The TGV transgenic vectors for single-copy gene expression from the Escherichia coli chromosome

Gumbiner-Russo, Laura; Lombardo, Mary‐Jane; Ponder, Rebecca G.; Rosenberg, Susan M.

doi:10.1016/s0378-1119(01)00565-0

Cited by 23 publications

(25 citation statements)

References 27 publications

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“…The strains and plasmids used are shown in Table 1. SMR5222, an E. coli strain carrying the E. cloacae ampRC ϩ genes in the E. coli chromosome, was constructed using the TGV (transgenic vector) system for integrating linear DNA cassettes into the E. coli chromosome (14). E. cloacae strain MHN1 ampRC ϩ genes were isolated from plasmid pEc1c (35) by digestion with BamHI and SalI and were ligated into BglII-and XhoI-digested pTGV-light (14) plasmid DNA, creating pJP2.…”

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“…E. cloacae strain MHN1 ampRC ϩ genes were isolated from plasmid pEc1c (35) by digestion with BamHI and SalI and were ligated into BglII-and XhoI-digested pTGV-light (14) plasmid DNA, creating pJP2. pJP2 was digested with NdeI to generate an ampRC ϩ fragment flanked on both sides by homology to the E. coli attachment site for phage (att) for linear transformation in the TGV system (14). SMR5201, a transformant carrying ampRC ϩ replacing att (confirmed by PCR as described elsewhere [14]) was used as a P1 donor to move att::ampRC ϩ into SMR5156 by P1 transduction (as described elsewhere [14]) to create SMR5222.…”

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“…pJP2 was digested with NdeI to generate an ampRC ϩ fragment flanked on both sides by homology to the E. coli attachment site for phage (att) for linear transformation in the TGV system (14). SMR5201, a transformant carrying ampRC ϩ replacing att (confirmed by PCR as described elsewhere [14]) was used as a P1 donor to move att::ampRC ϩ into SMR5156 by P1 transduction (as described elsewhere [14]) to create SMR5222. Subsequent strains are isogenic to SMR5222 and were created using standard phage P1 transduction (referenced elsewhere [14]), and the constructions are outlined in Table 1.…”

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Chromosomal System for Studying AmpC-Mediated β-Lactam Resistance Mutation in Escherichia coli

Petrosino¹,

Pendleton²,

Weiner

et al. 2002

Antimicrob Agents Chemother

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In some enterobacterial pathogens, but not in Escherichia coli, loss-of-function mutations in the ampD gene are a common route to ␤-lactam antibiotic resistance. We constructed an assay system for studying mechanism(s) of enterobacterial ampD mutation using the well-developed genetics of E. coli. We integrated the Enterobacter ampRC genes into the E. coli chromosome. These cells acquire spontaneous recombination-and SOS response-independent ␤-lactam resistance mutations in ampD. This chromosomal system is useful for studying mutation mechanisms that promote antibiotic resistance.

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Chromosomal System for Studying AmpC-Mediated β-Lactam Resistance Mutation in Escherichia coli

Petrosino¹,

Pendleton²,

Weiner

et al. 2002

Antimicrob Agents Chemother

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“…The strains and plasmids used are shown in Table 1. SMR5222, an E. coli strain carrying the E. cloacae ampRC + genes in the E. coli chromosome, was constructed using the TGV (transgenic vector) system for integrating linear DNA cassettes into the E. coli chromosome (14). E. cloacae strain MHN1 ampRC + genes were isolated from plasmid pEclc (35) by digestion with BarriHl and Sail and were ligated into Bglll-and ATioI-digested pTGV-light (14) plasmid DNA, creating pJP2.…”

Section: Discussionmentioning

confidence: 99%

“…SMR5222, an E. coli strain carrying the E. cloacae ampRC + genes in the E. coli chromosome, was constructed using the TGV (transgenic vector) system for integrating linear DNA cassettes into the E. coli chromosome (14). E. cloacae strain MHN1 ampRC + genes were isolated from plasmid pEclc (35) by digestion with BarriHl and Sail and were ligated into Bglll-and ATioI-digested pTGV-light (14) plasmid DNA, creating pJP2. pJP2 was digested with Ndel to generate an ampRC + fragment flanked on both sides by homology to the E. coli attachment site for phage \ (att\) for linear transformation in the TGV system (14).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Mutation in Non-Dividing Cells

Petrosino¹,

Rosenberg²

2003

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. Public reposing burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. 13. Abstract Understanding how mutations arise in non-growing cells will help illuminate mechanisms of oncogenesis, tumor progression, and resistance to chemotherapeutic drugs. To this end, I have been addressing how antibiotic resistance mutations occur in non-, or slowly-growing enterobacteria cells. Previously, our laboratory discovered that RecA (an hRAD51 homolog) and RecBCD recombination repair proteins are necessary for the acquisition of ß-lactam drug-resistant mutations in the Escherichia coli chromosome during stationary-phase. The data suggest that either the SOS DNA damage-repair response, recombinational DNA repair, or both, are involved in the mutation pathway.

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