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Sp homozygous mice were used as experimental models to study the programming of skeletal myogenesis. The results of the loss-of-function approach demonstrated that the bHLH myogenic regulatory factor Myf-5 and the paired box transcription factor Pax-3 are required by progenitor cells to generate muscles. Another bHLH myogenic regulatory factor, MyoD, on the other hand, was found to act genetically downstream of both Pax-3 and Myf-5 for the establishment of skeletal muscles in the body.

Molecular biological techniques were used to study the role of ectopically expressed FasL in the autoimmune destruction of insulin-producing pancreatic beta cells in transgenic nonobese diabetic strain of mice which was used as the disease model for insulin-dependent diabetes mellitus. The results indicated that some animals expressing Fasl in pancreatic islets showed higher rates of developing spontaneous diabetes while all transgenic mice exhibited greater sensitivity to diabetogenic T cells. The latter event is thought to be due to self-destruction of beta cells upon T cell-mediated induction of Fas.

The mechanism involved in the T cell lineage decision was studied using transgenic mice as host systems, supplemented with flow cytometry and polymerase chain reaction-restriction fragment length polymorphism. The results revealed that T cells that are heterozygous for a mutation of the Notch1 gene have a greater tendency to develop as gamma-delta T cells rather than as alpha-beta T cells. A constitutively activated form of Notch gene, on the other hand, stimulates the thymocytes to adopt the alpha-beta T cell fate. Notch, together with the newly formed T cell antigen receptor are thus identified as determinants of T cell lineage decision.

Mice which are double heterozygous for null alleles in the insulin receptor and insulin receptor substrate-1 genes which rendered them highly insulin resistant, were used as experimental disease model for non-insulin-dependent diabetes mellitus (NIDDM). The mice were observed to develop NIDDM in an age-dependent manner. The results of immunoprecipitation assay and Western blot analysis revealed that the genetic and molecular mechanisms behind NIDDM involve the combination of two mild effects in the insulin signaling cascade, leading to insulin resistance and subsequent progression to a diabetic phenotype.