Welcome to the Bolterstein Lab!
Every day substances such as chemicals and radiation damage our DNA. If left unchecked, this damage can lead to mutations that can increase cancer risk and lead to accelerated aging. To counteract this DNA damage, cells contain numerous proteins responsible for DNA repair. My lab studies the genetic interactions of these proteins using Drosophila melanogaster (fruit flies) as a model organism and techniques in genetics, cell biology, and toxicology. There are two main areas of research that my lab is currently pursuing:
- Response to oxidative stress: Free radicals are unstable molecules that can be generated both inside the cell as byproducts of cellular metabolism, or outside of the cell through environmental and chemical exposure. While small amounts of free radicals are essential to normal cell function, an excess of free radicals causes oxidative stress, leading to DNA damage. Because inaccurate repair of damaged DNA causes genomic instability and cancer, it is unsurprising that many cancers include alterations in the expression of DNA repair genes. For example, a clear link has been established between mutations in the DNA repair genes, BRCA1 and BRCA2, and breast cancer. Therefore it is crucial that we have a clear understanding of universal DNA repair mechanisms to better understand cancer progression and to predict cellular responses to chemotherapeutics in all cancer patients.
- The role of DNA repair mechanisms in aging: As cells age, they accumulate DNA damage in the form of mutations, lesions, and breaks in DNA. Double strand breaks can be repaired by one of two main mechanisms: homologous recombination, which is generally believed to be error-free, and non-homologous end-joining, which may lead to imprecise repair and mutations. I’m interesting in investigating the “choice” between error-free and error-prone DNA repair and how this decision may change during aging.
Other research interests: physiological responses to environmental toxins and stress