作者: Kuo Song , Martin Hagemann , Xiaoming Tan , Xuefeng Lu
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摘要: 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 spsA gene encoding sucrose-phosphate synthase and mutation of slr1588 also affected tolerance Synechocystis (Chen et al., 2014). The latter finding contrary to earlier observations (Hagemann 1997a). Here, we observed ectopic expression did not restore mutant, making essential function this questionable. Subsequent experiments showed deletion entire coding sequence compromised downstream situated ggpP gene, encodes glucosylglycerol-phosphate phosphatase synthesis primary osmolyte glucosylglycerol. Mutation by deleting N-terminal part protein (∆slr1588-F976) affect expression, glucosylglycerol accumulation as well salt-tolerance, while resulted in previously reported sensitive phenotype. In ∆slr1588-F976 mutant was up-regulated but content lowered due increased invertase activity. Our results reveal acting a repressor suggested it crucial overall acclimation Synechocystis.