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Hik36–Hik43 and Rre6 act as a two-component regulatory system to control cell aggregation in Synechocystis sp. PCC6803
Hik36–Hik43 and Rre6 act as a two-component regulatory system to control cell aggregation in Synechocystis sp. PCC6803
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Hik36–Hik43 and Rre6 act as a two-component regulatory system to control cell aggregation in Synechocystis sp. PCC6803
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Hik36–Hik43 and Rre6 act as a two-component regulatory system to control cell aggregation in Synechocystis sp. PCC6803
Hik36–Hik43 and Rre6 act as a two-component regulatory system to control cell aggregation in Synechocystis sp. PCC6803

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Hik36–Hik43 and Rre6 act as a two-component regulatory system to control cell aggregation in Synechocystis sp. PCC6803
Hik36–Hik43 and Rre6 act as a two-component regulatory system to control cell aggregation in Synechocystis sp. PCC6803
Journal Article

Hik36–Hik43 and Rre6 act as a two-component regulatory system to control cell aggregation in Synechocystis sp. PCC6803

2020
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Overview
In response to environmental stress the model cyanobacterium, Synechocystis sp. PCC6803 can switch from a planktonic state to autoaggregation and biofilm formation. The precise mechanism of this transition remains unknown. Here we investigated the role of a candidate two-component regulatory system (TCS) in controlling morphological changes, as a way to understand the intermediate molecular steps that are part of the signaling pathway. A bacterial two-hybrid assay showed that the response regulator Rre6 formed a TCS together with a split histidine kinase consisting of Hik36 and Hik43. Individual disruption mutants displayed autoaggregation in a static culture. In contrast, unlike in the wild type, high salinity did not induce biofilm formation in Δhik36 , Δhik43 and Δrre6 . The expression levels of exopolysaccharide (EPS) production genes were higher in Δhik36 and Δhik43 , compared with the wild type, but lower in Δrre6 , suggesting that the TCS regulated EPS production in Synechocystis . Rre6 interacted physically with the motor protein PilT2, that is a component of the type IV pilus system. This interaction was enhanced in a phosphomimic version of Rre6. Taken together, Hik36–Hik43–Rre6 function as an upstream component of the pili-related signal transduction cascade and control the prevention of cell adhesion and biofilm formation.