Daniel Kane, Ph.D.

Education

Postdoctoral Research Associate, University of Nebraska Medical Center, Eppley Institute for Research in Cancer and Allied Diseases
Ph.D., Biology, Tufts University
B.S., Biology, Genetics option; Biotechnology Certification; Ball State University

Areas of Specialization

The Kane Lab uses the common fruit fly – Drosophila melanogaster – to better understand DNA replication, recombination and repair in all organisms, including humans.

Every day, the cells in our human bodies experience thousands of DNA damaging events. These can be caused by either exposure to damaging agents in our environment or by mistakes that occur naturally in the day-to-day operations of the cell. Most of us are able to correct these damage events perfectly fine before mutations arise. Others are not as fortunate and have diseases, disorders and cancers develop.

Our lab studies how cells function to repair DNA damage. Flies are a great model organism to explore these questions in due to their quick generation time and the quality of genetic assays available to determine repair mechanisms. Additionally, because many factors of repair mechanisms are conserved, the knowledge learned from the fly will help the larger research community and can be applied towards human understanding and possible treatment.

Undergraduates interested in joining this research program should email Dr. Kane or pop into his office for more information on how to get started.

Publications

Xing X, Kane DP, Bulock CR, Moore EA, Sharma S, Chabes A and Shcherbakova PV. (2019). A recurrent cancer-associated substitution in DNA Polymerase ε produces a hyperactive enzyme. Nat Commun 10, 374.

Barbari SR, Kane DP, Moore EA and Shcherbakova PV. (2018). Functional analysis of cancer-associated DNA polymerase ε variants in Saccharomyces cerevisiae. G3 (Bethesda) 8, 1019-1029.

Kane DP and Shcherbakova PV. (2014). A common cancer-associated DNA polymerase ε mutation causes an exceptionally strong mutator phenotype, indicating fidelity defects distinct from loss of proofreading. Cancer Res 74, 1895-1901.

Kane DP. (2012). Multiple DNA polymerases act during homologous recombination repair in Drosophila melanogaster. PhD Dissertation, Tufts University. ProQuest, UMI 3512134.

Kane DP, Shusterman M*, Rong Y, McVey M. (2012). Competition between replicative and translesion polymerases during homologous recombination repair in Drosophila. PLoS Genet 8, e1002659.
Witsell A, Kane DP, McVey M. (2010). Super-sized deletions: improved transposon excision screens using a mus309 mutant background. Fly (Austin) 4, 137-40.

Witsell A, Kane DP, Rubin S*, McVey M. (2009). Removal of the Bloom syndrome DNA helicase extends the utility of imprecise transposon excision for making null mutations in Drosophila. Genetics 183, 1187-1193.

Muñiz Ortiz JG, Opoka R*, Kane D*, Cartwright IL. (2009). Investigating arsenic susceptibility from a genetic perspective in Drosophila reveals a key role for glutathione synthetase. Toxicological Sciences 107, 416-426.

Conrad LJ, Bai L, Ahern K, Dusinberre K*, Kane DP*, Brutnell TP. (2007). State II Dissociation element formation following Activator excision in maize. Genetics 177, 737-747.