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Exploring systemic RNA interference in insects: a genome-wide survey for RNAi genes in Tribolium

Yoshinori Tomoyasu12*, Sherry C Miller12, Shuichiro Tomita3, Michael Schoppmeier4, Daniela Grossmann5 and Gregor Bucher5

Author affiliations

1 Division of Biology, Kansas State University, Manhattan, Kansas 66506, USA

2 K-State Arthropod Genomics Center, Kansas State University, Manhattan, Kansas 66506, USA

3 Insect Genome Research Unit, National Institute of Agrobiological Sciences, 1-2, Owashi, Tsukuba, Ibaraki 305-8634, Japan

4 Universitat Erlangen, Institut fur Biologie, Abteilung fur Entwicklungsbiologie, Staudtstr., D-91058 Erlangen, Germany

5 Johann-Friedrich-Blumenbach-Institut für Zoologie und Anthropologie, Georg-August-Universität Göttingen, Abteilung Entwicklungsbiologie, Justus-von-Liebig-Weg, 37077 Göttingen, Germany

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Citation and License

Genome Biology 2008, 9:R10  doi:10.1186/gb-2008-9-1-r10

Published: 17 January 2008



RNA interference (RNAi) is a highly conserved cellular mechanism. In some organisms, such as Caenorhabditis elegans, the RNAi response can be transmitted systemically. Some insects also exhibit a systemic RNAi response. However, Drosophila, the leading insect model organism, does not show a robust systemic RNAi response, necessitating another model system to study the molecular mechanism of systemic RNAi in insects.


We used Tribolium, which exhibits robust systemic RNAi, as an alternative model system. We have identified the core RNAi genes, as well as genes potentially involved in systemic RNAi, from the Tribolium genome. Both phylogenetic and functional analyses suggest that Tribolium has a somewhat larger inventory of core component genes than Drosophila, perhaps allowing a more sensitive response to double-stranded RNA (dsRNA). We also identified three Tribolium homologs of C. elegans sid-1, which encodes a possible dsRNA channel. However, detailed sequence analysis has revealed that these Tribolium homologs share more identity with another C. elegans gene, tag-130. We analyzed tag-130 mutants, and found that this gene does not have a function in systemic RNAi in C. elegans. Likewise, the Tribolium sid-like genes do not seem to be required for systemic RNAi. These results suggest that insect sid-1-like genes have a different function than dsRNA uptake. Moreover, Tribolium lacks homologs of several genes important for RNAi in C. elegans.


Although both Tribolium and C. elegans show a robust systemic RNAi response, our genome-wide survey reveals significant differences between the RNAi mechanisms of these organisms. Thus, insects may use an alternative mechanism for the systemic RNAi response. Understanding this process would assist with rendering other insects amenable to systemic RNAi, and may influence pest control approaches.