REV1 inhibition-dependent autophagy primes senescence phenotypes
Abstract
Translesion synthesis (TLS) is a DNA damage bypass pathway that replicates over damaged sites. TLS is manipulated by cancer cells to resist DNA-damaging cancer therapies. In REV1-deficient cells, different DNA damaging cancer therapies trigger various cell death phenotypes, although it is unknown how REV1 regulates these mechanisms. We hypothesize that REV1 inhibition-dependent induction of autophagy primes cells to undergo senescence and helps switch cell death mechanisms in response to different DNA damaging treatments. By quantifying switches in cell death pathway choice in REV1 deficient cells over time, we will address novel REV1-dependent functions beyond DNA damage tolerance.
Primary Faculty Mentor Name
Yolanda Chen
Status
Graduate
Student College
College of Agriculture and Life Sciences
Program/Major
Biology
Primary Research Category
Life Sciences
REV1 inhibition-dependent autophagy primes senescence phenotypes
Translesion synthesis (TLS) is a DNA damage bypass pathway that replicates over damaged sites. TLS is manipulated by cancer cells to resist DNA-damaging cancer therapies. In REV1-deficient cells, different DNA damaging cancer therapies trigger various cell death phenotypes, although it is unknown how REV1 regulates these mechanisms. We hypothesize that REV1 inhibition-dependent induction of autophagy primes cells to undergo senescence and helps switch cell death mechanisms in response to different DNA damaging treatments. By quantifying switches in cell death pathway choice in REV1 deficient cells over time, we will address novel REV1-dependent functions beyond DNA damage tolerance.
