PUBLICATION
Human MLL-AF9 Overexpression Induces Aberrant Hematopoietic Expansion in Zebrafish
- Authors
- Tan, J., Zhao, L., Wang, G., Li, T., Li, D., Xu, Q., Chen, X., Shang, Z., Wang, J., Zhou, J.
- ID
- ZDB-PUB-180714-6
- Date
- 2018
- Source
- BioMed Research International 2018: 6705842 (Journal)
- Registered Authors
- Keywords
- none
- 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
- PubMed
- 30003105 Full text @ Biomed Res. Int.
Citation
Tan, J., Zhao, L., Wang, G., Li, T., Li, D., Xu, Q., Chen, X., Shang, Z., Wang, J., Zhou, J. (2018) Human MLL-AF9 Overexpression Induces Aberrant Hematopoietic Expansion in Zebrafish. BioMed Research International. 2018:6705842.
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.
Errata / Notes
This article is corrected by ZDB-PUB-220202-35
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping