Evolutionary conservation of redundancy between a diverged pair of forkhead transcription factor homologues

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Abstract
The Caenorhabditis elegans gene pes-1 encodes a transcription factor of the forkhead family and is expressed in specific cells of the early embryo. Despite these observations suggesting pes-1 to have an important regulatory role in embryogenesis, inactivation of pes-1 caused no apparent phenotype. This lack of phenotype is a consequence of genetic redundancy. Whereas a weak, transitory effect was observed upon disruption of just T14G12.4 (renamed fkh-2) gene function, simultaneous disruption of the activity of both fkh-2 and pes-1 resulted in a penetrant lethal phenotype. Sequence comparison suggests these two forkhead genes are not closely related and the functional association of fkh-2 and pes-1 was only explored because of the similarity of their expression patterns. Conservation of the fkh-2/pes-1 genetic redundancy between C. elegans and the related species C. briggsae was demonstrated. Interestingly the redundancy in C. briggsae is not as complete as in C. elegans and this could be explained by alterations of pes-1 specific to the C. briggsae ancestry. With overlapping function retained on an evolutionary time-scale, genetic redundancy may be extensive and expression pattern data could, as here, have a crucial role in characterization of developmental processes.