A Flp/FRT EMS mutagenesis screen was conducted in the eye of Drosophila melanogaster on chromosome 2R to identify negative regulators of cell growth and cell division. In addition to the EMS mutation in the mosaic eye, an ark loss of function allele (ark 82 ) was utilized to block apoptosis in the homozygous mutant cells, setting up a screen for conditional regulators of cell growth and cell division. In the present study, we focus on the characterization and mapping of one mutant that resulted from this screen, Cruella (cru). A cross between flies with the flippase enzyme directed to the developing eye and flies with the mutations cru, ark 82 , revealed an unusual phenotype that resulted in the homozygous mutant tissue appearing black, in contrast to the expected red. To map the location of this mutation, complementation tests against the Bloomington deficiency kit were conducted. Cru failed to complement previously characterized alleles of capping protein α (cpa). Thus, cpa cru is a novel allele of cpa and displays phenotypes similar to previously characterized alleles such as cpa 107E, cpa 69E, and cpa scrd . The human homolog, Cap Z, is conserved in humans and serves a similar role in act in filament regulation.