The chlorosis response is governed by a complex and poorly understood regulatory network, which converges at the expression of the nblA gene, the triggering factor for phycobiliprotein degradation. We used a precise dosage of L-methionine-sulfoximine (MSX) which inhibits the glutamine synthetase mimicking the metabolic situation of nitrogen starvation. Addition of nitrate to such MSX-inhibited cells eliminates the associated redox-stress by enabling electron flow towards nitrate/nitrite reduction and thereby, prevents the induction of nblA expression and the associated chlorosis response. This work further established a cryptic role of nitrate/nitrite reductases as electron sinks to balance conditions of over-reduction (Klotz et al 2015).
Polyhydroxybutyrate (PHB) is a common carbon storage polymer among heterotrophic bacteria as well as for the model organism Synechocystis sp. PCC 6803 upon the limitation of macronutrients. We have previously reported a mutation in the gene sll0783 that impairs PHB accumulation in this cyanobacterium (Schlebusch & Forchhammer 2010). Metabolome analysis revealed a difference in sorbitol levels between the wild type and the mutant, indicating a more oxidizing intracellular environment than in the wild type. We confirmed this by directly measuring the NADPH/NADP ratio and by altering the intracellular redox state of wild type and sll0783 mutant and we were able to physiologically complement the mutant phenotype by making the intracellular environment more reducing. The NADPH pool is an important factor for regulation of PHB biosynthesis and metabolism, which is also of interest for potential biotechnological applications (Hauf et al 2013).