INDUCTION OF LACTOSE TRANSPORT SYSTEM IN A LIPID-SYNTHESIS-DEFECTIVE MUTANT OF ESCHERICHIA-COLI
INDUCTION OF LACTOSE TRANSPORT SYSTEM IN A LIPID-SYNTHESIS-DEFECTIVE MUTANT OF ESCHERICHIA-COLI
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DOI：
10.1128/jb.103.2.410-416.1970
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发表时间：
1970-01-01
影响因子：
3.2
通讯作者：
FOX, CF
中科院分区：
文献类型：
--
作者：
HSU, CC;FOX, CF
为了将乳糖转运系统的生物发生与脂质合成联系起来，分离并鉴定了一个在1-甘油-3-磷酸合成中具有特异性缺陷的需要甘油的大肠杆菌K-12突变体。有缺陷的酶是生物合成1-甘油-3-磷酸脱氢酶[1-甘油-3-磷酸：NAD（P）氧化还原酶，EC 1.1.1.8]，其作为二羟丙酮磷酸还原酶发挥功能，为脂质合成提供1-甘油-3-磷酸。在该突变体中，从生长培养基中去除甘油导致蛋白质、脱氧核糖核酸和磷脂的合成受到抑制。甘油去除后立即抑制磷脂合成，而脱氧核糖核酸和蛋白质合成的抑制之前有一个短暂的滞后期。甘油饥饿不会改变以前合成的磷脂的周转模式。通过甘油饥饿阻断脂质合成导致相对于β-半乳糖苷酶的β-半乳糖苷转运活性的诱导急剧降低，表明乳糖转运的诱导需要从头脂质合成。
In order to relate the biogenesis of the lactose transport system to lipid synthesis, a glycerol-requiring mutant ofEscherichia coliK-12 with a specific defect inl-glycerol-3-phosphate synthesis was isolated and characterized. The defective enzyme is the biosyntheticl-glycerol-3-phosphate dehydrogenase [l-glycerol-3-phosphate: NAD (P) oxidoreductase, EC 1.1.1.8] which functions as a dihydroxyacetone phosphate reductase to providel-glycerol-3-phosphate for lipid synthesis. In this mutant, removal of glycerol from the growth medium results in inhibition of the synthesis of protein, deoxyribonucleic acid, and phospholipid. Inhibition of phospholipid synthesis immediately follows glycerol removal, whereas the inhibition of deoxyribonucleic acid and protein synthesis is preceded by a short lag period. Glycerol starvation does not change the turnover pattern of previously synthesized phospholipids. The blocking of lipid synthesis by glycerol starvation causes a drastic decrease in inducibility of β-galactoside transport activity relative to β-galactosidase, indicating that induction of lactose transport requires de novo lipid synthesis.