Metabolic engineering of the freshwater cyanobacterium Synechococcus elongatus PCC 7942 (Syn7942), synthesizing sucrose as the only compatible solute upon salt stress, has greatly improved its sucrose productivity. However, the signaling and regulatory mechanisms of this physiological process are still unknown. To know more about these aspects, a library of inactivation mutants for all 44 predicted signal transduction genes of Syn7942 was constructed. By evaluating sucrose production, two two-component signal transduction mutants Δ1125 and Δ1404, in which Synpcc7942_1125 and Synpcc7942_1404 was inactivated, respectively, were identified. They exhibited stably enhanced sucrose production, but the growth and the expression of sps encoding sucrose-phosphate synthase under salt stress were not affected, indicating that the corresponding signal transduction proteins do not regulate salt-induced sucrose synthesis by directly regulating sps expression. Moreover, the glycogen accumulation was enhanced in Δ1125 and Δ1404, and the salt stress-intensified photodamage of these mutants was also found to be relieved. These results indicated that the basic cell metabolisms such as glycogen metabolism and photosynthesis of the mutants were affected by gene inactivation, which might further affect salt-induced sucrose synthesis. Further studies on gene functions and signaling pathways or networks of Synpcc7942_1125 and Synpcc7942_1404 would reveal more details about the molecular bases for the observed phenotypes of Δ1125 and Δ1404.