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Figure Legends for Supplementary Figures Figure SI 1. An early map of the mouse genome. Presented by The Roscoe B. Jackson Memorial Laboratory at the Tenth International Congress of Genetics, McGill University, Montreal, Canada, 1958, the map was sparse, but rich in visual impact. This remarkable exhibit showed the linkage groups of the mouse genome as they were known at the time, with each locus on the exhibit represented by live mutant mice (in their cages) and corresponding to the known genetic markers of the day. (Courtesy of The Jackson Laboratory Archives.) Figure SI 2. Human and mouse c-kit mutations show similar phenotypes. The utility of mouse as a biomedical model for human disease is enhanced when mutations in orthologous genes give similar phenotypes in both organisms. In a visually striking example of this, the same pattern of hypopigmentation is seen in (a) a patient with the piebald trait and (b) a mouse with dominant spotting, both resulting from heterozygous mutations of the c-kit proto-oncogene. This figure was reprinted with permission from Dr. Zneimer1. Figure SI 3. Genetic map versus draft sequence of Chromosome 5. The order of 2,605 genetic markers in the genetic map and the full assembly was compared. As shown in this example of Chromosome 5 the agreement between the two maps was very high (only 1.8% disagreed in chromosomal assignment and 0.7% had conflicts in local order). As was noted for human chromosomes, the recombination frequency per physical length was often (but not always) elevated near the telomeres. The relationship was complicated, however, by regions over which little or no recombination was evident. These regions may reflect rearrangements between the two strains used in the genetic cross (Ob, the strain where the obese mutation spontaneously occurred in the C57BL/6J inbred laboratory strain and CAST/Ei an inbred wild-derived M. m. castaneus strain). Two markers matching another chromosome are seen at the top. Testing of random examples of such discrepant markers showed that 90% of them resulted from errors in the genetic map. Figure SI 4. A schematic representation of the roles of gene clusters known to be involved in pheromonal and hormonal responses in the mouse. Red text denotes mouse-specific gene clusters whose definition is included in the text. Additional moderately expanded gene clusters of interest, which do not fall within our criteria, are shown in black. Blue lines represent neuronal connections between the highlighted organs. Red arrows represent the proposed pathway of interactions between expanded genes (intervening steps are not shown). Green arrows represent the proposed pathway by which metabolism of hormones may influence physiology. It is not assumed that all of these genes will influence physiology or behaviour at any one time point. The diagram represents a gender non-specific mouse, where 1 represents the vomeronasal organ, 2 the accessory olfactory bulb, 3 the hypothalamus and 4 the pituitary gland. Figure SI 5. The dinucleotide SSR density over 50 equal-sized fractions of each chromosome, as well as an average over all chromosomes for each relative position. The density varies considerably for regions in individual chromosomes, but on average it remains constant until it increases two-fold toward the telomere. Please note that mouse chromosomes are acrocentric with only one telomere shown to the right. Figure SI 6. Fraction of repeats lost at family substitution level derived using Jukes-Cantor in human (a) and mouse (b). For 270 LTR elements in human and 150 LTR elements in mouse, there is a decent linear correlation between the estimated fraction lost and the substitution level of each family, giving 1.2 % and 1.5% sequence loss per % substitution, for human (R2 = 0.39) and mouse (R2 = 0.46) respectively. This would estimate that since the human-mouse split, at least 20% of Mesozoic non-functional DNA has been lost in human and over 50% in mouse. 1. Fleischman, R. A., Saltman, D. L., Stastny, V. & Zneimer, S. Deletion of the c-kit protooncogene in the human developmental defect piebald trait. Proc Natl Acad Sci U S A 88, 10885-10889. (1991).