Abstract
The A-to-I (adenosine to inosine) RNA editing changing RNA sequence is a post-transcriptional modification mechanism which increases complexities of gene products. ADADs (adenosine deaminase that act on RNA) are the enzymes catalyzed the deamination of A to I. The e1b/i1b antisense morpholino which annealed to the junction between exon1b and intron1b of ADAR2 pre-mRNA was injected into zebrafish embryos to block the splicing of ADAR2 RNA. E1b/i1b morphant embryos developed abnormally. The abnormal phenotypes inclued small bodies, bulging hindbrain and brain ventricles, touch insensitivity, and death before 7 dpf. To understand the defects of neuronal development in the e1b/i1b morphant, the expression patterns of several neuronal markers were studied by in situ hybridization. No significant differences in the expression patterns of the midbrain hindbrain boundary (MHB), forebrain, hindbrain, neuroblast and neuronal markers between wild-type and e1b/i1b morphant embryos were observed. These results showed that ADAR2 e1b/i1b antisense morpholino has no apparent influence on the gene expressions in the MHB, forebrain, hindbrain and neurons, suggesting that the regionalization and development of these brain regions were not perturbed in the e1b/i1b morphant. The results observed in the e1b/i1b morphant. The results observed in the e1b/i1b morphant, however, differed from those observed in the 5'-UTR morphant created by injecting antisense morpholino complementary to the 5'-UTR.