Kevin Culligan, Ph.D.

Kevin Culligan, Ph.D.

Research Assistant Professor

Educational Background:

 Ph.D., Oregon State University, 2000

Research Overview:

Cellular DNA is continually altered by mutagenic agents from the environment (e.g. UV light, radiation etc.) and cellular metabolism (e.g. reactive oxygen). This DNA damage, and the resulting mutation, contributes to many interesting phenomena in biology– evolution, antibiotic resistance in bacteria, toxicity, initiation of cancerous cells in animals, treatments for cancer, to name a few. My lab is focused on the mechanisms that protect genes and genomes from excess DNA damage and mutation, using the plant Arabidopsis thaliana as a model system. Because the types of damage to DNA are so diverse, it is not surprising that the mechanisms and molecular pathways that monitor and repair DNA damage are very complex. What may be surprising, however, is that DNA maintenance and repair pathways are very well conserved, from single-celled microorganisms (such as yeasts), to plants, to humans. In other words, yeast and plant genomes encode the same general DNA repair pathways that are present in humans. Therefore, organisms such as yeasts and plants are useful “model systems” for the study of DNA repair and genome maintenance.

Two general mechanisms that we are actively pursuing in the lab are the regulation of DNA repair pathways, and how cells monitor and regulate cell-cycle progression in response to DNA damage. When a cell incurs DNA damage, the cell must first recognize the type of damage, and then mount an appropriate response. This response is not simply just a decision of the type of repair pathway to activate (Non-homologous end joining versus recombinational repair, for example), but also involves activating so-called cell-cycle “checkpoints” if DNA damage persists, and in the case of animals often involves a cellular life or death decision termed apoptosis. Consequently, we are interested in identifying novel genes and pathways involved in the initial response to DNA damage in Arabidopsis thaliana to gain insights into how plant cells protect themselves from genomic stress, potentially leading to insights into animal DNA repair and maintenance.

The protein kinases ATR and ATM are known master regulators of both the DNA repair and cell-cycle checkpoint responses to DNA damage in mammalian cells. These master regulators are key components of cellular decisions in how to respond appropriately to cellular DNA damage. Currently, my lab is interested in upstream activators of ATR and ATM. One example is activation of ATR pathways through Replication Protein A (RPA) by DNA damage. We have recently characterized a unique plant gene family of RPA, and are interested in how the various functions of RPA are integrated into the DNA damage response.

Overall, our goal is to better understand the highly complex pathways involved in DNA repair and genome maintenance in Arabidopsis, and apply this knowledge to better improve crop species, and potentially aid in the understanding of these pathways in humans as it relates to disease and cancer biology.

Undergraduate Research:

If you are currently an undergraduate (preferably majoring in biological sciences) in good academic standing, and would like to gain some research experience, please visit the COLSA Research Opportunities Webpage, to see what current opportunities are available in the lab.



Defective meiosis I (anaphase I) in the atr atm double mutant.
You can see the centromeres being pulled apart toward the poles
of the daughter cells but the damaged DNA is stuck on the metaphase
plate in the middle. See reference 3 and 6 for more information.






Selected Publications:

  1. Aklilu, B.B. and Culligan K.M. (2015) “Evolutionary Origin and Functional Diversification of Replication Protein A1 in Plants.” Manuscript Submitted.
  2. Missirian V., Conklin P.A., Culligan K.M., Huefner N.D., and Britt A.B.  (2014) “High atomic weight, high-energy radiation (HZE) induces transcriptional responses shared with conventional stresses in addition to a core DSB response specific to clastogenic treatments.” Front Plant Sci. Aug 1;5:364.  {DOI: 10.3389/fpls.2014.00364.}
  3. Aklilu B.B., Soderquist R.A., and Culligan K.M. (2013) “Genetic Analysis of the Replication Protein A (RPA) Large Subunit Family in Arabidopsis Reveals Unique and Overlapping Roles in DNA Repair, Meiosis, and DNA Replication.” Nucleic Acids Research 42(5):3104-18.  {DOI: 10.1093/nar/gkt1292.}
  4. Sweeney, P.R., A.B. Britt, and Culligan K.M. (2009) “The Arabidopsis ATRIP ortholog is required for a programmed response to replication inhibitors.” The Plant Journal 60(3): 518-526.  {DOI:10.1111/j.1365-313X.2009.03975.x}
  5. Roa, H., J. Lang, K.M. Culligan, M. Keller, S. Holec, V. Cognat, M.H. Montane, G. Houlne, and M.E. Chaboute. (2009) “Ribonucleotide reductase regulation in response to genotoxic stress in Arabidopsis.” Plant Physiology 151(1), 461-71.   {DOI:10.1104/pp.109}
  6. Culligan, K.M. and A.B. Britt. (2008) “Both ATM and ATR promote the efficient and accurate processing of programmed meiotic double-strand breaks.” The Plant Journal 55(4): 629–638. {DOI:10.1111/j.1365-313X.2008.03530.x}
  7. Culligan, K.M., C.E. Robertson, J. Foreman, P. Doerner, and A.B. Britt. (2006) “ATR and ATM play both distinct and additive roles in response to ionizing radiation.” The Plant Journal 48(6): 947-961. {DOI:10.1111/j.1365-313X.2006.02931.x}
  8. Friesner, J.D., B. Liu, K.M. Culligan, and A.B. Britt.  (2005) ”Ionizing radiation-dependent {gamma}-H2AX focus formation requires ataxia telangiectasia mutated and ataxia telangiectasia mutated and Rad3-related.” Molecular Biology of the Cell 16(5): 2566-76.   {DOI:10.1091/mbc.E04-10-0890}
  9. Culligan, K.M., A. Tissier, and A.B. Britt. (2004) “ATR regulates a G2-phase cell-cycle checkpoint in Arabidopsis thaliana.” The Plant Cell 16(5): 1091-104.   {DOI:10.​1105/​tpc.​018903}
  10. Culligan, K.M. and J. Hays. (2000) “Arabidopsis MutS homologs - tMSH2, AtMSH3, AtMSH6, and a novel AtMSH7—form three distinct protein heterodimers with different specificities for mismatched DNA.”  The Plant Cell 12(6): 991-1002.   {DOI:10.​1105/​tpc.​12.​6.​991}


Kevin Culligan
Rudman Hall, Room 302
Durham, NH 03824
(603) 862-2430