Fig. 4.

Apical markers are not disrupted, but Nod:LacZ is mislocalized, in Glued mutants. Third instar eye discs are stained with anti-Elav (blue), anti-Armadillo (red), and anti-PATJ (green) (A–D). Views from the apical surface (A,B) show evenly spaced apical markers in wild type (A), with each ommatidial cluster (dashed outline) centered under a concentration of Armadillo (arrowhead). Armadillo staining is largely normal in Glued¹ (B), despite the presence of ommatidia devoid of nuclei (arrowhead). Side views show that in wild type (C), each ommatidium (dashed line) has a distinct apical clustering of Armadillo and PATJ (arrowhead). Glued animals appear to retain apical markers (arrowheads) even when photoreceptor nuclei are mispositioned (D). Nod:LacZ (yellow) expressed in postmitotic photoreceptor neurons under the control of the Glass_38-1 promotor localizes apical to photoreceptor nuclei (anti-Elav, blue) in the most mature photoreceptor neurons (E, apical surface, and F, side view) and is not found in axons or in the optic stalk (G). When dominant-negative Glued is expressed in photoreceptor neurons using the Glass_38-1 promoter, Nod:LacZ staining is distributed throughout the axons of the most mature cells (H, arrowhead). In (I), consequences of Dynactin disruption are summarized, synthesizing the data obtained in Fig 2–Fig 4. Inhibition of Dynactin function in the postmitotic neuron causes the photoreceptor nucleus (blue) to be displaced toward the axon terminal. Despite nuclear movement, a trailing process remains and apical markers (PATJ in green, Armadillo in red) are retained. Nod: LacZ (yellow), however, becomes mislocalized from its wild-type apical position and enters the axon.