New insights in cyanobacterial cold stress responses: Genes, sensors, and molecular triggers.

BACKGROUND

Cold stress strongly induces the expression of ~100 genes in cyanobacteria. Some of these genes are necessary to protect cellular functions by adjustment of membranes, as well as transcriptional and translational machineries. About a half of cold-induced genes are not functionally characterized. A part of cold-induced genes is under control of a two-component regulatory system, consisting of histidine kinase Hik33 and response regulator Rre26. The mechanism(s) that control another part of cold-inducible genes are still unknown.

SCOPE OF REVIEW

The aim of this review is to summarise the latest findings in cyanobacterial cold-stress responses including transcriptomics, cold sensing, and molecular triggers.

MAJOR CONCLUSIONS

A feedback loop between the membrane fluidity and transcription of genes for fatty acid desaturases operates via the transmembrane red-light-activated cold sensor Hik33, which perceives cold-induced membrane rigidification as a change in its thickness. The cold-induced kinase activity of Hik33 is facilitated by interaction with a small protein, Ssl3451 - the third contributor to a canonical two-component regulatory system, which may explain the ability of some cyanobacterial histidine kinases to interact with different response regulators under different stress conditions. Other regulatory systems that control cold-stress responses operate via Ser/Thr protein kinase, SpkE, and via temperature-dependent changes in DNA supercoiling. Transcriptomic analysis shows that universal triggers of stress responses are reactive oxygen species and changes in redox status of plastoquinone pool.

GENERAL SIGNIFICANCE

Deeper understanding of molecular mechanisms of temperature sensing and regulation of cold-stress responses in photosynthetic cells provide a background for generation of cold-resistant crops.