Evolutionarily conserved human targets of adenosine to inosine RNA editing

EY Levanon, M Hallegger, Y Kinar… - Nucleic acids …, 2005 - academic.oup.com
EY Levanon, M Hallegger, Y Kinar, R Shemesh, K Djinovic-Carugo, G Rechavi, MF Jantsch
Nucleic acids research, 2005academic.oup.com
Abstract A-to-I RNA editing by ADARs is a post-transcriptional mechanism for expanding the
proteomic repertoire. Genetic recoding by editing was so far observed for only a few
mammalian RNAs that are predominantly expressed in nervous tissues. However, as these
editing targets fail to explain the broad and severe phenotypes of ADAR1 knockout mice,
additional targets for editing by ADARs were always expected. Using comparative genomics
and expressed sequence analysis, we identified and experimentally verified four additional …
Abstract
A-to-I RNA editing by ADARs is a post-transcriptional mechanism for expanding the proteomic repertoire. Genetic recoding by editing was so far observed for only a few mammalian RNAs that are predominantly expressed in nervous tissues. However, as these editing targets fail to explain the broad and severe phenotypes of ADAR1 knockout mice, additional targets for editing by ADARs were always expected. Using comparative genomics and expressed sequence analysis, we identified and experimentally verified four additional candidate human substrates for ADAR-mediated editing: FLNA, BLCAP, CYFIP2 and IGFBP7. Additionally, editing of three of these substrates was verified in the mouse while two of them were validated in chicken. Interestingly, none of these substrates encodes a receptor protein but two of them are strongly expressed in the CNS and seem important for proper nervous system function. The editing pattern observed suggests that some of the affected proteins might have altered physiological properties leaving the possibility that they can be related to the phenotypes of ADAR1 knockout mice.
Oxford University Press