Format

Send to

Choose Destination
PeerJ. 2019 Feb 26;7:e6459. doi: 10.7717/peerj.6459. eCollection 2019.

Two membrane-bound transcription factors regulate expression of various type-IV-pili surface structures in Sulfolobus acidocaldarius.

Author information

1
Institute of Biology II, Molecular Biology of Archaea, University of Freiburg, Freiburg, Germany.
2
Spemann Graduate School of Biology and Medicine (SGBM), Freiburg, Germany.
3
Department of Molecular Microbiology, Washington University, School of Medicine in St. Louis, St. Louis, MO, USA.

Abstract

In Archaea and Bacteria, gene expression is tightly regulated in response to environmental stimuli. In the thermoacidophilic crenarchaeon Sulfolobus acidocaldarius nutrient limitation induces expression of the archaellum, the archaeal motility structure. This expression is orchestrated by a complex hierarchical network of positive and negative regulators-the archaellum regulatory network (arn). The membrane-bound one-component system ArnR and its paralog ArnR1 were recently described as main activators of archaellum expression in S. acidocaldarius. They regulate gene expression of the archaellum operon by targeting the promoter of flaB, encoding the archaellum filament protein. Here we describe a strategy for the isolation and biochemical characterization of these two archaellum regulators. Both regulators are capable of forming oligomers and are phosphorylated by the Ser/Thr kinase ArnC. Apart from binding to pflaB, ArnR but not ArnR1 bound to promoter sequences of aapF and upsX, which encode components of the archaeal adhesive pilus and UV-inducible pili system, demonstrating a regulatory connection between different surface appendages of S. acidocaldarius.

KEYWORDS:

Archaea; Cell motility; Membrane protein; One-component system; Signal transduction; Transcription regulation

Conflict of interest statement

Sonja-Verena Albers is an Academic Editor for PeerJ.

Supplemental Content

Full text links

Icon for PeerJ, Inc. Icon for PubMed Central
Loading ...
Support Center