Kara Boltz
Hometown:
Butler, PA
Undergraduate Degree:
B.S. Biology; Georgia Tech
Research Synopsis
One function of telomeres is to differentiate chromosome ends from DNA double-strand breaks. Telomere deprotection can result in an inappropriate DNA damage response. This attempt to “repair” chromosome ends can result in end-to-end chromosome fusions or aberrant recombination events and eventually could lead to genomic instability. Paradoxically, some DNA repair proteins are required for normal telomere function. I am interested in understanding how these DNA repair proteins function at telomeres and how the CST (CTC1/STN1/TEN1) end-protection complex may regulate DNA damage proteins. One potential role for some of the DNA damage response proteins may be to ensure efficient replication of telomeres. Telomeres pose a challenge to the regular DNA replication machinery because they are repeat-rich and can contain structures such as G-quadruplexes and T-loops. DNA damage proteins and other telomere-specific replication proteins may localize to telomeres to resolve these problems. One consequence of slowed or stalled telomere replication is an increase in the amount of single-stranded telomeric DNA. Thus, I am also interested in whether the CST complex, which binds single-stranded telomeric DNA, plays a role in telomere replication.