PT  - JOURNAL ARTICLE
AU  - Jun Jie Wong
AU  - Kelvin K.L. Chong
AU  - Foo Kiong Ho
AU  - Chee Meng Benjamin Ho
AU  - Ramesh Neelakandan
AU  - Pei Yi Choo
AU  - Damien Keogh
AU  - John Chen
AU  - Chuan Fa Liu
AU  - Kimberly A. Kline
TI  - <em>Escherichia coli</em> BarA-UvrY regulates the <em>pks</em> island and kills Staphylococci via the genotoxin colibactin
AID  - 10.1101/2021.12.17.473262
DP  - 2021 Jan 01
TA  - bioRxiv
PG  - 2021.12.17.473262
4099  - http://biorxiv.org/content/early/2021/12/18/2021.12.17.473262.short
4100  - http://biorxiv.org/content/early/2021/12/18/2021.12.17.473262.full
AB  - Wound infections are often polymicrobial in nature and are associated with poor disease prognoses. Escherichia coli and Staphylococcus aureus are among the top five most cultured pathogens from wound infections. However, little is known about the polymicrobial interactions between E. coli and S. aureus during wound infections. In this study, we show that E. coli kills S. aureus both in vitro and in a mouse excisional wound model via the genotoxin, colibactin. We also show that the BarA-UvrY two component system (TCS) is a novel regulator of the pks island, which acts through the carbon storage global regulatory (Csr) system. Together, our data demonstrate the role of colibactin in inter-species competition and show that it is regulated by BarA-UvrY TCS, a previously uncharacterized regulator of the pks island.Competing Interest StatementThe authors have declared no competing interest.