The transformation of non-motile epithelial cells to a migratory state plays a significant role in normal development and diseases such as cancer. During Drosophila oogenesis, a specialized group of cells termed border cells (BCs) acquire the ability to detach from their host epithelium and migrate through surrounding cells to the posterior end of the oocyte. The steroid receptor transcriptional co-activator taiman (tai) plays an important role in promoting this motility process, but its downstream transcriptional targets remain poorly defined. Here we introduce a novel, pathogenic model of Tai-driven tissue invasion that allows for rapid genetic screening for elements of the Tai-induced transcriptional program. Overexpression of tai in non-motile pupal wing cells causes these cells to invade through adjacent thoracic cuticle and into internal tissues, leading to a high-penetrance adult phenotype of wing tips embedded into the thorax. Using this phenotype as the basis for a dominant-modifier screen led to identification of alleles of genes in the Hippo pathway as modulators of Tai-driven tissue invasion. Our published work shows that Tai and Yki (the downstream effector of the Hippo pathway) bind together and co-regulate target genes (Zhang et al, 2015). In support of this model, a version of Tai that cannot bind to Yki also cannot efficiently drive invasion of wing cells into the thorax. Genetic and transcriptomic analysis has identified candidate Tai-target genes involved in promoting wing cell invasiveness, including the extracellular serine protease gastrulation defective (gd) and the actin-remodeling complex protein Arpc3B. Data on gd and Arpc3B as putative transcriptional targets of Tai and Yki, and the roles of the Gd and Arpc3B proteins in driving the invasive process will be presented.