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. Author manuscript; available in PMC: 2013 Apr 22.
Published in final edited form as: J Pathol. 2011 Jun 14;224(4):540–552. doi: 10.1002/path.2891

Figure 1.

Figure 1

Meiotic mapping and identification of the mutation responsible for the SFA phenotype. (A) Meiotic mapping of the SFA locus performed after a two-generation backcross onto the 129S6/SvEv background from the C57BL/6J parent strain. C57BL/6J genotypes are represented by black boxes and 129S6/SvEv by white boxes. Polymorphic microsatellite marker designation is shown on the left, while physical location is shown on the right of the box genotype diagram. Numbers of both SFA/+ and WT mice of each genotype combination for the nine microsatellite markers are shown underneath the box genotype diagram. (B) The first two panels are sequence chromatograms of mice of indicated genotypes. The bottom panel represents the intron–exon structure of the Rpl27a gene. The white boxes illustrate the untranslated exons and the red boxes illustrate the coding exons. The ENU-induced point mutation (IVS4 -15A > G) within the intron four-splice acceptor is represented by a red star. (C) Expression levels of Rpl27a (mean + SEM) in SFA/+ P3 cerebellum (n = 8, p = 0.0388), P23-25 BM (n = 6, p = 0.0426) and P3 footpad skin (n = 9, p = 0.0283) in comparison to levels in WT tissue indicated by the dotted line (set at 1; n = 6 for cerebellum, n = 7 for BM and n = 5 for skin). (d) Variably penetrant low body weight and size in P35 SFA/+ mice. (E) Postnatal growth and survival curves of WT and SFA/+ mice.