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大肠杆菌中缺乏Ca2+、Mg2+刺激的三磷酸腺苷酶的突变体中转运缺陷的生理抑制。

Physiological suppression of a transport defect in Escherichia coli mutants deficient in Ca2+, Mg2+-stimulated adenosine triphosphatase.

作者信息

Boonstra J, Gutnick D L, Kaback H R

出版信息

J Bacteriol. 1975 Dec;124(3):1248-55. doi: 10.1128/jb.124.3.1248-1255.1975.

DOI:10.1128/jb.124.3.1248-1255.1975
PMID:127784
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC236034/
Abstract

Transport properties of membrane vesicles isolated from two adenosine triphosphatase-deficient mutants of Escherichia coli, NR70 and DL54, were compared with those of vesicles prepared from the corresponding parental strains. As reported previously (Rosen, 1973; Altendorf et al., 1974), vesicles prepared from these mutants grown under aerobic conditions exhibited defective amino acid transport, and activity was restored after treatment with dicyclohexylcarbodiimide. In sharp contrast, however, vesicles isolated from the same mutants grown anaerobically in the presence of nitrate exhibited completely normal transport activity when assayed under either anaerobic or aerobic conditions. Suppression of the transport defect was not due to the manner by which the vesicles were prepared, and the adenosine triphosphatase deficiency was not ameliorated by anaerobic growth in the presence of nitrite. Finally, the transport activity of vesicles prepared from the mutants grown under aerobic conditions was relatively resistant to the effect of 1.0 M guanidine hydrochloride extraction, whereas the activity of vesicles prepared from mutants grown anaerobically was totally refractory to the effect of the chaotrope.

摘要

将从大肠杆菌的两个三磷酸腺苷酶缺陷型突变体NR70和DL54中分离出的膜囊泡的转运特性,与从相应亲本菌株制备的膜囊泡的转运特性进行了比较。如先前报道(罗森,1973年;阿尔滕多夫等人,1974年),由在有氧条件下生长的这些突变体制备的膜囊泡表现出有缺陷的氨基酸转运,在用二环己基碳二亚胺处理后活性得以恢复。然而,与之形成鲜明对比的是,当在厌氧或有氧条件下进行测定时,从在硝酸盐存在下厌氧生长的相同突变体中分离出的膜囊泡表现出完全正常的转运活性。转运缺陷的抑制并非由于制备膜囊泡的方式,并且在亚硝酸盐存在下厌氧生长并没有改善三磷酸腺苷酶缺陷。最后,由在有氧条件下生长的突变体制备的膜囊泡的转运活性对1.0 M盐酸胍提取的影响相对具有抗性,而由厌氧生长的突变体制备的膜囊泡的活性对离液剂的影响则完全不敏感。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4ca/236034/28d97907e4bc/jbacter00325-0224-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4ca/236034/28d97907e4bc/jbacter00325-0224-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4ca/236034/28d97907e4bc/jbacter00325-0224-a.jpg

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Physiological suppression of a transport defect in Escherichia coli mutants deficient in Ca2+, Mg2+-stimulated adenosine triphosphatase.大肠杆菌中缺乏Ca2+、Mg2+刺激的三磷酸腺苷酶的突变体中转运缺陷的生理抑制。
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引用本文的文献

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Carbodiimide-resistant mutant of Escherichia coli: suppression of resistance to dicyclohexylcarbodiimide by growth on glucose or glycerol.大肠杆菌对碳二亚胺的抗性突变体:通过在葡萄糖或甘油上生长来抑制对二环己基碳二亚胺的抗性
J Bacteriol. 1978 May;134(2):687-9. doi: 10.1128/jb.134.2.687-689.1978.

本文引用的文献

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Mutants of Escherichia coli requiring methionine or vitamin B12.需要甲硫氨酸或维生素B12的大肠杆菌突变体。
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Anaerobic transport in Escherichia coli membrane vesicles.大肠杆菌膜囊泡中的厌氧转运
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The energy-linked transhydrogenase reaction in respiratory mutants of Escherichia coli K12.大肠杆菌K12呼吸突变体中的能量偶联转氢酶反应。
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