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Cyanobacterial sucrose biosynthesis is stimulated under salt stress, which could be used for biotechnological sugar production. It has been shown that the response regulator Slr1588 negatively regulates the  spsA  gene encoding sucrose-phosphate synthase and mutation of the  slr1588  gene also affected the salt tolerance of  Synechocystis  ( Chen et al., 2014 ). The latter finding is contrary to earlier observations ( Hagemann et al., 1997b ). Here, we observed that ectopic expression of  slr1588  did not restore the salt tolerance of the  slr1588  mutant, making the essential function of this response regulator for salt tolerance questionable. Subsequent experiments showed that deletion of the entire coding sequence of  slr1588  compromised the expression of the downstream situated  ggpP  gene, which encodes glucosylglycerol-phosphate phosphatase for synthesis of the primary osmolyte glucosylglycerol. Mutation of  slr1588  by deleting the N-terminal part of this protein (Δ slr1588 -F976) did not affect  ggpP  expression, glucosylglycerol accumulation as well as salt tolerance, while the mutation of  ggpP  resulted in the previously reported salt-sensitive phenotype. In the Δ slr1588 -F976 mutant  spsA  was up-regulated but sucrose content was lowered due to increased invertase activity. Our results reveal that Slr1588 is acting as a repressor for  spsA  as previously suggested but it is not crucial for the overall salt acclimation of  Synechocystis .

The Response Regulator Slr1588 Regulates spsA But Is Not Crucial for Salt Acclimation of Synechocystis sp. PCC 6803