Vasopressin, and not oxytocin, receptor gene methylation is associated with individual differences in receptive joint attention in chimpanzees (Pan troglodytes)

Author:

Hopkins William D.1,Staes Nicky234,Guevara Elaine E.2,Mulholland Michele M.1ORCID,Sherwood Chet C.2,Bradley Brenda J.2

Affiliation:

1. Michale E. Keeling Center for Comparative Medicine and Research The University of Texas MD Anderson Cancer Center Bastrop Texas USA

2. Center for the Advanced Study of Human Paleobiology, Department of Anthropology The George Washington University Washington DC USA

3. Behavioral Ecology and Ecophysiology Group, Department of Biology University of Antwerp Wilrijk Belgium

4. Centre for Research and Conservation Royal Zoological Society of Antwerp Antwerp Belgium

Abstract

AbstractJoint attention (JA) is an important milestone in human infant development and is predictive of the onset of language later in life. Clinically, it has been reported that children at risk for or with a diagnosis of autism spectrum disorder (ASD) perform more poorly on measures of JA compared to neurotypical controls. JA is not unique to humans but has also been reported in great apes and to a lesser extent in more distantly related monkeys. Further, individual differences in JA among chimpanzees are associated with polymorphisms in the vasopressin and oxytocin genes, AVPR1A and OXTR. Here, we tested whether individual variation in DNA methylation of OXTR and AVPR1A were associated with performance on JA tasks in chimpanzees. We found that individual differences in JA performance was associated with AVPR1A methylation, but not OXTR methylation in the chimpanzees. The collective results provide further evidence of the role of AVPR1A in JA abilities in chimpanzees. The results further suggest that methylation values for AVPR1A may be useful biomarkers for identifying individuals at risk for ASD or related neurodevelopmental disorders associated with impairments in JA abilities.

Funder

National Institutes of Health

National Science Foundation

Publisher

Wiley

Subject

Genetics (clinical),Neurology (clinical),General Neuroscience

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