Abstract Heme oxygenase function is highly conserved between vertebrates where it plays important roles in normal embryonic development and controls oxidative stress. Expression of the zebrafish heme oxygenase 1 genes are known to be responsive to oxidative stress suggesting a conserved physiological function. Here we generate a knockout allele of zebrafish hmox1a and characterize the effects of hmox1a and hmox1b loss on embryonic development. We find that loss of hmox1a or hmox1b causes developmental defects in only a minority of embryos, in contrast to Hmox1 gene deletions in mice that causes loss of most embryos. Using a tail wound inflammation assay we find a conserved role for hmox1a , but not hmox1b , in normal macrophage migration to the wound site. Together our results indicate zebrafish hmox1a has clearly a partitioned role from hmox1b that is more consistent with conserved functions of mammalian Heme oxygenase 1.

Zebrafish heme oxygenase 1a is necessary for normal development and macrophage migration