Control of the lux regulon of Vibrio fischeri.

Control of the lux regulon of Vibrio fischeri.
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DOI:
10.1002/bio.1170050205
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发表时间:
1990-04
期刊:
Journal of bioluminescence and chemiluminescence
影响因子:
--
通讯作者:
G. Shadel;J. Devine;T. Baldwin
G. Shadel;J. Devine;T. Baldwin
中科院分区:
其他
文献类型:
--
作者:
G. Shadel;J. Devine;T. Baldwin

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大肠杆菌中费氏弧菌lux调节子对生物发光表达的调节是一种独特形式的正反馈叠加在定义不清的顺式作用抑制机制上的结果。勒克斯调节子由两个转录趋异的操纵子组成。该操纵子仅包含单个基因luxR,其编码转录激活蛋白。该操纵子包含luxI,其与luxR和分隔两个操纵子的218个碱基对一起构成初级调节回路,以及生物发光活性所需的五个结构基因luxC、luxD、luxA、luxB和luxE。PL的luxR转录受E. coli crp基因产物与推测启动子上游的序列TGTGACAAAAATCCAA连接。纯E.已经通过体外足迹法证明了大肠杆菌CAP蛋白在对费氏弧菌lux调节区的cAMP依赖性反应中的作用。luxI基因产物是催化细胞质底物缩合反应以产生自诱导物N-(3-氧代-己酰基)高丝氨酸内酯的酶。可自由扩散的自诱导物的积累导致与LuxR形成复合物。该复合物与PR上游的序列ACCTGTAGGATCGTACAGGT结合以刺激转录操纵子的转录。PR转录的增加应产生增加的LuxI水平和更高水平的自诱导物,其将进一步激活LuxR。LuxR结合位点也是莱克萨结合位点,如通过体外足迹法所证明的。PL和PR的基础转录受到luxR编码区内序列的抑制。(250字处删节)
Regulation of expression of bioluminescence from the Vibrio fischeri lux regulon in Escherichia coli is a consequence of a unique form of positive feedback superimposed on a poorly defined cis-acting repression mechanism. The lux regulon consists of two divergently transcribed operons. The leftward operon contains only a single gene, luxR, which encodes a transcriptional activator protein. The rightward operon contains luxI, which together with luxR and the 218 base pairs separating the two operons comprises the primary regulatory circuit, and the five structural genes, luxC, luxD, luxA, luxB and luxE, which are required for the bioluminescence activity. Transcription of luxR from PL is stimulated by binding of the E. coli crp gene product to the sequence TGTGACAAAAATCCAA upstream of the presumed promoter. Binding of pure E. coli CAP protein in a cAMP-dependent reaction to the V. fischeri lux regulatory region has been demonstrated by in vitro footprinting. The luxI gene product is an enzyme which catalyses a condensation reaction of cytoplasmic substrates to yield the autoinducer, N-(3-oxo-hexanoyl) homoserine lactone. Accumulation of autoinducer, which is freely diffusible, results in formation of a complex with LuxR. The complex binds to the sequence ACCTGTAGGATCGTACAGGT upstream of PR to stimulate transcription of the rightward operon. Increased transcription from PR should yield increased levels of LuxI and higher levels of autoinducer which would further activate LuxR. The LuxR binding site is also a LexA binding site, as demonstrated by in vitro footprinting. Basal transcription from both PL and PR is repressed by sequences within the luxR coding region.(ABSTRACT TRUNCATED AT 250 WORDS)