Research in the laboratory investigates the evolution and development of morphology. We’re particularly interested in the interplay of nature and nurture in affecting final adult morphology. We use a variety of approaches including genetics, genomics, and developmental biology.

Our study system is the pea aphid. Aphids are remarkable insects, able to produce a variety of morphologies across their complex life cycles that alternate between asexual and sexual development. During the asexual phase, females are often wingless and specialize in the mass production of genetically identical wingless daughters. However, if their host plant becomes too crowded, those same females can switch to producing daughter that have wings as adults so that those daughters can fly away and find better food sources. Thus, winged and wingless females of pea aphids are genetically identical yet morphologically very different. How these alternative morphologies are produced is one of the main questions we address in the lab.

During their sexual phase in the fall, pea aphids produce winged and wingless males as well. However, unlike the females the males are not genetically identical and their morphology is not determined by environmental circumstances. Rather, adult male morphology appears to be under the control of a single locus on the X chromosome called aphicarus.

Ongoing projects in the lab include:

1. Understanding the male wing dimorphism system. Males are winged and wingless in some species, but monomorphic in others. How has this trait evolved across aphid species? What is the genetic basis of wing dimorphism and is that mechanism the same or different across species?

2. Discovering the molecular mechanisms underlying developmental plasticity in pea aphid asexual females. How does a pea aphid mother sense her environment and pass that information on to her developing embryos? How does the developmental timing of environmental sensitivity differ among aphid species?

3. Investigating genetic variation for the female polyphenism. We’ve observed that aphid lines respond to high density environments differently. How extensive is this variation in nature? What genes underlie this plasticity variation?

What have we found so far?

Work in the lab has contributed to the evo-devo/evolutionary genomics field by identifying the genetic basis of winged versus wingless pea aphid males: a derived insertion carrying a duplicated follistatin homolog. This is the first time the molecular basis of a wing polymorphism has been identified, despite their repeated evolution across most Orders of insects. We have also demonstrated that this dramatic phenotypic difference is due to a structural variant, and thus have shown that mutations of relatively large effect can play an important role in adaptive evolution. The discovery of these types of structural variants underlying morphological adaptations have largely gone undetected to date (at least, compared to SNPs) due to limitation of genomic and sequencing methods. Future work by us and others is likely to uncover additional cases of structural variants underlying morphological evolution in the future. See Li et al. (2020) for more information.

The lab has also contributed important information to the field’s understanding of the mechanistic basis of phenotypic plasticity. Historically, this information has been limited and primarily focused on the hormonal basis of plasticity in a handful of systems. We have developed the pea aphid female wing/wingless dimorphism as a model system for studying the mechanistic basis of phenotypic plasticity. This system provides a worthwhile addition because aphids have a transgenerational plasticity–the mother aphid processes environmental cues and transmits that information to her developing embryos; analogous to maternal effects in humans. We’ve determined the endocrine basis of the aphid plasticity (see Vellichirammal et al. 2017) and intensively interrogated the transcriptional response to environmental cues (e.g., see Grantham et al. 2019 and Parker et al. 2021). As a result of this work, we have generalized what is known about plasticities: we’ve shown that ecdysone and insulin signaling remain important even in this transgenerational plasticity. We have also significantly extended the field by showing not only that variation for the plasticity exists, but that some of that variation is mediated by a horizontally transferred gene (see Parker et al. 2019). An open question that remains in the field is: how does plasticity evolve? Does it evolve by changes to genes within the developmental network that controls the plasticity or by genes outside that network? Horizontally transferred genes are clearly outside the network, so we’ve provided an intriguing answer to that question.