These authors contributed equally to this work.
YopK controls both rate and fidelity of Yop translocation
Article first published online: 4 DEC 2012
© 2012 Blackwell Publishing Ltd
Volume 87, Issue 2, pages 301–317, January 2013
How to Cite
Dewoody, R., Merritt, P. M. and Marketon, M. M. (2013), YopK controls both rate and fidelity of Yop translocation. Molecular Microbiology, 87: 301–317. doi: 10.1111/mmi.12099
- Issue published online: 14 JAN 2013
- Article first published online: 4 DEC 2012
- Manuscript Accepted: 12 NOV 2012
- NIH/NIAID. Grant Number: R21AI083660
- NIH Training Grant. Grant Number: T32 GM007757
- Region V ‘Great Lakes’ RCE. Grant Number: 2-U54-AI-057153
Yersinia pestis, the causative agent of plague, utilizes a type III secretion system (T3SS) to intoxicate host cells. The injection of T3SS substrates must be carefully controlled, and dysregulation leads to altered infection kinetics and early clearance of Y. pestis. While the sequence of events leading up to cell contact and initiation of translocation has received much attention, the regulatory events that take place after effector translocation is less understood. Here we show that the regulator YopK is required to maintain fidelity of substrate specificity, in addition to controlling translocation rate. YopK was found to interact with YopD within targeted cells during Y. pestis infection, suggesting that YopK's regulatory mechanism involves a direct interaction with the translocation pore. In addition, we identified a single amino acid in YopK that is essential for translocation rate regulation but is dispensable for maintaining fidelity of translocation. Furthermore, we found that expression of YopK within host cells was sufficient to downregulate translocation rate, but it did not affect translocation fidelity. Together, our data support a model in which YopK is a bifunctional protein whose activities are genetically and spatially distinct such that fidelity control occurs within bacteria and rate control occurs within host cells.