Human MLL-AF9 Overexpression Induces Aberrant Hematopoietic Expansion in Zebrafish

Biomed Res Int. 2018 May 30:2018:6705842. doi: 10.1155/2018/6705842. eCollection 2018.

Abstract

The 11q23 of the mixed lineage leukemia 1 (MLL1) gene plays a crucial role in early embryonic development and hematopoiesis. The MLL-AF9 fusion gene, resulting from chromosomal translocation, often leads to acute myeloid leukemia with poor prognosis. Here, we generated a zebrafish model expressing the human MLL-AF9 fusion gene. Microinjection of human MLL-AF9 mRNA into zebrafish embryos resulted in enhanced hematopoiesis and the activation of downstream genes such as meis1 and hox cluster genes. Embryonic MLL-AF9 expression upregulated HSPC and myeloid lineage markers. Doxorubicin and MI-2 (a menin inhibitor) treatments significantly restored normal hematopoiesis in MLL-AF9-expressing animals. This study provides insight into the role of MLL-AF9 in zebrafish hematopoiesis and establishes a robust and efficient in vivo model for high-throughput drug screening.

MeSH terms

  • Animals
  • Disease Models, Animal
  • Hematopoiesis / genetics*
  • Histone-Lysine N-Methyltransferase
  • Humans
  • Leukemia, Myeloid, Acute / genetics*
  • Myeloid-Lymphoid Leukemia Protein / physiology*
  • Oncogene Proteins, Fusion / physiology*
  • Translocation, Genetic*
  • Zebrafish

Substances

  • KMT2A protein, human
  • MLL-AF9 fusion protein, human
  • Oncogene Proteins, Fusion
  • Myeloid-Lymphoid Leukemia Protein
  • Histone-Lysine N-Methyltransferase