Evolutionary developmental biology and genomics

Abstract

Evolutionary developmental biology faces reciprocal paradoxes: the conservation of similar developmental genetic toolkits despite a diversity of life forms, and the inverse paradox — the development of similar morphologies despite the phylogenetically variable presence of the genetic tools that are thought to be responsible for those forms. Phylogenomic analysis, when carried out with care for possible pitfalls, can indicate the orientation of trait gain and loss among diverging lineages. Comparative genomic analysis correlated to the loss of an ancestral trait can identify candidate genes that are responsible for the development of that trait. Genome contractions in various lineages have diminished genetic toolkits for DNA methylation and for retinoic acid signalling, providing examples of the inverse paradox. It is thought that changes in genome architecture might have disrupted regulatory mechanisms that depend on chromosome territories or long-range enhancers, which would have decreased the importance of genome methylation and patterning by distantly diffusible signals in some animals with determinative development and rapid life cycles. Genome expansion, for example, by whole-genome duplication events, can result in the complementary degeneration of gene subfunctions leading to the reduction of pleiotropy and subsequent evolution of toolkit components that are specialized for precise developmental functions, as illustrated by fibroblast growth factor (Fgf) family genes. Genome architecture can, in some cases, be related to conserved non-coding elements that act as enhancers located far from the genes they encode; fitness penalties for disrupting these relationships can explain certain human developmental diseases and syntenies that have been conserved over evolutionary time. These examples show that genomics bridges the gap between evolutionary biology and developmental biology.