Abstract
The Drosophila melanogaster pair-rule gene odz (odd Oz, or Ten-m) is expressed in distinct patterns in the larval eye imaginal disc. Its earliest eye expression occurs in ommatidial precursors starting from the posterior edge of the morphogenetic furrow. Loss of function of odz activity leads to visible light photoreceptor loss; R7 photoreceptor loss; ommatidial size, shape, and rotation defects; ommatidial disorder and fusions; interommatidial bristle defects; and ommatidial lens defects. The same effects are seen in odz eye mitotic clones, in odz-Ten-a transheterozygous combinations, and in eyes expressing an Odz-Dominant Negative transgene (Odz-DN). Effects of the same strength are also seen when the Odz-DN transgene is driven only in regions of scabrous expression, which overlaps the four columns of Odz expression clusters behind the furrow. Small odz mitotic clones suggest an odz role in cell proliferation or survival. Senseless is expressed in odz mutant clones, in a fairly ordered manner, indicating that Odz acts downstream of R8 specification. Disorder within each ommatidium in odz clones is accompanied by some loss of R7 precursors and visible photoreceptor precursor order.
