Figure 11

A mechanistic model for Spen function. The cartoon illustrates our conclusions to explain the defects seen in the presence of spen mutant clones. Wild type or heterozygote cells are depicted with green nuclei, and spen mutant cells with gray nuclei. The appearance of spen mutant cells in fields that will give rise to specific structures such as bristles or veins would imply the lack of an instructive signal to remain in place during growth of the disc. This will finally result in a progressive mis-localization of cells, ultimately leading to the abnormal positioning of structures after development is completed. Such a model would explain that, in some cases as in the proneural clusters, a change of fate is generated because negative instructive signals that depend on cell to cell contact are lost, resulting in the formation of two sensory organ precursor (SOP) cells within the same pro neural cluster (shown as red cells in B and C). The same situation may occur in the formation of wing veins, where similar Notch dependent regulatory mechanisms take place (E). Loss of or veins (or bristles) may occur when vein-forming cells move into intervein regions after their commitment has taken place, therefore leaving a hole where they should have been, which has been filled with cells that are unable to form vein at that spot.