From the ‡Interfaculty Institute for Microbiology and Infection Medicine, Eberhard-Karls University Tübingen, Auf der Morgenstelle 28, 72076 Tübingen, Germany.
¶Proteome Center Tuebingen, Eberhard-Karls-University Tübingen, Auf der Morgenstelle 15, 72076 Tübingen, Germany.
Mol Cell Proteomics. 2018 Sep;17(9):1650-1669. doi: 10.1074/mcp.RA118.000699. Epub 2018 May 30.
Cyanobacteria that do not fix atmospheric nitrogen gas survive prolonged periods of nitrogen starvation in a chlorotic, dormant state where cell growth and metabolism are arrested. Upon nutrient availability, these dormant cells return to vegetative growth within 2-3 days. This resuscitation process is highly orchestrated and relies on the stepwise reinstallation and activation of essential cellular structures and functions. We have been investigating the transition to chlorosis and the return to vegetative growth as a simple model of a cellular developmental process and a fundamental survival strategy in biology. In the present study, we used quantitative proteomics and phosphoproteomics to describe the proteomic landscape of a dormant cyanobacterium and its dynamics during the transition to vegetative growth. We identified intriguing alterations in the set of ribosomal proteins, in RuBisCO components, in the abundance of central regulators and predicted metabolic enzymes. We found O-phosphorylation as an abundant protein modification in the chlorotic state, specifically of metabolic enzymes and proteins involved in photosynthesis. Nondegraded phycobiliproteins were hyperphosphorylated in the chlorotic state. We provide evidence that hyperphosphorylation of the terminal rod linker CpcD increases the lifespan of phycobiliproteins during chlorosis.
不固定大气氮气的蓝细菌在缺铁的休眠状态下可以存活很长时间，此时细胞生长和代谢停滞。一旦营养物质可用，这些休眠细胞会在 2-3 天内恢复到营养生长状态。这个复苏过程是高度协调的，依赖于必要细胞结构和功能的逐步重新安装和激活。我们一直在研究向缺铁状态的转变和向营养生长的恢复，将其作为细胞发育过程的简单模型和生物学中基本的生存策略。在本研究中，我们使用定量蛋白质组学和磷酸化蛋白质组学来描述休眠蓝细菌的蛋白质组景观及其在向营养生长过渡过程中的动态变化。我们发现核糖体蛋白、RuBisCO 成分、中央调节剂和预测代谢酶的丰度发生了有趣的变化。我们发现 O-磷酸化是缺铁状态下一种丰富的蛋白质修饰，特别是代谢酶和光合作用相关蛋白。在缺铁状态下，藻胆蛋白的降解产物被高度磷酸化。我们提供的证据表明，末端杆状链接蛋白 CpcD 的高度磷酸化增加了藻胆蛋白在缺铁状态下的寿命。
