Slc9a6 (solute carrier family 9 (sodium/hydrogen exchanger), member 6 or NHE6) encodes a proton leakage channel (Na+/H+ exchanger) that localizes to early and recycling endosomes and functions to regulate endosomal pH and volume. Mutations in SLC9A6 are associated with X-linked mental retardation, Christianson syndrome (an X-linked neurodevelopmental disorder), and tauopathies like corticobasal degeneration and Parkinson's disease. The conditional Slc9a6fl mice possess loxP sites flanking exon 1. Mice homozygous for the mutation are viable and fertile. When bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exon 1 deleted in cre-expressing tissues. Deletion of exon 1 is expected to result in a null allele that abolishes Slc9a6 expression in a tissue-specific manner. In addition, when bred to a strain with widespread tamoxifen-inducible Cre recombinase (such as Tg(CAG-cre/Esr1*)5Amc, Stock No. <a href="https://www.jax.org/strain/004586">004586</a>), the resulting double mutant progeny treated with tamoxifen at 2 months of age exhibit Purkinje cell loss.

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Slc9a6fl conditional mutant mice possess loxP sites flanking exon 1 of the X-linked Slc9a6 (solute carrier family 9 (sodium/hydrogen exchanger), member 6 or NHE6) gene and may be useful in generating conditional mutations to study the development of amyloid plaques and corticobasal degeneration.

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