Connie J. Mulligan, Ph.D.
Phone: (352) 273-8092
Lab: 415 Genetics Institute, CGRC
- Ph.D., Molecular Biophysics and Biochemistry, Yale University, 1990
- M.Phil., Molecular Biophysics and Biochemistry, Yale University, 1985
- B.S., Honors Biology and Chemistry, University of Illinois,1983
Human genetics, epigenetics, complex phenotypes, biocultural investigation, impact of stress, risk and resilience, Syrian refugees, human evolution
Broadly, I am interested in understanding the basis of patterns and levels of human genetic variation. My lab analyzes genetic variation in order to reconstruct human evolutionary history and the basis of different diseases and pathogens. In order to understand complex disease, we take a biocultural approach. We investigate a broad range of data types, including genetic (candidate genes and genetic ancestry), epigenetic (specific genes and genome-wide), biological (blood pressure, biomarkers), psycho-social (stress exposures, anxiety, depression) and socio-cultural (discrimination experiences, personal social networks) data. We use these data to create the most comprehensive picture of blood pressure variation (African Americans living in Tallahassee, FL) and the impact of stress on health outcomes (new mothers and their newborns in the Democratic Republic of Congo). I recently began a new project (with Catherine Panter-Brick, Yale University) to look at the genetics and epigenetics of risk and resilience in Syrian refugee youth who have fled to Jordan. For the study of population history, we assay genetic variants in the mitochondrial genome, autosomes and sex chromosomes, and ancient DNA in order to provide the most complete representation of human evolution. We are particularly interested in the first migrations of anatomically modern humans out of Africa as well as the recent colonization of the New World. We study populations from around the world with an emphasis on the Arabian Peninsula, Horn of Africa, Mongolia and the New World for our population history studies and the continental US and Democratic Republic of Congo for our disease studies.
Positions and Honors
Positions and Employment
- 2010 – present Professor, Department of Anthropology
- 2005 – 2010 Associate Professor, Department of Anthropology, University of Florida
- 1999 – 2005 Assistant Professor, Department of Anthropology, University of Florida
- 1998 – 2000 National Research Council Senior Research Associate, NIAAA, NIH
- 1995 – 1998 Research Biologist, Smithsonian Center for Materials Research and Education
- 1991 – 1995 Postdoctoral Fellow, Smithsonian Tropical Research Institute, Republic of Panamá
- 1990 – 1991 Postdoctoral Fellow, Molecular Biophysics and Biochemistry, Yale University
Other Experience and Professional Memberships
- 2012 – 2016 Co-graduate coordinator, UF Genetics & Genomics Graduate Program
- 2011 – 2016 Associate Chair, Department of Anthropology
- 2008 – present Affiliate Professor, Center for African Studies, University of Florida
- 2003 – 2015 Associate Director, University of Florida Genetics Institute
- 2017-2018 President, American Association of Anthropological Genetics
- 2016 UF Postdoctoral Mentoring Award
- 2013-2016 University of Florida Foundation Research Professor
- 2013 University of Florida Honors Professor of the Year
- 2012-2013 Elizabeth Wood Dunlevie Honors Term Professor
- 2010 HHMI Science for Life Distinguished Mentor Award
- 2007-2008 Colonel Allan R. and Margaret G. Crow Term Professor
Quinlan J, Pearson LN, Clukay CJ, Mitchell MM, Boston Q, Gravlee CC, Mulligan CJ. 2016. Genetic loci and novel discrimination measures associated with blood pressure variation in African Americans living in Tallahassee, PLoS ONE, 11(12):e0167700.
Mulligan CJ. 2016. Early environments, stress, and the epigenetics of human health, Annual Review Anthro, 45:233-249.
Mulligan CJ, D’Errico NS, Stees J, Hughes DA. 2012. Methylation changes at NR3C1 in newborns associate with maternal prenatal stress exposure and newborn birthweight, Epigenetics, 7:853-857, doi: 10.4161/epi.21180.
