Melcher T, Maas S, Herb A, Sprengel R, Seeburg P H, Higuchi M
Laboratory of Molecular Neuroendocrinology, University of Heidelberg, Germany.
Nature. 1996 Feb 1;379(6564):460-4. doi: 10.1038/379460a0.
Editing of RNA by site-selective adenosine deamination alters codons in brain-expressed pre-messenger RNAs for glutamate receptor (GluR) subunits including a codon for a channel determinant (Q/R site) in GluR-B, which controls the Ca2+ permeability of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors. Editing of GluR pre-mRNAs requires a double-stranded RNA (dsRNA) structure formed by exonic and intronic sequences and is catalysed by an unknown dsRNA adenosine deaminase. Here we report the cloning of complementary DNA for RED1, a dsRNA adenosine deaminase expressed in brain and peripheral tissues that efficiently edits the Q/R site in GluR-B pre-mRNA in vitro. This site is poorly edited by DRADA, which is distantly sequence-related to RED1. Both deaminases edit the R/G site in GluR-B pre-mRNA, indicating that members of an emerging gene family catalyse adenosine deamination in nuclear transcripts with distinct but overlapping substrate specificities.
通过位点选择性腺苷脱氨作用对RNA进行编辑,会改变大脑中表达的谷氨酸受体(GluR)亚基前体信使RNA中的密码子,其中包括GluR-B中一个通道决定簇(Q/R位点)的密码子,该位点控制着α-氨基-3-羟基-5-甲基异恶唑-4-丙酸(AMPA)受体的Ca2+通透性。GluR前体信使RNA的编辑需要由外显子和内含子序列形成的双链RNA(dsRNA)结构,并由一种未知的dsRNA腺苷脱氨酶催化。在此,我们报告了RED1互补DNA的克隆,RED1是一种在大脑和外周组织中表达的dsRNA腺苷脱氨酶,它在体外能有效地编辑GluR-B前体信使RNA中的Q/R位点。该位点被与RED1序列关系较远的DRADA编辑的效率很低。这两种脱氨酶都能编辑GluR-B前体信使RNA中的R/G位点,表明一个新出现的基因家族成员催化核转录本中的腺苷脱氨作用,其底物特异性不同但有重叠。