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Disc1基因的缺失多态性在所有129小鼠亚系中都很常见：对脑功能基因靶向研究的启示。

Deletion polymorphism of Disc1 is common to all 129 mouse substrains: implications for gene-targeting studies of brain function.

作者信息

Clapcote Steven J, Roder John C

机构信息

Mount Sinai Hospital Research Institute, Department of Molecular and Medical Genetics, University of Toronto, Toronto, Ontario M5S 1A8, Canada.

出版信息

Genetics. 2006 Aug;173(4):2407-10. doi: 10.1534/genetics.106.060749. Epub 2006 Jun 4.

DOI:10.1534/genetics.106.060749
PMID:16751659
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1569715/
Abstract

We report that the Disc1 gene in all extant 129 mouse inbred substrains has a deletion, previously considered specific to the 129S6/SvEv substrain, which is predicted to abolish production of the full-length protein. This finding has implications for the study of knockout mice generated from 129-derived embryonic stem cells.

摘要

我们报告称，所有现存的129小鼠近交亚系中的Disc1基因都有一个缺失，该缺失以前被认为是129S6/SvEv亚系所特有的，预计会导致全长蛋白无法产生。这一发现对源自129胚胎干细胞的基因敲除小鼠的研究具有重要意义。

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Deletion polymorphism of Disc1 is common to all 129 mouse substrains: implications for gene-targeting studies of brain function.Disc1基因的缺失多态性在所有129小鼠亚系中都很常见：对脑功能基因靶向研究的启示。
Genetics. 2006 Aug;173(4):2407-10. doi: 10.1534/genetics.106.060749. Epub 2006 Jun 4.
2
Genetic variation among 129 substrains and its importance for targeted mutagenesis in mice.129个亚系之间的遗传变异及其在小鼠定向诱变中的重要性。
Nat Genet. 1997 May;16(1):19-27. doi: 10.1038/ng0597-19.
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Disc1 is mutated in the 129S6/SvEv strain and modulates working memory in mice.Disc1在129S6/SvEv品系小鼠中发生突变，并调节小鼠的工作记忆。
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Phenotypic characterization of C57BL/6J mice carrying the Disc1 gene from the 129S6/SvEv strain.携带来自129S6/SvEv品系Disc1基因的C57BL/6J小鼠的表型特征分析。
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Behavioral alterations associated with targeted disruption of exons 2 and 3 of the Disc1 gene in the mouse.与在小鼠中靶向破坏 Disc1 基因外显子 2 和 3 相关的行为改变。
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The natural Disc1-deletion present in several inbred mouse strains does not affect sleep.几种近交系小鼠中存在的自然 Disc1 缺失并不影响睡眠。
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本文引用的文献

1
Disrupted in schizophrenia 1: building brains and memories.精神分裂症相关基因1：构建大脑与记忆
Trends Mol Med. 2006 Jun;12(6):255-61. doi: 10.1016/j.molmed.2006.04.009. Epub 2006 May 6.
2
Genetic modifiers of the phenotype of mice deficient in mitochondrial superoxide dismutase.线粒体超氧化物歧化酶缺陷小鼠表型的遗传修饰因子
Hum Mol Genet. 2006 Apr 1;15(7):1187-94. doi: 10.1093/hmg/ddl034. Epub 2006 Feb 23.
3
Disc1 is mutated in the 129S6/SvEv strain and modulates working memory in mice.Disc1在129S6/SvEv品系小鼠中发生突变，并调节小鼠的工作记忆。
Proc Natl Acad Sci U S A. 2006 Mar 7;103(10):3693-7. doi: 10.1073/pnas.0511189103. Epub 2006 Feb 16.
4
Genetic association between schizophrenia and the DISC1 gene in the Scottish population.苏格兰人群中精神分裂症与DISC1基因之间的遗传关联。
Am J Med Genet B Neuropsychiatr Genet. 2006 Mar 5;141B(2):155-9. doi: 10.1002/ajmg.b.30274.
5
A schizophrenia-associated mutation of DISC1 perturbs cerebral cortex development.DISC1基因的一种与精神分裂症相关的突变扰乱了大脑皮层发育。
Nat Cell Biol. 2005 Dec;7(12):1167-78. doi: 10.1038/ncb1328. Epub 2005 Nov 20.
6
DISC1 and PDE4B are interacting genetic factors in schizophrenia that regulate cAMP signaling.DISC1和PDE4B是精神分裂症中相互作用的遗传因素，可调节环磷酸腺苷（cAMP）信号传导。
Science. 2005 Nov 18;310(5751):1187-91. doi: 10.1126/science.1112915.
7
Association of DISC1/TRAX haplotypes with schizophrenia, reduced prefrontal gray matter, and impaired short- and long-term memory.DISC1/TRAX单倍型与精神分裂症、前额叶灰质减少以及短期和长期记忆受损之间的关联。
Arch Gen Psychiatry. 2005 Nov;62(11):1205-13. doi: 10.1001/archpsyc.62.11.1205.
8
A frameshift mutation in Disrupted in Schizophrenia 1 in an American family with schizophrenia and schizoaffective disorder.一个患有精神分裂症和分裂情感性障碍的美国家庭中，精神分裂症1号基因（Disrupted in Schizophrenia 1）发生了移码突变。
Mol Psychiatry. 2005 Aug;10(8):758-64. doi: 10.1038/sj.mp.4001667.
9
Variation in DISC1 affects hippocampal structure and function and increases risk for schizophrenia.DISC1基因的变异会影响海马体的结构和功能，并增加患精神分裂症的风险。
Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8627-32. doi: 10.1073/pnas.0500515102. Epub 2005 Jun 6.
10
DISC1 and DISC2: discovering and dissecting molecular mechanisms underlying psychiatric illness.DISC1与DISC2：发现并剖析精神疾病背后的分子机制
Ann Med. 2004;36(5):367-78. doi: 10.1080/07853890410033603.