Search for: All records

Abstract Environmental factors early in life can have lasting influence on the development and phenotypes of animals, but the underlying molecular modifications remain poorly understood. We examined cross‐sectional associations among early life socioecological factors and global DNA methylation in 293 wild spotted hyenas (Crocuta crocuta) in the Masai Mara National Reserve, Kenya, grouped according to three age classes (cub, subadult and adult). Explanatory variables of interest included annual maternal rank based on outcomes of dyadic agonistic interactions, litter size, wild ungulate prey density and anthropogenic disturbance in the year each hyena was born based on counts of illegal livestock in the Reserve. The dependent variable of interest was global DNA methylation, assessed via the LUminometric Methylation Assay, which provides a percentage methylation value calculated at CCGG sites across the genome. Among cubs, we observed approximately 2.75% higher CCGG methylation in offspring born to high‐ than low‐ranking mothers. Among cubs and subadults, higher anthropogenic disturbance corresponded with greater %CCGG methylation. In both cubs and adults, we found an inverse association between prey density measured before a hyena was 3 months old and %CCGG methylation. Our results suggest that maternal rank, anthropogenic disturbance and prey availability early in life are associated with later life global DNA methylation. Future studies are required to understand the extent to which these DNA methylation patterns relate to adult phenotypes and fitness outcomes. 

In ecology and evolutionary biology (EEB), the study of developmental plasticity seeks to understand ontogenetic processes underlying the phenotypes upon which natural selection acts. A central challenge to this inquiry is ascertaining a causal effect of the exposure on the manifestation of later-life phenotype due to the time elapsed between the two events. The exposure is a potential cause of the outcome—i.e. an environmental stimulus or experience. The later phenotype might be a behaviour, physiological condition, morphology or life-history trait. The latency period between the exposure and outcome complicates causal inference due to the inevitable occurrence of additional events that may affect the relationship of interest. Here, we describe six distinct but non-mutually exclusive conceptual models from the field of lifecourse epidemiology and discuss their applications to EEB research. The models include Critical Period with No Later Modifiers, Critical Period with Later Modifiers, Accumulation of Risk with Independent Risk Exposures, Accumulation of Risk with Risk Clustering, Accumulation of Risk with Chains of Risk and Accumulation of Risk with Trigger Effect. These models, which have been widely used to test causal hypotheses regarding the early origins of adult-onset disease in humans, are directly relevant to research on developmental plasticity in EEB.