Furrow M H, Pizer L I
J Virol. 1968 Jun;2(6):594-605. doi: 10.1128/JVI.2.6.594-605.1968.
After infection of Escherichia coli with T4 phage, phospholipid synthesis continued but at a reduced rate. The same phospholipid components were synthesized as in uninfected cells; however, the relative rates of (32)P(i) incorporation into phosphatidylglycerol (PG) and phosphatidylethanolamine (PE) were altered. This alteration was most pronounced during the first 10 min after infection. Under these conditions, the isotope incorporated into PG equaled or exceeded that found in PG from uninfected cells. Chloramphenicol (CM) added before, but not 5 min after, infection inhibited the relative increase in PG synthesis, and CM added at different times after infection indicated that a protein synthesized between 3 and 6 min was required for this change to occur. Supplies of exogenous l-serine or l-alpha-glycerol-P failed to affect the relative rates of (32)P(i) incorporation into PG and PE by infected or uninfected cells. Phospholipid synthesis was somewhat higher after infection with T4rII mutants than after infection with wild-type phage. After infection with these mutants or several amber mutants, the relative synthesis of PG and PE was characteristic of T4r(+)-infected cells. The phospholipid synthesized after infection did not rapidly turn over, but infection accelerated the loss of PG synthesized prior to infection.
用T4噬菌体感染大肠杆菌后,磷脂合成继续进行,但速率降低。合成的磷脂成分与未感染细胞中的相同;然而,(32)P(i)掺入磷脂酰甘油(PG)和磷脂酰乙醇胺(PE)的相对速率发生了改变。这种改变在感染后的最初10分钟最为明显。在这些条件下,掺入PG的同位素等于或超过未感染细胞中PG的含量。在感染前而非感染后5分钟添加氯霉素(CM)可抑制PG合成的相对增加,感染后不同时间添加CM表明,这种变化发生需要在3至6分钟之间合成一种蛋白质。外源性l-丝氨酸或l-α-甘油-P的供应未能影响感染或未感染细胞中(32)P(i)掺入PG和PE的相对速率。用T4rII突变体感染后的磷脂合成比用野生型噬菌体感染后略高。用这些突变体或几个琥珀突变体感染后,PG和PE的相对合成具有T4r(+)感染细胞的特征。感染后合成的磷脂不会迅速周转,但感染加速了感染前合成的PG的损失。