Yoakum G, Ferron W, Eisenstark A, Webb R B
J Bacteriol. 1974 Jul;119(1):62-9. doi: 10.1128/jb.119.1.62-69.1974.
Near-ultraviolet photoproducts of l-tryptophan (TP) differentially inhibited deoxyribonucleic acid (DNA) replication in wild-type cells and uvrA, polA1, and recA recB double mutants of Escherichia coli. Wild-type cells labeled in their DNA with [(3)H]thymidine in the presence of TP produced small pieces of DNA (7 x 10(6) daltons), which corresponded in size to late replicative intermediates of discontinuous DNA synthesis. Moreover, when TP was present, it took five times longer to chase the low-molecular-weight DNA pieces into high-molecular-weight DNA. The observation of replicative intermediates in the presence of TP, and their slow chase into high-molecular-weight DNA in the presence of TP, is strong evidence that TP stabilizes replication gaps in E. coli DNA. Although TP slowed DNA replication in wild-type cells, this effect was transient and DNA synthesis eventually resumed at a normal rate. However, in polA1 and recA recB mutants, DNA synthesis was completely inhibited. Determinations of size and total counts of cells incubated in TP suggested that TP uncouples cell division from DNA replication in recA recB mutants, whereas these processes remain coupled in wild-type cells and in uvrA and polA1 mutants. The slow chase of TP-stabilized pieces of DNA in the presence of TP suggested that the selective effect of TP on DNA synthesis and viability in repair-deficient mutants is a result of TP inhibition of replication gap closure.
L-色氨酸（TP）的近紫外光产物对大肠杆菌野生型细胞以及uvrA、polA1和recA recB双突变体中的脱氧核糖核酸（DNA）复制有不同程度的抑制作用。在TP存在的情况下，用[³H]胸腺嘧啶标记DNA的野生型细胞产生了小片段DNA（7×10⁶道尔顿），其大小与不连续DNA合成的晚期复制中间体相对应。此外，当存在TP时，将低分子量DNA片段追踪转化为高分子量DNA所需的时间延长了五倍。在TP存在的情况下观察到复制中间体，以及它们在TP存在时缓慢追踪转化为高分子量DNA，有力地证明了TP能稳定大肠杆菌DNA中的复制缺口。虽然TP减缓了野生型细胞中的DNA复制，但这种作用是短暂的，DNA合成最终会以正常速率恢复。然而，在polA1和recA recB突变体中，DNA合成被完全抑制。对在TP中孵育的细胞大小和总数的测定表明，TP使recA recB突变体中的细胞分裂与DNA复制解偶联，而在野生型细胞以及uvrA和polA1突变体中，这些过程仍然是偶联的。在TP存在的情况下，TP稳定的DNA片段的缓慢追踪表明，TP对修复缺陷型突变体中DNA合成和生存能力的选择性作用是TP抑制复制缺口闭合的结果。
