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Population-scale proteome variation in human induced pluripotent stem cells.

Bogdan Andrei Mirauta1, Daniel D Seaton1, Dalila Bensaddek2

  • 1European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Genome Campus, Hinxton, United Kingdom.

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Summary

This study provides the first comprehensive proteomic analysis of human induced pluripotent stem cells (iPSC). It identifies 654 protein quantitative trait loci (pQTLs), revealing genetic and non-genetic factors influencing protein levels and disease associations.

Keywords:
deleterious variantsgeneticsgenomicshumaninduced pluripotent stem cellsproteomics

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Area of Science:

  • Genomics
  • Proteomics
  • Stem Cell Biology
  • Human Disease Genetics

Background:

  • Human disease phenotypes are linked to protein expression and function alterations.
  • Understanding proteome variability and its relation to mRNA expression and disease loci is crucial but limited.
  • Human induced pluripotent stem cells (iPSCs) are vital for disease modeling.

Purpose of the Study:

  • To conduct the first comprehensive proteomic analysis of human iPSCs.
  • To integrate proteomic data with transcriptome and genomic data from the same iPSC lines.
  • To characterize determinants of proteome variation and regulatory mechanisms in iPSCs.

Main Methods:

  • Proteomic analysis of 202 iPSC lines from 151 donors.
  • Integration of transcriptome and genomic sequence data.
  • Identification and characterization of protein quantitative trait loci (pQTLs).

Main Results:

  • Identified 654 pQTLs in iPSCs.
  • Characterized major genetic and non-genetic determinants of proteome variation.
  • Discovered pQTLs linked to GWAS variants not detectable at the mRNA level.

Conclusions:

  • Proteomic analysis of iPSCs reveals significant genetic and non-genetic influences on protein variation.
  • Peptide-level resolution of pQTLs provides insights into disease-linked variants missed by mRNA analysis.
  • This study enhances understanding of proteome variability and its role in human disease.