Deletion mapping of four loci defined by N-ethyl-N-nitrosourea-induced postimplantation-lethal mutations within the pid-Hbb region of mouse chromosome 7.
Deletion mapping of four loci defined by N-ethyl-N-nitrosourea-induced postimplantation-lethal mutations within the pid-Hbb region of mouse chromosome 7.
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小鼠 7 号染色体 pid-Hbb 区域内由 N-乙基-N-亚硝基脲诱导的植入后致死突变定义的四个位点的缺失图谱。
DOI：
10.1093/genetics/135.4.1117
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发表时间：
1993
期刊：
影响因子：
3.3
通讯作者：
Long,CL
中科院分区：
文献类型：
--
作者：
Rinchik,EM;Carpenter,DA;Long,CL
作为完善小鼠 7 号染色体 Fes-Hbb 区域物理和功能图谱的长期努力的一部分，通过与携带小鼠 7 号染色体白化病致死缺失的小鼠进行反式互补杂交，绘制了由 N-乙基-N-亚硝基脲 (ENU) 诱导的产前致死突变定义的四个位点 [l(7)1Rn、l(7)2Rn、l(7)3Rn、l(7)4Rn]。 (c) 轨迹。每个基因座被分配到 Fes-Hbb 区间远端缺失图谱的定义子区域。该映射特别有用的是具有位于 pid 和 Omp 之间的远端断点的植入前致死缺失。发现每个 ENU 诱导的致死的半合子或纯合子会在子宫着床后阻止发育；植入后死亡的具体时间各不相同，并且取决于突变本身以及它是半合子还是纯合子。根据它们在植入前阶段导致死亡的缺失之外和远端的图谱位置，这些 ENU 诱导的突变识别了植入后发育所必需的基因座，而这些基因座是通过对任何白化缺失纯合小鼠的表型分析无法发现的。将这些基因座映射到由删除断点定义的特定遗传区间，提出了许多用于分子分离这些基因的定位克隆策略。这些突变的表型和遗传分析应该提供有关人类基因组相应片段（可能是人类 11q13.5）功能组成的有用信息。
As part of a long-term effort to refine the physical and functional maps of the Fes-Hbb region of mouse chromosome 7, four loci [l(7)1Rn, l(7)2Rn, l(7)3Rn, l(7)4Rn] defined by N-ethyl-N-nitrosourea (ENU)-induced, prenatally lethal mutations were mapped by means of trans complementation crosses to mice carrying lethal deletions of the mouse chromosome-7 albino (c) locus. Each locus was assigned to a defined subregion of the deletion map at the distal end of the Fes-Hbb interval. Of particular use for this mapping were preimplantation-lethal deletions having distal breakpoints localized between pid and Omp. Hemizygosity or homozygosity for each of the ENU-induced lethals was found to arrest development after uterine implantation; the specific time of postimplantation death varied, and depended on both the mutation itself and on whether it was hemizygous or homozygous. Based on their map positions outside of and distal to deletions that cause death at preimplantation stages, these ENU-induced mutations identify loci, necessary for postimplantation development, that could not have been discovered by phenotypic analyses of mice homozygous for any albino deletion. The mapping of these loci to specific genetic intervals defined by deletion breakpoints suggests a number of positional-cloning strategies for the molecular isolation of these genes. Phenotypic and genetic analyses of these mutations should provide useful information on the functional composition of the corresponding segment of the human genome (perhaps human 11q13.5).