Submitted by Rachel B BREM on
The over-arching goal of the Brem lab is to understand mechanisms of evolution in the context of long-diverged species. Organisms landing in a new niche often acquire genetic changes that allow them to thrive in their environment. Sometimes this process takes millions of years, and reconstructing it after the fact is a challenge for modern evolutionary geneticists. As a consequence, the field knows surprisingly little about how evolution works on these timescales.
We have an opening for an undergraduate researcher to contribute to a project on the evolution of species of house mice. But this project doesn't study whole organism mouse phenotypes like behavior or disease; instead we use simple cellular models in a dish. Our focus is on a stress resistance program called cellular senescence. Upon exposure to DNA damage or other stresses, mammalian cells convert to a senescent state, where they stop growing and secrete signaling factors to recruit immune cells to clear damage in tissues. In vivo, with age, the clearance gets more and more faulty, and senescent cells accumulate in the body, giving rise to "collateral damage" that has been shown to drive aging pathologies.
Our preliminary work has begun to reveal that cells from different mouse species exhibit different characteristics in senescence assays—some secrete more cytokines, some less, and some appear to die off altogether instead of entering the senescent state. The ongoing project seeks to characterize these changes more fully and map the underlying genetic basis.
This project is a good fit for SPUR students who want intensive training in mammalian cell genetics, with additional opportunities for computational scripting. Students working on the project will carry out cell culture, cell phenotyping (in bulk and using flow cytometry), and microscopy.
Interest in evolution, aging, and/or cell biology is a must.