Sato Norihiro, Endo Mizuki, Nishi Hiroki, Fujiwara Shoko, Tsuzuki Mikio
School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, Japan.
Front Plant Sci. 2024 Jul 31;15:1441626. doi: 10.3389/fpls.2024.1441626. eCollection 2024.
Polyphosphate is prevalent in living organisms. To obtain insights into polyphosphate synthesis and its physiological significance in cyanobacteria, we characterize , a homolog of the polyphosphate-kinase-1 gene, in the freshwater cyanobacterium sp. PCC 6803. The Sll0290 protein structure reveals characteristics of Ppk1. A disruptant and -overexpressing transformant demonstrated loss and gain of polyphosphate synthesis ability, respectively. Accordingly, is identified as . The disruptant (Δ) grows normally with aeration of ordinary air (0.04% CO), consistent with its photosynthesis comparable to the wild type level, which contrasts with a previously reported high-CO (5%) requirement for Δ in an alkaline hot spring cyanobacterium, OS-B'. Δ is defective in polyphosphate hyperaccumulation and survival competence at the stationary phase, and also under sulfur-starvation conditions, implying that sulfur limitation is one of the triggers to induce polyphosphate hyperaccumulation in stationary cells. Furthermore, Δ is defective in the enhancement of total phosphorus contents under sulfur-starvation conditions, a phenomenon that is only partially explained by polyphosphate hyperaccumulation. This study therefore demonstrates that in , is not essential for low-CO acclimation but plays a crucial role in dynamic P-metabolic regulation, including polyP hyperaccumulation, to maintain physiological fitness under sulfur-starvation conditions.
多聚磷酸盐在生物体内普遍存在。为了深入了解多聚磷酸盐在蓝藻中的合成及其生理意义,我们对淡水蓝藻集胞藻PCC 6803中的多聚磷酸激酶-1基因的同源物Sll0290进行了表征。Sll0290蛋白结构揭示了Ppk1的特征。一个Sll0290缺失突变体和一个Sll0290过表达转化体分别表现出多聚磷酸盐合成能力的丧失和增加。因此,Sll0290被鉴定为Ppk1。该缺失突变体(ΔSll0290)在普通空气(0.04% CO₂)曝气条件下正常生长,这与其光合作用与野生型水平相当一致,这与之前报道的碱性温泉蓝藻温泉红藻OS-B'中的ΔSll0290对高浓度CO₂(5%)的需求形成对比。ΔSll0290在稳定期以及硫饥饿条件下的多聚磷酸盐过度积累和生存能力方面存在缺陷,这意味着硫限制是诱导静止细胞中多聚磷酸盐过度积累的触发因素之一。此外,ΔSll0290在硫饥饿条件下总磷含量的增加方面存在缺陷,这一现象仅部分由多聚磷酸盐过度积累来解释。因此,本研究表明,在集胞藻PCC 6803中,Sll0290对于低CO₂适应并非必不可少,但在动态磷代谢调节中起着关键作用,包括多聚磷酸盐过度积累,以在硫饥饿条件下维持生理适应性。