Sandlin R C, Danaher R J, Stein D C
Department of Microbiology, University of Maryland, College Park 20742.
J Bacteriol. 1994 Nov;176(22):6869-76. doi: 10.1128/jb.176.22.6869-6876.1994.
The genetic basis for pyocin resistance in Neisseria gonorrhoeae 1291d, 1291e, and FA5100 was determined by Southern blot and DNA sequence analyses. The genes defective in these strains are present as single copies in the gonococcal chromosome. The mutant regions of 1291d, 1291e, and FA5100 were amplified by the PCR. Sequence analysis of the mutant regions demonstrated that strain 1291d contains a 12-bp deletion that results in the loss of four amino acids in phosphoglucomutase, while strain 1291e contains a point mutation that results in the change of an uncharged glycine residue to a charged glutamic acid residue in the same protein. FA5100 contains a nonsense mutation in the gene encoding heptosyltransferase II. The gene previously described as lsi-1 was shown to complement an rfaF mutation in Salmonella typhimurium and has been renamed rfaF.
通过Southern印迹法和DNA序列分析确定了淋病奈瑟菌1291d、1291e和FA5100对绿脓菌素耐药的遗传基础。这些菌株中存在缺陷的基因在淋球菌染色体中以单拷贝形式存在。通过PCR扩增了1291d、1291e和FA5100的突变区域。对突变区域的序列分析表明，1291d菌株存在一个12bp的缺失，导致磷酸葡萄糖变位酶中四个氨基酸缺失，而1291e菌株存在一个点突变，导致同一蛋白质中一个不带电荷的甘氨酸残基变为带电荷的谷氨酸残基。FA5100在编码庚糖基转移酶II的基因中存在一个无义突变。先前被描述为lsi-1的基因被证明可互补鼠伤寒沙门氏菌中的rfaF突变，并已重新命名为rfaF。