Kitchen D, Miyamoto MM, Mulligan CJ. 2008. A three-stage colonization model for the peopling of the Americas, PLoS ONE, 3(2):e1596.
Kolman CJ, Sambuughin N, Bermingham E. 1996. Mitochondrial DNA analysis of Mongolian populations and implications for the origin of New World founders, Genetics, 142: 1321-1334.
Contribution to Science
Biocultural Investigations of Human Health and Disease
Working with Dr. Lance Gravlee, a cultural anthropologist in the Department of Anthropology, we have demonstrated that integrating genetic and sociocultural data provides a more comprehensive picture of human health and disease. We have studied blood pressure variation in African Americans living in Tallahassee and in Puerto Ricans. In both studies, we detected numerous interactions between genetic and sociocultural measures that identify relevant biological and cultural factors that would not have been detected without including both types of data. Significantly, we used a novel measure of discrimination (unfair treatment of individuals close to the study participant) that is a significant predictor of blood pressure variation and interacts with genetic variants involved in psychosocial stress and mood disorders, suggesting that racial discrimination might underlie some of the racial disparities seen in complex diseases like hypertension. This research was funded by NSF grants BCS 0820687 and 1540372.
- Quinlan J, Pearson LN, Clukay CJ, Mitchell MM, Boston Q, Gravlee CC, Mulligan CJ.2016. Genetic loci and novel discrimination measures associated with blood pressure variation in African Americans living in Tallahassee, PLoS ONE, 11(12):e0167700.
- Boulter AC, Quinlan JA, Miró-Herrans AT, Pearson L, Todd NL, Gravlee CC, Mulligan CJ. 2015. Interaction of Alu polymorphisms and novel measures of discrimination in association with blood pressure in African Americans living in Tallahassee, Hum Biol 87(4):295-305.
- Gravlee CC, Non AL, Mulligan CJ. 2009. Genetic ancestry, social classification, and racial inequalities in blood pressure in Southeastern Puerto Rico, PLoS ONE, 4(9):e6821.
Epigenetic Markers of Psychosocial Stress
My research in the Democratic Republic of Congo has provided some of the first evidence that psychosocial stressors, such as sexual violence, can leave an epigenetic imprint (specifically DNA methylation) that may influence health outcomes and may be transmitted to future generations. We study new mothers and their newborns in the Democratic Republic of Congo, where ongoing civil war and its aftermath has created one of the most traumatic environments in the world for women. We find that maternal stress is associated with a genome-wide change in methylation in mothers, but a more focused, gene-specific effect on methylation in newborns. A change in methylation at particular genes in newborns that is not seen in mothers is consistent with the Developmental Origins of Health and Disease (DOHaD) hypothesis in which maternal stress modifies offspring biology. Our research suggests that events experienced during one’s life may leave an epigenetic imprint that may impact gene expression in future generations. This research is funded by NSF grants BCS 1231264 and 1540372.
- Mulligan CJ. 2016. Early environments, stress, and the epigenetics of human health, Annual Review Anthro, 45:233-249.
- Kertes DA, Kamin HS, Hughes DA, Rodney NC, Mulligan CJ. 2016. Prenatal maternal stress predicts methylation of genes regulating the hypothalamic-pituitary-adrenocortical system in mothers and newborns, Child Development, special issue on “Epigenetics in Child and Adolescent Development”, 87:61-72.
- Rodney NC and Mulligan CJ. 2014. A biocultural study of the effects of maternal stress on mother and newborn health in the Democratic Republic of Congo, Amer J Phys Anthropol, 155(2):200-209.
- Mulligan CJ, D’Errico NS, Stees J, Hughes DA. 2012. Methylation changes at NR3C1 in newborns associate with maternal prenatal stress exposure and newborn birthweight, Epigenetics, 7:853-857, doi: 10.4161/epi.21180.
