Abstract
The Drosophila paired (prd) gene, the founding member of the PAX gene family, is required for normal embryonic segmentation and is re-expressed later in development in the head and developing CNS. As for most embryonically active genes, global defects resulting from loss of early prd function obscure an analysis of the role of later expression phases. We used inducible targeted ribozymes to functionally 'knock-out' prd at late stages. When prd protein levels in the head are reduced in this fashion, the maxillary chemosensory ventral organs fail to develop and dorsal-lateral cirri rows are disrupted. These studies reveal a role for prd in sensory organ development that appears to be conserved in PAX genes throughout the animal kingdom.
