Skip to main content
Advertisement
Browse Subject Areas
?

Click through the PLOS taxonomy to find articles in your field.

For more information about PLOS Subject Areas, click here.

< Back to Article

Autoregulation of RNA Helicase Expression in Response to Temperature Stress in Synechocystis sp. PCC 6803

Figure 8

Schematic summary of crhR expression and regulation.

crhR expression is controlled by a complex interaction between temperature-regulation of both transcript accumulation and protein degradation. crhR transcript. crhR transcript half-lives are equal and short in both wild type and ΔcrhR Synechocystis cells which contributes to a basal level of transcript accumulation at 30°C. A temperature downshift to 20°C rapidly induces crhR transcript accumulation associated with enhanced half-life and with similar kinetics in both cell types, suggesting that CrhR is not required for temperature sensing or induction of its own transcript accumulation. At low temperature, crhR is transiently accumulated in wild type cells whereas conversely, transcript remains elevated at 20°C in the ΔcrhR mutant, suggesting that CrhR activity is required for the transient expression. Although crhR half-life is influenced by temperature, being significantly longer at 20°C, it is identical in both cell types. This suggests that CrhR is not directly involved in degradation of its own transcript but functional CrhR is directly associated with repression of crhR transcript accumulation, most likely through another mechanism, possibly altered regulation of transcription. CrhR protein. CrhR protein levels correspond to transcript levels in wild type Synechocystis, accumulating to a basal level at 30°C and increasing significantly at 20°C. This is distinctly not the case in the ΔcrhR mutant in which CrhR protein remains elevated and constant at both temperatures. CrhR protein accumulates to the level observed in wild type Synechocystis at 20°C, irrespective of transcript accumulation or temperature. Combined, these results suggest that the reduced level of CrhR at 30°C is caused by proteolytic degradation which is temperature- and CrhR-dependent as this process is inactive in the ΔcrhR mutant. In addition, there appears to be a maximal level of CrhR that can accumulate in cells, irrespective of the transcript level, a process that is CrhR independent. This accumulation appears to be a default level as it was never observed to increase above the level detected in wild type cells at 20°C.

Figure 8

doi: https://doi.org/10.1371/journal.pone.0048683.g008