HSP90 buffers newly induced mutations in massively mutated plant lines
Robustness to both genetic and environmental change is an emergent feature of living systems. Loss of phenotypic robustness can be associated with increased penetrance of genetic variation. In model organisms and in humans, the phenotypic consequences of standing genetic variation can be buffered by the molecular chaperone HSP90. However, it has been argued that HSP90 has the opposite effect on newly introduced genetic variation. To test the buffering effect of HSP90 on new mutations, we introduced vast numbers of mutations into wild-type and HSP90-reduced plants and assessed embryonic lethality and early seedling phenotypes for thousands of offspring. Although the levels of newly introduced mutations were similar in the two backgrounds, the HSP90-reduced plants showed a significantly greater frequency of embryonic lethality and severe phenotypic abnormalities, consistent with higher penetrance and expressivity of newly introduced genetic variation. We further demonstrate that some mutant phenotypes were heritable in an HSP90-dependent manner, and we map candidate HSP90-dependent polymorphisms. Moreover, both sequence and phenotypic analyses of wild-type and HSP90-reduced plants suggest that the HSP90-dependent phenotypes are largely due the newly introduced mutations rather than to an increased mutation rate in HSP90-reduced plants. Taken together, our results support a model in which HSP90 buffers newly introduced mutations, and the phenotypic consequences of such mutations outweigh those of mutations arising de novo in response to HSP90 perturbation.