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.
Keywords: Cold stress; Cyanobacteria; Protein kinases; ROS; Red light; Universal triggers.
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