cells.
  • To investigate the role and impact of IpA isoforms in B-cell development and multiple myeloma (MM).
  • To assess the clinical significance of IpA alterations in MM progression and treatment response.

Main Methods:

  • Analysis of 46 3'-seq and RNA-seq profiles from normal human tissues, primary immune cells, and multiple myeloma (MM) samples.
  • Identification and high-confidence mapping of 4927 intronic polyadenylation (IpA) events.
  • Differential expression analysis of IpA isoforms in various cellular contexts, including B-cell development and MM.

Main Results:

  • A comprehensive atlas of 4927 high-confidence IpA events was generated across diverse human cell types.
  • IpA isoforms are broadly expressed in immune cells and show differential usage during B-cell development.
  • Multiple myeloma cells exhibit a significant reduction in IpA isoforms found in plasma cells, linked to shorter progression-free survival and altered gene expression relevant to MM biology and lenalidomide response.

Conclusions:

  • Intronic polyadenylation (IpA) generates transcript variants that can produce truncated proteins, affecting protein function and cellular processes.
  • IpA plays a dynamic role in immune cell differentiation and is significantly dysregulated in multiple myeloma.
  • The loss of IpA in MM is a potential biomarker for disease progression and may influence therapeutic strategies.