During vertebrate development, the facial skeleton forms from the segmental pharyngeal arches. Hox genes specify segmental identity throughout the pharyngeal arches: altered Hox expression causes homeotic transformations of facial skeletal elements. Now, Miller and co-workers report that Moz(monocytic leukaemia zinc finger) regulates Hox expression and pharyngeal segmental identity in zebrafish (see ). To identify genes involved in specifying segmental identity, the researchers looked for mutations affecting cartilage patterning in the zebrafish larval pharynx. They homed in on a mutant with a mirror image duplication of jaw cartilages in place of the normal second-arch cartilages, a pattern seen in zebrafish with reduced hox2 expression. They identify the mutated gene as a zebrafish orthologue of the human oncogene MOZ, a histone acetyltransferase. Inhibition of histone deacetylase activity rescues the defective Hox gene expression and homeosis in moz mutants. These results indicate that Moz maintains Hox gene expression through a process involving chromatin remodelling.
