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Widespread intronic polyadenylation diversifies immune cell transcriptomes

Author

Listed:
  • Irtisha Singh

    (Memorial Sloan Kettering Cancer Center
    Weill Cornell Graduate College)

  • Shih-Han Lee

    (Memorial Sloan Kettering Cancer Center)

  • Adam S. Sperling

    (Harvard Medical School)

  • Mehmet K. Samur

    (Harvard Medical School)

  • Yu-Tzu Tai

    (Harvard Medical School)

  • Mariateresa Fulciniti

    (Harvard Medical School)

  • Nikhil C. Munshi

    (Harvard Medical School)

  • Christine Mayr

    (Memorial Sloan Kettering Cancer Center)

  • Christina S. Leslie

    (Memorial Sloan Kettering Cancer Center)

Abstract

Alternative cleavage and polyadenylation (ApA) is known to alter untranslated region (3ʹUTR) length but can also recognize intronic polyadenylation (IpA) signals to generate transcripts that lose part or all of the coding region. We analyzed 46 3ʹ-seq and RNA-seq profiles from normal human tissues, primary immune cells, and multiple myeloma (MM) samples and created an atlas of 4927 high-confidence IpA events represented in these cell types. IpA isoforms are widely expressed in immune cells, differentially used during B-cell development or in different cellular environments, and can generate truncated proteins lacking C-terminal functional domains. This can mimic ectodomain shedding through loss of transmembrane domains or alter the binding specificity of proteins with DNA-binding or protein–protein interaction domains. MM cells display a striking loss of IpA isoforms expressed in plasma cells, associated with shorter progression-free survival and impacting key genes in MM biology and response to lenalidomide.

Suggested Citation

  • Irtisha Singh & Shih-Han Lee & Adam S. Sperling & Mehmet K. Samur & Yu-Tzu Tai & Mariateresa Fulciniti & Nikhil C. Munshi & Christine Mayr & Christina S. Leslie, 2018. "Widespread intronic polyadenylation diversifies immune cell transcriptomes," Nature Communications, Nature, vol. 9(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-04112-z
    DOI: 10.1038/s41467-018-04112-z
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    Cited by:

    1. Emily Kunce Stroup & Zhe Ji, 2023. "Deep learning of human polyadenylation sites at nucleotide resolution reveals molecular determinants of site usage and relevance in disease," Nature Communications, Nature, vol. 14(1), pages 1-17, December.
    2. Siddharth Sethi & David Zhang & Sebastian Guelfi & Zhongbo Chen & Sonia Garcia-Ruiz & Emmanuel O. Olagbaju & Mina Ryten & Harpreet Saini & Juan A. Botia, 2022. "Leveraging omic features with F3UTER enables identification of unannotated 3’UTRs for synaptic genes," Nature Communications, Nature, vol. 13(1), pages 1-15, December.
    3. Timofey A. Karginov & Antoine Ménoret & Anthony T. Vella, 2022. "Optimal CD8+ T cell effector function requires costimulation-induced RNA-binding proteins that reprogram the transcript isoform landscape," Nature Communications, Nature, vol. 13(1), pages 1-13, December.
    4. Xiaochuan Liu & Hao Chen & Zekun Li & Xiaoxiao Yang & Wen Jin & Yuting Wang & Jian Zheng & Long Li & Chenghao Xuan & Jiapei Yuan & Yang Yang, 2024. "InPACT: a computational method for accurate characterization of intronic polyadenylation from RNA sequencing data," Nature Communications, Nature, vol. 15(1), pages 1-15, December.
    5. Richard Taylor & Fursham Hamid & Triona Fielding & Patricia M. Gordon & Megan Maloney & Eugene V. Makeyev & Corinne Houart, 2022. "Prematurely terminated intron-retaining mRNAs invade axons in SFPQ null-driven neurodegeneration and are a hallmark of ALS," Nature Communications, Nature, vol. 13(1), pages 1-14, December.

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