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Background Kdm6b, a specific histone 3 lysine 27 (H3K27) demethylase, has been reported to be implicated in a variety of developmental processes including cell differentiation and cell fate determination and multiple organogenesis. Here, we regulated the transcript level of  kdm6bb  to study the potential role in controlling the hearing organ development of zebrafish. Methods A morpholino antisense oligonucleotide (MO) strategy was used to induce Kdm6b deficiency; immunohistochemical staining and in situ hybridization analysis were conducted to figure out the morphologic alterations and embryonic mechanisms. Results Kdm6bb  is expressed in the primordium and neuromasts at the early stage of zebrafish embryogenesis, suggesting a potential function of Kdm6b in the development of mechanosensory organs. Knockdown of  kdm6bb  severely influences the cell migration and proliferation in posterior lateral line primordium, abates the number of neuromasts along the trunk, and mRNA-mediated rescue test can partially renew the neuromasts. Loss of  kdm6bb  might be related to aberrant expressions of chemokine genes encompassing  cxcl12a  and  cxcr4b/cxcr7b  in the migrating primordium. Moreover, inhibition of  kdm6bb  reduces the expression of genes in Fgf signaling pathway, while it increases the  axin2  and  lef1  expression level of Wnt/β-catenin signaling during the migrating stage. Conclusions Collectively, our results revealed that Kdm6b plays an essential role in guiding the migration of primordium and in regulating the deposition of zebrafish neuromasts by mediating the gene expression of chemokines and Wnt and Fgf signaling pathway. Since histone methylation and demethylation are reversible, targeting Kdm6b may present as a novel therapeutic regimen for hearing disorders.

The H3K27 demethylase controls the lateral line embryogenesis of zebrafish