Akimitsu N, Mizushima T, Suzuki E, Miki T, Sekimizu K
Faculty of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Biol Pharm Bull. 1996 Oct;19(10):1275-8. doi: 10.1248/bpb.19.1275.
We identified novel phenotypes of a pgsA3 mutant lacking the potential to synthesize phosphatidylglycerophosphate, a precursor of phosphatidylglycerol. The first phenotype is limited cell growth at a high temperature, under the condition of low salt. The phenotype was co-transduced with a phenotype lacking the potential to synthesize phosphatidylglycerol in a P1 transduction experiment, and was restored by transformation with a plasmid containing a wild type pgsA gene. The second phenotype of the pgsA3 mutant was resistant to growth in the presence of a low concentration of kanamycin (4 micrograms/ml). P1 transduction and transformation with the plasmid containing the wild-type pgsA gene revealed that the pgsA3 mutation was also responsible for the second phenotype.
我们鉴定出了pgsA3突变体的新表型，该突变体缺乏合成磷脂酰甘油磷酸（磷脂酰甘油的前体）的能力。第一个表型是在低盐条件下高温时细胞生长受限。在P1转导实验中，该表型与缺乏合成磷脂酰甘油能力的表型共转导，并通过用含有野生型pgsA基因的质粒转化得以恢复。pgsA3突变体的第二个表型是在低浓度卡那霉素（4微克/毫升）存在下生长具有抗性。用含有野生型pgsA基因的质粒进行P1转导和转化表明，pgsA3突变也导致了第二个表型。
