Home About us Contact
|
Home About us Contact | ||
|
|
||
RNA Editing (rna + editing)
Selected AbstractsRNA editing in plant mitochondria: 20 years laterIUBMB LIFE, Issue 12 2009Michael W. Gray Abstract In 1989, three laboratories (in Canada, France and Germany) independently and simultaneously reported the discovery of C-to-U RNA editing in plant mitochondria (1,3). To mark the 20th anniversary of this finding, the leaders of the three research teams have written personal essays describing the events leading up to the discovery in each of their laboratories. These essays are intended not only to capture historical facts but also to illustrate unexpected convergence in the process of scientific discovery, with different groups coming to the same conclusion, often very close together in time, drawing on different types of evidence and via sometimes quite different hypotheses and approaches. Essential background information pertaining to RNA editing in general and RNA editing in plant organelles in particular is provided in this overview. © 2009 IUBMB IUBMB Life, 61: 1101,1104, 2009 [source] The long and winding road to RNA editing in plant mitochondria: The Tübingen-Berlin chapter,IUBMB LIFE, Issue 12 2009Axel Brennicke Abstract It took several independent observations of C-to-T differences between genomic mtDNA sequences and corresponding complementary DNA (cDNA) sequences before RNA editing in plant mitochondria was accepted as a fact by the group at Tübingen and later Berlin (Hiesel et al., Science246 (1989) 1632,1634). The first such deviating sequence runs were critically viewed in the lab as being errors of some kind, most likely cloning artifacts, which occur only too frequently. Several such cDNA-mtDNA differences identified in independent cDNA clones in different libraries and finally CGG to TGG codon changes dispelled the skeptical view, and this phenomenon was finally recognized as plant mitochondrial RNA editing of a type similar to the apolipoprotein B RNA editing in mammals. © 2009 IUBMB IUBMB Life, 61: 1105,1109, 2009. [source] RNA editing and alternative splicing of human serotonin 2C receptor in schizophreniaJOURNAL OF NEUROCHEMISTRY, Issue 6 2003Stella Dracheva Abstract Serotonin 2C receptor (5-HT2CR) heterogeneity in the brain occurs mostly from two different sources: (i) 5-HT2CR mRNA undergoes adenosine-to-inosine editing events at five positions, which leads to amino acid substitutions that produce receptor variants with different pharmacological properties; (ii) 5-HT2CR mRNA is alternatively spliced, resulting in a truncated mRNA isoform (5-HT2CR-tr) which encodes a non-functional serotonin receptor. 5-HT2CR mRNA editing efficiencies and the expression of the full-length and the truncated 5-HT2CR mRNA splice isoforms were analyzed in the prefrontal cortex of elderly subjects with schizophrenia vs. matched controls (ns = 15). No significant differences were found, indicating that there are no alterations in editing or alternative splicing of 5-HT2CRs that are associated with schizophrenia in persons treated with antipsychotic medications. Quantitation of 5-HT2CR and 5-HT2CR-tr mRNA variants revealed that the expression of 5-HT2CR-tr was ,,50% of that observed for the full-length isoform. [source] The large form of ADAR 1 is responsible for enhanced hepatitis delta virus RNA editing in interferon- , -stimulated host cellsJOURNAL OF VIRAL HEPATITIS, Issue 3 2006D. Hartwig Summary., Hepatitis delta virus (HDV) RNA editing controls the formation of hepatitis-delta-antigen-S and -L and therefore indirectly regulates HDV replication. Editing is thought to be catalysed by the adenosine deaminase acting on RNA1 (ADAR1) of which two different forms exist, interferon (IFN)- , -inducible ADAR1-L and constitutively expressed ADAR1-S. ADAR1-L is hypothesized to be a part of the innate cellular immune system, responsible for deaminating adenosines in viral dsRNAs. We examined the influence of both forms on HDV RNA editing in IFN- , -stimulated and unstimulated hepatoma cells. For gene silencing, an antisense oligodeoxyribonucleotide against a common sequence of both forms of ADAR1 and another one specific for ADAR1-L alone were used. IFN- , treatment of host cells led to approximately twofold increase of RNA editing compared with unstimulated controls. If ADAR1-L expression was inhibited, this substantial increase in editing could no longer be observed. In unstimulated cells, ADAR1-L suppression had only minor effects on editing. Inhibition of both forms of ADAR1 simultaneously led to a substantial decrease of edited RNA independently of IFN- , -stimulation. In conclusion, the two forms of ADAR1 are responsible almost alone for HDV editing. In unstimulated cells, ADAR1-S is the main editing activity. The increase of edited RNA under IFN- , -stimulation is because of induction of ADAR1-L, showing for the first time that this IFN-inducible protein is involved in the base modification of replicating HDV RNA. Thus, induction of ADAR1-L may at least partially cause the antiviral effect of IFN- , in natural immune response to HDV as