Large-scale mRNA sequencing determines global regulation of RNA editing during brain development Export

@article{citeulike:4510784, abstract = {10.1101/gr.089409.108 RNA editing by adenosine deamination has been shown to generate multiple isoforms of several neural receptors, often with profound effects on receptor function. However, little is known about the regulation of editing activity during development. We have developed a large-scale RNA sequencing protocol to determine adenosine-to-inosine (A-to-I) editing frequencies in the coding region of genes in the mammalian brain. Using the 454 Life Sciences (Roche) Amplicon Sequencing technology, we were able to determine even low levels of editing with high accuracy. The efficiency of editing for 28 different sites was analyzed during the development of the mouse brain from embryogenesis to adulthood. We show that, with few exceptions, the editing efficiency is low during embryogenesis, increasing gradually at different rates up to the adult mouse. The variation in editing gave receptors like HTR2C and GABA (gamma-aminobutyric acid type A) a different set of protein isoforms during development from those in the adult animal. Furthermore, we show that this regulation of editing activity cannot be explained by an altered expression of the ADAR proteins but, rather, by the presence of a regulatory network that controls the editing activity during development.}, author = {Wahlstedt, Helene and Daniel, Chammiran and Enster\~{A}{\P}, Mats and \~{A}–hman, Marie}, citeulike-article-id = {4510784}, citeulike-linkout-0 = {http://dx.doi.org/10.1101/gr.089409.108}, citeulike-linkout-1 = {http://genome.cshlp.org/content/gr.089409.108v1//.abstract}, citeulike-linkout-2 = {http://genome.cshlp.org/content/gr.089409.108v1//.full.pdf}, citeulike-linkout-3 = {http://view.ncbi.nlm.nih.gov/pubmed/19420382}, citeulike-linkout-4 = {http://www.hubmed.org/display.cgi?uids=19420382}, day = {6}, doi = {10.1101/gr.089409.108}, journal = {Genome Research}, keywords = {454, fourstar, sequencing, subassemblypaper, transcriptomics}, month = {June}, number = {6}, pages = {978--986}, posted-at = {2009-05-13 22:02:34}, priority = {2}, title = {Large-scale mRNA sequencing determines global regulation of RNA editing during brain development}, url = {http://dx.doi.org/10.1101/gr.089409.108}, volume = {19}, year = {2009} }

TY - JOUR ID - citeulike:4510784 L3 - citeulike-article-id:4510784 N2 - 10.1101/gr.089409.108 RNA editing by adenosine deamination has been shown to generate multiple isoforms of several neural receptors, often with profound effects on receptor function. However, little is known about the regulation of editing activity during development. We have developed a large-scale RNA sequencing protocol to determine adenosine-to-inosine (A-to-I) editing frequencies in the coding region of genes in the mammalian brain. Using the 454 Life Sciences (Roche) Amplicon Sequencing technology, we were able to determine even low levels of editing with high accuracy. The efficiency of editing for 28 different sites was analyzed during the development of the mouse brain from embryogenesis to adulthood. We show that, with few exceptions, the editing efficiency is low during embryogenesis, increasing gradually at different rates up to the adult mouse. The variation in editing gave receptors like HTR2C and GABA (gamma-aminobutyric acid type A) a different set of protein isoforms during development from those in the adult animal. Furthermore, we show that this regulation of editing activity cannot be explained by an altered expression of the ADAR proteins but, rather, by the presence of a regulatory network that controls the editing activity during development. IS - 6 JF - Genome Research EP - 986 TI - Large-scale mRNA sequencing determines global regulation of RNA editing during brain development VL - 19 SP - 978 KW - 454 KW - fourstar KW - sequencing KW - subassemblypaper KW - transcriptomics AU - Wahlstedt, Helene AU - Daniel, Chammiran AU - Ensterö, Mats AU - Öhman, Marie PY - 2009/06/06/ UR - http://dx.doi.org/10.1101/gr.089409.108 ER -