This week’s BEACON Researchers at Work post is by Michigan State University graduate student Austin Dreyer.
Variation is one of the most obvious themes in biology. From variation between taxonomic groups, morphological traits, behavioral responses, habitats, and so on, we are constantly bombarded by the presence and importance of variability in the world around us. An oftentimes less obvious component of biology, however, is how populations maintain an optimal trait value in the face of inevitable environmental and genetic disturbance. Answering this question has been the focus of research for decades, and has caught my attention as well. Indeed, the first time I really considered how any sort of constancy in phenotype is achieved through time given how unpredictable nature can be I was surprised I had not recognized this impressive feat sooner.
One of the pioneering ideas to describe how phenotypic constancy occurs comes from C.H. Waddington in the early part of the 20th century. His conceptualization of phenotypes revolved around developmental ‘channels’ being formed through generations of selection for a consistent trait value. Waddington postulated that the deeper those channels became through repeated selection, the more resistant the trait was to genetic or environmental perturbations. He termed this phenomenon ‘canalization’ in direct reference to the channels of development that helped to ensure beneficial traits were reproduced with a high degree of fidelity. Since Waddington’s introduction of this concept, much research has been done on the topic, and it is likely no surprise that there is considerable contention regarding what the meaning of canalization really is and how it arises. For the purposes of this discussion, however, I stick to a broad definition of canalization as developmental buffering, or, any mechanism that reduces the effect of environmental and genetic variation on a trait.
The interest in canalization over the years encompasses not only how it has evolved, but also its potential as a driver of evolutionary divergence. Given a working definition of canalization as developmental buffering from environmental and genetic effects, it is possible for genetic variation to accumulate under the umbrella of a trait’s development being canalized. This cryptic genetic variation can then be exposed given a large enough environmental perturbation, potentially acting as a source of novel phenotypes. It is a bit counterintuitive that a process defined as reducing phenotypic variance could contribute to the introduction of new variance, but the buildup of genetic variation made possible by canalization is thought to do just that. Additionally, canalization is often divided into two types, environmental and genetic, and there are numerous mechanisms through which canalization is thought to occur including basic genetic principles such as dominance, molecular chaperones, a result of the complexity of gene networks and due to components of developmental pathways. While much has been studied, clearly much research remains to be done.
My research focuses on looking for canalization mechanisms that are intrinsic to the developmental pathways they occur in, that is, canalization of a trait as a result of the composition of the pathways giving rise to that trait. Specifically, I am looking at canalization mechanisms using the Avida system in collaboration with Carlos Anderson and the model organism Drosophila melanogaster.
To test for the presence of intrinsic genetic canalization mechanisms in Avida, we first evolved populations of Avidians in environments with various mutation rates. We then measured genetic canalization by generating every single-mutant for each population and measuring their fitness. Mutationally canalized organisms should be robust to these introduced mutations and we did find that populations evolved under high mutation rates were more canalized than populations evolved under low mutation rates (Figure 1). To test for the presence of intrinsic environmental canalization mechanisms we evolved several digital populations in environments with various probabilities of instruction failure (“disturbed environment”). Environmental canalization was measured by subjecting the ancestral and evolved populations to a disturbed environment and calculating their respective fitnesses. We found that the evolved populations were more environmentally canalized than the ancestral population. For both types of canalization, our next step is to determine whether the mutations that helped canalize these populations were also involved in performing tasks, classifying them as intrinsic mechanisms.
The Drosophila portion of my research involves modifying expression of a known developmental pathway, the insulin-signaling pathway, to test for intrinsic genetic canalization. Using the standard genetic tools that make Drosophila such a powerful study system I will be tinkering with the expression levels of an important component of the insulin-signaling pathway. To establish causation of a specific component of the insulin-signaling pathway controlling genetic canalization, I predict that there will be a relationship between expression levels of the pathway and expressed genetic variation. This research is ongoing, but when completed it has the potential to be one of the first demonstrations of a genetic canalization mechanism that is part of the developmental pathway it canalizes.
The far-reaching implications of canalization have sustained its study for decades, and the attention is well deserved. From its enigmatic potential as a source of evolutionary novelty to the range of mechanisms it can act through to its contested explanation for how constancy of phenotype is maintained, the concept of canalization continues to promise great discoveries relating to development and evolution. For me, I am most excited about unpacking another biological concept that explains how life persists in the face of so much change.
For more information about Austin’s work, you can contact him at dreyerau at gmail dot com.