Fournier B, Hooper D C
Infectious Disease Division and Medical Services, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114-2696, USA.
Antimicrob Agents Chemother. 1998 Aug;42(8):2109-12. doi: 10.1128/AAC.42.8.2109.
The grlA genes of Staphylococcus aureus ISP794 (wild type), MT5224c4 (grlA [Phe-80]), MT5224c2 (grlA [Pro-116]), and MT111 (grlA [Glu-116]) were cloned in pSK950, a shuttle vector, and introduced into S. aureus strains derived from strain RN4220. The mutations at position 116 of GrlA (Ala-->Pro or Glu) caused an increase in the level of fluoroquinolone resistance and a decrease in the level of coumarin susceptibility, whereas the mutation at position 80 (Ser-->Phe) caused only an increase in the level of fluoroquinolone resistance. In multicopy alleles, both types of mutations were codominant for fluoroquinolone resistance, and mutations at position 116 were also codominant for coumarin resistance.
金黄色葡萄球菌ISP794(野生型)、MT5224c4(grlA [Phe-80])、MT5224c2(grlA [Pro-116])和MT111(grlA [Glu-116])的grlA基因被克隆到穿梭载体pSK950中,并导入源自RN4220菌株的金黄色葡萄球菌菌株。GrlA第116位的突变(Ala→Pro或Glu)导致氟喹诺酮耐药水平增加,香豆素敏感性水平降低,而第80位的突变(Ser→Phe)仅导致氟喹诺酮耐药水平增加。在多拷贝等位基因中,两种类型的突变对氟喹诺酮耐药均为共显性,第116位的突变对香豆素耐药也为共显性。