Abstract
Simple SummaryPolyphenism is a widespread phenomenon in insects that allows organisms to produce alternative and discrete phenotypes in response to environmental conditions. Epigenetic mechanisms, including histone post-translational modifications, DNA methylation and non-coding RNAs, are essential mechanisms that can promote rapid and flexible changes in the expression of transcriptional programs associated with the production of alternative phenotypes. This review summarizes knowledge regarding the contribution of those mechanisms in the regulation of the most-studied examples of polyphenism in insects.Many insect species display a remarkable ability to produce discrete phenotypes in response to changes in environmental conditions. Such phenotypic plasticity is referred to as polyphenism. Seasonal, dispersal and caste polyphenisms correspond to the most-studied examples that are environmentally-induced in insects. Cues that induce such dramatic phenotypic changes are very diverse, ranging from seasonal cues, habitat quality changes or differential larval nutrition. Once these signals are perceived, they are transduced by the neuroendocrine system towards their target tissues where gene expression reprogramming underlying phenotypic changes occur. Epigenetic mechanisms are key regulators that allow for genome expression plasticity associated with such developmental switches. These mechanisms include DNA methylation, chromatin remodelling and histone post-transcriptional modifications (PTMs) as well as non-coding RNAs and have been studied to various extents in insect polyphenism. Differential patterns of DNA methylation between phenotypes are usually correlated with changes in gene expression and alternative splicing events, especially in the cases of dispersal and caste polyphenism. Combinatorial patterns of histone PTMs provide phenotype-specific epigenomic landscape associated with the expression of specific transcriptional programs, as revealed during caste determination in honeybees and ants. Alternative phenotypes are also usually associated with specific non-coding RNA profiles. This review will provide a summary of the current knowledge of the epigenetic changes associated with polyphenism in insects and highlights the potential for these mechanisms to be key regulators of developmental transitions triggered by environmental cues.
Highlights
We focus on environmentally-induced polyphenisms in well-studied insect models, classified as three different groups: seasonal, dispersal and caste polyphenisms
Regarding the contribution of epigenetic mechanisms in wing polyphenism, little is known so far apart from a handful of genes involved in chromatin remodelling that are differentially expressed in the heads of crowded and uncrowded parthenogenetic females
Caste polyphenism has far received the main attention and especially in well-studied organisms, such as ants and bees, several studies pointing out the role of DNA methylation and alternative splicing in the establishment of castespecific transcriptional programs underlying alternative phenotypes
Summary
Once the target tissues/organs receive the signal, the genome of the corresponding cells will modify its expression allowing the transcription of new sets of genes and proteins necessary for the production of the alternative phenotype. Epigenetic mechanisms mainly involving chromatin regulation and DNA methylation are activated in specific cells of the target tissue(s) These mechanisms modulate gene expression, ending up with the setup of alternative transcriptional programs underlying the production of discrete phenotypes. Epigenetic mechanisms are major regulators of gene expression in all organisms, including insects [8], and are involved in the production of alternative phenotypes. The combination of these three major epigenetic mechanisms can have a strong impact on the coordinated regulation of gene expression in the context of alternative phenotype production associated with polyphenism in insects. We start with a brief description of the neuro-endocrine transduction of the triggering signals and follow with a picture of the transcriptional and epigenetic modifications that contribute to the production of alternative phenotypes
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