Modulation of bacterial cell size and growth rate via activation of a cell envelope stress response
Abstract
Fluctuating conditions and diverse stresses are typical in natural environments. In response, cells mount complex responses across multiple scales, including adjusting their shape to withstand stress. In enterobacteria, the Rcs phosphorelay is activated by cell envelope damage and by changes to periplasmic dimensions and cell width. Here, we investigated the physiological and morphological consequences of Rcs activation in Escherichia coli in the absence of stresses, using an inducible version of RcsF that mislocalizes to the inner membrane, RcsFIM. Expression of RcsFIM immediately reduced cellular growth rate and the added length per cell cycle in a manner that was directly dependent on induction levels, but independent of Rcs-induced capsule production. At the same time, cells increased intracellular concentration of the cell division protein FtsZ, and decreased the distance between division rings in filamentous cells. Depletion of the Rcs negative regulator IgaA phenocopied RcsFIM induction, indicating that IgaA is essential due to growth inhibition in its absence. However, A22 treatment did not affect growth rate or FtsZ intracellular concentration, despite activating the Rcs system. These findings suggest that the effect of Rcs activation on FtsZ levels is mediated indirectly through growth-rate changes, and highlight feedbacks among the Rcs stress response, growth dynamics, and cell-size control.
Additional Information
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. The authors thank the Huang and Typas labs for useful discussions. This work was supported by a National Science Foundation Graduate Research Fellowship (to A.M.), an ARCS Fellowship (to A.M.), a James McDonnell Postdoctoral Fellowship (to H.S.), EMBL core funding and a DFG grant (TY 116/2-1) for SPP1617 (to A.T.), NIH Director's New Innovator Award DP2OD006466 (to K.C.H.), NSF CAREER Award MCB-1149328 and grant EF-2125383 (to K.C.H.), and the Allen Discovery Center at Stanford on Systems Modeling of Infection (to K.C.H.). K.C.H. is a Chan Zuckerberg Biohub Investigator. This work was also supported in part by the National Science Foundation under Grant PHYS-1066293 and the hospitality of the Aspen Center for Physics. The authors have declared no competing interest.Attached Files
Submitted - 2022.07.26.501648v1.full.pdf
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Additional details
- Eprint ID
- 115931
- Resolver ID
- CaltechAUTHORS:20220728-119864000
- NSF Graduate Research Fellowship
- ARCS Foundation
- James McDonnell Foundation
- European Molecular Biology Laboratory (EMBL)
- Deutsche Forschungsgemeinschaft (DFG)
- TY 116/2-1
- NIH
- DP2OD006466
- NSF
- MCB-1149328
- NSF
- EF-2125383
- Stanford University
- Chan Zuckerberg Biohub
- NSF
- PHY-1066293
- Created
-
2022-07-28Created from EPrint's datestamp field
- Updated
-
2022-07-28Created from EPrint's last_modified field
- Caltech groups
- Division of Biology and Biological Engineering