Our research centers on understanding the mechanisms governing gene expression and morphogenesis. Specifically, we investigate the roles of two transcription factors, HNF1alpha and HNF1beta, encoded by the HNF1A and HNF1B genes. Mutations in these genes are associated with diabetes and renal developmental disorders.

Cell growth, differentiation, and morphogenesis are critical events, and their disruption can result in severe developmental pathologies. These intricate processes are predominantly regulated by complex transcriptional networks in which transcription factors play a pivotal role. Analyzing the functions of transcription factors and understanding the mechanisms underlying their actions provide a unique perspective for comprehending intricate biological processes and pathophysiology. In recent years, as a paradigm for our research, we have focused on investigating the roles of HNF1alpha and HNF1beta, a small family of transcription factors known for their association with severe human diseases.

Our research objectives can be summarized in the following areas:

• Genetic Programs - Explore the genetic programs controlled by HNF1A and HNF1B, particularly in epithelial morphogenesis and differentiation, with a focus on kidney development.
• Epigenetic Inheritance - Investigate the unique epigenetic "bookmarking" properties of HNF1A and HNF1B.
• Phenotypic Variability - Identify the mechanisms underlying the diverse phenotypes associated with HNF1A and HNF1B deficiencies, including the involvement of modifier genes.
• Pharmacological Intervention - Evaluate the potential therapeutic benefits of specific compounds to restore HNF1B activity.

In pursuing these objectives, our research aims to shed light on the fundamental biological processes controlled by HNF1A and HNF1B, ultimately contributing to a better understanding of the complex mechanisms underlying severe human diseases and potential therapeutic interventions