Contribution of retrotransposable elements to aging

Abstract

Retrotransposable elements (RTEs) are abundant in the genomes of most species and continue to evolve and adapt to the defense mechanisms of their host cells. RTEs have contributed to the evolution of their hosts by creating germline genomic diversity, but under most circumstances retrotransposition has deleterious consequences. Our understanding of RTE activity in somatic cells and tissues has lagged, largely because we lacked effective tools to study them in these contexts. Recent evidence indicates that RTEs are more active in somatic cells than anticipated, for example in the nervous system, during the development of cancer, or in senescent cells and aging tissues. This raises the important question of whether RTEs contribute actively to these processes and the development of pathologies, and if so, how. In this review we focus on the role of RTEs in the biology of aging: the evidence for their activation, the host defense mechanisms whose failure may allow this, the consequences of the ensuing RTE activity, and the prospects that targeting RTEs may provide new avenues of treating some age-associated disorders.