Jo Anne Powell-Coffman
Professor and Chair
Dr. Powell-Coffman received her Bachelor’s Degree in Animal Physiology from the University of California-Davis, and her Ph.D. in Biology from the University of California-San Diego (1993). After a postdoctoral fellowship at the University of Colorado in Boulder, Dr. Powell-Coffman joined the faculty at Iowa State University in 1998. Recent honors include an Established Investigator Award from the American Heart Association and a Bailey Research Career Development Award from ISU. Dr. Powell-Coffman served as the GDCB ADVANCE Professor from 2007-2009 and was Chair of the Interdepartmental Genetics graduate program 2010 - 2011. She is also co-investigator for a HHMI Science Education grant to increase student engagement in introductory undergraduate science courses. Dr. Powell-Coffman has served as the GDCB Interim Department Chair since July 2011 and formally accepted the position of Department Chair on January 1, 2013.
The Powell-Coffman research group employs a powerful genetic model system, the nematode C. elegans, to study how animals sense and adapt to their environment. Currently, the lab's research is focused on two biomedically important transcription factors: the aryl hydrocarbon receptor (AHR) and the hypoxia-inducible factor (HIF).
The hypoxia-inducible factor plays a central role in the response to hypoxia (low oxygen). Using genetic strategies in C. elegans, we have identified novel regulators of HIF-1 and have gained important insights to the regulatory circuits that control HIF-1. This research project is currently supported by a grant from the National Institutes of Health.
The aryl hydrocarbon receptor (AHR) mediates the toxic effects of dioxins in vertebrates. C. elegans AHR has a role in neuronal development, and we have shown that AHR activity in key neurons is required for specific behaviors in C. elegans. This is of particular interest because these behaviors are also regulated by environmental oxygen levels.
2108 Molecular Biology
Ames, IA 50011-3260
B.S., University of California, Davis, 1986
Ph.D., University of California, San Diego, 1993
- Park, E.C., Ghose, P., Shao, Z., Kang, L., Xu, S., Powell-Coffman, J.A., and Rongo, C. (2012) EGL-9 Regulates Glutamate Receptor Trafficking in a HIF-Independent Manner by Modulating CDK-5 Phosphorylation of LIN-10. EMBO Journal 31: 1379-1393.
- Powell-Coffman, J.A. and Qin H. (2011) Invertebrate AHR homologs: Ancestral functions in sensory systems. In The AH Receptor in Biology and Toxicolgy. Ed R. Pohjanvirta, Wiley & Sons pp 405-411.
- Powell-Coffman, JA and CR Coffman (2010) Lack of oxygen aids cell survival. Nature 465: 554-555.
- Shao, Z., Zhang, Y., Ye, Q, Saldanha, J. and Powell-Coffman JA (2010) C. elegans SWAN-1 binds to EGL-9 and regulates HIF-1-mediated resistance to the bacterial pathogen Pseudomonas aeruginosa PAO1. PLoS Pathogens, 6(8) e1001075
- Powell-Coffman, JA (2010) Hypoxia signaling and resistance in C. elegans. Trends Endocrinol Metab. 21 (7): 435-440.
- Shao, Z., Zhang, Y., and Powell-Coffman JA. (2009) Two distinct roles for EGL-9 in the regulation of HIF-1-mediated gene expression in Caenorhabditis elegans. Genetics 183: 821 - 829.
- Zhang, Y., Shao, Z., Zhai, Z., Shen, C., and Powell-Coffman JA. 2009. The HIF-1 Hypoxia-Inducible Factor Modulates Lifespan in C. elegans. PLoS ONE 4(7):e6348.
- Qian, H., Robertson, A. P., Powell-Coffman, J. A., and R. J. Martin . 2008. In situ recordings of C. elegans levamisole receptor channels. Faseb Journal 22(9):3247 - 3254.
- Hoogewijs D, Terwilliger NB, Webster KA, Powell-Coffman JA, Tokishita S, Yamagata H, Hankeln T, Burmester T, Rytkönen KT, Nikinmaa M, Abele D, Heise K, Lucassen M, Fandrey J, Maxwell PH, Påhlman S and Gorr TA. 2007. From Critters to Cancer: Bridging trajectories between comparative and clinical research of oxygen sensing: HIF signaling and adaptations towards hypoxia. Integrative and Comparative Biology 47:552 - 577.
- Shen, C., Shao, Z., and J. A. Powell-Coffman. 2006. The Caenorhabditis elegans rhy-1 gene inhibits HIF-1 hypoxia-inducible factor activity in a negative feedback loop that does not include vhl-1. Genetics 174(3):1205 - 1214.
- Qin, H., Zhai, Z., and J. A. Powell-Coffman. 2006. The Caenorhabditis elegans AHR-1 transcription complex controls expression of soluble guanylate cyclase genes in the URX neurons and regulates aggregation behavior. Developmental Biology 298(2):606 - 615.
- Shen, C., Nettleton, D, Jiang, M., Kim, S. and Powell-Coffman, J.A.. 2005. Roles of HIF-1/hypoxia inducible factor and VHL-1/ Von Hippel tumor suppressor during hypoxia response in C. elegans. J. Biol. Chem 280:20580-8.
- Huang, X., Powell-Coffman, J. A., and Y. Jin. 2004. Specification of GABAnergic subtypes by the AHR-1 aryl hydrocarbon receptor complex in C. elegans. Development 131: 819-28.
- Qin, H. and Powell-Coffman, J.A.. 2004. Regulation of neuronal development by AHR-1, the C. elegans aryl hydrocarbon receptor. Developmental Biology 270: 64-75.
- Powell-Coffman, J.A.. 2003. bHLH-PAS proteins in C. elegans. In, PAS Proteins: Regulators and Sensors of Development and Physiology (Editor S. Crews). Kluwer Academic Publishers. Norwell, MA. pp 51 - 68 .
- Shen, C. and Powell-Coffman, J. A.. 2003. Genetic analysis of hypoxia signaling and response in C. elegans. Ann. New York Acad. Sci. 995: 191 - 199.
- Treinin, M., Schleyer, J., Jiang, H., Powell-Coffman, J. A., Bromberg, Z., and M. Horowitz. 2003. HIF-1 is required for heat acclimation in the nematode C. elegans. Physiological Genomics 14, 17-24.
- Jiang, H., Guo, R., and J. A. Powell-Coffman. 2001. The Caenorhabditis elegans hif-1 gene encodes a bHLH-PAS protein that is required for adaptation to hypoxia. Proc. Natl. Acad. Sci. U. S. A. 98: 7916 – 7921.
- Powell-Coffman, J.A., Bradfield, C.A., and W.B. Wood. 1998. C. elegans orthologs of the aryl hydrocarbon receptor and its heterodimerization partner the aryl hyrdrocarbon receptor nuclear translocator. Proc. Natl. Acad. Sci. U. S. A. 95: 2844-2849.
- Powell-Coffman, J.A., Knight, J., and W.B. Wood. 1996. Onset of C. elegans gastrulation is blocked by inhibition of embryonic transcription with an RNA polymerase antisense RNA. Dev. Biol. 178: 472-483.