Meeting Abstract
Canalization is a result of intrinsic developmental buffering that ensures phenotypic robustness under genetic variation and environmental perturbation. As a consequence, animal phenotypes are remarkably consistent within a species under a wide range of conditions, a property that seems contradictory to evolutionary change. Study of laboratory model species has uncovered several possible canalization mechanisms, however we still do not understand how the level of buffering is controlled or whether these mechanisms are important for natural populations. We exploit wild populations of the marine chordate Ciona intestinalis to show that levels of buffering are maternally inherited. Comparative transcriptomics show expression levels of genes encoding canonical chaperones such as HSP70 and HSP90 do not correlate with buffering. However the expression of genes encoding endoplasmic reticulum (ER) chaperones does correlate. Furthermore, pharmacological impairment of ER function also reduces buffering levels. We also show that these ER chaperone genes are widely conserved amongst animals, and that their experimental knockdown compromises developmental robustness in the nematode Caenorhabditis elegans. These results show ER associated chaperones comprise a cellular basis for canalization, and that variation in their expression in natural populations may explain variation in the ability of embryos to buffer environmental insult. ER chaperones have been neglected by the fields of development, evolution and ecology, but their study will enhance understanding of both our evolutionary past and the impact of global environmental change.
