Elf1 Deficiency Impairs Macrophage Development in Zebrafish Model Organism

Elf1缺陷会损害斑马鱼模式生物的巨噬细胞发育

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Abstract

The Ets (E-twenty-six) family of transcription factors plays a critical role in hematopoiesis and myeloid differentiation. However, the specific functions of many family members in these processes remain largely underexplored and poorly understood. Here, we identify Elf1 (E74-like factor 1), an Ets family member, as a critical regulator of macrophage development in the zebrafish model organism, with minimal impact on neutrophil differentiation. Through morpholino knockdown screening and CRISPR/Cas9-mediated gene editing, we demonstrate that Elf1 is critical for macrophage development and tissue injury responses. Specific overexpression of dominant-negative Elf1 (DN-Elf1) in macrophages demonstrated a cell-autonomous effect on macrophage infiltration. Furthermore, the overexpression of cxcr4b, a gene downstream of Elf1 regulation and essential for cell migration and injury response, significantly rescued this defect, indicating Elf1 as a key regulator of macrophage function. Our findings shed light on the roles of Elf1 in macrophage development and injury response and also highlight zebrafish as a powerful model for immunity research.

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