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首页> 外文期刊>Molecular and Cellular Biology >Snm1-Deficient Mice Exhibit Accelerated Tumorigenesis and Susceptibility to Infection
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Snm1-Deficient Mice Exhibit Accelerated Tumorigenesis and Susceptibility to Infection

机译：Snm1缺陷小鼠表现出加速的肿瘤发生和感染的易感性。

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The eukaryotic SNM1 gene family has been implicated in a number of cellular pathways, including repair of DNA interstrand cross-links, involvement in VDJ recombination, repair of DNA double-strand breaks, and participation in cell cycle checkpoint pathways. In particular, mammalian SNM1 has been shown to be required in a mitotic checkpoint that causes arrest of cells in prophase prior to chromosome condensation in response to spindle poisons. Here, we report on the phenotype of a knockout of Snm1 in the mouse. Snm1?/? mice are viable and fertile but exhibit a complex phenotype. Both homozygous and heterozygous mice show a decline in survival compared to wild-type littermates. In homozygous mutant males, this reduction in survival is principally due to bacterial infections in the preputial and mandibular glands and to a lesser extent to tumorigenesis, while in homozygous and heterozygous females, it is due almost solely to tumorigenesis. The high incidence of bacterial infections in the homozygous mutant males suggests an immune dysfunction; however, examinations of T- and B-cell development and immunoglobulin class switching did not reveal a defect in these pathways. Crossing of Snm1 mutant mice with a Trp53 null mutant resulted in an increase in mortality and a restriction of the tumor type to lymphomas, particularly those of the thymus. Taken together, these findings demonstrate that Snm1 is a tumor suppressor in mice that in addition has a role in immunity.
机译：真核 SNM1 基因家族与许多细胞途径有关，包括DNA链间交联的修复，VDJ重组的参与，DNA双链断裂的修复以及参与细胞周期检查点的参与。途径。特别是，哺乳动物 SNM1 已显示在有丝分裂检查点中是必需的，该检查点可导致梭形毒物使染色体凝结之前的前期细胞停滞。在这里，我们报道了在小鼠中 Snm1 的敲除的表型。 Snm1 ？ / ？小鼠是活的和可育的，但表现出复杂的表型。与野生型同窝小鼠相比，纯合和杂合小鼠均显示存活率下降。在纯合突变的雄性中，这种存活率的降低主要归因于包皮和下颌腺中的细菌感染，并且在较小程度上归因于肿瘤发生，而在纯合和杂合性雌性中，这几乎完全归因于肿瘤发生。纯合突变型男性中细菌感染的高发生率表明存在免疫功能障碍。然而，对T细胞和B细胞发育以及免疫球蛋白类别转换的检查并未揭示这些途径的缺陷。 Snm1 突变小鼠与 Trp53 null突变体的杂交导致死亡率增加，并且肿瘤类型仅限于淋巴瘤，尤其是胸腺。综上所述，这些发现表明 Snm1 是小鼠的肿瘤抑制因子，此外还具有免疫功能。

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