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2
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3
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3
Complementation analyses for 45 mutations encompassing the pink-eyed dilution (p) locus of the mouse.对涵盖小鼠粉红眼稀释（p）基因座的45个突变进行互补分析。
Genetics. 1995 Dec;141(4):1547-62. doi: 10.1093/genetics/141.4.1547.
4
A gene for the mouse pink-eyed dilution locus and for human type II oculocutaneous albinism.一种与小鼠粉红眼稀释位点以及人类II型眼皮肤白化病相关的基因。
Nature. 1993 Jan 7;361(6407):72-6. doi: 10.1038/361072a0.
5
A cluster of three GABAA receptor subunit genes is deleted in a neurological mutant of the mouse p locus.在小鼠p位点的一个神经学突变体中，一组三个GABAA受体亚基基因被删除。
Nature. 1993 Jul 29;364(6436):448-50. doi: 10.1038/364448a0.
6
N-ethyl-N-nitrosourea-induced prenatally lethal mutations define at least two complementation groups within the embryonic ectoderm development (eed) locus in mouse chromosome 7.N-乙基-N-亚硝基脲诱导的产前致死突变在小鼠7号染色体的胚胎外胚层发育（eed）基因座内定义了至少两个互补群。
Mamm Genome. 1993;4(7):349-53. doi: 10.1007/BF00360583.
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A complete YAC contig of the Prader-Willi/Angelman chromosome region (15q11-q13) and refined localization of the SNRPN gene.普拉德-威利/安吉尔曼综合征染色体区域（15q11-q13）的完整酵母人工染色体连续克隆系及SNRPN基因的精细定位。
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Deletion mapping of four loci defined by N-ethyl-N-nitrosourea-induced postimplantation-lethal mutations within the pid-Hbb region of mouse chromosome 7.对由N-乙基-N-亚硝基脲诱导的小鼠7号染色体pid-Hbb区域内植入后致死突变所定义的四个基因座进行缺失定位。
Genetics. 1993 Dec;135(4):1117-23. doi: 10.1093/genetics/135.4.1117.
9
Mutations of the P gene in oculocutaneous albinism, ocular albinism, and Prader-Willi syndrome plus albinism.眼皮肤白化病、眼白化病以及普拉德-威利综合征合并白化病中P基因的突变。
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10
Imprinting mutations suggested by abnormal DNA methylation patterns in familial Angelman and Prader-Willi syndromes.在家族性安吉尔曼综合征和普拉德-威利综合征中，由异常DNA甲基化模式提示的印记突变。
Am J Hum Genet. 1994 May;54(5):741-7.

小鼠粉红眼稀释（p）位点36个突变的分子分析。

Molecular analysis of 36 mutations at the mouse pink-eyed dilution (p) locus.

作者信息

Johnson D K, Stubbs L J, Culiat C T, Montgomery C S, Russell L B, Rinchik E M

机构信息

Biology Division, Oak Ridge National Laboratory, Tennessee 37831-8077, USA.

出版信息

Genetics. 1995 Dec;141(4):1563-71. doi: 10.1093/genetics/141.4.1563.

DOI:10.1093/genetics/141.4.1563
PMID:8601494
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1206887/
Abstract

Thirty-six radiation- or chemically induced homozygous-lethal mutations at the p locus in mouse chromosome 7 have been analyzed at 17 loci defined by molecular probes to determine the types of lesions, numbers of p-region markers deleted or rearranged, regions of overlap of deletion mutations, and genetic distances between loci. A linear deletion map of the [Myod1, Ldh3]-[Snrpn, Znf127] region has been constructed from the molecular analyses of the p-locus deletions. The utility of these deletions as tools for the isolation and characterization of the genes specifying the neurological, reproductive, and developmental phenotypes genetically mapped to this region will grow as more detailed molecular analyses continue.

摘要

对小鼠7号染色体p位点上36个辐射或化学诱导的纯合致死突变进行了分析，这些突变位于由分子探针定义的17个位点，以确定损伤类型、缺失或重排的p区域标记数量、缺失突变的重叠区域以及位点之间的遗传距离。通过对p位点缺失的分子分析，构建了[Myod1, Ldh3]-[Snrpn, Znf127]区域的线性缺失图谱。随着更详细的分子分析不断进行，这些缺失作为分离和鉴定在遗传上定位于该区域的神经、生殖和发育表型相关基因的工具，其效用将会增加。