207-288-9880 ext 444
Chronic psychosocial stress experienced very early in life—even in utero during prenatal development—increases the risk of developing inflammatory disease in adulthood, leading to unhealthy aging. Chronically elevated neuroendocrine stress signaling is one mechanism hypothesized to account for that correlation. We are testing that hypothesis and investigating the mechanisms underlying the causal link between chronic early life stress and adult health by examining how chronic exposure to the stress hormone cortisol during early development affects the immune system. To do this we are using zebrafish as an experimental model, as the cortisol-mediated stress response is conserved between zebrafish and humans, and zebrafish are exceptionally amenable to mechanistic studies of early development, adult regeneration, and immunoregulation.
Partnership with EMMC Cancer Care Provides Clinical Laboratory Training
Press Release · June 15, 2017
Sea Urchin Regeneration May Help Us Understand Aging
NIGMS Biomedical Beat · May 31, 2017
Sea Urchin Regeneration May Help Us Understand Aging
Breaking Through · May 31, 2017
James A. Coffman, Ph.D., Discusses How Stress Experienced During Early Development Programs Adult Disease Risk Featured in Webinar
Breaking Through · April 13, 2017
How Chronic Stress Experienced During Early Development Epigenetically Programs Adult Disease Risk
Neurology Central · April 13, 2017
Webinar to Feature MDI Biological Laboratory Scientist James A. Coffman, Ph.D.
Press Release · April 5, 2017
Introduction to the MDI Biological Laboratory’s Center for Science Entrepreneurship
Regenerative Medicine Network · March 7, 2017
A Biomedical Rationale for Having Strong Social Safety Nets
Breaking Through · February 21, 2017
Q&A with James A. Coffman, Ph.D.: Early-Life Stress in Adult Illness
Breaking Through · January 27, 2017
Interview with James Coffman: Early Life Stress in Adult Illness
Future Neurology · January 27, 2017
Zebrafish May Hold the Answer to Why Early-Life Stress Can Make You Sick When You’re an Adult
Breaking Through · January 23, 2017
Zebrafish May Hold the Answer to Why Early Life Stress Can Make You Sick When You’re an Adult
Catching Health · January 23, 2017
How Childhood Stress Leads to Adult Disease
WABI TV5/The CW · December 1, 2016
How Early Childhood Stress Could Lead to Costly Adult Illnesses
Mainebiz · October 25, 2016
Research at MDI Biological Laboratory Examines Role of Early-Life Stress in Adult Illness
Press Release · October 24, 2016
A Healthy Old Age May Trump Immortality
Science News · July 13, 2016
MDI Scientists Investigating Ways to Slow Aging
Fox 22/ABC 7 · July 3, 2016
Is Aging Inevitable? Not Necessarily for Sea Urchins: Study Shows That Sea Urchins Defy Aging, Regardless of Lifespan
Breaking Through · June 29, 2016
Maine Scientist Seeks Keys to How Sea Urchins Avoid Aging Process
Portland Press Herald · June 1, 2016
MDIBL Scientists Study ‘Ocean Methuselahs’ to Learn About Aging
Mainebiz · May 26, 2016
Do Sea Urchins Hold the Secret to Anti-Aging?
News Beat Social · May 26, 2016
Is Ageing Inevitable? Sea Urchins Could Hold the Key to Living Forever
Huffington Post UK · May 26, 2016
Is Aging Inevitable? Not Necessarily for Sea Urchins
Press Release · May 24, 2016
Cortisol-treated zebrafish embryos develop into pro-inflammatory adults with aberrant immune gene regulation. Hartig, E.I., Zhu, S., King, B.L, and Coffman, J.A. (2016). Biology Open 5: 1134-1141.
An Elk transcription factor is required for Runx-dependent survival signaling in the sea urchin embryo. Rizzo, F., Coffman, J.A., and Arnone, M.I. (2016). Dev. Biol. 416: 173-186.
Comparative biology of tissue repair, regeneration, and aging. Coffman, J.A., Rieger, S., Rogers, A.N., Updike, D.L, and Yin, V.P. (2016). npj Regen. Med., 1: 16003.
Maintenance of somatic tissue regeneration with age in short- and long-lived species of sea urchins. Bodnar, A.G. and Coffman, J.A. (2016). Aging Cell 15: 778-787.
Developmental control of transcriptional and proliferative potency during the evolutionary emergence of animals. Arenas-Mena, C. and Coffman, J.A. (2015). Dev. Dyn. 244: 1193-1201.
