A partner-switching regulatory system controls hormogonium development in the filamentous cyanobacterium Nostoc punctiforme

Mol Microbiol. 2018 Aug;109(4):555-569. doi: 10.1111/mmi.14061. Epub 2018 Aug 27.

Abstract

Filamentous cyanobacteria exhibit developmental complexity, including the transient differentiation of motile hormogonia in many species. Using a forward genetic approach, a trio of genes unique to filamentous cyanobacteria encoding a putative Rsb-like partner-switching regulatory system (PSRS) was implicated in regulating hormogonium development in the model filamentous cyanobacterium Nostoc punctiforme. Analysis of in-frame deletion strains indicated that HmpU (putative serine phosphatase) and HmpV (STAS domain) enhance, while HmpW (putative serine kinase) represses motility and persistence of the hormogonium state. Protein-protein interaction studies demonstrated specificity between HmpW and HmpV. Epistasis analysis between hmpW and hmpV was consistent with HmpV acting as the downstream effector of the system, rather than regulation of a sigma factor by HmpW. Deletion of hmpU or hmpV reduced accumulation of extracellular PilA and hormogonium polysaccharide (HPS), and expression of type IV pilus- and HPS-specific genes was reduced in the ΔhmpV strain. Expression of the Hmp PSRS is induced in hormogonia, and the cytoplasmic localization of HmpV-GFPuv implies that its downstream target is probably cytoplasmic as well. Collectively, these results support a model where HmpU and HmpW antagonistically regulate the phosphorylation state of HmpV, and subsequently, unphosphorylated HmpV positively regulates an undefined downstream target to affect hormogonium-specific gene expression.

Keywords: Nostoc punctiforme; gliding motility; hormogonia; partner-switching system; signal transduction; type IV pili.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Bacterial Adhesion / physiology
  • Fimbriae, Bacterial / genetics
  • Fimbriae, Bacterial / metabolism*
  • Gene Expression Regulation, Bacterial / genetics*
  • Nostoc / genetics
  • Nostoc / metabolism*
  • Phosphoserine / metabolism*
  • Polysaccharides, Bacterial / genetics
  • Polysaccharides, Bacterial / metabolism
  • Protein Serine-Threonine Kinases / metabolism*

Substances

  • Polysaccharides, Bacterial
  • Phosphoserine
  • Protein Serine-Threonine Kinases