Development and evolution of insect pigmentation: Genetic mechanisms and the potential consequences of pleiotropy

Insect pigmentation is a premier model system in evolutionary and developmental biology. It has been at the heart of classical studies as well as recent breakthroughs. In insects, pigments are produced by epidermal cells through a developmental process that includes pigment patterning and synthesis. Many aspects of this process also impact other phenotypes, including behavior and immunity

Genomics of Developmental Plasticity in Animals

Developmental plasticity refers to the property by which the same genotype produces distinct phenotypes depending on the environmental conditions under which development takes place. By allowing organisms to produce phenotypes adjusted to the conditions that adults will experience, developmental plasticity can provide the means to cope with environmental heterogeneity. Developmental plasticity can be adaptive and its evolution can be shaped by natural selection. It has also been suggested that developmental plasticity can facilitate adaptation and promote diversification. Here, we summarize current knowledge on the evolution of plasticity and on the impact of plasticity on adaptive evolution, and we identify recent advances and important open questions about the genomics of developmental plasticity in animals. We give special attention to studies using transcriptomics to identify genes whose expression changes across developmental environments and studies using genetic mapping to identify loci that contribute to variation in plasticity and can fuel its evolution.Fundação para a Ciência e Tecnologia (FCT)info:eu-repo/semantics/publishedVersio

Thermal Plasticity in Insects’ Response to Climate Change and to Multifactorial Environments

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Developmental Plasticity in Butterfly Eyespot Mutants: Variation in Thermal Reaction Norms across Genotypes and Pigmentation Traits

Developmental plasticity refers to the property by which a genotype corresponds to distinct phenotypes depending on the environmental conditions experienced during development. This dependence of phenotype expression on environment is graphically represented by reaction norms, which can differ between traits and between genotypes. Even though genetic variation for reaction norms provides the basis for the evolution of plasticity, we know little about the genes that contribute to that variation. This includes understanding to what extent those are the same genes that contribute to inter-individual variation in a fixed environment. Here, we quantified thermal plasticity in butterfly lines that differ in pigmentation phenotype to test the hypothesis that alleles affecting pigmentation also affect plasticity therein. We characterized thermal reaction norms for eyespot color rings of distinct Bicyclus anynana genetic backgrounds, corresponding to allelic variants affecting eyespot size and color composition. Our results reveal genetic variation for the slope and curvature of reaction norms, with differences between eyespots and between eyespot color rings, as well as between sexes. Our report of prevalent temperature-dependent and compartment-specific allelic effects underscores the complexity of genotype-by-environment interactions and their consequence for the evolution of developmental plasticity.info:eu-repo/semantics/publishedVersio

Editorial: Evolution of Postembryonic Development

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Effects ofWolbachiaon Transposable Element Expression Vary BetweenDrosophila melanogasterHost Genotypes

Transposable elements (TEs) are repetitive DNA sequences capable of changing position in host genomes, thereby causing mutations. TE insertions typically have deleterious effects but they can also be beneficial. Increasing evidence of the contribution of TEs to adaptive evolution further raises interest in understanding what factors impact TE activity. Based on previous studies associating the bacterial endosymbiont Wolbachia with changes in the abundance of piRNAs, a mechanism for TE repression, and to transposition of specific TEs, we hypothesized that Wolbachia infection would interfere with TE activity. We tested this hypothesis by studying the expression of 14 TEs in a panel of 25 Drosophila melanogaster host genotypes, naturally infected with Wolbachia and annotated for TE insertions. The host genotypes differed significantly in Wolbachia titers inside individual flies, with broad-sense heritability around 20%, and in the number of TE insertions, which depended greatly on TE identity. By removing Wolbachia from the target host genotypes, we generated a panel of 25 pairs of Wolbachia-positive and Wolbachia-negative lines in which we quantified transcription levels for our target TEs. We found variation in TE expression that was dependent on Wolbachia status, TE identity, and host genotype. Comparing between pairs of Wolbachia-positive and Wolbachia-negative flies, we found that Wolbachia removal affected TE expression in 21.1% of the TE-genotype combinations tested, with up to 2.3 times differences in the median level of transcript. Our data show that Wolbachia can impact TE activity in host genomes, underscoring the importance this endosymbiont can have in the generation of genetic novelty in hosts.info:eu-repo/semantics/publishedVersio

Many ways to make darker flies: Intra- and inter-specific variation in Drosophila body pigmentation components

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Genomic Sequence around Butterfly Wing Development Genes: Annotation and Comparative Analysis

, where a whole-genome BAC library allows targeted access to large genomic regions. genes. Comparative analysis with orthologous regions of the lepidopteran reference genome allowed assessment of conservation of fine-scale synteny (with detection of new inversions and translocations) and of DNA sequence (with detection of high levels of conservation of non-coding regions around some, but not all, developmental genes)., both involved in multiple developmental processes including wing pattern formation

The combined effect of two mutations that alter serially homologous color pattern elements on the fore and hindwings of a butterfly

<p>Abstract</p> <p>Background</p> <p>The ability for serially homologous structures to acquire a separate identity has been primarily investigated for structures dependent on Hox gene input but is still incompletely understood in other systems. The fore and hindwings of butterflies are serially homologous structures as are the serially homologous eyespots that can decorate each of these wings. Eyespots can vary in number between fore and hindwings of the same individual and mutations of large effect can control the total number of eyespots that each of the wings displays. Here we investigate the genetics of a new spontaneous color pattern mutation, <it>Missing</it>, that alters eyespot number in the nymphalid butterfly, <it>Bicyclus anynana</it>. We further test the interaction of <it>Missing </it>with a previously described mutation, <it>Spotty</it>, describe the developmental stage affected by <it>Missing</it>, and test whether <it>Missing </it>is a mutant variant of the gene <it>Distal-less </it>via a linkage association study.</p> <p>Results</p> <p><it>Missing </it>removes or greatly reduces the size of two of the hindwing eyespots from the row of seven eyespots, with no detectable effect on the rest of the wing pattern. Offspring carrying a single <it>Missing </it>allele display intermediate sized eyespots at these positions. <it>Spotty </it>has the opposite effect of <it>Missing</it>, i.e., it introduces two extra eyespots in homologous wing positions to those affected by <it>Missing</it>, but on the forewing. When <it>Missing </it>is combined with <it>Spotty </it>the size of the two forewing eyespots decreases but the size of the hindwing spots stays the same, suggesting that these two mutations have a combined effect on the forewing such that <it>Missing </it>reduces eyespot size when in the presence of a <it>Spotty </it>mutant allele, but that <it>Spotty </it>has no effect on the hindwing. <it>Missing </it>prevents the complete differentiation of two of the eyespot foci on the hindwing. We found no evidence for any linkage between the <it>Distal-less </it>and <it>Missing </it>genes.</p> <p>Conclusion</p> <p>The spontaneous mutation <it>Missing </it>controls the differentiation of the signaling centers of a subset of the serial homologous eyespots present on both the fore and the hindwing in a dose-dependent fashion. The effect of <it>Missing </it>on the forewing, however, is only observed when the mutation <it>Spotty </it>introduces additional eyespots on this wing. <it>Spotty</it>, on the other hand, controls the differentiation of eyespot centers only on the forewing. <it>Spotty</it>, unlike <it>Missing</it>, may be under Ubx gene regulation, since it affects a subset of eyespots on only one of the serially homologous wings.</p