IP3 signalling regulates exogenous RNAi in Caenorhabditis elegans.
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Authors
Nagy, Anikó I
Vázquez-Manrique, Rafael P
Lopez, Marie
Christov, Christo P
Sequedo, María Dolores
Abstract
RNA interference (RNAi) is a widespread and widely exploited phenomenon. Here, we show that changing inositol 1,4,5-trisphosphate (IP3) signalling alters RNAi sensitivity in Caenorhabditis elegans. Reducing IP3 signalling enhances sensitivity to RNAi in a broad range of genes and tissues. Conversely up-regulating IP3 signalling decreases sensitivity. Tissue-specific rescue experiments suggest IP3 functions in the intestine. We also exploit IP3 signalling mutants to further enhance the sensitivity of RNAi hypersensitive strains. These results demonstrate that conserved cell signalling pathways can modify RNAi responses, implying that RNAi responses may be influenced by an animal's physiology or environment.
Description
Keywords
C. elegans, RNA interference, calcium signalling, enhanced RNAi, inositol 1,4,5‐trisphosphate, Animals, Caenorhabditis elegans, Image Processing, Computer-Assisted, Inositol 1,4,5-Trisphosphate, Intestinal Mucosa, Microscopy, Fluorescence, Models, Biological, RNA Interference, RNA, Double-Stranded, Signal Transduction
Journal Title
EMBO Rep
Conference Name
Journal ISSN
1469-221X
1469-3178
1469-3178
Volume Title
16
Publisher
Wiley-VCH Verlag
Publisher DOI
Sponsorship
Medical Research Council (G0601106)
We thank A. Fire, K. Ford, S. Mitani and H. Peterkin for the provision of plasmids and strains. Some strains were provided by the CGC, which is funded by NIH Office of Research Infrastructure Programs (P40 OD010440). Other strains were provided by the Mitani Lab through the National Bio‐Resource Project of the MEXT, Japan. We are grateful to J. Ahringer, B. Olofsson and members of the Baylis group for helpful discussions. AIN was funded by Trinity Hall College, Cambridge and the Cambridge European Trust. The work of MDS and RPV‐M was partially funded by a Miguel Servet Grant (CP11/00090) from the Health Research Institute Carlos III, which is partially supported by the European Regional Development Fund. RPV‐M is a Marie Curie fellow (CIG322034). RG was funded by the MRC (G0601106).