Migration of Anatomically Modern Humans out of Africa
In collaboration with archaeologists in the department, I became interested in identifying the route by which the first anatomically modern humans left Africa and successfully colonized the rest of the planet. We have compared genetic support for migration routes along the northern vs southern extent of the Red Sea. Using the largest set of samples collected from Yemen, the first step along the southern migration route, we have determined that multiple migrations out of, and back into, Africa have erased most of the signals of the first migration out of Africa. We have also investigated introgression of archaic DNA into the modern human gene pool and find strikingly similar levels of Neanderthal introgression throughout the Arabian Peninsula. This research was funded by NSF grants BCS 0518530 and 1258965.
- Vyas D, Kitchen A, MIró-Herrans AT, Pearson L, Al-Meeri A, Mulligan CJ, 2016. Bayesian analyses of Yemeni mitochondrial genomes suggest multiple migration events with Africa and Eurasia, Am J Phys Anthropol, 159:382-393.
- Miró-Herrans AT, AL-Meeri A, Mulligan CJ. 2014. Human migration patterns in Yemen and implications for reconstructing prehistoric population movements. PLoS ONE, 9(4): e95712.
- Hodgson JA, Mulligan CJ, Al-Meeri A, Raaum R. 2014. Early back-to-Africa migration into the Horn of Africa, PLoS Genetics, 10(6):e1004393.
- Kitchen A, Ehret D, Assefa S, Mulligan CJ. 2009. Bayesian phylogenetic analysis of Semitic languages identifies an Early Bronze Age origin of Semitic in the Near East, Proc R Soc B 276:2703-10
- Cerný V, Mulligan CJ, Rídl J, Zaloudková M, Edens CM, Hájek M, Pereira L. 2008. Regional differences in the distribution of the sub-Saharan, West Eurasian, and South Asian mtDNA lineages in Yemen, Am J Phys Anthropol, 136:128-137.
Peopling of the New World
Before I came to UF, my research provided some of the first evidence to suggest that the New World was colonized by a single wave of migration that most likely originated in east Central Asia around Mongolia. While at UF, my colleagues and I have expanded that model to specify three separate stages of migration that include an extended period of population isolation and genetic differentiation on Beringia. Specifically, we propose that Amerinds first diverged from the Asian gene pool about 40,000 years ago, occupied Beringia for approximately 10,000 years, and then rapidly expanded in the New World approximately 16,000 years ago. Expansion into the New World was accomplished by a large population increase that reached the southern tip of South America within several thousand years.
- Mulligan CJ, Szathmáry EJE. 2017. The peopling of the Americas and the origin of the Beringian occupation model, Am J Phys Anthropol, 162: 403-408.
- Mulligan CJ, Kitchen A, Miyamoto MM. 2008. Updated three-stage model for the peopling of the Americas, PLoS ONE, 3(9):e3199.
- Kitchen D, Miyamoto MM, Mulligan CJ. 2008. A three-stage colonization model for the peopling of the Americas, PLoS ONE, 3(2):e1596.
Ongoing Research Support
- “Epigenetic alterations, gene expression, and stress among new mothers and neonates in the Democratic Republic of Congo: A biocultural investigation of the intergenerational effects of stress”
- 02/01/17-01/31/19 (PI)
- “Doctoral Dissertation Research: Effect of intrauterine environment on newborn telomere length”
- PI, (student co-PI – Peter Rej)
- “US/UK joint workshop on social and behavioral epigenetics”
- 6/15/14-5/31/15 (PI)
- “Doctoral dissertation research: Testing for archaic hominid introgression in Eritrean and Yemeni modern human genomes”
- PI (student co-PI – Deven Vyas)
Completed Research Support (within the past three years)
- “Epigenetic alterations and stress among new mothers and neonates in the Democratic Republic of Congo: A biocultural investigation of the intergenerational effects of war”