Gene expression changes associated with the developmental plasticity of sea urchin larvae in response to food availability. Carrier, T.J., King, B.L., and Coffman, J.A. (2015). Biological Bulletin 228: 171-180.
On the meaning of chance in biology. Coffman, J.A. (2014). Biosemiotics 7: 377-388.
Oral-aboral axis specification in the sea urchin embryo IV. Hypoxia radializes embryos by preventing the initial spatialization of nodal activity. Coffman, J.A., Wessels, A., DeSchiffart, C., and Rydlizky, K. (2014). Dev. Biol. 386: 302-307.
Developmental cis-regulatory analysis of the cyclin D gene in the sea urchin Strongylocentrotus purpuratus. McCarty, C.M., and Coffman, J.A. (2013). Biochem. Biophys. Research Comm. 440: 413-418.
Sea urchin akt activity is Runx-dependent and required for post-cleavage stage cell division. Robertson, A.J., Coluccio, A., Jensen, S., Rydlizky, K., and Coffman, J.A. (2013). Biology Open, 2: 472-478.
Global Insanity: How Homo sapiens Lost Touch with Reality while Transforming the World. Coffman, J.A. and Mikulecky, D.C. (2012). Emergent Publications (ISBN 9781938158049).
Nodal-mediated epigenesis requires dynamin-mediated endocytosis. Ertl, R.P., Robertson, A.J., Saunders, D., and Coffman, J.A. (2011). Dev. Dyn. 240: 704-711.
Oxygen, pH, and oral-aboral axis specification in the sea urchin embryo. Coluccio, A.E., LaCasse, T.J., and Coffman, J.A. (2011). Mol. Rep. & Dev. 78: 68.
On causality in non-linear complex systems: the developmentalist perspective. Coffman, J.A. (2011). In: Philosophy of Complex Systems (Cliff Hooker, ed.): pp. 287-309. North Holland/Elsevier, Oxford, UK (ISBN 9780444520760).
The evolution of Runx genes. II. The C-terminal Groucho recruitment motif is present in both eumetazoans and homoscleromorphs but absent in a haplosclerid demosponge. Robertson, A.J., Larroux, C., Degnan, B.M., and Coffman, J.A. (2009). BMC Research Notes 2: 59.
Oral-aboral axis specification in the sea urchin embryo III. Role of mitochondrial redox signaling via H2O2. Coffman, J.A., Coluccio, A., Planchart, A., and Robertson, A.J. (2009). Dev. Biol. 330: 123-130.
Is Runx a linchpin for developmental signaling in metazoans? Coffman, J.A. (2009). J. Cellular Biochem. 107: 194-202.
Mitochondria and metazoan epigenesis. Coffman, J.A. (2009). Semin. Cell Dev. Biol. 20: 321-329.
Runx expression is mitogenic and mutually linked to wnt activity in blastula-stage sea urchin embryos. Robertson, A.J., Coluccio, A., Knowlton, P., Dickey-Sims, C., and Coffman, J.A. (2008). PLoS One 3: 11.
Mitochondria, redox signaling, and axis specification in metazoan embryos. Coffman, J.A. and Denegre, J.M. (2007). Dev. Biol. 308: 266-280.
CBF-beta is a facultative Runx partner in the sea urchin embryo. Robertson, A.J., Dickey-Sims, C., Ransick, A., Rupp, D.E., McCarthy, J.J., and Coffman, J.A. (2006). BMC Biol. 4: 4.
Developmental ascendency: from bottom-up to top-down control. Coffman, J.A. (2006). Biological Theory 1 (2):165-178.
The genomic underpinnings of apoptosis in Strongylocentrotus purpuratus. Robertson, A.J., Croce, J., Carbonneau, S., Voronina, E., Miranda, E., McClay, D.R. and Coffman, J.A. (2006). Dev. Biol. 300: 321-334.
The genome of the sea urchin Strongylocentrotus purpuratus. Sodergren E., Weinstock G. M., Davidson E. H., Cameron R. A., Gibbs R. A., Angerer R. C., Angerer L. M., Arnone M. I., Burgess D. R., Burke R. D., Coffman J.A., et al. (The Sea Urchin Genome Sequencing Consortium) (2006). Science 314: 941-952.
- Shusen Zhu, M.S., Research Assistant
- Ellen Hartig, B.S., B.A., Research Assistant
- Ian Gans, B.S., Graduate Student