Phenotypic plasticity is an important mechanism for populations to buffer themselves from environmental change. While it has long been appreciated that natural populations possess genetic variation in the extent of plasticity, a surge of recent evidence suggests that epigenetic variation could also play an important role in shaping phenotypic responses. Compared with genetic variation, epigenetic variation is more likely to have higher spontaneous rates of mutation and a more sensitive reaction to environmental inputs. In our review, we first provide an overview of recent studies on epigenetically encoded thermal plasticity in animals to illustrate environmentally-mediated epigenetic effects within and across generations. Second, we discuss the role of epigenetic effects during adaptation by exploring population epigenetics in natural animal populations. Finally, we evaluate the evolutionary potential of epigenetic variation depending on its autonomy from genetic variation and its transgenerational stability. Although many of the causal links between epigenetic variation and phenotypic plasticity remain elusive, new data has explored the role of epigenetic variation in facilitating evolution in natural populations. This recent progress in ecological epigenetics will be helpful for generating predictive models of the capacity of organisms to adapt to changing climates.

Abstract-Cardiac hypertrophy involves a remodeling process of the heart in response to diverse pathological stimuli. Both calcineurin/nuclear factor of activated T cells pathway and microRNA-133 (miR-133) have been shown to play a critical role in cardiac hypertrophy. It has been recognized that the expression and activity of calcineurin increases and miR-133 expression decreases in the hypertrophic heart, and inhibition of calcineurin or increase of miR-133 expression protects against cardiac hypertrophy. miR-133, miR-195, miR-1, miR-208, miR-21, and so forth. 2-6 Carè et al 2 reported that the expression of microRNA-133 (miR-133) decreased in mouse and human models of cardiac hypertrophy. Overexpression of miR-133 in vitro inhibited cardiac hypertrophy. In contrast, suppression of miR-133 by "decoy" sequences induced hypertrophy. Therefore, changes of miR-133 were considered as the requisites for determining cardiac hypertrophy. Calcineurin is a calcium/calmodulin-activated serinethreonine phosphatase that dephosphorylates the transcription factor, nuclear factor of activated T cells (NFAT), which translocates into the nucleus to bind to DNA and activate hypertrophic response genes. Cardiac-specific activation of calcineurin or its downstream effector NFAT is sufficient to induce cardiac hypertrophy, 7,8 and calcineurin protein levels and phosphatase activities increase in hypertrophic hearts. 9,10 In light of the antithetical functions of calcineurin and miR-133, we hypothesized that calcineurin is the target of miR-133, and the expression of miR-133 is regulated by the calcineurin/NFAT signaling pathway.

A 63-day feeding trial was conducted in northern snakehead to observe the effects of a dietary soybean meal substitution on the microbiota community, morphology and inflammatory cytokine gene expression in the intestine. Four isonitrogenous and isoenergetic diets containing increasing levels of soybean meal were used to replace 0%, 25%, 50% and 75% of the defatted fishmeal (diets are referred to G1, G2, G3 and G4, respectively). Different dietary soybean meal substitutions significantly affected the intestinal microbiota composition. At the phylum level, Firmicutes abundance was the lowest in the G4 group, in contrast with Proteobacteria, Bacteroidetes and Planctomycetes. At the genus level, significantly lower abundance of Lactococcus, Geobacillus, Pseudomonas, Streptococcus, Bacillus and Acinetobacter,but higher abundance of Cetobacterium, Planctomyces, Shewanella, Thermomonas, Rubrivivax and Carnobacterium was observed in fish fed the G4 diet. With increased dietary soybean meal, the thickness of the muscularis, the height of the fold and the height of the microvillus in the distal intestine decreased, but the relative expression of IL-1β, IL-10 and IL-17F was significantly up-regulated. In conclusion, more emphasis should be placed on the functionality of intestinal microbiota and the pathogenesis of mucosal inflammation to assess the effects of diet and fish intestinal health through intestinal microbiota profiling.

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