Fig. 1. SSPN-Tg mice display kyphosis and reduced body mass. (A) Schematic diagram of construct used to generate SSPN-Tg mice. A human skeletal muscle -actin promoter (HSA) was used to control muscle-specific expression of the human SSPN (hSSPN) transgene. A SV40 VP1 intron serves as a splice acceptor and is located downstream of the HSA promoter. Polyadenylation sites (pA) were inserted at the 3' end of the hSSPN cDNA. (B) Representative photographs of phenotypic Tg and non-Tg littermates reveal dramatic differences in body size and length. Severe kyphosis is evident in the phenotypic Tg mouse, as illustrated in the side view. Phenotypic SSPN-Tg mice appear atrophic and have limited mobility. Non-phenotypic SSPN-Tg mice were indistinguishable from their non-Tg controls (data not shown). (C) Phenotypic SSPN-Tg mice are nearly 50% lighter than non-Tg controls. Body mass (g) of 4-week-old non-Tg (n=14), non-phenotypic SSPN-Tg (n=3), and phenotypic SSPN-Tg (n=5) is plotted. Values are means and s.e.m.; ^*P=0.0015.