Fraley Cresson D, Rashid M Harunur, Lee Sam S K, Gottschalk Rebecca, Harrison Janine, Wood Pauline J, Brown Michael R W, Kornberg Arthur
*Department of Biochemistry, Stanford University School of Medicine, 279 West Campus Drive, Stanford, CA 94305-5307.
Proc Natl Acad Sci U S A. 2007 Feb 27;104(9):3526-31. doi: 10.1073/pnas.0609733104. Epub 2007 Feb 22.
Pseudomonas aeruginosa, of medical, environmental, and industrial importance, depends on inorganic polyphosphate (poly P) for a wide range of functions, especially survival. Mutants of PAO1 lacking poly P kinase 1, PPK1, the enzyme responsible for most poly P synthesis in Escherichia coli and other bacteria, are defective in motility, quorum sensing, biofilm formation, and virulence. We describe here multiple defects in the ppk1 mutant PAOM5, including a striking compaction of the nucleoid, distortion of the cell envelope, lack of planktonic motility and exopolymer production, and susceptibility to the beta-lactam antibiotic carbenicillin as well as desiccation. We propose that P. aeruginosa with reduced poly P levels undergoes ultrastructural changes that contribute to profound deficiencies in cellular functions.
铜绿假单胞菌在医学、环境和工业领域都具有重要意义，它依赖无机多聚磷酸盐（多聚P）来实现多种功能，尤其是生存。PAO1的缺乏多聚P激酶1（PPK1）的突变体，PPK1是负责大肠杆菌和其他细菌中大多数多聚P合成的酶，该突变体在运动性、群体感应、生物膜形成和毒力方面存在缺陷。我们在此描述了ppk1突变体PAOM5的多种缺陷，包括拟核的显著压缩、细胞壁的扭曲、浮游运动和胞外聚合物产生的缺乏，以及对β-内酰胺抗生素羧苄青霉素和干燥的敏感性。我们提出，多聚P水平降低的铜绿假单胞菌会发生超微结构变化，这导致细胞功能出现严重缺陷。
