A Genome-Wide Screen Identifies 27 Genes Involved in Transposon Silencing in C. elegans

• Published in: Current biology Vol. 13; no. 15; pp. 1311 - 1316
• Main Authors: Vastenhouw, Nadine L., Fischer, Sylvia E.J., Robert, Valérie J.P., Thijssen, Karen L., Fraser, Andrew G., Kamath, Ravi S., Ahringer, Julie, Plasterk, Ronald H.A.
• Format: Journal Article
• Language: English
• Published: England Elsevier Inc 05.08.2003
• Subjects: Animals; Caenorhabditis elegans - genetics; Chromosome Mapping; DNA Transposable Elements - genetics; Gene Expression Profiling; Genome; Genomic Instability - genetics; RNA Interference; Suppression, Genetic - genetics
• ISSN: 0960-9822; 1879-0445
• DOI: 10.1016/S0960-9822(03)00539-6

Transposon jumps are a major cause of genome instability. In the C. elegans strain Bristol N2, transposons are active in somatic cells, but they are silenced in the germline [1], presumably to protect the germline from mutations. Interestingly, the transposon-silencing mechanism shares factors with the RNAi machinery [2]. To better understand the mechanism of transposon silencing, we performed a genome-wide RNAi screen for genes that, when silenced, cause transposition of Tc1 in the C. elegans germline. We identified 27 such genes, among which are mut-16, a mutator that was previously found but not identified at the molecular level, ppw-2, a member of the argonaute family, and several factors that indicate a role for chromatin structure in the regulation of transposition. Some of the newly identified genes are also required for cosuppression and therefore represent the shared components of the two pathways. Since most of the newly identified genes have clear homologs in other species, and since transposons are found from protozoa to human, it seems likely that they also protect other genomes against transposon activity in the germline.