Abstract

It is generally accepted that new genes arise via duplication and functional divergence of existing genes, in accordance with Ohno's model [1], now called “Mutation During Redundancy,” or MDR [2]. In this model, one of the two gene copies is free to acquire novel (although likely related) activities through mutation, since only one copy is required for its original function. However, duplication within a genome is not the only process that might give rise to this situation: acquisition of a functionally redundant gene by lateral gene transfer (LGT) could also initiate the MDR process. Here we describe a probable instance, involving LGT of an archaeal or eukaryotic elongation factor 1α (EF-1α) gene. The large subunit of ATP sulfurylase (CysN or the N-terminal portion of NodQ), found mainly in proteobacteria, is clearly related to translation elongation factors [3, 4]. However, our analyses show that cysN arose from an EF-1α gene initially acquired by LGT, not from a within-genome duplication of the resident EF-Tu gene. To our knowledge, this is the first unequivocal case of LGT followed by functional modification to be described; this mechanism could be a potentially important force in establishing genes with novel functions in genomes.

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