Biology:Mouse Genetics Project
The Mouse Genetics Project (MGP) is a large-scale mutant mouse production and phenotyping programme aimed at identifying new model organisms of disease.[1][2][3][4]
Based at the Wellcome Trust Sanger Institute, the project uses knockout mice most of which were generated by the International Knockout Mouse Consortium. For each mutant line, groups of seven male and seven female mice move through a standard analysis pipeline aimed at detecting traits that differ from healthy C57BL/6 mice.[1] The pipeline collects many measurements of viability, fertility, body weight, infection, hearing, morphology, haematology, behaviour, blood chemistry and immunity and compares them to wild type controls using a statistical mixed model.[5] These data are immediately shared among the scientific and medical research community through a bespoke open access database,[6] and summaries are displayed in other online resources, including the Mouse Genome Informatics database and the Wikipedia-based Gene Wiki.[4]
As of July 2013, the MGP reports having over 900 mutant lines openly available to the international research community,[4] and have "substantively complete" analysis for over 650 mutant lines,[6] of which over 75 per cent have at least one abnormal phenotype.[1] Among these are new discoveries of genes implicated in disease, including finding:
- Mutation of SLX4 causes a new type of Fanconi anemia.[3][7][8]
- Nine new genes that influence bone strength.[9]
- Mutation of CENPJ models Seckel syndrome.[10]
- SPNS2 is important in mammalian immune system function.[11]
- MYSM1 is important for hematopoiesis and lymphocyte differentiation.[12]
See also
References
- ↑ 1.0 1.1 1.2 "Mouse large-scale phenotyping initiatives: overview of the European Mouse Disease Clinic (EUMODIC) and of the Wellcome Trust Sanger Institute Mouse Genetics Project". Mamm. Genome 23 (9–10): 600–10. October 2012. doi:10.1007/s00335-012-9418-y. PMID 22961258.
- ↑ Gerdin AK (2010). "The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice". Acta Ophthalmologica 88 (S248). doi:10.1111/j.1755-3768.2010.4142.x.
- ↑ 3.0 3.1 "The mouse genetics toolkit: revealing function and mechanism.". Genome Biol 12 (6): 224. 2011. doi:10.1186/gb-2011-12-6-224. PMID 21722353.
- ↑ 4.0 4.1 4.2 "Genome-wide Generation and Systematic Phenotyping of Knockout Mice Reveals New Roles for Many Genes". Cell 154 (2): 452–64. July 2013. doi:10.1016/j.cell.2013.06.022. PMID 23870131.
- ↑ "Robust and sensitive analysis of mouse knockout phenotypes". PLoS ONE 7 (12): e52410. 2012. doi:10.1371/journal.pone.0052410. PMID 23300663. Bibcode: 2012PLoSO...752410K.
- ↑ 6.0 6.1 Mouse Resources Portal, Wellcome Trust Sanger Institute.
- ↑ Alderton GK (March 2011). "Genomic instability: Expanding the reach of Fanconi anaemia". Nat. Rev. Cancer 11 (3): 158–159. doi:10.1038/nrc3027. PMID 21451554.
- ↑ "Disruption of mouse Slx4, a regulator of structure-specific nucleases, phenocopies Fanconi anemia". Nat. Genet. 43 (2): 147–52. February 2011. doi:10.1038/ng.752. PMID 21240276.
- ↑ "Rapid-throughput skeletal phenotyping of 100 knockout mice identifies 9 new genes that determine bone strength". PLoS Genet. 8 (8): e1002858. 2012. doi:10.1371/journal.pgen.1002858. PMID 22876197.
- ↑ "Disruption of mouse Cenpj, a regulator of centriole biogenesis, phenocopies Seckel syndrome". PLOS Genet. 8 (11): e1003022. 2012. doi:10.1371/journal.pgen.1003022. PMID 23166506.
- ↑ "The role of sphingosine-1-phosphate transporter Spns2 in immune system function". J. Immunol. 189 (1): 102–11. July 2012. doi:10.4049/jimmunol.1200282. PMID 22664872.
- ↑ "The critical role of histone H2A-deubiquitinase Mysm1 in hematopoiesis and lymphocyte differentiation". Blood 119 (6): 1370–9. February 2012. doi:10.1182/blood-2011-05-352666. PMID 22184403.
External links
- The Sanger Mouse Portal, containing all MGP data
- The MGP Biomart, for extracting phenotypic data
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