由质粒携带的耐药二氢蝶酸合酶介导的R因子对磺胺类药物的耐药性。
R-factor-mediated resistance to sulfonamides by a plasmid-borne, drug-resistant dihydropteroate synthase.
作者信息
Sköld O
出版信息
Antimicrob Agents Chemother. 1976 Jan;9(1):49-54. doi: 10.1128/AAC.9.1.49.
Abstract
Evidence was found for the existence of an episome-specified variant of the enzyme dihydropteroate synthase involved in folic acid formation. Since the plasmid-borne enzyme showed a decreased susceptibility for sulfonamide inhibition and was transferable together with resistance to this drug, it is proposed that diploidy for the target enzyme in some cases could be the mechanism of R-factor-mediated resistance to sulfonamides. Two types of evidence were obtained. One was the rescue from temperature sensitivity of bacterial mutants with a lesion in the chromosomal dihydropteroate synthase by the R factor R1dr19 mediating sulfonamide resistance. The other evidence was found by the determination of dihydropteroate forming activity in extracts from R(-) and R(+) bacteria. Cells harboring R1dr19 were found to contain an enzyme activity which was far less susceptible to sulfonamide inhibition than the corresponding activity from R(-) cells.
摘要
已发现存在一种参与叶酸形成的二氢蝶酸合酶的附加体特异性变体的证据。由于质粒携带的酶对磺胺类药物抑制的敏感性降低，并且可与对该药物的抗性一起转移，因此有人提出在某些情况下靶酶的二倍体可能是R因子介导的对磺胺类药物抗性的机制。获得了两类证据。一类证据是由介导磺胺类药物抗性的R因子R1dr19拯救了染色体二氢蝶酸合酶有损伤的细菌突变体的温度敏感性。另一类证据是通过测定R（-）和R（+）细菌提取物中二氢蝶酸形成活性而发现的。发现携带R1dr19的细胞含有一种酶活性，该酶活性比来自R（-）细胞的相应活性对磺胺类药物抑制的敏感性要低得多。
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