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Microbial genetics

Amplified origins of antibiotic resistance

Nature Reviews Genetics volume 15, page 362 (2014)Cite this article

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Slager et al. studied the response of Streptococcus pneumoniae (which causes pneumonia and other diseases) to the bacterial DNA polymerase inhibitor 6-(p-hydroxyphenylazo)-uracil (HPUra). The resulting replication stress caused competence, as shown by the transcriptional induction of competence genes and by the ability to import and integrate exogenous DNA. From a global analysis of the transcriptional response to HPUra, the authors found that it was specifically genes proximal to the DNA replication origin (oriC) that were upregulated, including known com genes.

Interestingly, fluorescence microscopy and DNA copy-number analysis showed that HPUra slowed replisome progression away from oriC while allowing repeated firing of new DNA replication at oriC, thus increasing the copy number of oriC-proximal genes relative to genes elsewhere on the chromosome and providing an explanation for their selective transcriptional upregulation. Further evidence for this mechanism came from engineered strains, in which moving com genes away from oriC blocked antibiotic-induced competence, whereas additional copies of oriC-proximal com genes speeded up the response.

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References

  1. Slager, J. et al. Antibiotic-induced replication stress triggers bacterial competence by increasing gene dosage near the origin. Cell 157, 395–406 (2014)

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  1. Darren J. Burgess
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Burgess, D. Amplified origins of antibiotic resistance. Nat Rev Genet 15, 362 (2014). https://doi.org/10.1038/nrg3740

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