Organ-wide profiling in mouse reveals high editing levels of Filamin B mRNA in the musculoskeletal system

RNA Biol. 2018;15(7):877-885. doi: 10.1080/15476286.2018.1480252. Epub 2018 Jul 31.


Adenosine to inosine RNA editing in protein-coding messenger RNAs (mRNAs) potentially leads to changes in the amino acid composition of the encoded proteins. The mRNAs encoding the ubiquitously expressed actin-crosslinking proteins Filamin A and Filamin B undergo RNA editing leading to a highly conserved glutamine to arginine exchange at the identical position in either protein. Here, by targeted amplicon sequencing we analysed the RNA editing of Filamin B across several mouse tissues during post-natal development. We find highest filamin B editing levels in skeletal muscles, cartilage and bones, tissues where Filamin B function seems most important. Through the analysis of Filamin B editing in mice deficient in either ADAR1 or 2, we identified ADAR2 as the enzyme responsible for Filamin B RNA editing. We show that in neuronal tissues Filamin B editing drops in spliced transcripts indicating regulated maturation of edited transcripts. We show further that the variability of Filamin B editing across several organs correlates with its mRNA expression.

Keywords: ADARs; Adenosine to inosine RNA editing; Filamin B; amplicon sequencing; mouse development.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine / genetics
  • Adenosine Deaminase / genetics
  • Adenosine Deaminase / metabolism
  • Animals
  • Bone and Bones / metabolism*
  • Cartilage / metabolism*
  • Filamins / genetics*
  • Humans
  • Inosine / genetics
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Muscle, Skeletal / metabolism*
  • Neurons / metabolism
  • RNA Editing*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism*
  • RNA-Binding Proteins / genetics
  • RNA-Binding Proteins / metabolism


  • FLNB protein, mouse
  • Filamins
  • RNA, Messenger
  • RNA-Binding Proteins
  • Inosine
  • ADAR1 protein, mouse
  • ADAR2 protein, mouse
  • Adenosine Deaminase
  • Adenosine

Grants and funding

This work was supported by the Austrian Science Fund [F4313, P26882, P26845] grants to MFJ. FA was funded by the Austrian Science Fund [FWF SFB F43]. LC was supported by the Mahlke-Obermann Stiftung and the European Union's Seventh Framework Programme (FP7) Marie Curie Actions / INDICAR - Interdisciplinary Cancer Research [609431].