well as in case of therapeutic administration of IFN. [source] Substrate and cofactor requirements for RNA editing of chloroplast transcripts in Arabidopsis in vitroTHE PLANT JOURNAL, Issue 1 2005Carla E. Hegeman Summary None of the macromolecular components of the chloroplast RNA editing apparatus has yet been identified. In order to facilitate biochemical purification and characterization of the chloroplast RNA editing apparatus, we have identified conditions suitable for production of chloroplast extracts from the model plant Arabidopsis that are capable of editing exogenous substrates produced by in vitro transcription. A simple poisoned primer extension assay readily quantified editing extent of mutated and wild-type substrates. Maximum editing efficiency typically varied from 10 to 40% with different chloroplast preparations. Substrates carrying as little as 47 nt surrounding the psbE editing site were as efficiently edited as longer substrates. Editing activity was stimulated when either ATP, CTP, or dCTP was provided to the extract, an unusual observation also recently seen with plant mitochondrial editing extracts. Editing was sensitive to a zinc chelator, also a characteristic of the mammalian APOBEC editing enzyme, which is a zinc-dependent cytidine deaminase. [source] Notice of Retraction: ,RNA editing in human cancer: review' (APMIS 2009;117:551,7)APMIS, Issue 4 2010Article first published online: 20 MAR 2010 No abstract is available for this article. [source] RNA editing in human cancer: reviewAPMIS, Issue 8 2009JOZEF, KARDA Notice of Retraction: ,RNA editing in human cancer: review' (APMIS 2009;117:551,7) The following article from APMIS, ,RNA editing in human cancer: review' by Jozef Skarda, Ninette Amariglio and Gideon Rechavi, published online (2 July 2009) in Wiley InterScience (http://www.interscience.wiley.com) and in Volume 117, Issue 8 (August 2009), has been retracted by agreement between the authors, the journal Editors-in-Chief E. Ralfkiær and B. Norrild and John Wiley & Sons A/S. The retraction has been agreed as a result of textual overlap with a paper published in the journal RNA Biology, ,A-to-I RNA editing and cancer: from pathology to basic science' by Angela Gallo and Silvia Galardi, published in Volume 5, Issue 3 (September 2008). Jozef Skarda takes full responsibility for the textual overlap. [source] RNA editing: a driving force for adaptive evolution?BIOESSAYS, Issue 10 2009Willemijn M. Gommans Abstract Genetic variability is considered a key to the evolvability of species. The conversion of an adenosine (A) to inosine (I) in primary RNA transcripts can result in an amino acid change in the encoded protein, a change in secondary structure of the RNA, creation or destruction of a splice consensus site, or otherwise alter RNA fate. Substantial transcriptome and proteome variability is generated by A-to-I RNA editing through site-selective post-transcriptional recoding of single nucleotides. We posit that this epigenetic source of phenotypic variation is an unrecognized mechanism of adaptive evolution. The genetic variation introduced through editing occurs at low evolutionary cost since predominant production of the wild-type protein is retained. This property even allows exploration of sequence space that is inaccessible through mutation, leading to increased phenotypic plasticity and provides an evolutionary advantage for acclimatization as well as long-term adaptation. Furthermore, continuous probing for novel RNA editing sites throughout the transcriptome is an intrinsic property of the editing machinery and represents the molecular basis for increased adaptability. We propose that higher organisms have therefore evolved to systems with increasing RNA editing activity and, as a result, to more complex systems. [source] Dinoflagellate mitochondrial genomes: stretching the rules of molecular biologyBIOESSAYS, Issue 2 2009Ross F. Waller Abstract Mitochondrial genomes represent relict bacterial genomes derived from a progenitor ,-proteobacterium that gave rise to all mitochondria through an ancient endosymbiosis. Evolution has massively reduced these genomes, yet despite relative simplicity their organization and expression has developed considerable novelty throughout eukaryotic evolution. Few organisms have reengineered their mitochondrial genomes as thoroughly as the protist lineage of dinoflagellates. Recent work reveals dinoflagellate mitochondrial genomes as likely the most gene-impoverished of any free-living eukaryote, encoding only two to three proteins. The organization and expression of these genomes, however, is far from the simplicity their gene content would suggest. Gene duplication, fragmentation, and scrambling have resulted in an inflated and complex genome organization. Extensive RNA editing then recodes gene transcripts, and trans-splicing is required to assemble full-length transcripts for at least one fragmented gene. Even after these processes, messenger RNAs (mRNAs) lack canonical start codons and most transcripts have abandoned stop codons altogether. [source] | |||||||||||||