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New derivatives of TOL plasmid pWW0

I Sarand1, A Mäe, R Vilu

  • 1Institute of Molecular and Cell Biology, University of Tartu, Republic of Estonia.

Insights

Two Pseudomonas putida strains, PPW1-1 and PPW161-1, were studied for TOL plasmid gene deletions. Strain PPW161-1 maintained TOL substrate utilization despite gene loss, suggesting chromosomal integration of catabolic genes.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Biochemistry

Background:

  • Pseudomonas putida utilizes TOL plasmids for aromatic hydrocarbon degradation.
  • TOL plasmids contain operons encoding enzymes for xylene and toluene metabolism.
  • Genetic instability and rearrangements in TOL plasmids can affect bacterial catabolic capabilities.

Purpose of the Study:

  • To characterize new segregants of Pseudomonas putida with altered TOL plasmids.
  • To investigate the genetic basis for changes in substrate utilization in these strains.
  • To understand the implications of plasmid gene deletions and potential chromosomal integration.

Main Methods:

  • Isolation and characterization of Pseudomonas putida segregants (PPW1-1, PPW161-1).
  • Plasmid DNA analysis to identify deletions in transposon Tn4651 and TOL operons.
  • Growth studies on various aromatic substrates (m-xylene, m-toluate, benzoate).
  • Phenotypic analysis of TOL+ (TOL plasmid) substrate utilization.

Main Results:

  • Strain PPW1-1 showed a deletion in the TOL plasmid's upper-operon genes, losing m-xylene growth ability but retaining m-toluate utilization.
  • Strain PPW161-1 exhibited deletions in both upper- and meta-operon genes of its TOL plasmid.
  • PPW161-1 cells retained the ability to grow on all TOL plasmid substrates, indicating a stable Tol+ phenotype.
  • The catabolic genes deleted from the plasmid in PPW161-1 were proposed to have integrated into the bacterial chromosome.

Conclusions:

  • Plasmid gene deletions in Pseudomonas putida can lead to altered substrate utilization patterns.
  • Chromosomal integration of TOL catabolic genes can compensate for plasmid-borne gene loss.
  • This integration mechanism may explain the stable Tol+ phenotype observed in strain PPW161-1 despite plasmid deletions.

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