Research: Oxidative Stress, Genome Stability, DNA Repair, Nucleic Acids Enzymology
Ph.D from Bogazici University, Istanbul, Turkey, 2010
Office: ARB R3-226A
Office Phone: 352-294-8383
Lab: ARB R3-171
Lab Phone: 352-294-8391
Dr. Caglayan’s Ph.D. work focused on bacterial DNA replication and thermostable DNA polymerases. In 2013, she joined the laboratory of Dr. Samuel H. Wilson at National Institutes of Health (NIH), National Institutes of Environmental Health (NIEHS), to study the base excision repair. Dr. Caglayan joined the faculty at the University of Florida in July 2018.
Oxidative stress is a prevalent and dangerous cellular condition resulting in deleterious modifications to the structure of DNA. These modifications promote mutagenesis and consequently the development of numerous human diseases including cancer. We are particularly interested in oxidative DNA damage. Base Excision Repair (BER) is the major cellular defense mechanism against base damage generated by reactive oxygen species, alkylating agents, and ionizing radiation. BER pathway involves sequential enzymatic steps and substrate channeling mechanism that protect the cell from the accumulation of toxic and mutagenic DNA intermediates.
While the roles of individual enzymes are largely established, it remains unknown how the repair proteins function together to specifically recognize, remove, and repair a base damage in a multi-protein/DNA complex. The overall goal of the lab is to better understand the biological importance and molecular mechanism of the sequential flow of DNA intermediates through the BER pathway under oxidative stress cellular conditions.
Using multi-disciplinary approach including X-ray crystallography, biochemistry, enzyme kinetics, and molecular biology, we will cast light on previously understudied DNA repair protein/protein and protein/DNA interactions to uncover the abnormalities in the functional interplay between BER proteins, its importance for genome stability, and characterize how they contribute to malignant phenotype of tumor cells.
Funding and Awards
- NIH Pathway to Independence Award (K99/R00)
- UF, College of Medicine 2020 Thomas Maren Junior Investigator
- Caglayan M. Interplay between DNA polymerases and DNA ligases: Influence on substrate channeling and the fidelity of DNA ligation.Journal of Molecular Biology (2019) 31(11): 2068 – 2081.
- Caglayan M.and Wilson S.H. Pol μ dGTP mismatch insertion opposite T coupled with ligation reveals a promutagenic DNA intermediate during double strand break repair. Nature Communications(2018) 9: 4213.
- Caglayan M., Horton J.K., Da-Peng D., Stefanick D.F., Wilson S.H. Oxidized nucleotide insertion by pol β confounds ligation during base excision repair. Nature Communications (2017) 8: 14045.
- Caglayan M., Batra V.K., Sassa A., Prasad R., Wilson S.H. Role of polymerase β in complementing aprataxin deficiency during abasic-site base excision repair. Nature Structural and Molecular Biology(2014) 21: 497 – 499.