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

Author:

Chen Jiahao12ORCID,Wang Honggao2ORCID,Wu Shuting3ORCID,Zhang Ao4ORCID,Qiu Zhongkai2ORCID,Huang Peng5ORCID,Qu Jianan Y.6ORCID,Xu Jin12ORCID

Affiliation:

1. Department of Neurology, the Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou 510006, China.

2. Innovation Centre of Ministry of Education for Development and Diseases, School of Medicine, South China University of Technology, Guangzhou 510006, China.

3. Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.

4. Division of Life Science, State Key Laboratory of Molecular Neuroscience, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong, PRC.

5. Department of Biochemistry and Molecular Biology, Alberta Children’s Hospital Research Institute, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada.

6. Department of Electronic and Computer Engineering, The Hong Kong University of Science and Technology, Kowloon, China.

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 csf1a and csf1b mutants altered xanthophore countershading differently: csf1a mutants lack ventral xanthophores, while csf1b mutants have reduced dorsal xanthophores. Further study revealed that csf1a is expressed throughout the trunk, whereas csf1b is expressed dorsally. Ectopic expression of csf1a or csf1b in neurons attracted xanthophores into the spinal cord. Blocking csf1 signaling by csf1ra mutants disrupts spinal cord distribution and normal xanthophores countershading. Single-cell RNA sequencing identified two col1a2 + populations: csf1a high csf1b high muscle progenitors and csf1a high csf1b low fibroblast progenitors. Ablation of col1a2 + fibroblast and muscle progenitors abolished xanthophore patterns. Our study suggests that fibroblast and muscle progenitors differentially express csf1a and csf1b to modulate xanthophore patterning, providing insights into the mechanism of countershading.

Publisher

American Association for the Advancement of Science (AAAS)

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