Figure 1.

Nbce1b/c is specifically disrupted in Nbce1b/c-null (KO_b/c) mice. (A) Cartoon depicting the structure of the Slc4a4 gene (not to scale) and its major products Nbce1a, Nbce1b, and Nbce1c (minor products Nbce1d and e are produced by choice of an alternate 5′ splice site within exon 6 of a and b).¹⁴ Numbered gray boxes are exons. Exons that are included in each gene product are reproduced below the gene cartoon: Noncoding exons are colorless, exons common to all variants are colored dark gray, exons encoding sequence unique to individual exons are colored orange, blue, or red. Exons 7–22 are included in all variants and are omitted to highlight the variable regions. (B) Genomic DNA and encoded protein sequence around the 5 bp deletion in the described strain of Nbce1b/c-null mouse. (C) Example of a genotyping gel showing the shift in molecular weight of the amplicon caused by the 5 bp deletion. (D) Western blots showing the effect of the 5 bp deletion upon the abundance of Nbce1 in lysates prepared from the kidneys, brains, and hearts of Nbce1b/c-null mice. Each blot is representative of results obtained from lysates prepared from three pairs of wild-type versus KO_b/c littermates and probed with the anti-Slc4a4 antibody. Four further paired kidney lysates were probed with the anti–NBCe1-A/B antibody αrb1NBC (a gift from Walter Boron at Case Western Reserve University⁸) with similar results. WT, wild-type.