The Fifth one-day Evolutionary Developmental Biology Meeting was recently held in Oxford (September 13, 2004) and attracted a considerable crowd of researchers in the field from the UK and from overseas. The talks represented a variety of different approaches and perspectives in evolutionary developmental biology: from the mechanisms that produce developmental variation within populations to the patterns and processes of evolution across phyla and even the animal kingdom as a whole. Many of the speakers used some combination of mechanistic and comparative approaches, and the integration of these methods will surely produce further progress in the field. The program started with a talk by Tim Littlewood (Natural History Museum, London) on the evolution of life cycles in flatworms. Littlewood used a phylogenetic approach to track the history of the evolution of parasitic life styles. He demonstrated that drastic changes of life cycles and modes of transfer between hosts have occurred multiple times, and switches even between higher taxa of hosts have repeatedly occurred. As a result, the phylogenetic ‘‘ages’’ of the parasite and their host taxa do not coincide, contrary to a widespread view. Parasitism is an intriguing opportunity for studying the evolution of development, because the development of the parasite is intimately tied to that of its hosts throughout the life cycle. Peter Holland (University of Oxford) discussed the origin of multicellular animals. He first briefly discussed whether the origin of multicellularity might have coincided with a wholesale genome duplication. Comparisons between metazoan and yeast genomes do not support this hypothesis, but indicate that metazoans possess many families of genes that are not found in yeast or other eucaryotes. The problem with this comparison is that yeast is too distantly related to the metazoans to be fully informative. This gives a new urgency to the long-standing problem regarding the uncertainty about the sister-group of metazoans. Holland’s lab has conducted phylogenetic analyses that clearly point to choanoflagellates, a heterogenous group with mainly single-celled and a few colonial species, as the sister-group of the metazoans. First results from genome studies in the choanoflagellate Monosiga ovata are most promising. Holland presented the example of the Hoglet gene of M. ovata and its similarity to the hedgehog gene family of the metazoans. Hoglet and the hedgehog genes share an autocatalytic domain with similar characteristics. Hoglet is a protein that undergoes autocatalytic cleavage just as hedgehog genes do, but it differs from them because it is not a signaling molecule. Its function is unclearFit contains a CBD-II (cellulose-binding domain) not found in metazoans, as well as a very long threonine repeat. Hoglet and the hedgehogs provide a fascinating opportunity for studying the evolution of signaling, one of the central features of multicellularity. Further studies of the genomes of choanoflagellates and the basal metazoans (sponges, Placozoa, etc.) are likely to shed more light on this question in the near future. Claudio Alonso (University of Cambridge) and Adam Wilkins (BioEssays) presented a shared talk in which they challenged the view that enhancer elements are the only, or the predominant, sites for genetic control of gene regulation, and therefore are the primary target for the evolution of developmental processes. In the first section of the talk, Alonso showed some quotes from prominent evo-devo researchers stating forcefully that cis-regulatory control is all evolution is about, and that indeed there is a sort of ‘‘enhancer cult.’’ He then went on to point out how many different players are involved in the regulation of gene expression, both at the transcriptional and posttranscriptional levels: the whole transcriptional machinery and the basal promoter to which it binds, translational regulation, and alternative splicing. All these components, or alternative regulatory points (ARPs), might well contribute to variation that is relevant for the evolution of gene expression. But do they? A short survey of some examples illustrated that mutations of ARPs have been described often, and that a large proportion of mutations may affect ARPs. Around 10–15% of known human disease mutations are at splice sites, and it is likely that splicing is also affected by additional mutations that are not located directly at these sites. Moreover, about 75% of human genes undergo alternative splicing, providing scope for considerable variation in expression. And splicing is just one example of an ARP. Wilkins outlined that ARPs have many of the features, like flexibility and modularity, which have made enhancers attractive as a mechanism for explaining standing genetic EVOLUTION & DEVELOPMENT 7:1, 1–2 (2005)
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Jan 1, 2006
Maximilian J Telford + 1
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