Abstract
Although two related species may have extremely similar phenotypes, the genetic networks underpinning this conserved biology may have diverged substantially since they last shared a common ancestor. This is termed Developmental System Drift (DSD) and reflects the plasticity of genetic networks. One consequence of DSD is that some orthologous genes will have evolved different in vivo functions in two such phenotypically similar, related species and will therefore have different loss of function phenotypes. Here we report an RNAi screen in C. elegans and C. briggsae to identify such cases. We screened 1333 genes in both species and identified 91 orthologues that have different RNAi phenotypes. Intriguingly, we find that recently evolved genes of unknown function have the fastest evolving in vivo functions and, in several cases, we identify the molecular events driving these changes. We thus find that DSD has a major impact on the evolution of gene function and we anticipate that the C. briggsae RNAi library reported here will drive future studies on comparative functional genomics screens in these nematodes.
Highlights
As genomes evolve, new genes are born and older genes may adopt novel functions, fuse, or disappear altogether
We decided to construct a library targeting only the set of 1437 C. briggsae genes that had direct 1:1 orthologues with the 1640 genes which were previously shown to have a robust, readily detectable RNAmediated interference (RNAi) phenotype in C. elegans [14]. This excludes a small number of genes that have no apparent phenotype in C. elegans but that have a phenotype in C. briggsae, this set will cover the great majority of genes that have phenotypes in C. briggsae
We made the library according to the same design principles as the C. elegans RNAi library [13,14], and as far as possible targeted an orthologous region of the C. briggsae gene as was targeted by the C. elegans RNAi fragment (Figure S1B)
Summary
New genes are born and older genes may adopt novel functions, fuse, or disappear altogether. New organism-level phenotypes can result from the rewiring of already existing activities such as the shuffling of existing domains into novel combinations (e.g. the rapidly evolving architectures of chromatin regulators [1]) or through changes in the regulation of expression of otherwise conserved genes — for example, evolution of lin-48 expression affects salt tolerance in C. elegans [2], evolution of the yellow gene alters wing spots in different Drosophila species [3], and evolution at the Pitx locus causes adaptive loss of pelvic spines in sticklebacks [4]. Many genomic changes have no impact on the phenotype of the organism since they do not have any impact on the molecular phenotype, that is, on the functions encoded in the genome and their precise regulation Such changes are under no selection — while they may disappear or become fixed in a species, neither outcome is a consequence of their effect on phenotype
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