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通过N-甲基-N-亚硝基脲诱导的姐妹染色单体交换分析揭示小鼠中Msh2单倍体不足的证据。

Evidence for Msh2 haploinsufficiency in mice revealed by MNU-induced sister-chromatid exchange analysis.

作者信息

Bouffler S D, Hofland N, Cox R, Fodde R

机构信息

Radiation Effects Department, National Radiological Protection Board, Chilton, Didcot, Oxfordshire, OX11 0RQ, UK.

出版信息

Br J Cancer. 2000 Nov;83(10):1291-4. doi: 10.1054/bjoc.2000.1422.

DOI:10.1054/bjoc.2000.1422
PMID:11044352
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2408782/
Abstract

The role of Msh2 in chromosome stability has been investigated in a targeted mouse model for HNPCC, Msh2Delta7N. Chromosome aberration frequencies were similar in bone marrow of Msh2(+/+), Msh2(+/-)and Msh2(-/-)mice and no differential effects of in vivo X-irradiation were noted. By contrast, the induction of sister-chromatid exchanges (SCEs) by methyl nitrosourea (MNU) was reduced in Msh2(-/-)and Msh2(+/-)cells to approximately 20% and approximately 45% wild-type levels respectively indicating a phenotypic effect of haploinsufficiency of the mouse Msh2 gene.

摘要

在一种针对遗传性非息肉病性结直肠癌（HNPCC）的靶向小鼠模型Msh2Delta7N中，研究了Msh2在染色体稳定性中的作用。Msh2(+/+)、Msh2(+/-)和Msh2(-/-)小鼠骨髓中的染色体畸变频率相似，且未观察到体内X射线照射的差异效应。相比之下，甲基亚硝基脲（MNU）诱导的姐妹染色单体交换（SCE）在Msh2(-/-)和Msh2(+/-)细胞中分别降至约20%和约45%的野生型水平，这表明小鼠Msh2基因单倍剂量不足具有表型效应。

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