Androgens are required for the male reproductive tissues. In addition, androgens regulate gene ex-pression in several non-reproductive tissues. Defects in androgen signaling are linked to diseases, such as prostate cancer. Androgens act through androgen receptor, AR, a hormone-inducible nuclear receptor. Upon ligand binding, AR is shuttled to the nucleus where it binds to the androgen response elements to regulate gene transcription. Specificity of spatiotemporal androgen regulation in different tissues is achieved by differential usage of coregulators. However, in many target tissues the regulation of cell type specific responses to androgen action remains poorly understood. Given the importance of androgen action, it is necessary to understand how androgen actions are normally regulated. We are especially interested in how tissue-specific androgen responses are mediated via AR SUMOylation, pioneer factors, collaborating transcription factors and small RNAs, namely microRNAs in the male reproductive tissues.

As a part of the FinnDisMice research consortium we have also generated disease model for Cartilage-hair hypoplasia, which is one of the rare Finnish heritage diseases with poorly known pathophysiology. The disease is manifested by growth disorder, defective immunity and increased risk for cancer. Cartilage-hair hypoplasia is caused by mutations in a long non-coding RNA, RMRP, the functions of which are poorly known. Our focus is to discover novel functions and interactors of Rmrp, ultimately to contribute to the discovery of biomarkers as well as development of diagnostic and therapeutic strategies for Cartilage-hair hypoplasia.