Martin N, Jaubert J, Glaser P, Szatanik M, Guénet J L
Unité de Génétique des Mammiferes, Institut Pasteur, 25 Rue du Docteur Roux, F-75724 Paris Cedex 15, France.
Genomics. 2001 Jul;75(1-3):9-16. doi: 10.1006/geno.2001.6595.
The mouse autosomal recessive mutation progressive motor neuropathy (pmn) results in early onset motor neuron disease with rapidly progressing hindlimb paralysis, severe muscular wasting, and death at 4--6 weeks of age. pmn is thus considered a good animal model for motor neuron diseases and the characterization of the causative gene should help in understanding the biological causes of human spinal muscular atrophies. Here we report the generation of a physical map based on a high-resolution and high-density genetic map encompassing the pmn locus on mouse chromosome 13. We have positioned the pmn locus and a cluster of markers cosegregating with it within a genetic interval of 0.30 cM, delineated by two clusters of markers. We have constructed an approximately 850-kb contig of BACs spanning the pmn critical region. This BAC contig contains the breakpoint of synteny between mouse chromosome 13 and human 1q and 7p regions and lays the foundation for identifying at the molecular level such a breakpoint region. The physical and genetic maps provided a support for the identification of five transcription units positioned in the nonrecombinant interval, and constitute invaluable tools for the identification of other candidate genes for the pmn mutation.
小鼠常染色体隐性突变进行性运动神经病(pmn)会导致早发性运动神经元疾病,伴有后肢迅速瘫痪、严重肌肉萎缩,并在4至6周龄时死亡。因此,pmn被认为是运动神经元疾病的良好动物模型,对致病基因的特征描述应有助于理解人类脊髓性肌萎缩症的生物学病因。在此,我们报告基于高分辨率和高密度遗传图谱构建的物理图谱,该遗传图谱涵盖小鼠13号染色体上的pmn位点。我们已将pmn位点及其共分离的一组标记定位在由两组标记划定的0.30 cM的遗传区间内。我们构建了一个跨越pmn关键区域的约850 kb的BAC重叠群。这个BAC重叠群包含小鼠13号染色体与人类1q和7p区域之间的同线性断点,为在分子水平上鉴定此类断点区域奠定了基础。物理图谱和遗传图谱为鉴定位于非重组区间的五个转录单位提供了支持,并构成了鉴定pmn突变其他候选基因的宝贵工具。