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. 2002 Jun;22(12):4147–4157. doi: 10.1128/MCB.22.12.4147-4157.2002

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Copyright © 2002, American Society for Microbiology

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FIG. 6. — Sim2 has no obvious genetic interaction with Sim1 in PVN development and energy homeostasis. Brains of wild-type (Sim1^+/+/Sim2^+/+) (A), Sim2 mutant (Sim1^+/+/Sim2^−/−) (B), Sim1 heterozygous (Sim1^+/−/Sim2^+/+) (C), Sim1 heterozygote/Sim2 mutant (Sim1^+/−/Sim2^−/−) (D), and Sim1 mutant (Sim1^−/−) (E) mice were embedded in paraffin, sectioned, and stained with hematoxylin. SCN, suprachiasmatic nucleus. An asterisk labels the medial preoptic nucleus as a reference. Dashed lines outline the ventral boundary of the PVN. Arrowheads in panel E indicate the lack of PVN and SON in Sim1^−/− mice. (F and G) ³⁵S radioactive in situ hybridization of the PVN/SON region with Sim1 and Sim2 probes. (H) Six females (left) and five males (right) of each of the following genotypes were used in this study: wild type (wt, triangles), Sim1^+/− (diamonds), Sim2^+/− (circles), and Sim1^+/−/Sim2^+/− (squares). Animals were weighed every 4 weeks after birth, continuing on until 30 weeks. The average weight (in grams) was plotted, and the error bars represent standard errors. By Student's t test, there is no significant difference between wild-type and Sim2 heterozygous mice (P > 0.75) or between Sim1^+/− and Sim2^+/−/Sim1^+/− mice (P > 0.8).