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Plasticity is found in all domains of life and is particularly relevant when populations experience variable environmental conditions. Traditionally, evolutionary models of plasticity are non-mechanistic: they typically view reactions norms as the target of selection, without considering the underlying genetics explicitly. Consequently, there have been difficulties in understanding the emergence of plasticity, and in explaining its limits and costs. In this paper, we offer a novel mechanistic approximation for the emergence and evolution of plasticity. We simulate random "epigenetic mutations" in the genotype–phenotype mapping, of the kind enabled by DNA-methylations/demethylations. The frequency of epigenetic mutations at loci affecting the phenotype is sensitive to organism stress (trait–environment mismatch), but is also genetically determined and evolvable. Thus, the "random motion" of epigenetic markers enables developmental learning-like behaviors that can improve adaptation within the limits imposed by the genotypes. However, with random motion being "goal-less," this mechanism is also vulnerable to developmental noise leading to maladaptation. Our individual-based simulations show that epigenetic mutations can hide alleles that are temporarily unfavorable, thus enabling cryptic genetic variation. These alleles can be advantageous at later times, under regimes of environmental change, in spite of the accumulation of genetic loads. Simulations also demonstrate that plasticity is favored by natural selection in constant environments, but more under periodic environmental change. Plasticity also evolves under directional environmental change as long as the pace of change is not too fast and costs are low. [ABSTRACT FROM AUTHOR]

The neritid snail Theodoxus fluviatilis is found across habitats differing in salinity, from shallow waters along the coast of the Baltic Sea to lakes throughout Europe. Living close to the water surface makes this species vulnerable to changes in salinity in their natural habitat, and the lack of a free-swimming larval stage limits this species' dispersal. Together, these factors have resulted in a patchy distribution of quite isolated populations differing in their salinity tolerances. In preparation for investigating the mechanisms underlying the physiological differences in osmoregulation between populations that cannot be explained solely by phenotypic plasticity, we present here an annotated draft genome assembly for T. fluviatilis , generated using PacBio long reads, Illumina short reads, and transcriptomic data. While the total assembly size (1045 kb) is similar to those of related species, it remains highly fragmented (N scaffolds = 35,695; N50 = 74 kb) though moderately high in complete gene content (BUSCO single copy complete: 74.3%, duplicate: 2.6%, fragmented: 10.6%, missing: 12.5% using metazoa n = 954). Nevertheless, we were able to generate gene annotations of 21,220 protein-coding genes (BUSCO single copy complete: 65.1%, duplicate: 16.7%, fragmented: 9.1%, missing: 9.1% using metazoa n = 954). Not only will this genome facilitate comparative evolutionary studies across Gastropoda, as this is the first genome assembly for the basal snail family Neritidae, it will also greatly facilitate the study of salinity tolerance in this species. Additionally, we discuss the challenges of working with a species where high molecular weight DNA isolation is very difficult. [ABSTRACT FROM AUTHOR]