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ADAM12‐deficient zebrafish exhibit retardation in body growth at the juvenile stage without developmental defects
Author(s) -
Tokumasu Yudai,
Iida Atsuo,
Wang Zi,
Ansai Satoshi,
Kinoshita Masato,
SeharaFujisawa Atsuko
Publication year - 2016
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1111/dgd.12286
Subject(s) - zebrafish , biology , vertebrate , microbiology and biotechnology , myogenesis , synteny , juvenile , in situ hybridization , genetics , gene , gene expression , genome
ADAM ( a d isintegrin a nd m etalloprotease) constitutes a family of multi‐domain proteins that are involved in development, homeostasis, and disease. ADAM 12 plays important roles in myogenesis and adipogenesis in mice; however, the precise physiological mechanisms are not known, and the function of this gene in other vertebrates has not been examined. In this study, we used a simple model vertebrate, the zebrafish, to investigate the functions of ADAM 12 during development. Zebrafish adam12 is conserved with those of mammals in the synteny and the amino‐acid sequence. We examined adam12 expression in zebrafish embryos by whole mount in situ hybridization and the promoter activity of the adam12 upstream sequence. We found that adam12 is strongly expressed in the cardiovascular system, erythroid progenitors, brain, and jaw cartilage during zebrafish development, and adam12‐ knockout zebrafish exhibited reduced body size in the juvenile stage without apparent morphological defects. Taken together, these results suggest that adam12 plays a significant role in the regulation of body growth during juvenile stage in zebrafish, although the precise molecular mechanisms await further study.