ABS 2022
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Socioecological adversity is associated with differential immune gene regulation in rhesus macaques
Marina M. Watowich1, Elisabeth A. Goldman2, Christina E. Costa3, Kenneth L. Chiou4, Michael J. Montague5, Angelina V. Ruiz-Lambides6, Melween I. Martinez6, Julie E. Horvath7, Kirstin N. Sterner2, Michael L. Platt5, James P. Higham3, Lauren J.N. Brent8, Amanda J. Lea9, Noah Snyder-Mackler4. 1University of Washington, Seattle, WA, United States; 2University of Oregon, Eugene, OR, United States; 3New York University, New York, NY, United States; 4Arizona State University, Tempe, AZ, United States; 5University of Pennsylvania, Philadelphia, PA, United States; 6University of Puerto Rico, San Juan, PR, United States; 7North Carolina Central University, Raleigh, NC, United States; 8University of Exeter, Exeter, , United Kingdom; 9Vanderbilt University, Nashville, TN, United States

Individuals of the same chronological age can vary in “biological” age, reflecting acceleration of age-related processes that are well-captured by DNA methylation and gene expression. While there is mounting evidence that socioecological adversities accelerate biological aging, few studies have comprehensively addressed how these adversities affect molecular mechanisms of aging. We quantified immune cell epigenomic (CpG methylation) and transcriptomic variation across a population of free-ranging rhesus macaques that varied in chronological age and adversity exposure. Over 35% of CpG sites were differentially methylated with age (FDR< 5%, n sites=74,073) and these sites were more likely to be differentially methylated in animals exposed to a major hurricane (odds ratio=1.3, p=9.2 x 10-119), hinting that ecological adversity may exert similar effects to aging on the epigenome. We also found that female macaques with more social partners had an epigenomic profile that was, on average, 0.5 years younger than those with fewer partners (p=0.04). Our results indicate that both ecological and social influences may moderate aging via epigenetic gene regulatory processes.