When do factors promoting genetic diversity also promote population persistence? A demographic perspective on Gillespie's SAS-CFF model.

Classical stochastic demography predicts that environmental stochasticity reduces population growth rates and, thereby, can increase extinction risk. In contrast, in a 1978 Theoretical Population Biology paper, Gillespie demonstrated with his stochastic additive scale and concave fitness function (SAS-CFF) model that environmental stochasticity can promote genetic diversity. Extending the SAS-CFF to account for demography, I examine the simultaneous effects of environmental stochasticity on genetic diversity and population persistence. Explicit expressions for the per-capita growth rates of rare alleles and the population at low-density are derived. Consistent with Gillespie's analysis, if the log-fitness function is concave and allelic responses to the environment are not perfectly correlated, then per-capita growth rates of rare alleles are positive and genetic diversity is maintained in the sense of stochastic persistence i.e. allelic frequencies tend to stay away from zero almost-surely and in probability. Alternatively, if the log-fitness function is convex, then per-capita growth rates of rare alleles are negative and an allele asymptotically fixates with probability one. If the population's low-density, per-capita growth rate is positive, then the population persists in the sense of stochastic persistence, else it goes asymptotically extinct with probability one. In contrast to per-capita growth rates of rare alleles, the population's per-capita growth rate is a decreasing function of the concavity of the log-fitness function. Moreover, when the log-fitness function is concave, allelic diversity increases the population's per-capita growth rate while decreasing the per-capita growth rate of rare alleles; when the log-fitness function is convex, environmental stochasticity decreases the per-capita growth rate of rare alleles, but increases the population's per-capita growth rate. Collectively, these results (i) highlight how mechanisms promoting population persistence may be at odds with mechanisms promoting genetic diversity, and (ii) provide conditions under which population persistence relies on existing standing genetic variation.