Cell division of germline cells throughout the animal kingdom is characterized by incomplete cytokinesis resulting in clusters of sibling cells connected by intercellular bridges called ring canals (RC). In the Drosophila melanogaster female germline, ring canals acquire a robust actin cytoskeleton that supports the dramatic increase in ring canal lumen diameter over the course of egg chamber development. Genetic studies show that the hts gene is involved in the accumulation of ring canal F-actin, and a product of this gene, HtsRC, could be the substrate of the Kelch-Cullin3 RING ubiquitin ligase, whose function is also essential for ring canal growth. We demonstrate that HtsRC, produced by a germline-specific hts transcript, is necessary for actin accumulation. Using CRISPR/Cas9 directed mutagenesis of HtsRC, we obtained a series of alleles in the HtsRC coding region that block accumulation of F-actin to RCs and cause a dramatic reduction in RC size. Homozygous mutant females have severely reduced fertility. Ectopic expression of HtsRC in somatic follicle cells results in accumulation of filamentous actin aggregates. These results support the conclusion that HtsRC is necessary and sufficient for recruiting F-actin assemblies. We are now carrying out biochemical and functional analyses of the HtsRC protein in order to determine how it affects actin organization. The predicted protein contains no known functional domains and is conserved only in the Drosophila family. Therefore studying HtsRC should enhance our understanding of existing actin regulatory mechanisms, and provide new insights into the regulation of F-actin structures.