Major intrinsic protein (MIP) functions as a water channel and a cell-junction molecule in the vertebrate eye lens. The pathogenic mechanism behind the loss of MIP function in the lens, which leads to degraded optical quality and cataract formation, is still unclear. In this study, a zebrafish model with the mipb mutant was produced. The expression of mipb mRNA and protein was dramatically reduced in the mutant. Immunological analysis reveals that loss function of mip leads to the diffuse distribution of ZL-1 in the mutant lens. Furthermore, in situ hybridization reveals that mip knockout results in a decrease in the transcripts of beaded filament structural protein 2 (Bfsp2) in the lens. Histology study shows that lens fibers in the mutants are less uniform in shape and the fiber arrangement is disrupted. The presented data provides evidence for the essential role of mipb in the development of lens fibers. The absence of mipb during lens formation is likely to result in aberrant lens fiber formation and impaired lens function.

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.