Notch3 and the Notch3-upregulated RNA-binding protein HuD regulate Ikaros alternative splicing

EMBO J. 2007 Mar 21;26(6):1670-80. doi: 10.1038/sj.emboj.7601626. Epub 2007 Mar 1.

Abstract

Constitutive activation of the transmembrane receptor, Notch3, and loss of function of the hematopoietic transcription repressor, Ikaros (IK), play direct roles in T-cell differentiation and leukemogenesis that are dependent on pre-T-cell receptor (pre-TCR) signaling. We demonstrate the occurrence of crosstalk between Notch3 and IK that results in transcriptional regulation of the gene encoding the pTalpha chain of the pre-TCR. We also show that, in the presence of the pre-TCR, constitutive activation of Notch3 in thymocytes causes increased expression of dominantnegative non-DNA-binding IK isoforms, which are able to restrain the IK inhibition of Notch3's transcriptional activation of pTalpha. This effect appears to be mediated by Notch3's pre-TCR-dependent upregulation of the RNA-binding protein, HuD. Notch3 signaling thus appears to play a critical role in the diminished IK activity described in several lymphoid leukemias. By exerting transcription-activating and transcription-repressing effects on the pTalpha promoter, Notch3 and IK cooperate in the fine-tuning of pre-TCR expression and function, which has important implications for the regulation of thymocyte differentiation and proliferation.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alternative Splicing / genetics
  • Alternative Splicing / physiology*
  • Animals
  • Blotting, Western
  • Cell Differentiation / physiology
  • Cell Proliferation
  • Chromatin Immunoprecipitation
  • DNA Primers
  • ELAV Proteins / metabolism*
  • ELAV-Like Protein 4
  • Electrophoretic Mobility Shift Assay
  • Flow Cytometry
  • Gene Expression Regulation / genetics
  • Gene Expression Regulation / physiology*
  • Ikaros Transcription Factor / genetics
  • Ikaros Transcription Factor / physiology*
  • Luciferases
  • Membrane Glycoproteins / metabolism
  • Mice
  • RNA Interference
  • Receptor, Notch3
  • Receptors, Antigen, T-Cell, alpha-beta / metabolism
  • Receptors, Notch / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction / genetics
  • Signal Transduction / physiology*
  • T-Lymphocytes / cytology*
  • T-Lymphocytes / metabolism

Substances

  • DNA Primers
  • ELAV Proteins
  • ELAV-Like Protein 4
  • Elavl4 protein, mouse
  • Membrane Glycoproteins
  • Notch3 protein, mouse
  • Receptor, Notch3
  • Receptors, Antigen, T-Cell, alpha-beta
  • Receptors, Notch
  • Zfpn1a1 protein, mouse
  • pre-T cell receptor alpha
  • Ikaros Transcription Factor
  • Luciferases