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Deletion of Mtg16, a target of t(16;21), alters hematopoietic progenitor cell proliferation and lineage allocation.

While a number of DNA binding transcription factors have been identified that control hematopoietic cell fate decisions, only a limited number of transcriptional corepressors (e.g., the retinoblastoma protein [pRB] and the nuclear hormone corepressor [N-CoR]) have been linked to these functions. Here, we show that the transcriptional corepressor Mtg16 (myeloid translocation gene on chromosome 16), which is targeted by t(16;21) in acute myeloid leukemia, is required for hematopoietic progenitor cell fate decisions and for early progenitor cell proliferation. Inactivation of Mtg16 skewed early myeloid progenitor cells toward the granulocytic/macrophage lineage while reducing the numbers of megakaryocyte-erythroid progenitor cells. In addition, inactivation of Mtg16 impaired the rapid expansion of short-term stem cells, multipotent progenitor cells, and megakaryocyte-erythroid progenitor cells that is required under hematopoietic stress/emergency. This impairment appears to be a failure to proliferate rather than an induction of cell death, as expression of c-Myc, but not Bcl2, complemented the Mtg16(-/-) defect.

Pubmed ID: 18710942


  • Chyla BJ
  • Moreno-Miralles I
  • Steapleton MA
  • Thompson MA
  • Bhaskara S
  • Engel M
  • Hiebert SW


Molecular and cellular biology

Publication Data

October 1, 2008

Associated Grants

  • Agency: NCI NIH HHS, Id: R01 CA064140
  • Agency: NCI NIH HHS, Id: R01-CA112005
  • Agency: NCI NIH HHS, Id: R01-CA64140
  • Agency: NHLBI NIH HHS, Id: R01-HL088494
  • Agency: NCI NIH HHS, Id: T32CA009385-24

Mesh Terms

  • Anemia
  • Animals
  • Antigens, CD34
  • Bone Marrow Cells
  • Cell Lineage
  • Cell Proliferation
  • Chromosomes, Mammalian
  • Colony-Forming Units Assay
  • Female
  • Gene Deletion
  • Gene Regulatory Networks
  • Hematopoietic Stem Cells
  • Humans
  • Male
  • Megakaryocytes
  • Mice
  • Multipotent Stem Cells
  • Myeloid Progenitor Cells
  • Nuclear Proteins
  • Phenylhydrazines
  • Proto-Oncogene Proteins c-kit
  • Proto-Oncogene Proteins c-myc
  • Receptors, IgG
  • Time Factors
  • Transcription Factors
  • Translocation, Genetic