A mutant of Salmonella enterica serovar Typhimurium was isolated that simultaneously affected two metabolic pathways as follows: NAD metabolism and DNA repair. The mutant was isolated as resistant to a nicotinamide analog and as temperature-sensitive for growth on minimal glucose medium. In this mutant, Salmonella's 94-kb virulence plasmid pSLT had recombined into the chromosome upstream of the NAD salvage pathway gene pncA. This insertion blocked most transcription of pncA, which reduced uptake of the nicotinamide analog. The pSLT insertion mutant also exhibited phenotypes associated with induction of the SOS DNA repair system, including an increase in filamentous cells, higher exonuclease III and catalase activities, and derepression of SOS gene expression. Genome sequencing revealed increased read coverage extending out from the site of pSLT insertion. The two pSLT replication origins are likely initiating replication of the chromosome near the normal replication terminus. Too much replication initiation at the wrong site is probably causing the observed growth defects. Accordingly, deletion of both pSLT replication origins restored growth at higher temperatures.

中文翻译：

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由于异常的DNA复制，将pSLT质粒整合到沙门氏菌染色体中会导致温度敏感的生长缺陷。

分离到一个沙门氏菌血清型鼠伤寒沙门氏菌的突变体，该突变体同时影响以下两个代谢途径：NAD代谢和DNA修复。分离出该突变体具有对烟酰胺类似物的抗性，并且对在最小葡萄糖培养基上的生长具有温度敏感性。在该突变体中，沙门氏菌的94 kb毒力质粒pSLT已重组到NAD打捞途径基因pncA上游的染色体中。该插入阻止了大多数pncA转录，减少了烟酰胺类似物的摄取。pSLT插入突变体还表现出与SOS DNA修复系统的诱导相关的表型，包括丝状细胞的增加，更高的核酸外切酶III和过氧化氢酶活性以及SOS基因表达的抑制。基因组测序显示，从pSLT插入位点开始延伸的阅读覆盖范围有所增加。这两个pSLT复制起点可能会启动正常复制末端附近染色体的复制。在错误的位置进行过多的复制起始可能会导致观察到的生长缺陷。因此，两个pSLT复制起点的缺失在较高温度下恢复了生长。