Sedliakova M
Cancer Research Institute, Slovak Academy of Sciences, Bratislava, Slovak Republic.
J Photochem Photobiol B. 1998 Sep;45(2-3):75-81. doi: 10.1016/s1011-1344(98)00159-6.
In UV-irradiated excision-proficient (uvr+) Escherichia coli, pre-induced by simultaneous pre-starvation for thymine (T) and amino acids (AAs), and/or a low UV pre-dose applied after prestarvation for AAs, pyrimidine dimer excision (PDE) is reduced without an adequate increase of UV sensitivity and UV mutagenesis. The unexcised lesions are tolerated by a putative repair pathway that is uvr dependent but does not involve excision. The process consists of PDE inhibition, which requires outer membrane protease OmpT, and subsequent pyrimidine dimer (PD) toleration, which may be mediated by interaction with a sister duplex using a number of SOS and stress-inducible proteins.
在经紫外线照射的切除 proficient(uvr+)大肠杆菌中,通过同时对胸腺嘧啶(T)和氨基酸(AAs)进行预饥饿,和/或在对 AAs 预饥饿后施加低剂量紫外线预照射进行预诱导,嘧啶二聚体切除(PDE)减少,而紫外线敏感性和紫外线诱变没有相应增加。未切除的损伤由一种推定的修复途径耐受,该途径依赖于 uvr 但不涉及切除。该过程包括 PDE 抑制,这需要外膜蛋白酶 OmpT,以及随后的嘧啶二聚体(PD)耐受,这可能通过使用多种 SOS 和应激诱导蛋白与姐妹双链相互作用来介导。