By Dudoit S., Speed T. P.

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Additional resources for A score test for the linkage analysis of qualitative and quantitative traits based on identity [...]

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However, these results that appear inconsistent may be such only super¢cially and a deeper understanding will be necessary to compile a consistent picture; thus, one should not jump to premature conclusions on the utility of both genetics and functional studies for shedding light on complex disease mechanisms. For example, the results on IL4 make complete sense when one considers that the control of IL4 expression may not be in cis in the gene itself but instead operate in trans from another important locus that may remain uncharacterized.

If you could demonstrate that certain genes have more amino acid substitutions or that their alleles have much longer lineage coalescence times than would be predicted by neutrality, then this would indicate that their polymorphisms have functional consequences, which would make them excellent candidates for common disease involvement. Foote: There are examples of that in the mouse. If you do a mouse cross there are certain things you don’t see because presumably they are lethal. There are obviously loci that work synergistically, where you have to have two given alleles or you can’t have either.

We are looking at large pedigrees. Goldstein: An at-risk haplotype is unlikely to have been present in a single copy in your original founding population of 10 000. It will have been present in multiple copies. So the time since ¢nding the Tasmanian population is not relevant. Foote: I disagree: it is completely relevant. Goldstein: To the extent that there are multiple at-risk haplotypes in the founding population, then the genealogical relationship among those haplotypes at the time of ¢nding is relevant, not the time since.

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