<i>col1a2⁺</i> fibroblasts/muscle progenitors finetune xanthophore countershading by differentially expressing <i>csf1a/1b</i> in embryonic zebrafish.

Abstract

Animals evolve diverse pigment patterns to adapt to the natural environment. Countershading, characterized by a dark-colored dorsum and a light-colored ventrum, is one of the most prevalent pigment patterns observed in vertebrates. In this study, we reveal a mechanism regulating xanthophore countershading in zebrafish embryos. We found that <i>csf1a</i> and <i>csf1b</i> mutants altered xanthophore countershading differently: <i>csf1a</i> mutants lack ventral xanthophores, while <i>csf1b</i> mutants have reduced dorsal xanthophores. Further study revealed that <i>csf1a</i> is expressed throughout the trunk, whereas <i>csf1b</i> is expressed dorsally. Ectopic expression of <i>csf1a</i> or <i>csf1b</i> in neurons attracted xanthophores into the spinal cord. Blocking <i>csf1</i> signaling by <i>csf1ra</i> mutants disrupts spinal cord distribution and normal xanthophores countershading. Single-cell RNA sequencing identified two <i>col1a2⁺</i> populations: <i>csf1a^highcsf1b^high</i> muscle progenitors and <i>csf1a^highcsf1b^low</i> fibroblast progenitors. Ablation of <i>col1a2⁺</i> fibroblast and muscle progenitors abolished xanthophore patterns. Our study suggests that fibroblast and muscle progenitors differentially express <i>csf1a</i> and <i>csf1b</i> to modulate xanthophore patterning, providing insights into the mechanism of countershading.