FEBS Letters
Volume 582, Issue 18 , Pages 2761-2767, 6 August 2008

A novel interaction between the proto-oncogene Evi1 and histone methyltransferases, SUV39H1 and G9a

Edited by Gianni Cesareni

Department of Hematology, Erasmus University Medical Center, Dr. Molewaterplein 50, 3015 GE Rotterdam, The Netherlands

Received 14 March 2008; received in revised form 16 June 2008; accepted 20 June 2008. published online 10 July 2008.

Abstract 

The transcription factor ecotropic viral integration site 1 (Evi1) is associated with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) in patients due to chromosomal aberration of chromosome 3. Here we show that Evi1 interacts with the histone methyltransferase SUV39H1. The interaction requires the N-terminal part of Evi1 and the H3-specific histone methyltransferase domain, SET, of SUV39H1 without Evi1 having an inhibitory effect on SUV39H1 methyltransferase activity. Presence of SUV39H1 enhances Evi1 transcriptional repression in a dose dependent manner. In addition, Evi1 also interacts with another histone methyltransferase, G9a, but not with SET9. Our data establish an epigenetic role of Evi1 in cell transformation by recruiting higher order chromatin remodeling complexes.

Keywords: Evi1, SUV39H1, G9a, Histone methyltransferase, Transcription, Repression, AML

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

PII: S0014-5793(08)00582-6

doi:10.1016/j.febslet.2008.06.056

FEBS Letters
Volume 582, Issue 18 , Pages 2761-2767, 6 August 2008