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. 2002 Oct 21;196(8):1113–1119. doi: 10.1084/jem.20020959

Figure 5.

Figure 5.

Intronic point mutation in NF-κB2 results in aberrant mRNA splicing and premature stop codons. (A) Chromosomal mapping of xdr/xdr mutation. Haplotypes of individual xdr/xdr affected mice are shown. Black squares indicate C57BL/6 homozygote; white squares indicate C57BL/6/NOD heterozygote. (B) Amplification of NF-κB2 cDNA reveals multiple aberrant spliced products between exons 5–8 in xdr/xdr mice. Spleen cDNA from WT and xdr/xdr mice was amplified by PCR using the indicated primer pairs. Primer pair 204F and 550R amplifies exons 2–5, 457F and 872R amplifies exons 5–8 and 791F and 3013R amplify exons 8–23. (C) The PCR products resulting from amplification of exons 5–8 from WT and xdr/xdr mice were cloned and sequenced. Intronic base number 3163 mutated in xdr/xdr mice shown as bold A. (D) Absence of NFκB2 protein in xdr/xdr mice. Cell lysates were prepared from the spleens of WT and xdr/xdr mice and probed with a polyclonal antibody against NF-κB2. (E) T to A conversion of Nf-κb2 intronic base 3163 in amplified genomic DNA in xdr/xdr mice. (F) Schematic representation of the effect of the ENU-induced point mutation in Nf-κb2.