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Summary: Erwinia amylovora, the causative agent of fire blight, uses flagella‐based motilities to translocate to host plant natural openings; however, little is known about how this bacterium migrates systemically in the apoplast. Here, we reveal a novel surface motility mechanism, defined as sliding, in E. amylovora. Deletion of flagella assembly genes did not affect this movement, whereas deletion of biosynthesis genes for the exopolysaccharides (EPSs) amylovoran and levan resulted in non‐sliding phenotypes. Since EPS production generates osmotic pressure that potentially powers sliding, we validated this mechanism by demonstrating that water potential positively contributes to sliding. In addition, no sliding was observed when the water potential of the surface was lower than −0.5 MPa. Sliding is a passive motility mechanism. We further show that the force of gravity plays a critical role in directing E. amylovora sliding on unconfined surfaces but has a negligible effect when cells are sliding in confined microcapillaries, in which EPS‐dependent osmotic pressure acts as the main force. Although amylovoran and levan are both required for sliding, we demonstrate that they exhibit different roles in bacterial communities. In summary, our study provides fundamental knowledge for a better understanding of mechanisms that drive bacterial sliding motility. [ABSTRACT FROM AUTHOR]

Summary: Dickeya dadantii is a plant pathogen that causes soft rot disease on vegetable and potato crops. To successfully cause infection, this pathogen needs to coordinately modulate the expression of genes encoding several virulence determinants, including plant cell wall degrading enzymes (PCWDEs), type III secretion system (T3SS) and flagellar motility. Here, we uncover a novel feed‐forward signalling circuit for controlling virulence. Global RNA chaperone Hfq interacts with an Hfq‐dependent sRNA ArcZ and represses the translation of pecT, encoding a LysR‐type transcriptional regulator. We demonstrate that the ability of ArcZ to be processed to a 50 nt 3′‐ end fragment is essential for its regulation of pecT. PecT down‐regulates PCWDE and the T3SS by repressing the expression of a global post‐transcriptional regulator‐ (RsmA‐) associated sRNA encoding gene rsmB. In addition, we show that the protein levels of two cyclic di‐GMP (c‐di‐GMP) diguanylate cyclases (DGCs), GcpA and GcpL, are repressed by Hfq. Further studies show that both DGCs are essential for the Hfq‐mediated post‐transcriptional regulation on RsmB. Overall, our report provides new insights into the interplays between ubiquitous signalling transduction systems that were most studied independently and sheds light on multitiered regulatory mechanisms for a precise disease regulation in bacteria. [ABSTRACT FROM AUTHOR]

Dickeya dadantii is a globally dispersed phytopathogen which causes diseases on a wide range of host plants. This pathogen utilizes the type III secretion system (T3SS) to suppress host defense responses, and secretes pectate lyase (Pel) to degrade the plant cell wall. Although the regulatory small RNA (sRNA) RsmB, cyclic diguanylate monophosphate (c-di-GMP) and flagellar regulator have been reported to affect the regulation of these two virulence factors or multiple cell behaviours such as motility and biofilm formation, the linkage between these regulatory components that coordinate the cell behaviours remain unclear. Here, we revealed a sophisticated regulatory network that connects the sRNA, c-di-GMP signalling and flagellar master regulator FlhDC. We propose multi-tiered regulatory mechanisms that link the FlhDC to the T3SS through three distinct pathways including the FlhDC-FliAYcgR3937 pathway; the FlhDC-EcpC-RpoN-HrpL pathway; and the FlhDC-rsmB-RsmA-HrpL pathway. Among these, EcpC is the most dominant factor for FlhDC to positively regulate T3SS expression. [ABSTRACT FROM AUTHOR]