ArticleProceedings of the National Academy of Sciences of the United States of America2006
Genomic anatomy of the Tyrp1 (brown) deletion complex.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 33 citations in OpenAlex.
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- Identification of Susceptibility Loci for Cutaneous Squamous Cell Carcinoma.The Journal of investigative dermatology · 2016Article
- GRASP: analysis of genotype-phenotype results from 1390 genome-wide association studies and corresponding open access database.Bioinformatics (Oxford, England) · 2014Article
- Comprehensive candidate gene study highlights UGT1A and BNC2 as new genes determining continuous skin color variation in Europeans.Human genetics · 2013Article
- GILT modulates CD4+ T-cell tolerance to the melanocyte differentiation antigen tyrosinase-related protein 1.The Journal of investigative dermatology · 2012Article
- Differentiated melanocyte cell division occurs in vivo and is promoted by mutations in Mitf.Development (Cambridge, England) · 2011Article
- Complex interactions of Tyrp1 in the eye.Molecular vision · 2011Article
- Creating a "hopeful monster": mouse forward genetic screens.Methods in molecular biology (Clifton, N.J.) · 2011Article
- GILT accelerates autoimmunity to the melanoma antigen tyrosinase-related protein 1.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Naive tumor-specific CD4(+) T cells differentiated in vivo eradicate established melanoma.The Journal of experimental medicine · 2010Article
- Advances in genome studies: The PAG 2010 conference.Functional & integrative genomics · 2010Article
- Palmitoylation regulates epidermal homeostasis and hair follicle differentiation.PLoS genetics · 2009Article
- Basonuclin-2 requirements for zebrafish adult pigment pattern development and female fertility.PLoS genetics · 2009Article
- High-avidity autoreactive CD4+ T cells induce host CTL, overcome T(regs) and mediate tumor destruction.Journal of immunotherapy (Hagerstown, Md. : 1997) · 2009Article
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- Basonuclins 1 and 2, whose genes share a common origin, are proteins with widely different properties and functions.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
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60 authors at 5 institutions in 2 countries.
Funding
Abstract
Chromosome deletions in the mouse have proven invaluable in the dissection of gene function. The brown deletion complex comprises >28 independent genome rearrangements, which have been used to identify several functional loci on chromosome 4 required for normal embryonic and postnatal development. We have constructed a 172-bacterial artificial chromosome contig that spans this 22-megabase (Mb) interval and have produced a contiguous, finished, and manually annotated sequence from these clones. The deletion complex is strikingly gene-poor, containing only 52 protein-coding genes (of which only 39 are supported by human homologues) and has several further notable genomic features, including several segments of >1 Mb, apparently devoid of a coding sequence. We have used sequence polymorphisms to finely map the deletion breakpoints and identify strong candidate genes for the known phenotypes that map to this region, including three lethal loci (l4Rn1, l4Rn2, and l4Rn3) and the fitness mutant brown-associated fitness (baf). We have also characterized misexpression of the basonuclin homologue, Bnc2, associated with the inversion-mediated coat color mutant white-based brown (B(w)). This study provides a molecular insight into the basis of several characterized mouse mutants, which will allow further dissection of this region by targeted or chemical mutagenesis.
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