Identification and characterization of new molecular partners for the protein arginine methyltransferase 6 (PRMT6)

PLoS One. 2013;8(1):e53750. doi: 10.1371/journal.pone.0053750. Epub 2013 Jan 10.

Abstract

PRMT6 is a protein arginine methyltransferase that has been implicated in transcriptional regulation, DNA repair, and human immunodeficiency virus pathogenesis. Only few substrates of this enzyme are known and therefore its cellular role is not well understood. To identify in an unbiased manner substrates and potential regulators of PRMT6 we have used a yeast two-hybrid approach. We identified 36 new putative partners for PRMT6 and we validated the interaction in vivo for 7 of them. In addition, using invitro methylation assay we identified 4 new substrates for PRMT6, extending the involvement of this enzyme to other cellular processes beyond its well-established role in gene expression regulation. Holistic approaches create molecular connections that allow to test functional hypotheses. The assembly of PRMT6 protein network allowed us to formulate functional hypotheses which led to the discovery of new molecular partners for the architectural transcription factor HMGA1a, a known substrate for PRMT6, and to provide evidences for a modulatory role of HMGA1a on the methyltransferase activity of PRMT6.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Chromatography, Affinity
  • HMGA1a Protein / metabolism
  • Humans
  • Models, Biological
  • Nuclear Proteins / metabolism*
  • Protein Binding
  • Protein Interaction Domains and Motifs
  • Protein Interaction Mapping
  • Protein-Arginine N-Methyltransferases / metabolism*
  • Reproducibility of Results
  • Substrate Specificity
  • Two-Hybrid System Techniques

Substances

  • Nuclear Proteins
  • HMGA1a Protein
  • PRMT6 protein, human
  • Protein-Arginine N-Methyltransferases

Grants and funding

This work was supported by AIRC (Associazione Italiana per la Ricerca sul Cancro), Università degli Studi di Trieste, and project “Rete Nazionale Proteomica” FIRB 2008-RBRN07BMCT to G.M. E.M. is supported by a FIRC (Fondazione Italiana per la Ricerca sul Cancro) fellowship. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.