Jan Vijg
Jan Vijg is the Lola and Saul Kramer Chairperson in Molecular Genetics at the Department of Genetics at the Albert Einstein College of Medicine, New York City, United States. Prior to this appointment, he was a professor at the Buck Institute for Research on Aging (Novato, California). His research interests include studying genomic instability in aging. In 1989, he created the first transgenic mouse models for the study of "in vivo" mutagenesis. He discusses his genomic/epigenomic drift hypothesis as a cause of aging in his book "Aging of the Genome: The Dual Role of DNA in Life  and Death"'. In his second book, "The American Technological Challenge: Stagnation and Decline in the 21st Century", he argues that technological innovation has decelerated ever since 1970. Vijg is co-editor-in-chief of the journal "Aging" published by Impact Journals (Albany, New York). Genome instability in aging and disease. Genome instability, i.e., the tendency of the genome to acquire mutations and epimutations, underlies human genetic disease, causally contributes to cancer and has also been implicated in aging and age-related, degenerative conditions other than cancer. Little is known about the mechanisms that give rise to spontaneous changes in the  genome or epigenome and how this may lead, in somatic cells, to increased cancer risk and loss of organ and tissue function with age. We study genome and epigenome instability as a function of age in various model organisms, including mouse and fruit fly, and its consequences in terms of alterations in tissue-specific patterns of gene regulation. We developed transgenic reporter systems in mouse and fruit fly, which allow us to determine tissue-specific frequencies of various forms of genome instability, e.g., point mutations, deletions, translocations. By crossing the mutational reporter animals with mutants harboring specific defects in various  genome maintenance pathways, the relevance of these pathways for the accumulation of specific forms of genome instability is assessed, in relation to the pathophysiology of aging. Similarly, by using knockdown approaches we assess the effect of specific genes implicated in longevity and healthy aging, e.g., SOD, FOXO, SIR2, on genome integrity. More recently, we have begun to assess global gene mutation and epimutation loads in normal and disease tissues of both animal models and humans using massively parallel sequencing approaches.