The Micacocidin Production-Related Deletion Alters the Quorum Sensing-Dependent Gene Regulation of Strain OE1-1.

The soil-borne phytopathogenic gram-negative bacterium species complex (RSSC) produces staphyloferrin B and micacocidin as siderophores that scavenge for trivalent iron (Fe) in the environment, depending on the intracellular divalent iron (Fe) concentration. The staphyloferrin B-deficient mutant reportedly retains its virulence, but the relationship between micacocidin and virulence remains unconfirmed. To elucidate the effect of micacocidin on RSSC virulence, we generated the micacocidin productivity-deficient mutant (Δ) that lacks , which encodes a putative polyketide synthase/non-ribosomal peptide synthetase, using the RSSC phylotype I strain OE1-1. When incubated in the condition without Fe, Δ showed significantly lower Fe-scavenging activity, compared with OE1-1. Until 8 days after inoculation on tomato plants, Δ was not virulent, similar to the mutant (Δ) missing , which encodes the LysR-type transcriptional regulator PhcA that regulates the expression of the genes responsible for quorum sensing (QS)-dependent phenotypes including virulence. The transcriptome analysis revealed that deletion significantly altered the expression of more than 80% of the PhcA-regulated genes in the mutant grown in medium with or without Fe. Among the PhcA-regulated genes, the transcript levels of the genes whose expression was affected by the deletion of were strongly and positively correlated between the Δ and the -deletion mutant. Furthermore, the deletion of significantly modified QS-dependent phenotypes, similar to the effects of the deletion of . Collectively, our findings suggest that the deletion of micacocidin production-related alters the regulation of PhcA-regulated genes responsible for QS-dependent phenotypes including virulence as well as Fe-scavenging activity. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.