Widespread intronic polyadenylation diversifies immune cell transcriptomes

Irtisha Singh, Shih-Han Lee, Adam S. Sperling, Mehmet K. Samur, Yu-Tzu Tai, Mariateresa Fulciniti, Nikhil C. Munshi, Christine Mayr () and Christina S. Leslie ()
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Irtisha Singh: Memorial Sloan Kettering Cancer Center
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

Nature Communications, 2018, vol. 9, issue 1, 1-16

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-018-04112-z

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