Impact of SliP4 deletion on the high-light acclimation in Synechocystis sp. PCC 6803

TL;DR

Deleting the SliP4 protein in Synechocystis affects its ability to adjust to high light, but the organism compensates by activating alternative stress responses.

Contribution

This study reveals how Synechocystis compensates for SliP4 deletion through population-level acclimation mechanisms.

Findings

ΔsliP4 mutants show wild-type-like gene regulation 30 minutes after high-light exposure.

Mutant cells alter N and C metabolism and produce more extracellular polysaccharides.

Upregulated xssA-E and xssN-P genes suggest increased synechan production in the mutant.

Abstract

SliP4 is a small, 37 amino acids protein that is strongly induced when the cyanobacterium Synechocystis sp. PCC 6803 is exposed to high-light (HL) conditions. Deletion mutants manifest a light-sensitive phenotype due to impaired cyclic electron flow and state transitions. In this study, we aimed to investigate the consequences of SliP4 deficiency on the process of high-light acclimation on systems level. Transcriptomic data revealed that the deletion mutant ΔsliP4 exhibited a wild-type-like gene regulatory response 30 minutes after the light intensity was increased from 50 to 250 μmol photons m−2 s−1, a process that is controlled by the RpaB-PsrR1 system. Proteome analysis showed consistent expression changes of many HL-regulated proteins. Metabolome analysis provided hints for a changed N and C metabolism in mutant cells compared to wild type. In addition, the mutant increased the production of extracellular polysaccharides causing the mutant cells to aggregate after the shift to HL. This effect corresponds to the upregulated expression of xssA-E and xssN-P genes for the production of the sulfated exopolysaccharide synechan. We interpret these observations as a response that counteracts the potential light stress effects caused by the impaired capacity for cyclic electron flow and state transitions in the ΔsliP4 mutant. Our results demonstrate that the unicellular cyanobacterium Synechocystis compensates for the loss of SliP4 and its crucial role by activating a genetic program for a population-level response that helps the cells to cope with HL conditions.

The lack of the small high-light-induced protein SliP4 has a marked impact on the acclimation response of Synechocystis sp. PCC 6803 to high light.

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