Mechanisms of buffering of phenotypic variation in A. thaliana: Features of HSP90 and characterization of AGO1 as a new regulator of robustness

Abstract

Biological systems have molecular mechanisms that allow them to maintain a constant phenotype despite environmental and genetic perturbations. These mechanisms can take the form of master regulator of robustness, gene products that are epistatic to environmental and genetic perturbations. When these regulators are perturbed, the phenotypic variation of the biological systems increases. The best example of a master regulator of robustness is HSP90. HSP90 interacts with proteins involved in different biological pathways, and thus is a central node of many genetic networks. HSP90 provides robustness to environmental and genetic perturbations, and it has been hypothesized that influences the evolution of its clients. Here, I provide evidence that HSP90 impacts the evolutionary trajectories of clients belonging to pairs of duplicate genes or gene families. MicroRNAs (miRNAs) have been shown to provide robustness to environmental and genetic perturbations of specific phenotypic traits. The central node of the miRNA pathway in A. thaliana is AGO1. In my thesis, I show that AGO1 is another master regulator of robustness, since AGO1 can buffer both environmental and genetic perturbations for a variety of traits. I also show that AGO1-dependent variation is background specific. Two of the AGO1-revealed phenotypes, lesions in cotyledons and lack of correlation between days to flowering and leaf number were analyzed to further detail.