Hypotheses and models linking epigenetic transgenerational effects to population dynamics: Exploring oscillations and applications to wildlife cycles

Epigenetic transgenerational mechanisms underpin the imprinting of gamete origin during reproduction in mammals but are also hypothesized to transmit environmental exposures from parents to progeny in many life forms, which could have important consequences in population dynamics. Transgenerational hypotheses embody epigenetic alterations occurring in gametes, embryonic somatic cells, and embryonic primordial germ cells because most of the epigenome is erased and reconstituted during development. Four scenarios are described in this paper encompassing somatic and germline effects where each of these is either non-propagating or propagating in time. The non-propagating effects could result from environmental impulses such as toxicants, weather, epidemics, forest fires, etc. The propagating effects could result from continuous signals such as climate variations, food web abundances, population densities, predator numbers, etc. Focusing on the propagating mode, a population growth model is constructed incorporating the intrinsic delays associated with somatic or germline effects. Each exhibit oscillatory behavior over a wide range of the parameter space due to the inherent negative feedback of such delays. The somatic (maternal) model oscillates with a period of [~]6 generations while the germline (grandmaternal) model oscillates with a period of [~]10 generations. These models can be entrained by oscillatory external signals providing that the signals contain harmonic components near the intrinsic oscillations of the models. The 10-generation oscillation of the germline-effects model is similar to many wildlife cycles in mammals, bird, and insects. The possibility that such a transgenerational mechanism is a component of these wildlife cycles is discussed.