Cyanobacterial sigma factor controls biofilm-promoting genes through intra- and intercellular pathways
Cyanobacteria frequently constitute integral components of microbial communities known as phototrophic biofilms, which are widespread in various environments and hold significant industrial relevance. Previous studies of the model cyanobacterium Synechococcus elongatus PCC 7942 revealed that its planktonic growth habit results from a biofilm-suppression mechanism that depends on an extracellular inhibitor, an observation that opens the door to investigating cyanobacterial intercellular communication. Here, we demonstrate that the RNA polymerase sigma factor SigF1, is required for this biofilm-suppression mechanism and suggest that sigF1-inactivation impairs secretion of the biofilm inhibitor. The S. elongatus paralog SigF2, however, is not involved in biofilm regulation. Comprehensive transcriptome analyses identified distinct regulons under the control of each of these sigma factors. Additional data indicate that SigF1 regulates biofilm through its involvement in transcriptional induction of genes that include those for the primary pilus subunit: sigF1 inactivation both prevents pilus assembly and abrogates secretion of the biofilm inhibitor. Consequently, expression is significantly upregulated for the ebfG-operon that encodes matrix components and the genes that encode the corresponding secretion system. Thus, this study uncovers a basic regulatory component of cyanobacterial intercellular communication, a field that is in its infancy. Elevated expression of biofilm-promoting genes in a sigF1 mutant supports an additional layer of regulation by SigF1 that operates via an intracellular mechanism. Overall design: To uncover transcriptional changes associated with biofilm formation we compared the transcriptomes of WT and the biofilm-forming strains PilB::Tn5 and SigF1::Mu. In addition, SigF2 mutant was included in the analysis to define the transcriptional space of either one of these SigF factors.