Long interspersed nuclear element 1 (LINE1 or L1) are a class of transposable elements that comprise approximately 20% of the human genome and have gained increased scrutiny as a source of genomic instability influencing or driving the cellular aging process. Previous studies have demonstrated that a consequence of L1 activation includes accumulation of L1 cDNA transcripts in the cellular cytoplasm leading to accelerated aging phenotypes in mouse models.

My work centers around characterizing the cellular mechanisms that lead to the accumulation of cytoplasmic L1 cDNA transcripts. Additionally, we aim to utilize cGas and STING knockout mouse models in order to better understand the direct role that L1 inflammatory activation plays on health-span and longevity.