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The Journal of Neuroscience, February 25, 2009, 29(8):2440-2452; doi:10.1523/JNEUROSCI.4400-08.2009

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Cellular/Molecular
Functional Complementation of Glra1spd-ot, a Glycine Receptor Subunit Mutant, by Independently Expressed C-Terminal Domains

Carmen Villmann,1 Jana Oertel,1 Zhan-Lu Ma-Högemeier,2 Michael Hollmann,2 Rolf Sprengel,3 Kristina Becker,1 Hans-Georg Breitinger,1 and Cord-Michael Becker1

1Institut für Biochemie, Emil-Fischer-Zentrum, Universität Erlangen-Nürnberg, 91054 Erlangen, Germany, 2Rezeptorbiochemie, Lehrstuhl für Biochemie, Ruhr-Universität Bochum, 44780 Bochum, Germany, and 3Molekulare Neurobiologie, Max-Planck-Institut für Medizinische Forschung, 69120 Heidelberg, Germany

Correspondence should be addressed to Dr. Cord-Michael Becker, Institut für Biochemie, Emil-Fischer-Zentrum, Universität Erlangen-Nürnberg, Fahrstrasse 17, D-91054 Erlangen, Germany. Email: cmb{at}biochem.uni-erlangen.de

The oscillator mouse (Glra1spd-ot) carries a 9 bp microdeletion plus a 2 bp microinsertion in the glycine receptor {alpha}1 subunit gene, resulting in the absence of functional {alpha}1 polypeptides from the CNS and lethality 3 weeks after birth. Depending on differential use of two splice acceptor sites in exon 9 of the Glra1 gene, the mutant allele encodes either a truncated {alpha}1 subunit (spdot-trc) or a polypeptide with a C-terminal missense sequence (spdot-elg). During recombinant expression, both splice variants fail to form ion channels. In complementation studies, a tail construct, encoding the deleted C-terminal sequence, was coexpressed with both mutants. Coexpression with spdot-trc produced glycine-gated ion channels. Rescue efficiency was increased by inclusion of the wild-type motif RRKRRH. In cultured spinal cord neurons from oscillator homozygotes, viral infection with recombinant C-terminal tail constructs resulted in appearance of endogenous {alpha}1 antigen. The functional rescue of {alpha}1 mutants by the C-terminal tail polypeptides argues for a modular subunit architecture of members of the Cys-loop receptor family.

Key words: chloride channel; domain; glycine receptor; TM3–TM4 loop; rescue; inhibition

Received Sept. 11, 2008; revised Jan. 14, 2009; accepted Jan. 15, 2009.

Correspondence should be addressed to Dr. Cord-Michael Becker, Institut für Biochemie, Emil-Fischer-Zentrum, Universität Erlangen-Nürnberg, Fahrstrasse 17, D-91054 Erlangen, Germany. Email: cmb{at}biochem.uni-erlangen.de






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