Gfi1ab-Cebpβ axis promotes eosinophilopoiesis in zebrafish
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Updated: Nov 4, 2026

Microbead Implantation in the Zebrafish Embryo
Published on: July 30, 2015
Hao Wen1, Zihan Hu1,2, Mei Wu3,4
1The Innovation Centre of Ministry of Education for Development and Diseases, Division of Cell, Developmental and Integrative Biology, School of Medicine, South China University of Technology, Guangzhou 510006, China.
Abstract:
Eosinophils play essential roles in parasite defense, allergic responses, and tissue homeostasis, yet the regulatory mechanisms governing their development remain incompletely understood. GFI1 is an important regulator of multiple hematopoietic lineages, but its role in eosinophil development is unclear. Using zebrafish as a model, we demonstrate that Gfi1ab promotes eosinophil development, as gfi1ab mutation significantly reduces eosinophil numbers, whereas its overexpression enhances eosinophilopoiesis. This effect is probably eosinophil-specific, as gfi1ab mutation does not significantly affect erythrocyte, neutrophil, or macrophage development. Integrative RNA-Seq and Chromatin immunoprecipitation sequencing (ChIP-Seq) analyses identify cebpb as a potential downstream target of Gfi1ab. Mechanistically, gfi1ab deficiency reduces cebpb expression, and cebpb overexpression partially rescues the eosinophil defects in gfi1ab-deficient larvae. These findings identify a Gfi1ab-Cebpβ regulatory axis that promotes eosinophil development and provide new insight into the transcriptional control of eosinophilopoiesis.

