Cells of the cyanobacterium Synechocystis sp. PCC 6803 are equipped with a mechanosensitive ion channel MscL that is located in their plasma membrane. However, the exact function of the channel in this freshwater cyanobacterium is unknown.

High affinity transport of manganese ions (Mn) in cyanobacteria is carried by an ABC-type transporter, encoded by the mntCAB operon, which is derepressed by the deficiency of Mn. Transcription of this operon is negatively regulated by the two-component system consisting of a sensory histidine kinase ManS and DNA-binding response regulator ManR. In this study, we examined two Synechocystis mutants, defective in ManS and ManR. These mutants were unable to grow on high concentrations of manganese. Furthermore, they were sensitive to high light intensity and unable to recover after short-term photoinhibition. Under standard illumination and Mn concentration, mutant cells revealed the elevated levels of transcripts of genes involved in the formation of Photosystem II (psbA, psbD, psbC, pap-operon). This finding suggests that, in mutant cells, the PSII is sensitive to high concentrations of Mn even at relatively low light intensity.

Calcium plays an essential role in a variety of stress responses of eukaryotic cells; however, its function in prokaryotes is obscure. Bacterial ion channels that transport Ca(2+) are barely known. We investigated temperature-induced changes in intracellular concentration of Ca(2+), Na(+) and K(+) in the cyanobacterium Synechocystis sp. strain PCC 6803 and its mutant that is defective in mechanosensitive ion channel MscL. Concentration of cations rapidly and transiently increased in wild-type cells in response to cold and heat treatments. These changes in ionic concentrations correlated with the changes in cytoplasmic volume that transiently decreased in response to temperature treatments. However, no increase in ionic concentrations was observed in the MscL-mutant cells. It implies that MscL functions as a non-specific ion channel, and it participates in regulation of cell volume under temperature-stress conditions.

Late blight is one of the most economically important diseases affecting potato and causing a significant loss in yield. The development of transgenic potato plants with enhanced resistance to infection by Phytophthora infestans may represent a possible approach to solving this issue. A comparative study of the leaf response in control potato plants (S.tuberosum L. cultivar Skoroplodnyi), control transgenic plants expressing the reporter gene of thermostable lichenase (transgenic licBM3 line) and transgenic plants expressing cyanobacterial hybrid genes ∆9-acyl-lipid desaturase (transgenic desC lines) and ∆12-acyl-lipid desaturase (transgenic desA lines) to infection with P. infestans has been performed. The expression of desaturase genes in potato plants enhanced their tolerance to potato late blight agents as compared with the control. The lipid peroxidation level raised in the leaves of the control and transgenic desA plants on third day after inoculation with P. infestans zoospores and remained the same in the transgenic desC plants. The number of total phenolic compounds was increased as early as on the second day after infection in all studied variants and continued to remain the same, except for transgenic desC plants. Accumulation of flavonoids, the main components of the potato leaf phenolic complex, raised on the second day in all studied variants, remained unchanged on the third day in the control plants and decreased in most transgenic plants expressing desaturase genes. The results obtained in our study demonstrate that the expression of genes of Δ9- and Δ12-acyl-lipid desaturases in potato plants enhanced their resistance to P. infestans as compared with the control non-transgenic plants due to concomitant accumulation of phenolic compounds, including flavonoids, in the leaves. All these changes were more pronounced in transgenic desC plants, which indicates that the Δ9-acyllipid desaturase gene appears to be a potential inducer of the production of biological antioxidants in plant cells.