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Previous studies have shown that <jats:italic>prdm1a<\/jats:italic> is required for the specification and differentiation of neural crest cells in the zebrafish. <jats:styled-content>Results:<\/jats:styled-content> Here we examine other members of this family, specifically <jats:italic>prdm3, 5<\/jats:italic>, and <jats:italic>16<\/jats:italic>, in the differentiation of the zebrafish craniofacial skeleton. <jats:italic>prdm3<\/jats:italic> and <jats:italic>prdm16<\/jats:italic> are strongly expressed in the pharyngeal arches, while <jats:italic>prdm5<\/jats:italic> is expressed specifically in the area of the forming neurocranium. Knockdown of <jats:italic>prdm3<\/jats:italic> and <jats:italic>prdm16<\/jats:italic> results in a reduction in the neural crest markers <jats:italic>dlx2a<\/jats:italic> and <jats:italic>barx1<\/jats:italic> and defects in both the viscerocranium and the neurocranium. The knockdown of <jats:italic>prdm3<\/jats:italic> and <jats:italic>prdm16<\/jats:italic> in combination is additive in the neurocranium, but not in the viscerocranium. Injection of sub\u2010optimal doses of <jats:italic>prdm1a<\/jats:italic> with <jats:italic>prdm3<\/jats:italic> or <jats:italic>prdm16<\/jats:italic> Morpholinos together leads to more severe phenotypes in the viscerocranium and neurocranium. <jats:italic>prdm5<\/jats:italic> mutants have defects in the neurocranium and <jats:italic>prdm1a<\/jats:italic> and <jats:italic>prdm5<\/jats:italic> double mutants also show more severe phenotypes. <jats:styled-content>Conclusions:<\/jats:styled-content> Overall, our data reveal that <jats:italic>prdm3, 5<\/jats:italic>, and <jats:italic>16<\/jats:italic> are involved in the zebrafish craniofacial development and that <jats:italic>prdm1a<\/jats:italic> may interact with <jats:italic>prdm3, 5<\/jats:italic>, and <jats:italic>16<\/jats:italic> in the formation of the craniofacial skeleton in zebrafish. 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