text: People | Lynch Lab | The University of Chicago
  Published: Ancient Transposable Elements Transformed the Uterine Regulatory Landscape and Transcriptome during the Evolution of Mammalian Pregnancy
  Our latest preprint: Functional architecture of deleterious genetic variants in the Wrangel Island Mammoth
  Our latest preprint: A zombie LIF gene in elephants is up-regulated by TP53 to induce apoptosis in response to DNA damage
  920 E. 58th Street | CLSC 325B | Chicago, IL 60637
  920 E. 58th Street | CLSC 301 | Chicago, IL 60637
  I am interested in the evolutionary mechanisms that underlie the evolution of large body sizes and long life-spans in mammals, particularly the mechanisms by which long-lived, large-bodied species have evolved to enhance cancer resistance. I'm exploring these questions in two lineages – elephants, as a representative of large-bodied organisms with a closest living relative (the hyrax) that is small-bodied, and bats, in which long-lived species are closely related to short-lived species. We are using available genomes to identify genetic changes that may be associated with enhanced cancer resistance and using cell-culture based methods to functionally test our evolutionary predictions. I also resurrect mammoths.
  I am interested in the molecular mechanisms that underlie the origin of evolutionary novelties, particularly the origination of novel gene regulatory netwoks. I am currently exploring the role of transposable elements (TEs) in the genesis of new cis-regulatory elements.
  To determine the evolutionary effects of TE insertion, I am evaluating the regulatory potential of resurrected ancestral TEs as well as the regulatory functions of specific TEs located near genes important for regulation of the immune response during mammalian pregnancy.
  I am investigating the molecular mechanisms that underlie the expansion of the neocortex on the human lineage (since our common ancestor with chimpanzees). I utilize ancestral state reconstruction to identify and create regulatory elements with human-specific substitutions, followed by functional experimental approaches to validate the role of these substitutions in neuronal development.
  Marcus Soliai
  All living things have cells, and cell types between species have similar sizes; this means that animals that are large, like whales and elephants, are large because they have more cells. Since every cell in an organism's body will accumulate mutations throughout its life that could cause it to become cancerous, animals that are large or live long lives should be at an increased risk of cancer compared to smaller, shorter-lived animals. However, we see that there is no correlation between cancer risk and body size or lifespan, an observation titled "Peto's Paradox." This implies that large, long-lived animals must have evolved robust mechanism to either suppress or eliminate cancerous cells in order to live as long as they do, and reach their adult sizes without dying. My research looks at the evolutionary adaptations present in long-lived bats and whales that may explain how they live so long without cancer. To do this, I use a combination of computational genomics and live cell work to find and test duplications of cancer-suppression genes in these animals. https://www.vazquez.bio