English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Preprint

During heat stress in Myxococcus xanthus, the CdbS PilZ domain protein, along with two PilZ-DnaK chaperones, perturbs chromosome organization and accelerates cell death

MPS-Authors
/persons/resource/persons288697

Seidel,  Michael
Bacterial Adaption and Differentiation, Department of Ecophysiology, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

/persons/resource/persons254719

Skotnicka,  Dorota
Bacterial Adaption and Differentiation, Department of Ecophysiology, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

/persons/resource/persons261236

Glatter,  Timo       
Core Facility Mass Spectrometry and Proteomics, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

/persons/resource/persons254723

Søgaard-Andersen,  Lotte       
Bacterial Adaption and Differentiation, Department of Ecophysiology, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Seidel, M., Skotnicka, D., Glatter, T., & Søgaard-Andersen, L. (2023). During heat stress in Myxococcus xanthus, the CdbS PilZ domain protein, along with two PilZ-DnaK chaperones, perturbs chromosome organization and accelerates cell death. bioRxiv: the preprint server for biology, 2023.04.14.536847.


Cite as: https://hdl.handle.net/21.11116/0000-000C-F8ED-2
Abstract
C-di-GMP is a bacterial second messenger that regulates diverse processes in response to environmental or cellular cues. The nucleoid-associated protein (NAP) CdbA in Myxococcus xanthus binds c-di-GMP and DNA in a mutually exclusive manner in vitro. CdbA is essential for viability, and CdbA depletion causes defects in chromosome organization, leading to a block in cell division and, ultimately, cell death. Most NAPs are not essential; therefore, to explore the paradoxical cdbA essentiality, we isolated suppressor mutations that restored cell viability without CdbA. Most mutations mapped to cdbS, which encodes a stand-alone c-di-GMP binding PilZ domain protein, and caused loss-of-function of cdbS. Cells lacking CdbA and CdbS or only CdbS were fully viable and had no defects in chromosome organization. CdbA depletion caused post-transcriptional upregulation of CdbS accumulation, and this CdbS over-accumulation was sufficient to disrupt chromosome organization and cause cell death. CdbA depletion also caused increased accumulation of CsdK1 and CsdK2, two unusual PilZ-DnaK chaperones. During CdbA depletion, CsdK1 and CsdK2, in turn, stabilized CdbS, thereby enabling its increased accumulation and toxicity. Moreover, we demonstrate that heat stress, possibly involving an increased cellular c-di-GMP concentration, induces the CdbA/CsdK1/CsdK2/CdbA system, causing a CsdK1- and CsdK2-dependent increase in CdbS accumulation. Thereby this system accelerates heat stress-induced chromosome mis-organization and cell death. Collectively, this work describes a unique system that contributes to regulated cell death in M. xanthus and suggests a link between c-di-GMP signaling and regulated cell death in bacteria.Competing Interest StatementThe authors have declared no competing interest.