Populations adapt to novel environmental conditions by genetic changes or phenotypic plasticity. Plastic responses are generally faster and can buffer fitness losses under variable conditions. Plasticity is typically modelled as random noise and linear reaction norms that assume simple one-to-one genotype-phenotype maps and no limits to the phenotypic response. Most studies on plasticity have focused on its effect on population viability. However, it is not clear, whether the advantage of plasticity depends solely on environmental fluctuations or also on the genetic and demographic properties (life histories) of populations. Here we present an individual-based model and study the relative importance of adaptive and non-adaptive plasticity for populations of sexual species with different life histories experiencing directional stochastic climate change. Environmental fluctuations were simulated using differentially autocorrelated climatic stochasticity or noise color, and scenarios of directional climate change. Non-adaptive plasticity was simulated as a random environmental effect on trait development, while adaptive plasticity as a linear, logistic, or sinusoidal reaction norm. The last two imposed limits to the plastic response and emphasized flexible interactions of the genotype with the environment. Interestingly, this assumption led to (i) smaller phenotypic than genotypic variance in the population and the coexistence of polymorphisms, (ii) many-to-one genotype-phenotype map, and (iii) the maintenance of higher genetic variation – compared to linear reaction norms and genetic determinism – even when the population was exposed to a constant environment for several generations. Limits to plasticity led to genetic accommodation, when costs were negligible, and to the appearance of cryptic variation when limits were exceeded. We found that adaptive plasticity promoted population persistence under red noise stochasticity and was particularly important for life histories with low fecundity. Populations producing more offspring could cope with environmental fluctuations solely by genetic changes or random plasticity, unless environmental change was too fast.

A species’ response to thermal stress is an essential physiological trait that can determine occurrence and temporal succession in nature, including response to climate change. Environmental temperature affects zooplankton performance by altering life-spans and population growth rates, but the molecular mechanisms underlying these alterations are largely unknown. To compare temperature-related demography, we performed cross-temperature life-table experiments in closely related heat-tolerant and heat-sensitive Brachionus rotifer species that occur in sympatry. Within these same populations, we examined the genetic basis of physiological variation by comparing gene expression across increasing temperatures. We found significant cross-species and cross-temperature differences in heat response, with the heat-sensitive species adopting a strategy of high survival and low population growth, while the heat-tolerant followed an opposite strategy. Comparative transcriptomic analyses revealed both shared and opposing responses to heat. Most notably, expression of heat shock proteins (hsps) is strikingly different in the two species. In both species, hsp responses mirrored differences in population growth rates, showing that hsp genes are likely a key component of a species’ adaptation to different temperatures. Temperature induction caused opposing patterns of expression in further functional categories such as energy, carbohydrate and lipid metabolism, and in genes related to ribosomal proteins. In the heat-sensitive species, elevated temperatures caused up-regulation of genes related to induction of meiotic division as well as genes responsible for post-translational histone modifications. This work demonstrates the sweeping reorganizations of biological functions that accompany temperature adaptation in these two species and reveals potential molecular mechanisms that might be activated for adaptation to global warming.