Kurkela Juha, Vuorijoki Linda, Vakal Serhii, Turunen Otso, Koskinen Satu, Reimann Viktoria, Ray Mithila, Hess Wolfgang R, Salminen Tiina A, Tyystjärvi Taina
Department of Life Technologies/Molecular Plant Biology, University of Turku, Turku, FI-20014, Finland.
Structural Bioinformatics Laboratory, Biochemistry, Faculty of Science and Engineering, Åbo Akademi University, Tykistökatu 6A, Turku, 20520, Finland.
New Phytol. 2025 Sep;247(5):2118-2133. doi: 10.1111/nph.70328. Epub 2025 Jun 25.
Cyanobacterial growth depends on inorganic carbon (Ci; CO and bicarbonate) concentration, but mechanism(s) adjusting photosynthesis and growth according to Ci remain unclear. ΔrpoZ cells lacking the ω subunit of the RNA polymerase (RNAP) show a unique high-CO lethal phenotype in Synechocystis sp. PCC 6803. Bioinformatics, biochemical and 3D modeling studies were used to reveal how suppressor mutations rescue ΔrpoZ cells in 3% CO. Suppressor mutations were mapped to the ssr1600 gene. Ssr1600 was shown to function as an anti-σ factor antagonist. The Slr1861 protein was identified as an anti-σ factor and as an Ssr1600 kinase. The Slr1861/Ssr1600 pair was shown to control the formation of RNAP-SigC holoenzyme using a phosphorylation-controlled partner-switching mechanism. In high CO, excess formation of growth-limiting RNAP-SigC holoenzyme in ΔrpoZ reduces the expression of cell wall synthesis, photosynthetic and nutrient uptake genes, leading to low photosynthesis activity and cell lysis. In the suppressor mutants, drastically decreased Ssr1600 levels lowered the amounts of RNAP-SigC holoenzyme to similar levels as in the control strain, returning an almost normal transcriptome composition, photosynthesis and growth. The results indicate that SigC, Slr1861 and Ssr1600 proteins form a growth-regulating signaling cascade in cyanobacteria, which connects growth to environmental Ci levels.
蓝藻的生长依赖于无机碳（Ci；CO₂和碳酸氢盐）浓度，但根据Ci调节光合作用和生长的机制仍不清楚。缺乏RNA聚合酶（RNAP）ω亚基的ΔrpoZ细胞在集胞藻PCC 6803中表现出独特的高CO₂致死表型。利用生物信息学、生化和三维建模研究来揭示抑制突变如何在3% CO₂条件下拯救ΔrpoZ细胞。抑制突变被定位到ssr1600基因。结果表明Ssr1600作为一种抗σ因子拮抗剂发挥作用。Slr1861蛋白被鉴定为一种抗σ因子和Ssr1600激酶。研究表明，Slr1861/Ssr1600对通过磷酸化控制的伴侣切换机制控制RNAP-SigC全酶的形成。在高CO₂条件下，ΔrpoZ中生长限制型RNAP-SigC全酶的过量形成会降低细胞壁合成、光合作用和营养吸收基因的表达，导致光合作用活性降低和细胞裂解。在抑制突变体中，Ssr1600水平大幅降低，使RNAP-SigC全酶的量降至与对照菌株相似的水平，恢复了几乎正常的转录组组成、光合作用和生长。结果表明，SigC、Slr1861和Ssr1600蛋白在蓝藻中形成了一个生长调节信号级联，将生长与环境Ci水平联系起来。
