Mammalian Genome 10, 940 (1999). Incorporating Mouse Genome © Springer-Verlag New York Inc. 1999 Michael F. Seldin* Rowe Program in Genetics, Departments of Biological Chemistry and Medicine, University of California, Davis, Davis, CA 95616, USA Submitted: 13 January 1999 Introduction The eighth mouse Chromosome (Chr) 1 Committee report includes some). In general, for those markers designated with the highest 1437 entries of genes, anonymous sequences, chromosomal alter- confidence value the 95% confidence limit is ~ 1.5 cM. ations, mutations or traits that have been mapped to this chromo- some. The majority of these markers are defined by sequence and Comparative mapping relationships with the human genome are providing the basis for establishment of physical maps and The genes on mouse Chr 1 have been definitively mapped to 7 cloned contiguous segments of the genome. There have been 81 human chromosomes: Chr 8 (band 8q11.2) Chr 6 (bands q12–q14 new entries since the previous report including 18 recently mapped and p11–p12), Chr 2 (bands q12–q37), Chr 5 (bands 5q14–5q21), genes. Currently, there are map positions designated for 193 genes Chr 18 (band q21.3), and Chr 1 (bands q21–q42) and Chr 13 and over 40 expressed sequence tags. A single new mutation open (bands q32.3–q33). Multiple genes as well as ESTs have provided brain2 (opb2) has been identified since the last report. This new strong supporting evidence for 10 specific homology groups (one mutation that was induced in a mutagenesis experiment is allelic to for human Chrs 5, 6, 8, 18 and 13; and two for human Chrs 1 and the phenotypically similar opb mutation. Four new putative quan- three for 2). Recent data suggests a putative new homology rela- titative trait loci (QTL) are included in the new Chromosome 1 tionship with human Chr 22. The Limk2 gene and was mapped by map. As discussed in previous reports from this committee it is in situ hybridization to band D of mouse chromosome 1 and the difficult to assess the likelihood that putative QTLs are important. human orthologue of this gene was previously assigned to human New locus symbols and map positions (at low confidence) have chromosome 22q12. However, additional studies will be necessary been assigned for QTLs that may control circadian locomotor ac- to confirm this relationship. The individual positions of human tivity (Cplaq3, Cpaq4), autoimmune vasitis resistance (Vas) or egg gene homologues are included in Figure 1/Table 1 and more de- genomic imprinting (Egm1). tailed descriptions and references are provided in reports from Map construction previous years. The reader is referred to another database (http:// www.ncbi.nlm.nih.gov/Homology/) for relationships with respect The markers (Fig. 1) have been mapped by a variety of techniques to a composite human genetic map (Genethon sex-averaged map). including linkage studies using disparate mouse strain combina- This database also provides an easy method for selecting putative tions or recombinant inbred (RI) strains and in situ hybridization orthologues (primarily mouse ESTs) of human genes and ESTs and are shown arranged by chromosomal position. (Note: the on- based on their human map position determined by radiation hybrid line version of this report also contains an alpha-ordered version). mapping. As demonstrated by comparisons of linkage intervals of two dif- ferent crosses for a large segment of distal Chr 1 (4624), different Physical maps and contig development genetic crosses may result in significantly different recombination Previous studies on development of physical maps for regions of frequencies. Since many of the markers have not been mapped mouse Chromosome 1 were summarized in last years’ report with respect to a large number of other markers in the same cross, (36208). Partial physical contigs of regions of mouse Chromosome errors in gene order as well as relative intergenic distance may 1 have now also been constructed and the reader is referred to the occur. However, we have assigned a single map position for each on-line MIT data base for this information (www-genome.wi. marker except where there is insufficient data for analysis, to mit.edu/cgi-bin/mouse/index then choose Browse Physical Map). facilitate the use of the assembled information. The composite map was derived by calculating the recombination frequency between Gene families, mutations and diseases ordered loci. The map positions, in centi-Morgans (cM) were cal- Linkage maps of mouse chromosomes form the framework for a culated with respect to the position of the centromeric satellite more detailed understanding of genomic organization as well as DNA that is designated heterochromatin 1 (Hc1) (see 1997 report facilitating approaches to define the genetic bases for disease and (36208). In developing this map, the initial intervals were deter- developmental abnormalities. A review of gene families, visible mined using loci common to several different crosses and exam- mutations and diseases on mouse Chr 1 was presented in the first ined in large numbers of meiotic events. Distances within these Chr 1 Committee report (12012) and updated in the subsequent intervals were then calculated by interpolation using available Chr 1 Committee reports (23109, 20615, 25895, 36208). Interest- data. The confidence in map position is indicated in Table 1; ingly, recent studies have indicated that mutations in acyl- however, the relative order of markers and genes, including those CoA:cholesterol acyltransferase (Acact) are associated with the for which we have indicated a high confidence, can only be de- adrenocortical lipid depletion gene (ald)(42073) providing new termined in a single cross or by physical mapping studies. The insight into the pathogenesis of this disorder. reader is strongly urged to refer to individual haplotype data (ref- erences), and on-line data for individual large crosses (www. Acknowledgments. We are grateful for the assistance of the Jackson Labo- informatics.jax.org/crossdata.html then choose cross and chromo- ratory Informatics Group in providing relevant data and electronic refer- ences. We apologize for errors and omissions and welcome comments and corrections (Email: email@example.com or FAX 530-754-6015). Sup- port was provided by NIH grants HG00734. * Committee Chair
Mammalian Genome – Springer Journals
Published: Oct 1, 1999
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