The extracellular matrix protein TasA is a developmental cue that maintains a motile subpopulation within Bacillus subtilis biofilms

Nitai Steinberg, Alona Keren-Paz, Qihui Hou, Shany Doron, Keren Yanuka-Golub, Tsviya Olender, Rotem Hadar, Gili Rosenberg, Rakeshkumar Jain, Jesus Cámara-Almirón, Diego Romero, Sven van Teeffelen, Ilana Kolodkin-Gal

Research output: Contribution to journalArticlepeer-review

Abstract

In nature, bacteria form biofilms-differentiated multicellular communities attached to surfaces. Within these generally sessile biofilms, a subset of cells continues to express motility genes. We found that this subpopulation enabled Bacillus subtilis biofilms to expand on high-friction surfaces. The extracellular matrix (ECM) protein TasA was required for the expression of flagellar genes. In addition to its structural role as an adhesive fiber for cell attachment, TasA acted as a developmental signal stimulating a subset of biofilm cells to revert to a motile phenotype. Transcriptomic analysis revealed that TasA stimulated the expression of a specific subset of genes whose products promote motility and repress ECM production. Spontaneous suppressor mutations that restored motility in the absence of TasA revealed that activation of the biofilm-motility switch by the two-component system CssR/CssS antagonized the TasA-mediated reversion to motility in biofilm cells. Our results suggest that although mostly sessile, biofilms retain a degree of motility by actively maintaining a motile subpopulation.

Original languageEnglish
Article numbereaaw8905
JournalScience Signaling
Volume13
Issue number632
DOIs
StatePublished - 19 May 2020
Externally publishedYes

Bibliographical note

Publisher Copyright:
Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works

Keywords

  • Bacillus subtilis/physiology
  • Bacterial Proteins/metabolism
  • Biofilms/growth & development
  • Extracellular Matrix Proteins/metabolism

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