Bacteria sometimes hedge their survival bets by concurrently activating response circuits leading to different phenotypes in isogenic populations. We show that the cyanobacterium Nostoc punctiforme responds to UV-A by concurrently producing the sunscreen scytonemin and differentiating into motile hormogonia but segregating the responses at the filament level. Mutational studies show that a four-gene partner-switching regulatory system (hcyA-D) orchestrates the cross-talk between the respective regulatory circuitries. Transcription of hormogonium genes and hcyA-D is upregulated by UVA through the scytonemin two-component regulator (scyTCR), hcyA-D being directly involved in signal transduction into the hormogonium response and its modulation by visible light. The sigma factor cascade that regulates developmental commitment to hormogonia also upregulates hcyA-D transcription and strongly suppresses scytonemin synthesis through downregulation of the scyTCR itself. Through this complex bidirectional mechanism, Nostoc can concurrently deploy two fundamentally different UV stress mitigation strategies, either hunker down or flee, in a single population.
Keywords: Microbiology; Molecular Genetics; Molecular biology.
© 2022 The Author(s).