Genetic and molecular analysis of a regulatory region of the herbicide 2,4-dichlorophenoxyacetate catabolic plasmid pJP4.
Genetic and molecular analysis of a regulatory region of the herbicide 2,4-dichlorophenoxyacetate catabolic plasmid pJP4.
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除草剂 2,4-二氯苯氧基乙酸酯分解代谢质粒 pJP4 调控区的遗传和分子分析。
DOI：
10.1111/j.1365-2958.1995.tb02304.x
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发表时间：
1995
影响因子：
3.6
通讯作者：
Ghosal,D
中科院分区：
文献类型：
--
作者：
You,IS;Ghosal,D
在真养产碱菌 JMP134 中，pJP4 携带编码 2,4-二氯苯氧基乙酸酯 (2,4-D) 和 3-氯苯甲酸酯 (3-Cba) 降解以及耐汞性的基因。指定 2,4-D 和 3-Cba 分解代谢的质粒基因被组织在三个操纵子中：tfdA、tfdB 和 tfdCDEF。已经提出通过两个不连锁的基因 tfdR 和 tfdS 来调节这些操纵子。物理和 DNA 序列分析表明，tfdR 和 tfdS 基因是相同的，并且位于 1592bp 的较长反向重复序列内。在其他 2,4-D 质粒中也观察到类似的茎环结构。 tfdR基因长888bp，能够编码32kDa的多肽。推导的tfdR氨基酸序列表明它是LysR型激活剂的成员。通过构建 pJP4 定义的缺失突变体 pYG1010（缺少包含携带 tfdRandtfdS 调节基因的反向重复区域的 4.2 kilobaseXbal 片段）对分解代谢基因簇的调节进行研究表明，含有 pYG1010 的洋葱假单胞菌菌株变为 2,4-D 阴性，但 3-Cba 阳性。 pYG1010 和克隆的 tfdS 基因的体内重组体挽救了 2,4-D 表型，表明 TfdS 是 tfdA 表达的正调节因子，但不是 tfdCDEF 表达的正调节因子。
InAlcaligenes eutrophusJMP134, pJP4 carries the genes coding for 2,4‐dichlorophenoxyacetate (2,4‐D) and 3‐chlorobenzoate (3‐Cba) degradation plus mercury resistance. The plasmid genes specifying 2,4‐D and 3‐Cba catabolism are organized in three operons:tfdA, tfdB, andtfdCDEF.Regulation of these operons by two unlinked genes,tfdRandtfdS, has been proposed. Physical and DNA sequence analyses revealed that thetfdRandtfdSgenes were identical and were located within a longer inverted repeat of 1592bp. Similar stem‐loop structures were observed among other 2,4‐D plasmids. ThetfdRgene is 888 bp long and capable of encoding a polypeptide of 32kDa. The deduced amino acid sequence oftfdRindicates that it is a member of the LysR‐type activators. Investigation of the regulation of the catabolic gene clusters through the construction of a pJP4 defined deletion mutant, pYG1010, which lacks a 4.2 kilobaseXbalfragment containing the inverted repeat region carrying thetfdRandtfdSregulatory genes, showed thatPseudomonas cepaciastrains containing pYG1010 became 2,4‐D negative, but 3‐Cba positive.In vivorecombinants of pYG1010 and a clonedtfdSgene rescued the 2,4‐D phenotype, indicating that TfdS is a positive regulator oftfdAexpression, but not fortfdCDEFexpression.