A key challenge of the modern world relates to how our contribution to environmental degradation has a pervasive effect on our own health and the health of future generations. There is evidence from human epidemiological studies and animal models demonstrating that exposure to environmental agents prior to conception or during early development can increase disease susceptibility later in life and even transgenerationally in future generations . This seems to occur, at least partially, because of non-mutagenic alterations of the germline. Often, the exposure to environmental agents result in metabolic alterations such as obesity in the offspring of exposed individuals and even transgenerationally. Therefore, it is likely that the ramping rates of metabolic diseases worldwide have had a significant component that is associated with current and ancestral exposures to environmental agents. Nevertheless, the mechanisms through which exposure to these agents results in metabolic diseases in the offspring and future generations remain unclear.

The Chamorro-Garcia lab is interested in better understanding how environmental agents such as pollutants, diets, temperature or stress, shape our phenotype. Our main focus is to study mechanisms of genome-environment interactions using mouse models.

Deleted: Our work integrates epigenomic, transcriptomic, and physiological analyses to reveal how environmental stressors lead to the modulation of the expression of the genome. Our current emphasis is on alterations of chromatin organization during early embryonic development and how this disruption is propagated through development and across generations contributing to phenotypic variation and disease.