The kep1 gene encodes an RNA-binding protein containing a single maxi-KH domain. We have previously demonstrated that loss of the kep1 gene results in Drosophila females displaying a reduction in fertility and wished to further characterize the kep1 mutation in Drosophila males. Wild-type females mated to homozygous kep1- males resulted in 6% of the eggs laid hatching. This reduced reproductive success is due in part to a meiosis defect during spermatogenesis with approximately 10 % of sperm demonstrating a defect in cytokinesis. Utilizing indirect immunohistochemistry we found that the Kep1 protein is present in the nucleus of adult brain neuronal cells, suggesting a behavioural component contributing to the almost complete male sterility phenotype. We report that homozygote kep1- males display almost no courtship behaviour with a measured median courtship index of 0.005 relative to a median index of 0.77 for OreR wild-type controls. In order to better understand the behavioural role of kep1, we carried out gene profiling experiments to identify transcripts whose steady-state levels are altered in the kep1- homozygote males. Our gene profiling studies identified 61 transcripts whose steady-state levels are altered by at least 2 fold or more comparing RNA isolated from w1118 and kep1-/kep1- male heads. A large percentage of transcripts identified whose steady-state expression levels are depleted in kep1-/kep1- heads (10 out of 44) encode for proteins involved in some aspect of proteolysis. Our results show that the Kep1 protein has a pleiotropic effect in Drosophila males leading to cytokinesis defects and behavioural abnormalities. RNA was isolated from heads of 3-4 day old wild-type or homozygote mutant males. Three indepentent RNA samples were utilized to complete experiment.