Sumoylation of CCAAT/enhancer-binding protein α is implicated in hematopoietic stem/progenitor cell development through regulating runx1 in zebrafish
- Yuan, H., Zhang, T., Liu, X., Deng, M., Zhang, W., Wen, Z., Chen, S., Chen, Z., de The, H., Zhou, J., Zhu, J.
- Scientific Reports 5: 9011 (Journal)
- Registered Authors
- Chen, Zhu, Deng, Min, Wen, Zilong
- Developmental biology, Haematopoietic stem cells
- MeSH Terms
- CCAAT-Enhancer-Binding Protein-alpha/metabolism*
- Cell Differentiation*/genetics
- Core Binding Factor Alpha 2 Subunit/genetics*
- Embryo, Nonmammalian
- Gene Expression Regulation*
- Gene Knockdown Techniques
- Hematopoietic Stem Cells/cytology*
- Hematopoietic Stem Cells/metabolism*
- SUMO-1 Protein/deficiency
- SUMO-1 Protein/genetics
- SUMO-1 Protein/metabolism
- 25757417 Full text @ Sci. Rep.
Yuan, H., Zhang, T., Liu, X., Deng, M., Zhang, W., Wen, Z., Chen, S., Chen, Z., de The, H., Zhou, J., Zhu, J. (2015) Sumoylation of CCAAT/enhancer-binding protein α is implicated in hematopoietic stem/progenitor cell development through regulating runx1 in zebrafish. Scientific Reports. 5:9011.
The small ubiquitin-related modifier (SUMO) participates in various cellular processes, including maintenance of genome integrity, nuclear transport, transcription and signal transduction. However, the biological function of sumoylation in hematopoiesis has not been fully explored. We show here that definitive hematopoietic stem/progenitor cells (HSPCs) are depleted in SUMO-deficient zebrafish embryos. Impairment of sumoylation attenuates HSPC generation and proliferation. The hyposumoylation triggered HSPC defects are CCAAT/enhancer-binding protein α (C/ebpα) dependent. Critically, a SUMO-C/ebpα fusion rescues the defective hematopoiesis in SUMO-deficient embryos, at least in part through restored runx1 expression. While C/ebpα-dependent transcription is involved in myeloid differentiation, our studies here reveal that C/ebpα sumoylation is essential for HSPC development during definitive hematopoiesis.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes