Susan M. Bailey
Associate Professor

Phone: (970) 491-2944, (970) 491-5771
Fax: (970) 491-0623
Email: Susan.Bailey@colostate.edu
Office: 437 Molecular and Radiological Biosciences Building

 

Degrees

• Ph.D., Biomedical Sciences, University of New Mexico School of Medicine, Albuquerque, NM
• M.S., Biomedical Sciences, University of New Mexico School of Medicine, Albuquerque, NM
• B.S., Biological Sciences, Colorado State University, Fort Collins, CO

Research Interests

The focus of my research is on all things telomeres - fascinating features of the ends of chromosomes - and their many connections to DNA repair, cancer and aging. Cells must maintain functional telomeres in order to preserve genomic stability and prevent cancer. My research interests lie primarily in investigating the interactions between telomeres and DNA Repair, with the ultimate goal of shedding light on a key issue in these increasingly overlapping fields - how cells distinguish between natural chromosomal termini and broken DNA ends. Such studies and information also impact investigation of maintenance of telomere length by telomerase, not only in regards to tumorigenesis and its treatment, but in aging as well.

Telomeres are specialized nucleoprotein structures that are absolutely essential for the stabilization and protection of the ends of linear eukaryotic chromosomes. They are composed of deceptively simple tandem arrays of G-rich repetitive sequence (TTAGGG in all vertebrates) bound by a surprisingly vast array of telomere-specific proteins (TRF1, TRF2, TIN1, TANK1, TANK2, POT1...). Together, they form a dynamic terminal structure that "caps"the ends of the chromosome - preventing degradation and protecting against inappropriate recombination events. Interestingly, all of the subunits of the DNA repair protein DNA dependent protein kinase (Ku70, Ku80 and DNA-PKcs), as well as other members of the DNA-PK non-homologous end-joining (NHEJ) complex (XRCC4 and Ligase IV) have been shown to be required for effective telomeric end-capping of mammalian chromosomes. Other DNA repair proteins, including the MRE11/RAD50/NBS1 complex and ATM have also been implicated in telomere function. It is paradoxical that DNA repair proteins, which are in the business of joining ends together, are also involved in preventing telomeric ends from end joining types of events. Dr. Bailey's approach revolves around the use of specialized cytogenetic techniques such as Fluorescence in situ Hybridization (FISH), Chromosome Orientation FISH (CO-FISH) and combinatorial multi-fluor FISH (m-FISH and SKY) to explore the involvement of telomere dysfunction in the process of generating and/or contributing to genomic instability. To that end, the DNA-PKcs repair-deficient BALB/c mouse, which is susceptible to radiation-induced mammary carcinoma, serves as an informative experimental model system. RNA interference (RNAi) technology has allowed extension of such studies into human systems and the investigation of relevant deficiencies and individual susceptibilities. Dr. Bailey is currently interested in the identification of genes required for normal mammalian telomere function. The hope is that this approach will provide new insight into how the ends of chromosomes are normally protected from illegitimate recombination events, as well as lead to a greater understanding of the relationship between telomere dysfunction, end-capping failure and neoplastic development.

Selected Publications

 •  E.S. Williams, R. Klingler, B. Ponnaiya, T. Hardt, E. Schrock, S.P. Lees-Miller, K. Meek, R.L. Ullrich, and S.M. Bailey. Telomere Dysfunction and DNA-PKcs Deficiency: characterization and consequence. Cancer Res 69(5):2100-07, 2009.

 •  Hagelstrom RT, Askin KF, Williams AJ, Ramaiah L, Desaintes C, Goodwin EH, Ullrich RL, Bailey SM. DNA-PKcs and ATM influence generation of ionizing radiation-induced bystander signals. Oncogene 27(53):6761-9, 2008.

 •  Carsten RE, Bachand AM, Bailey SM, Ullrich RL. Resveratrol reduces radiation-induced chromosome aberration frequencies in mouse bone marrow cells. Radiation Research 169(6):633-8, 2008.

 •  Susan M. Bailey. 2007 Michael Fry Research Award Lecture: Telomeres and Double-Strand Breaks – all’s well that "Ends" well.". Radiation Research 169:1-7, 2008.

 •  Liu L, Bailey SM, Okuka M, Munoz P, Li C, Zhou L, Wu C, Czerwiec E, Sandler L, Seyfang A, Blasco MA, Keefe DL. Telomere lengthening early in development. Nature Cell Biology 9(12):1436-1441, 2007.

 •  Williams ES, Stap J, Essers J, Ponnaiya B, Luijsterburg MS, Krawczyk PM, Ullrich RL, Aten JA, Bailey SM. DNA double strand breaks are not sufficient to initiate recruitment of TRF2. Nature Genetics 39(6):696-698, 2007.

 •  S.M. Bailey and M.N. Cornforth. Telomeres and DNA double-strand breaks: ever the twin shall meet? Cell. Mol. Life Sci. 64(22):2956-2964, 2007.

 •  Wu L, Multani AS, He H, Cosme-Blanc W, Deng Y, Deng JM, Bachilo O, Pathak S, Tahara H, Bailey SM, Deng Y, Behringer RR, Chang S. Pot1 Deficiency Initiates DNA Damage Checkpoint Activation, Chromosomal Instability and Elevated Homologous Recombination at Telomeres. Cell 126(1):49-62, 2006.

 •  Susan M. Bailey and John P. Murnane. Survey and Summary: Telomeres, chromosome instability and cancer. Nucleic Acids Research 34(8):2408-2417 (2006).

 •  P.R. Laud, A.S. Multani, S.M. Bailey, L. Wu, J. Ma, C. Kingsley, M. Lebel, S. Pathak, R.A. DePinho and S. Chang. Elevated telomere-telomere recombination in WRN-deficient, telomere dysfunctional cells promotes escape from senescence and engagement of the ALT pathway. Genes & Development 19:2560-2570 (2005).

 •  Y. Zhang, C-U. Lim, E.S. Williams, J. Zhou, Q. Zhang, M.H. Fox, S.M. Bailey and H.L. Liber. NBS1 knockdown by siRNA increases ionizing radiation mutagenesis and telomere association in human cells. Can Research 65(13):5544-5553 (2005).

 •  Q. Zhang, E.S. Williams, K.F. Askin, Y. Peng, J.S. Bedford, H.L. Liber and S.M. Bailey. Suppression of DNA-PK by RNAi has different quantitative effects on telomere dysfunction and mutagenesis in human lymphoblasts treated with g-rays or HZE particles. Radiation Research 164: 497-504 (2005).

 •  S.M. Bailey, M.A. Brenneman and E.H. Goodwin. Frequent recombination in telomeric DNA may extend the proliferative life of telomerase-negative cells. Nucleic Acids Research, 32(12):3743-3751 (2004).

 •  S.M. Bailey, E.H. Goodwin and M.N. Cornforth. Strand-specific fluorescence in situ hybridization: the CO-FISH family. Cytogenet Genome Research 107:14-17 (2004).

 •  S.M. Bailey and E.H. Goodwin. DNA and telomeres: beginnings and endings. Cytogenet Genome Research 104:109-115 (2004).

 •  S.M. Bailey, M.N. Cornforth, R.L. Ullrich and E.H. Goodwin. Dysfunctional mammalian telomeres join with DNA double-strand breaks. DNA Repair 3:349-357 (2004).

 •  S.M. Bailey, M.A. Brenneman, J. Halbrook, J.A. Nickoloff, R.L. Ullrich, E.H. Goodwin. The kinase activity of DNA-PK is required to protect mammalian telomeres. DNA Repair 3:225-233 (2004).

 •  B.D. Loucas, R. Eberle, S.M. Bailey and M.N. Cornforth. Influence of dose rate on the induction of simple and complex chromosome exchanges by gamma rays. Radiation Research 162:339-349 (2004).

 •  I. Jaco, P. Munoz, F. Goytisolo, J. Wesoly, S. M. Bailey, G. Taccioli and M.A. Blasco. Role of mammalian Rad54 in telomere length maintenance. Molecular and Cellular Biology 23(16):5572-5580 (2003).

 •  S. Espejel, S. Franco, A. Sgura, D. Gae, S.M. Bailey, G.E. Taccioli and M.A. Blasco. Functional interaction between DNA-PKcs and telomerase in telomere length maintenance. EMBO Journal 21(22):1-13 (2002).

 •  M.N. Cornforth, S.M. Bailey and E.H. Goodwin. Dose responses for chromosome aberrations produced in noncycling primary human fibroblasts by alpha particles, and by gamma rays delivered at sublimiting low dose rates. Radiation Research 158:42-53 (2002).

 •  S.M. Bailey, M.N. Cornforth, A. Kurimasa, D.J. Chen, E.H. Goodwin. Strand-specific postreplicative processing of mammalian telomeres. Science 293:2462-2465 (2001).