Crooke E, Akiyama M, Rao N N, Kornberg A
Department of Biochemistry, Stanford University School of Medicine, California 94305.
J Biol Chem. 1994 Mar 4;269(9):6290-5.
The ppk gene encoding polyphosphate kinase (PPK), the enzyme in Escherichia coli that makes long chains of polyphosphate (polyP) reversibly from ATP, was disrupted by insertion of a kanamycin resistance gene. Expression of the exopolyphosphatase gene (ppx) immediately downstream of ppk in the operon was likewise disrupted. Cells were also transformed with a high-copy-number plasmid bearing ppk. Genetically altered polyP levels were estimated in cell extracts by the PPK conversion of ADP to ATP. PolyP levels (microgram/10(11) cells) near 2.0 were reduced in the ppk(-)-ppx- mutants to 0.16 and increased more than 100-fold (e.g. 220) in cells transformed with multiple copies of ppk. Mutant cells, lacking the long polyP chains, showed a growth lag following dilution of a stationary-phase culture. PolyP-deficient cells exhibit a striking phenotype in their failure to survive in stationary phase and loss of resistance to heat (55 degrees C) and to oxidants (42 mM H2O2). High polyP levels are also associated with reduced survival.
编码多聚磷酸激酶(PPK)的ppk基因被卡那霉素抗性基因插入破坏,PPK是大肠杆菌中一种能使ATP可逆地合成多聚磷酸(polyP)长链的酶。操纵子中ppk下游紧邻的外多聚磷酸酶基因(ppx)的表达同样被破坏。细胞还用携带ppk的高拷贝数质粒进行了转化。通过PPK将ADP转化为ATP来估计细胞提取物中基因改变后的多聚磷酸水平。ppk(-)-ppx-突变体中接近2.0的多聚磷酸水平(微克/10¹¹个细胞)降至0.16,而用多拷贝ppk转化的细胞中多聚磷酸水平增加了100多倍(例如220)。缺乏长链多聚磷酸的突变细胞在稳定期培养物稀释后表现出生长滞后。多聚磷酸缺陷型细胞在稳定期无法存活,对热(55℃)和氧化剂(42 mM H₂O₂)失去抗性,表现出显著的表型。高多聚磷酸水平也与存活率降低有关。