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大肠杆菌中维生素B12对metE和btuB进行抑制的独立调控系统。

Separate regulatory systems for the repression of metE and btuB by vitamin B12 in Escherichia coli.

作者信息

Lundrigan M D, De Veaux L C, Mann B J, Kadner R J

出版信息

Mol Gen Genet. 1987 Mar;206(3):401-7. doi: 10.1007/BF00428878.

Abstract

Synthesis of the btuB-encoded outer membrane receptor for vitamin B12 and the metE-encoded homocysteine methyltransferase is repressed by growth of Escherichia coli in the presence of vitamin B12. The regulation by vitamin B12 of the production of beta-galactosidase in strains carrying btuB-lac or metE-lac operon fusions indicated that repression of both genes operates at the transcriptional level. Selection for expression of these fusions under repressive conditions allowed isolation of second-site mutations in which repressibility by vitamin B12 had been lost. Mutations in metH and metF prevented vitamin B12-dependent regulation of metE, but not that of btuB. Mutations in btuB and other genes involved in uptake of the vitamin eliminated or reduced repression. Mutations in the newly identified gene, btuR, controlled the repressibility of btuB, but had no effect on metE regulation. The btuR gene resides at 27.9 min on the genetic map in the gene order cysB-topA-btuR-trp; it acts in a trans-dominant manner and appears to encode a repressor of btuB transcription.

摘要

维生素B12的btuB编码外膜受体和metE编码的同型半胱氨酸甲基转移酶的合成,在维生素B12存在的情况下,会受到大肠杆菌生长的抑制。在携带btuB-lac或metE-lac操纵子融合的菌株中,维生素B12对β-半乳糖苷酶产生的调节表明,这两个基因的抑制作用都在转录水平上起作用。在抑制条件下选择这些融合体的表达,使得能够分离出第二位点突变,其中维生素B12的可抑制性已经丧失。metH和metF中的突变阻止了维生素B12对metE的依赖性调节,但不影响btuB的调节。btuB和其他参与维生素摄取的基因中的突变消除或降低了抑制作用。新鉴定的基因btuR中的突变控制了btuB的可抑制性,但对metE的调节没有影响。btuR基因位于遗传图谱上27.9分钟处,基因顺序为cysB-topA-btuR-trp;它以反式显性方式起作用,似乎编码btuB转录的阻遏物。

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