High resolution transcriptome maps for wild-type and NMD mutant C. elegans through development
View / Open Files
Ramani, Arun K.
Nelson, Andrew C.
Gingeras, Thomas R.
Fraser, Andrew G.
MetadataShow full item record
Ramani, A. K., Nelson, A. C., Kapranov, P., Bell, I., Gingeras, T. R., & Fraser, A. G. (2009). High resolution transcriptome maps for wild-type and NMD mutant C. elegans through development. https://doi.org/10.1186/gb-2009-10-9-r101
RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are.
Abstract Background While many genome sequences are complete, transcriptomes are less well characterized. We used both genome-scale tiling arrays and massively parallel sequencing to map the Caenorhabditis elegans transcriptome across development. We utilized this framework to identify transcriptome changes in animals lacking the nonsense-mediated decay (NMD) pathway. Results We find that while the majority of detectable transcripts map to known gene structures, >5% of transcribed regions fall outside current gene annotations. We show that >40% of these are novel exons. Using both technologies to assess isoform complexity, we estimate that >17% of genes change isoform across development. Next we examined how the transcriptome is perturbed in animals lacking NMD. NMD prevents expression of truncated proteins by degrading transcripts containing premature termination codons. We find that approximately 20% of genes produce transcripts that appear to be NMD targets. While most of these arise from splicing errors, NMD targets are enriched for transcripts containing open reading frames upstream of the predicted translational start (uORFs). We identify a relationship between the Kozak consensus surrounding the true start codon and the degree to which uORF-containing transcripts are targeted by NMD and speculate that translational efficiency may be coupled to transcript turnover via the NMD pathway for some transcripts. Conclusions We generated a high-resolution transcriptome map for C. elegans and used it to identify endogenous targets of NMD. We find that these transcripts arise principally through splicing errors, strengthening the prevailing view that splicing and NMD are highly interlinked processes.
External DOI: https://doi.org/10.1186/gb-2009-10-9-r101
This record's URL: http://www.dspace.cam.ac.uk/handle/1810/238190
Rights Holder: Ramani et al.; licensee BioMed Central Ltd.