Dr. Jan Vijg was the first to develop transgenic mouse models for the study of mutagenesis in vivo (in 1989) and uses these models to study the possible relationship between damage to the genome and aging.
His current research interests are focused on genome instability and the mechanisms through which this may cause human disease and aging.
Current and future efforts involve the following:
- Mouse and Drosophila models for investigation into which genome rearrangements lead to disease by deregulating gene expression (e.g., through position effects, haploinsufficiencies or chromatin remodeling). These collaborative studies may lead to design novel strategies for suppressing genome rearrangements, in vitro and in vivo.
- In order to test if an increased frequency of genome rearrangements can causally contribute to the increased frequency of cancer and other, degenerative phenotypes during aging, novel mouse models are being generated in which DNA double-strand breaks - the likely source of genome rearrangements - can be regulated through the expression of genes encoding restriction enzymes.
- The study of transcriptional noise and its potential contribution to human disease (using advanced single-cell analysis techniques) is underway in the mouse, regarding expression levels of arbitrarily chosen housekeeping and heart-specific genes in the heart and how/why they vary significantly among cardiomyocytes (Bahar, R., et al., Nature, 2006).
- Development of objective standards embedded in new information science and data management technologies for the comparative analysis of pathophysiological characteristics over the murine life span.