| Literature DB >> 33691108 |
Maria Virginia Ruiz Cuevas1, Marie-Pierre Hardy2, Jaroslav Hollý3, Éric Bonneil2, Chantal Durette2, Mathieu Courcelles2, Joël Lanoix2, Caroline Côté2, Louis M Staudt4, Sébastien Lemieux1, Pierre Thibault5, Claude Perreault6, Jonathan W Yewdell7.
Abstract
Combining RNA sequencing, ribosome profiling, and mass spectrometry, we elucidate the contribution of non-canonical translation to the proteome and major histocompatibility complex (MHC) class I immunopeptidome. Remarkably, of 14,498 proteins identified in three human B cell lymphomas, 2,503 are non-canonical proteins. Of these, 28% are novel isoforms and 72% are cryptic proteins encoded by ostensibly non-coding regions (60%) or frameshifted canonical genes (12%). Cryptic proteins are translated as efficiently as canonical proteins, have more predicted disordered residues and lower stability, and critically generate MHC-I peptides 5-fold more efficiently per translation event. Translating 5' "untranslated" regions hinders downstream translation of genes involved in transcription, translation, and antiviral responses. Novel protein isoforms show strong enrichment for signaling pathways deregulated in cancer. Only a small fraction of cryptic proteins detected in the proteome contribute to the MHC-I immunopeptidome, demonstrating the high preferential access of cryptic defective ribosomal products to the class I pathway.Entities:
Keywords: computational biology; defective ribosomal products; major histocompatibility complex; mass spectrometry; non-canonical translation; peptides; protein isoforms; proteomic methods; ribosome profiling
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Year: 2021 PMID: 33691108 PMCID: PMC8040094 DOI: 10.1016/j.celrep.2021.108815
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423