Hls5 regulated erythroid differentiation by modulating GATA-1 activity

Blood. 2008 Feb 15;111(4):1946-50. doi: 10.1182/blood-2007-04-085746. Epub 2007 Dec 6.

Abstract

Hemopoietic lineage switch (Hls) 5 and 7 were originally isolated as genes up-regulated during an erythroid-to-myeloid lineage switch. We have shown previously that Hls7/Mlf1 imposes a monoblastoid phenotype on erythroleukemic cells. Here we show that Hls5 impedes erythroid maturation by restricting proliferation and inhibiting hemoglobin synthesis; however, Hls5 does not influence the morphology of erythroid cells. Under the influence of GATA-1, Hls5 relocates from cytoplasmic granules to the nucleus where it associates with both FOG-1 and GATA-1. In the nucleus, Hls5 is able to suppress GATA-1-mediated transactivation and reduce GATA-1 binding to DNA. We conclude that Hls5 and Hls7/Mlf1 act cooperatively to induce biochemical and phenotypic changes associated with erythroid/myeloid lineage switching.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis Regulatory Proteins / physiology*
  • Cell Cycle
  • Cell Differentiation / drug effects
  • Cell Differentiation / physiology*
  • Cell Line
  • Cell Line, Tumor
  • DNA Primers
  • Erythropoietin / pharmacology
  • GATA1 Transcription Factor / physiology*
  • Globins / genetics
  • Humans
  • Leukemia, Erythroblastic, Acute
  • Nuclear Proteins / physiology
  • Transcription Factors / physiology

Substances

  • Apoptosis Regulatory Proteins
  • DNA Primers
  • GATA1 Transcription Factor
  • GATA1 protein, human
  • Nuclear Proteins
  • TRIM35 protein, human
  • Transcription Factors
  • ZFPM1 protein, human
  • Erythropoietin
  • Globins