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Decanalizing thinking on genetic canalization.

ABSTRACT: The concept of genetic canalization has had an abiding influence on views of complex-trait evolution. A genetically canalized system has evolved to become less sensitive to the effects of mutation. When a gene product that supports canalization is compromised, the phenotypic impacts of a mutation should be more pronounced. This expected increase in mutational effects not only has important consequences for evolution, but has also motivated strategies to treat disease. However, recent studies demonstrate that, when putative agents of genetic canalization are impaired, systems do not behave as expected. Here, we review the evidence that is used to infer whether particular gene products are agents of genetic canalization. Then we explain how such inferences often succumb to a converse error. We go on to show that several candidate agents of genetic canalization increase the phenotypic impacts of some mutations while decreasing the phenotypic impacts of others. These observations suggest that whether a gene product acts as a 'buffer' (lessening mutational effects) or a 'potentiator' (increasing mutational effects) is not a fixed property of the gene product but instead differs for the different mutations with which it interacts. To investigate features of genetic interactions that might predispose them toward buffering versus potentiation, we explore simulated gene-regulatory networks. Similarly to putative agents of genetic canalization, the gene products in simulated networks also modify the phenotypic effects of mutations in other genes without a strong overall tendency towards lessening or increasing these effects. In sum, these observations call into question whether complex traits have evolved to become less sensitive (i.e., are canalized) to genetic change, and the degree to which trends exist that predict how one genetic change might alter another's impact. We conclude by discussing approaches to address these and other open questions that are brought into focus by re-thinking genetic canalization.

SUBMITTER: Geiler-Samerotte K

PROVIDER: S-EPMC6252154 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Decanalizing thinking on genetic canalization.

Geiler-Samerotte Kerry K Sartori Federica M O FMO Siegal Mark L ML

Seminars in cell & developmental biology 20180524

The concept of genetic canalization has had an abiding influence on views of complex-trait evolution. A genetically canalized system has evolved to become less sensitive to the effects of mutation. When a gene product that supports canalization is compromised, the phenotypic impacts of a mutation should be more pronounced. This expected increase in mutational effects not only has important consequences for evolution, but has also motivated strategies to treat disease. However, recent studies dem ...[more]

PMID: 29751086

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Project description:Natural populations exhibit substantial variation in quantitative traits. A quantitative trait is typically defined by its mean and variance, and to date most genetic mapping studies focus on loci altering trait means but not (co)variances. For single traits, the control of trait variance across genetic backgrounds is referred to as genetic canalization. With multiple traits, the genetic covariance among different traits in the same environment indicates the magnitude of potential genetic constraint, while genotype-by-environment interaction (GxE) concerns the same trait across different environments. While some have suggested that these three attributes of quantitative traits are different views of similar concepts, it is not yet clear, however, whether they have the same underlying genetic mechanism. Here, we detect quantitative trait loci (QTL) influencing the (co)variance of phenological traits in six distinct environments in Boechera stricta, a close relative of Arabidopsis. We identified nFT as the QTL altering the magnitude of phenological trait canalization, genetic constraint, and GxE. Both the magnitude and direction of nFT's canalization effects depend on the environment, and to our knowledge, this reversibility of canalization across environments has not been reported previously. nFT's effects on trait covariance structure (genetic constraint and GxE) likely result from the variable and reversible canalization effects across different traits and environments, which can be explained by the interaction among nFT, genomic backgrounds, and environmental stimuli. This view is supported by experiments demonstrating significant nFT by genomic background epistatic interactions affecting phenological traits and expression of the candidate gene, FT. In contrast to the well-known canalization gene Hsp90, the case of nFT may exemplify an alternative mechanism: Our results suggest that (at least in traits with major signal integrators such as flowering time) genetic canalization, genetic constraint, and GxE may have related genetic mechanisms resulting from interactions among major QTL, genomic backgrounds, and environments.

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Decanalizing thinking on genetic canalization.

Publications

Decanalizing thinking on genetic canalization.

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