Fig 1. Schematic representations of the Klhl18^lowf and Klhl18^tm1a alleles.

A.Klhl18^lowf is formed by a single base pair change on Chr9, at position 110455454, in exon 3 of the gene, with the wildtype C replaced with the mutant A. This produces an amino acid substitution in the resultant protein with the wildtype valine (conserved across species) being replaced by phenylalanine at position 55 (see [2] for further information). B. Klhl18^tm1a was generated at the Wellcome Sanger Institute by insertion of a large DNA cassette before the critical exon (exon 6) of the gene, which interrupts transcription of the gene into mRNA. The cassette is composed of a number of components; En2 SA (engrailed2 splice acceptor), IRES (internal ribosome entry site), lacZ (beta-galactosidase reporter gene), pA (polyadenylation site), hBactP (beta-actin promotor part) and neo (neomycin resistance gene), which are flanked by FRT (Flp-FRT) and loxP recombination sites to produce the promoter-driven Knockout First, reporter-tagged insertion with conditional potential allele (tm1a) of Klhl18 (see [15] for further information).