Nuclear Encoding of a Chloroplast RNA Polymerase Sigma Subunit in a Red Alga

Abstract

Homozygous weaver mice are profoundly ataxic because of the loss of granule cell neurons during cerebellar development. This granule cell loss appears to be caused by a genetic defect in the pore region (Gly¹⁵⁶ → Ser) of the heterotrimeric guanine nucleotide-binding protein (G protein)-gated inwardly rectifying potassium (K⁺) channel subunit (GIRK2). A related subunit, GIRK1, associates with GIRK2 to constitute a neuronal G protein-gated inward rectifier K⁺ channel. The weaver allele of the GIRK2 subunit (wvGIRK2) caused loss of K⁺ selectivity when expressed either as wvGIRK2 homomultimers or as GIRK1-wvGIRK2 heteromultimers. The mutation also led to loss of sensitivity to G protein βγ dimers. Expression of wvGIRK2 subunits led to increased cell death, presumably as a result of basal nonselective channel opening.