Identification of CTNNB1 in the lined seahorse, Hippocampus erectus, and its function in innate immunity and cell proliferation

Author:

Zhang Lele12,Wang Fang3,Lv Chunhui12,Yu Lanliang24,Ci Xiaojing24,Zhang Ning25,Jia Longwu12,Xue Yuanyuan12,Zhang Xu12,Su Xiaolei12ORCID,Wang Kai12

Affiliation:

1. School of Agriculture Ludong University Yantai China

2. Research and Development Center of Science, Technology and Industrialization of Seahorses Ludong University Yantai China

3. Department of Pathology The Affiliated Yantai Yuhuangding Hospital of Qingdao University Yantai China

4. Weihai Yinze Biotechnology Co., LTD Yantai China

5. Zongzhe Marine Technology Co. LTD. Yantai China

Abstract

Abstractβ‐Catenin (CTNNB) is a core downstream mediator in the Wnt/β‐catenin signaling pathway, which plays a role in immune regulation and cell differentiation. In the present study, two CTNNB genes were identified by genomic analysis of Hippocampus erectus and named He‐CTNNB1 and He‐CTNNB2. He‐CTNNB1 was more conserved than He‐CTNNB2. The full length of He‐CTNNB1 was 2369 bp, including an open reading frame of 2275 bp that encoded 737 amino acids containing 12 armadillo repeats. Phylogenetic analysis revealed that He‐CTNNB1 clusters had homologs in other bony fishes. Tissue distribution analysis showed the highest mRNA expression of He‐CTNNB1 in the ovary, liver, and kidney of the lined seahorse under normal physiological conditions. The transcription level of He‐CTNNB1 was significantly increased in the liver and kidney in response to LPS, poly I:C, and Edwardsiella tarda challenge (p < 0.05). In vitro overexpression of He‐CTNNB1 significantly upregulated the expression of key genes of the canonical Wnt/β‐catenin signaling pathway, such as axin2, cMyc, and cyclinD (p < 0.05), which increased cell proliferation during the wound‐healing process. Taken together, our results suggest that He‐CTNNB1 is essential for cell proliferation and the innate immune response in H. erectus.

Funder

National Natural Science Foundation of China

Publisher

Wiley

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