1. Uncovering buffered pleiotropy: a genome-scale screen for mel-28 genetic interactors in Caenorhabditis elegans.
- Author
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Fernandez AG, Mis EK, Lai A, Mauro M, Quental A, Bock C, and Piano F
- Subjects
- Animals, Caenorhabditis elegans growth & development, Caenorhabditis elegans Proteins antagonists & inhibitors, Caenorhabditis elegans Proteins metabolism, Chromosome Segregation, DNA-Binding Proteins, Dyneins metabolism, Heterozygote, Larva genetics, Larva metabolism, Nuclear Pore genetics, Nuclear Pore metabolism, Nuclear Proteins antagonists & inhibitors, Nuclear Proteins metabolism, Phenotype, RNA Interference, Transport Vesicles metabolism, Caenorhabditis elegans genetics, Caenorhabditis elegans Proteins genetics, Genetic Pleiotropy, Genome, Nuclear Proteins genetics
- Abstract
mel-28 (maternal-effect-lethal-28) encodes a conserved protein required for nuclear envelope function and chromosome segregation in Caenorhabditis elegans. Because mel-28 is a strict maternal-effect lethal gene, its function is required in the early embryo but appears to be dispensable for larval development. We wanted to test the idea that mel-28 has postembryonic roles that are buffered by the contributions of other genes. To find genes that act coordinately with mel-28, we did an RNA interference-based genetic interaction screen using mel-28 and wild-type larvae. We screened 18,364 clones and identified 65 genes that cause sterility in mel-28 but not wild-type worms. Some of these genes encode components of the nuclear pore. In addition we identified genes involved in dynein and dynactin function, vesicle transport, and cell-matrix attachments. By screening mel-28 larvae we have bypassed the requirement for mel-28 in the embryo, uncovering pleiotropic functions for mel-28 later in development that are normally provided by other genes. This work contributes toward revealing the gene networks that underlie cellular processes and reveals roles for a maternal-effect lethal gene later in development.
- Published
- 2014
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