OBLIGATORY FORMAT for Abstracts

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Sample abstract

EXPRESSION OF HUMAN FMR1 IN A MOUSE TRANSGENIC MODEL DECREASES COGNITIVE ABILITY AND FERTILITY

James Watson¹, Craig Venter¹, Walt Disney²

Dept. of Innovative Ideas, Disney World, Orlando, USA¹

Institute for Recognizing Good Ideas, Disney World, Paris, France²

We stably transformed murine ES cells with a viral vector containing the complete murine FMR1 sequence. The ES cells were injected into blastocytes of the inbreed Balb/C strain and the resultant transgenics were developed to term in utero. In age-matched comparisons between 50 transgenic and 50 control mice carried out at monthly intervals starting at 4 months, we show that in controls, transcription levels remain similar for the same tissue between individuals. The same is not true for transgenics, which exhibit statistically significant greater heterogeneity in expression (p < .002). Similar differences were also observed for FMRP production. Measurement of cognitive function using a swimming maze demonstrated that controls were much more adept at solving the maze than transgenics and required on average ~50% less time to solve the maze at 6 months; by 12 months, this difference had increased to 75%.  Further, the human trans-gene reduced fertility by 43% in females and 95% in males. We conclude that the processing of the human FMR1 gene is far less efficient than that of the mouse, even when the relative functioning of both genes is compared in the same genetic background. The apparent superiority of the murine gene in enhancing cognitive ability appears to reside in its greater stability in structure and uniformity between individuals, combined with a much more dependable trafficking of gene products, particularly in the brain. We suspect, but cannot confirm yet, that changes in length of an internal repeat are responsible for the variable function of the human FMR1 gene. Given that other human genes behave in the same unstable way as FMR1, this general phenomenon will undoubtedly lead to an ever-increasing load of both genetically determined morbidity and health insurance premiums. This brings into question the long-term sustainability of Homo sapiens as a viable species.

Acknowledgements: We thank the Walt Disney Foundation for supporting this research