Carol H. Pong, Jade E. Peace, Christopher J. Harmer, Ruth M. Hall
{"title":"is26介导的Tn4352B易位单元的丢失需要recA1等位基因的存在","authors":"Carol H. Pong, Jade E. Peace, Christopher J. Harmer, Ruth M. Hall","doi":"10.1016/j.plasmid.2022.102668","DOIUrl":null,"url":null,"abstract":"<div><p>The pseudo-compound transposon Tn<em>4352</em>B is unusual in that the translocatable unit (TU) consisting of one of the bounding IS<em>26</em> copies and the central portion containing the <em>aphA1a</em> gene has been found to be readily lost in the <em>Escherichia coli</em> strains used as host. Rapid loss required the presence of an additional 2 G residues adjacent to the internal end of one of the IS<em>26</em> that flank the central portion and an active Tnp26 transposase. However, Tn<em>4352</em>B was found to be stable in wild-type <em>Klebsiella pneumoniae</em> strains. Though it was concluded that the difference may be due to the species background, the <em>E. coli</em> strains used were recombination-deficient. Here, we have further investigated the requirements for TU loss in <em>E. coli</em> and found that Tn<em>4352</em>B was stable in recombination-proficient strains. Among several recombination-deficient strains examined, rapid loss occurred only in strains that carry the <em>recA1</em> allele but not in strains carrying different <em>recA</em> alleles, <em>recA13</em> and a novel <em>recA</em> allele identified here, that also render the strain deficient in homologous recombination. Hence, it appears that a specific property of the RecA1 protein underlies the observed TU loss from Tn<em>4352</em>B.</p></div>","PeriodicalId":49689,"journal":{"name":"Plasmid","volume":"125 ","pages":"Article 102668"},"PeriodicalIF":1.8000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"IS26-mediated loss of the translocatable unit from Tn4352B requires the presence of the recA1 allele\",\"authors\":\"Carol H. Pong, Jade E. Peace, Christopher J. Harmer, Ruth M. Hall\",\"doi\":\"10.1016/j.plasmid.2022.102668\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>The pseudo-compound transposon Tn<em>4352</em>B is unusual in that the translocatable unit (TU) consisting of one of the bounding IS<em>26</em> copies and the central portion containing the <em>aphA1a</em> gene has been found to be readily lost in the <em>Escherichia coli</em> strains used as host. Rapid loss required the presence of an additional 2 G residues adjacent to the internal end of one of the IS<em>26</em> that flank the central portion and an active Tnp26 transposase. However, Tn<em>4352</em>B was found to be stable in wild-type <em>Klebsiella pneumoniae</em> strains. Though it was concluded that the difference may be due to the species background, the <em>E. coli</em> strains used were recombination-deficient. Here, we have further investigated the requirements for TU loss in <em>E. coli</em> and found that Tn<em>4352</em>B was stable in recombination-proficient strains. Among several recombination-deficient strains examined, rapid loss occurred only in strains that carry the <em>recA1</em> allele but not in strains carrying different <em>recA</em> alleles, <em>recA13</em> and a novel <em>recA</em> allele identified here, that also render the strain deficient in homologous recombination. Hence, it appears that a specific property of the RecA1 protein underlies the observed TU loss from Tn<em>4352</em>B.</p></div>\",\"PeriodicalId\":49689,\"journal\":{\"name\":\"Plasmid\",\"volume\":\"125 \",\"pages\":\"Article 102668\"},\"PeriodicalIF\":1.8000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Plasmid\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0147619X2200052X\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"GENETICS & HEREDITY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Plasmid","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0147619X2200052X","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
IS26-mediated loss of the translocatable unit from Tn4352B requires the presence of the recA1 allele
The pseudo-compound transposon Tn4352B is unusual in that the translocatable unit (TU) consisting of one of the bounding IS26 copies and the central portion containing the aphA1a gene has been found to be readily lost in the Escherichia coli strains used as host. Rapid loss required the presence of an additional 2 G residues adjacent to the internal end of one of the IS26 that flank the central portion and an active Tnp26 transposase. However, Tn4352B was found to be stable in wild-type Klebsiella pneumoniae strains. Though it was concluded that the difference may be due to the species background, the E. coli strains used were recombination-deficient. Here, we have further investigated the requirements for TU loss in E. coli and found that Tn4352B was stable in recombination-proficient strains. Among several recombination-deficient strains examined, rapid loss occurred only in strains that carry the recA1 allele but not in strains carrying different recA alleles, recA13 and a novel recA allele identified here, that also render the strain deficient in homologous recombination. Hence, it appears that a specific property of the RecA1 protein underlies the observed TU loss from Tn4352B.
期刊介绍:
Plasmid publishes original research on genetic elements in all kingdoms of life with emphasis on maintenance, transmission and evolution of extrachromosomal elements. Objects of interest include plasmids, bacteriophages, mobile genetic elements, organelle DNA, and genomic and pathogenicity islands.