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Peer-reviewedCC BYBlood science (Baltimore, Md.)

Gfi1ab-Cebpβ axis promotes eosinophilopoiesis in zebrafish

  • Hao Wen1
  • Zihan Hu1
  • Mei Wu2
  • Wan Peng3
  • Yicong Sun1
  • Jing Li1
  • Junwei Lian4
  • Yubing Huang1
  • Yiyue Zhang1
  • Gaofei Li1
4 affiliations
  1. 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
  2. 2Department of Hematology, School of Medicine, The Second Affiliated Hospital of South China University of Technology (Guangzhou First People’s Hospital), Guangzhou 510180, China
  3. 3Blood Transfusion Department, Guangzhou Eighth People’s Hospital, Guangzhou Medical University, Guangzhou, 510440, China
  4. 4Department of Science and Research, School of Medicine, the Sixth Affiliated Hospital of South China University of Technology (Nanhai District People’s Hospital of Foshan), Foshan 528200, China
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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.

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Cite

BibTeXRIS
BibTeX
@article{wen2026gfi1abcebpβ,
  title = {{Gfi1ab-Cebpβ axis promotes eosinophilopoiesis in zebrafish}},
  author = {Hao Wen and Zihan Hu and Mei Wu and Wan Peng and Yicong Sun and Jing Li and Junwei Lian and Yubing Huang and Yiyue Zhang and Gaofei Li},
  journal = {Blood science (Baltimore, Md.)},
  year = {2026},
  month = nov,
  doi = {10.1097/bs9.0000000000000314},
  url = {https://europepmc.org/article/PMC/PMC13727250},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Gfi1ab-Cebpβ axis promotes eosinophilopoiesis in zebrafish
AU  - Hao Wen
AU  - Zihan Hu
AU  - Mei Wu
AU  - Wan Peng
AU  - Yicong Sun
AU  - Jing Li
AU  - Junwei Lian
AU  - Yubing Huang
AU  - Yiyue Zhang
AU  - Gaofei Li
PY  - 2026
DA  - 2026/11/02
JO  - Blood science (Baltimore, Md.)
DO  - 10.1097/bs9.0000000000000314
UR  - https://europepmc.org/article/PMC/PMC13727250
AB  - 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.
SN  - 2543-6368
ER  -