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在培养的中国仓鼠细胞中,X射线在次黄嘌呤磷酸核糖转移酶(HPRT)基因座诱导的突变大多是大片段缺失。

Mutations induced by X-rays at the HPRT locus in cultured Chinese hamster cells are mostly large deletions.

作者信息

Vrieling H, Simons J W, Arwert F, Natarajan A T, van Zeeland A A

出版信息

Mutat Res. 1985 Dec;144(4):281-6. doi: 10.1016/0165-7992(85)90065-x.

Abstract

We investigated the molecular basis of 19 X-ray-induced HPRT-deficient mutants of V79 Chinese hamster cells with Southern hybridisation techniques. 12 of those mutants suffer from a big deletion (greater than 10 kb) of HPRT DNA sequences. Cytological studies of chromosome preparations of those 12 deletion mutants showed that in at least 3 of these mutants part of the long arm of the X-chromosome was lost. After correction for spontaneous arising mutations we estimate that at least 70-80% of X-ray-induced mutations are caused by large deletions.

摘要

我们运用Southern杂交技术研究了19个X射线诱导的V79中国仓鼠细胞HPRT缺陷型突变体的分子基础。其中12个突变体存在HPRT DNA序列的大片段缺失(大于10 kb)。对这12个缺失型突变体的染色体标本进行细胞学研究表明,在这些突变体中至少有3个的X染色体长臂部分缺失。校正自发产生的突变后,我们估计至少70 - 80%的X射线诱导突变是由大片段缺失引起的。

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