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大肠杆菌中的DNA修复:uvr基因的双重功能。

DNA repair in Escherichia coli: the dual function of uvr genes.

作者信息

Masek F, Fridrichova I, Pirsel M, Sedliaková M

机构信息

Cancer Research Institute, Slovak Academy of Sciences, Bratislava, Slovakia.

出版信息

Neoplasma. 1995;42(6):317-23.

PMID:8592574
Abstract

It has been shown earlier that the starvation of E. coli for both amino-acids and thymine applied prior to UV irradiation inhibits pyrimidine dimer excision without affecting cell survival after UV irradiation. In such cells pyrimidine dimers are tolerated by a rather error-free process that depends on the activity of uvrB, recA and lexA genes. Data presented here show: (a) that the efficient toleration of unexcised dimers requires also the uvrA gene; (b) that the starvation increases the level of RecA protein about 4.7 times; (c) that the effect of starvation on subsequent pyrimidine dimer excision is reversed by a 2 h incubation in complete medium before the cells are UV irradiated. The data suggest that the uvrA, uvrB, recA, lexA dependent nonexcisional repair may be a pathway temporarily functioning in repeatedly damaged cells.

摘要

先前已经表明,在紫外线照射之前,对大肠杆菌进行氨基酸和胸腺嘧啶饥饿处理会抑制嘧啶二聚体切除,而不影响紫外线照射后的细胞存活。在这类细胞中,嘧啶二聚体通过一个相当无差错的过程被耐受,该过程依赖于uvrB、recA和lexA基因的活性。此处呈现的数据表明:(a)未切除二聚体的有效耐受也需要uvrA基因;(b)饥饿使RecA蛋白水平增加约4.7倍;(c)在细胞进行紫外线照射之前,在完全培养基中孵育2小时可逆转饥饿对后续嘧啶二聚体切除的影响。数据表明,uvrA、uvrB、recA、lexA依赖性非切除性修复可能是一条在反复受损细胞中暂时起作用的途径。

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