Ghiglione J F, Philippot L, Normand P, Lensi R, Potier P
Laboratoire d'Ecologie Microbienne du Sol, UMR C.N.R.S. 5557, Université Claude Bernard, Lyon 1, 69622 Villeurbanne Cedex, France.
J Bacteriol. 1999 Aug;181(16):5099-102. doi: 10.1128/JB.181.16.5099-5102.1999.
The Pseudomonas fluorescens YT101 gene narG, which encodes the catalytic alpha subunit of the respiratory nitrate reductase, was disrupted by insertion of a gentamicin resistance cassette. In the Nar(-) mutants, nitrate reductase activity was not detectable under all the conditions tested, suggesting that P. fluorescens YT101 contains only one membrane-bound nitrate reductase and no periplasmic nitrate reductase. Whereas N(2)O respiration was not affected, anaerobic growth with NO(2) as the sole electron acceptor was delayed for all of the Nar(-) mutants following a transfer from oxic to anoxic conditions. These results provide the first demonstration of a regulatory link between nitrate and nitrite respiration in the denitrifying pathway.
荧光假单胞菌YT101的narG基因编码呼吸型硝酸还原酶的催化α亚基,该基因通过插入庆大霉素抗性盒而被破坏。在Nar(-)突变体中,在所有测试条件下均未检测到硝酸还原酶活性,这表明荧光假单胞菌YT101仅含有一种膜结合硝酸还原酶,而没有周质硝酸还原酶。虽然N2O呼吸不受影响,但在从有氧条件转移到无氧条件后,所有Nar(-)突变体以NO2作为唯一电子受体的厌氧生长均延迟。这些结果首次证明了反硝化途径中硝酸盐呼吸和亚硝酸盐呼吸之间的调节联系。