Functional effects of the mouse weaver mutation on G protein-gated inwardly rectifying K+ channels

Paul A. Slesinger, Nila Patil, Y. Joyce Liao, Yuh Nung Jan, Lily Y. Jan, David R. Cox

Research output: Contribution to journalArticlepeer-review

226 Scopus citations

Abstract

The weaver mutation corresponds to a substitution of glycine to serine in the H5 region of a G protein-gated inwardly rectifying K+ channel gene (GIRK2). By studying mutant GIRK2 weaver homomultimeric channels and heteromultimeric channels comprised of GIRK2 weaver and GIRK1 in Xenopus oocytes, we found that GIRK2 weaver homomultimeric channels lose their selectivity for K+ ions, giving rise to inappropriate receptor-activated and basally active Na+ currents, whereas heteromultimers of GIRK2 weaver and GIRK1 appeared to have reduced current. Immunohistochemical localization indicates that GIRK2 and GIRK1 proteins are expressed in the cerebellar neurons of mice at postnatal day 4, at a time when these neurons normally undergo differentiation. Thus, the aberrant behavior of mutant GIRK2 weaver channels could affect the development of weaver mice in at least two distinct ways.

Original languageEnglish
Pages (from-to)321-331
Number of pages11
JournalNeuron
Volume16
Issue number2
DOIs
StatePublished - Feb 1996
Externally publishedYes

Fingerprint

Dive into the research topics of 'Functional effects of the mouse weaver mutation on G protein-gated inwardly rectifying K+ channels'. Together they form a unique fingerprint.

Cite this