Adaptation and plasticity within and across generations

The environment is seldom stable but often changes from one state to another and in order to survive and reproduce organisms need to respond to those changes. If the change is fast, genetic adaptations may not evolve quickly enough and organisms must adopt other strategies, such as phenotypic plasticity. As there are different types of environmental variations, the optimal type of plasticity also differs. However, plasticity is not always adaptive but can sometimes result in phenotype further away from the optimum. In the thesis I investigate how different types of environmental variation influence adaptation and phenotypic plasticity. I used experimental evolution approaches (Paper I, II) and RNA interference, (Paper III) in Caenorhabditis remanei (Paper I, II) and Caenorhabditis elegans (Paper III). In Paper IV I tested whether trade-offs with lifespan are caused by energy allocation, and if there are trans-generational fitness effects. In Paper I I show that the evolution of life histories, indeed, depends on whether organisms evolve in stable, fluctuating or variable temperatures. I also show, that the plastic response to temperature is in line with the temperature-size rule and that this response is adaptive. In Paper II I look closer on the evolutionary response to highly variable environments. I show that worms respond to fast changes in temperature by increasing the degree of phenotypic plasticity, rather than using bet-hedging. I again confirmed that plasticity in size follows the temperature size rule and that it is adaptive. In Paper III I examine how organisms respond to temperature changes that occur within their lifetime. I found that after initial decrease in growth rate as a response to cold temperatures, once temperature increases worms exhibit increased growth rate, which corresponds to the compensatory growth plasticity. Interestingly, the worms didn’t pay any cost in longevity or reproduction but had higher fitness. In addition, I show that temperature-induced compensatory growth is regulated by TRPA-1 ion channel (trpa-1gene). Finally, in Paper IV, I show that optimization of gene expression by down-regulation of insulin/IGF-1 signaling via daf-2 RNAi from sexual maturity in C. elegans can more than double longevity without imposing any cost on reproduction. This is not expected if investment in lifespan and reproduction compete for the same energy pool. Importantly, I also showed that the positive effects for the parents did not come at a trans-generational cost for the offspring, since they exhibited increased reproduction and fitness.