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Synopsis Gene duplicates, or paralogs, serve as a major source of new genetic material and comprise seeds for evolutionary innovation. While originally thought to be quickly lost or nonfunctionalized following duplication, now a vast number of paralogs are known to be retained in a functional state. Daughter paralogs can provide robustness through redundancy, specialize via sub-functionalization, or neo-functionalize to play new roles. Indeed, the duplication and divergence of developmental genes have played a monumental role in the evolution of animal forms (e.g., Hox genes). Still, despite their prevalence and evolutionary importance, the precise detection of gene duplicates in newly sequenced genomes remains technically challenging and often overlooked. This presents an especially pertinent problem for evolutionary developmental biology, where hypothesis testing requires accurate detection of changes in gene expression and function, often in nontraditional model species. Frequently, these analyses rely on molecular reagents designed within coding sequences that may be highly similar in recently duplicated paralogs, leading to cross-reactivity and spurious results. Thus, care is needed to avoid erroneously assigning diverged functions of paralogs to a single gene, and potentially misinterpreting evolutionary history. This perspective aims to overview the prevalence and importance of paralogs and to shed light on the difficulty of their detection and analysis while offering potential solutions. 

A fundamental focus of evolutionary-developmental biology is uncovering the genetic mechanisms responsible for the gain and loss of characters. One approach to this question is to investigate changes in the coordinated expression of a group of genes important for the development of a character of interest (a gene regulatory network). Here we consider the possibility that modifications to the wing gene regulatory network (wGRN), as defined by work primarily done in Drosophila melanogaster, were involved in the evolution of wing dimorphisms of the pea aphid (Acyrthosiphon pisum). We hypothesize that this may have occurred via changes in expression levels or duplication followed by sub-functionalization of wGRN components. To test this, we annotated members of the wGRN in the pea aphid genome and assessed their expression levels in first and third nymphal instars of winged and wingless morphs of males and asexual females. We find that only two of the 32 assessed genes exhibit morph-biased expression. We also find that three wing genes (apterous (ap), warts (wts), and decapentaplegic (dpp)) have undergone gene duplication. In each case, the resulting paralogs show signs of functional divergence, exhibiting either sex-, morph-, or stage-specific expression. Two gene duplicates, wts2 and dpp3, are of particular interest with respect to wing dimorphism, as they exhibit a wingless male-specific isoform and wingless male-biased expression, respectively. These results supplement our understanding of trends in developmental gene network evolution, such as side-stepping pleiotropic constraint via duplication and sub-functionalization, underlying the emergence of novel phenotypes. 

Understanding how morphology evolves requires identifying the types of mutations that contribute to changes in development. We integrated comparative genomics and transcriptomics to reconstruct the evolution and regulation offollistatinparalogs in relation to the evolution of aphid winged and wingless morphs. We find that different pea aphidfollistatinduplicates play an essential molecular role in both the male and female wing dimorphisms, linking the genetic and environmental control of morph determination in each sex, respectively. We also find that an ancestralfollistatingene likely had multiple promoters and that thefollistatinduplicates that evolved wingless-specific expression retained only the ancestral wingless-specific promoter. Our work provides a roadmap for how alternative promoter usage and subsequent gene duplication can enable the evolution of animal form. 

Aphids present a fascinating example of phenotypic plasticity, in which a single genotype can produce dramatically different winged and wingless phenotypes that are specialized for dispersal versus reproduction, respectively. Recent work has examined many aspects of this plasticity, including its evolution, molecular control mechanisms, and genetic variation underlying the trait. In particular, exciting discoveries have been made about the signaling pathways that are responsible for controlling the production of winged versus wingless morphs, including ecdysone, dopamine, and insulin signaling, and about how specific genes such as REPTOR2 and vestigial are regulated to control winglessness. Future work will likely focus on the role of epigenetic mechanisms, as well as developing transgenic tools for more thoroughly dissecting the role of candidate plasticity-related genes.