Walenga R W, Osborn M J
J Biol Chem. 1980 May 10;255(9):4257-63.
The effect of cerulenin on conversion of an acyl-deficient precursor of lipid A to lipopolysaccharide was investigated in a mutant of Salmonella typhimurium (PRX22H9) conditionally defective in synthesis of 3-deoxy-D-mannooctulosonate (KDO). The precursor lacks both KDO and the saturated O-fatty acyl chains of lipopolysaccharide and contains beta-hydroxymyristate as sole fatty acid. Concentrations of cerulenin which inhibited de novo synthesis of fatty acids and lipopolysaccharide more than 95% had no effect on the rate or extent of conversion of preformed lipid A precursor to a lipopolysaccharide product. The product was identified as a polymer containing the Rc type core polysaccharide of PRX22H9 linked to the acyl-deficient lipid A unit of the precursor. The acyl-deficient lipopolysaccharide was translocated to the outer membrane at a normal rate. Lipopolysaccharide deficient in saturated fatty acids was also produced by a fabD mutant of Escherichia coli under conditions of limited endogenous fatty acid synthesis. The results indicate that prior incorporation of the saturated O-acyl chains of lipid A is not necessary for extension of the core polysaccharide chain and that synthesis of underacylated lipopolysaccharides occurs under conditions of restricted fatty acid synthesis which permit formation of the beta-hydroxymyristate-containing lipid A precursor.
在鼠伤寒沙门氏菌(PRX22H9)的一个突变体中,研究了浅蓝菌素对脂质A的酰基缺陷前体转化为脂多糖的影响,该突变体在3-脱氧-D-甘露辛酮酸(KDO)合成方面存在条件缺陷。该前体既缺乏KDO,也缺乏脂多糖的饱和O-脂肪酸酰基链,并且仅含有β-羟基肉豆蔻酸作为唯一脂肪酸。抑制脂肪酸和脂多糖从头合成超过95%的浅蓝菌素浓度,对预先形成的脂质A前体转化为脂多糖产物的速率或程度没有影响。该产物被鉴定为一种聚合物,其含有与前体的酰基缺陷脂质A单元相连的PRX22H9的Rc型核心多糖。酰基缺陷的脂多糖以正常速率转运到外膜。在有限的内源性脂肪酸合成条件下,大肠杆菌的fabD突变体也产生了缺乏饱和脂肪酸的脂多糖。结果表明,脂质A的饱和O-酰基链预先掺入对于核心多糖链的延伸不是必需的,并且在限制脂肪酸合成的条件下会发生酰基化不足的脂多糖的合成,这种条件允许形成含β-羟基肉豆蔻酸的脂质A前体。