Open AccessTwo functionally dependent acetylcholine subunits are encoded in a single Caenorhabditis elegans operon
Author(s) -
Millet Treinin,
Boaz Gillo,
Lilach Liebman,
Martin Chalfie
Publication year - 1998
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.95.26.15492
Subject(s) - caenorhabditis elegans , biology , operon , nicotinic acetylcholine receptor , protein subunit , acetylcholine receptor , gene , mutant , genetics , microbiology and biotechnology , receptor
Thedeg-3 gene from the nematodeCaenorhabditis elegans encodes an α subunit of a nicotinic acetylcholine receptor that was first identified by a dominant allele,u662 , which produced neuronal degeneration. Becausedeg-3 cDNAs contain the SL2 trans-spliced leader, we suggested thatdeg-3 was transcribed as part of aC. elegans operon. Here we show thatdes-2 , a gene in which mutations suppressdeg-3(u662) , is the upstream gene in that operon. Thedes-2 gene also encodes an α subunit of a nicotinic acetylcholine receptor. As expected for genes whose mRNAs are formed from a single transcript, both genes have similar expression patterns. This coexpression is functionally important because (i )des-2 is needed for thedeg-3(u662) degenerationsin vivo ; (ii ) an acetylcholine-gated channel is formed inXenopus oocytes when both subunits are expressed but not when either is expressed alone; and (iii ) channel activity, albeit apparently altered from that of the wild-type channel, results from the expression of au662 -type mutant subunit but, again, only when the wild-type DES-2 subunit is present. Thus, the operon structure appears to regulate the coordinate expression of two channel subunits.