CGC Bibliography Paper 3080

ACR-3, A Caenorhabditis elegans nicotinic acetylcholine receptor subunit - Molecular cloning and functional expression.

Baylis HA, Matsuda K, Squire MD, Fleming JT, Harvey RJ, Darlison MG, Barnard EA, Sattelle DB

Medline:

98269564

Citation:

Receptors and Channels 5: 149-158 1997

Type:

ARTICLE

Genes:

acr-2 acr-3 lev-1 unc-29 unc-38

Abstract:

The molecular cloning and functional co-expression of a novel nicotinic acetylcholine receptor (nAChR) non-alpha subunit gene, acr-3, is described. Previously we determined the sequence and demonstrated the functional co-expression of acr-2, a nAChR non-alpha subunit gene from Caenorhabditis elegans. Analysis of the acr-2 genomic DNA revealed the existence of another potential nAChR subunit gene, acr-3, in the same orientation, only 281bp downstream of acr-2. A cDNA containing the entire acr-3 coding sequence was isolated by RT-PCR and sequenced. The predicted protein contains the conserved features typical of nAChR non-alpha subunits and most closely resembles other invertebrate nAChR non-alpha polypeptides, Unusually, the highly conserved glycine residue (equivalent to residue 240 in the Torpedo alpha subunit) upstream of transmembrane domain 2 (m(2)) is replaced by a serine residue in ACR-3. When acr-3 cDNA was injected alone into Xenopus oocytes no levamisole-gated channel activity was observed. However when co-expressed with a C. elegans alpha subunit (UNC-38), ACR-3 contributed to the formation of levamisole-gated channels. The response of this hetero-oligomer to levamisole (100 mu M) was reduced by the nAChR antagonists mecamylamine(1 mu M) and d-tubocurarine (10 mu M).