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Synthetic lethal analysis of Caenorhabditis elegans posterior embryonic patterning genes identifies conserved genetic interactions

L Ryan Baugh13, Joanne C Wen1, Andrew A Hill2, Donna K Slonim24, Eugene L Brown2 and Craig P Hunter1*

Author Affiliations

1 Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA

2 Department of Genomics, Wyeth Research, Cambridge, MA 02140, USA

3 Current address: Biology Division, California Institute of Technology, Pasadena, CA 91125

4 Current address: Department of Computer Science, Tufts University, Medford, MA 02155

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Genome Biology 2005, 6:R45  doi:10.1186/gb-2005-6-5-r45

Published: 11 April 2005


Phenotypic robustness is evidenced when single-gene mutations do not result in an obvious phenotype. It has been suggested that such phenotypic stability results from 'buffering' activities of homologous genes as well as non-homologous genes acting in parallel pathways. One approach to characterizing mechanisms of phenotypic robustness is to identify genetic interactions, specifically, double mutants where buffering is compromised. To identify interactions among genes implicated in posterior patterning of the Caenorhabditis elegans embryo, we measured synthetic lethality following RNA interference of 22 genes in 15 mutant strains. A pair of homologous T-box transcription factors (tbx-8 and tbx-9) is found to interact in both C. elegans and C. briggsae, indicating that their compensatory function is conserved. Furthermore, a muscle module is defined by transitive interactions between the MyoD homolog hlh-1, another basic helix-loop-helix transcription factor, hnd-1, and the MADS-box transcription factor unc-120. Genetic interactions within a homologous set of genes involved in vertebrate myogenesis indicate broad conservation of the muscle module and suggest that other genetic modules identified in C. elegans will be conserved.