Epigenetics encompasses mechanisms that dynamically modify gene expression in response to environmental change. This is a highly important mechanism, since its dysregulation can lead severe pathologies. A focus of our research has been on understanding how this type of alteration might contribute to obesity and neurological disorders, such as autism and mental retardation, which together affect over 30% of the global population.


We are using wild type and transgenic mice lacking the expression of Mecp2, a key gene in charge of sensing how much the genome has been modified in response to environmental changes. We are employing behavioural, physiological, and cellular and molecular biological approaches to study the effect of conditional deletion of Mecp2. Our principal findings showed that knocking out Mecp2 leads to the development of obesity, since the hypothalamus loses its ability to properly interpret metabolic signals, like leptin, that account for body energy reserves. Leptin-resistance observed in the absence of Mecp2 and the neurological phenotype associated to Rett syndrome, an epigenetic-associated disorder caused by mutations in Mecp2, can be importantly attenuated by improved cellular communication through environment enrichment. We hypothesise that it is possible to prevent the development of obesity or to revert mental retardation and autism by improving cell-cell communication into the brain.

Research Team Leader

Bredford Kerr


Research Assistant

Noemi Gutierrez



Gloria Alarcon

Luis Guzman

Sergio Hernandez


Doctoral Students

Rodrigo Torres

Patricia Ojeda

Camila Navia

Valdivia Shearim