STRUCTURE AND ORGANIZATION OF HIP, AN OPERON THAT AFFECTS LETHALITY DUE TO INHIBITION OF PEPTIDOGLYCAN OR DNA-SYNTHESIS
STRUCTURE AND ORGANIZATION OF HIP, AN OPERON THAT AFFECTS LETHALITY DUE TO INHIBITION OF PEPTIDOGLYCAN OR DNA-SYNTHESIS
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DOI：
10.1128/jb.173.18.5732-5739.1991
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发表时间：
1991-09-01
影响因子：
3.2
通讯作者：
MOYED, HS
中科院分区：
文献类型：
--
作者：
BLACK, DS;KELLY, AJ;MOYED, HS
高频率的持久性，无论是DNA或肽聚糖合成的抑制致死作用，髋关节表型，结果在髋关节位点的大肠杆菌K-12的突变。 与这些突变互补的DNA片段的核苷酸序列揭示了一个由可能的调节区组成的操纵子，包括与E. coli启动子和两个开放阅读框，它们在体外和体内都能翻译。 264-bp开放阅读框的终止密码子hipB和1，320-bp开放阅读框的起始密码子hipA共享一个腺嘌呤残基。 启动子强度的测定、可能启动子相对于转录起始的位置以及密码子使用都表明hipB和hipA是弱表达基因。 该启动子的活性受到包括hipB编码区的相邻下游序列的损害。 通过在hipB的编码区内插入过早的翻译终止信号，部分缓解了这种损伤，这表明HipB蛋白参与了该启动子的调节。 hipB和hipA的操纵子内的安排和hipA的菌株缺陷或缺乏hipB的毒性表明这些基因的产品之间的重要相互作用。
High-frequency persistence to the lethal effects of inhibition of either DNA or peptidoglycan synthesis, the Hip phenotype, results from mutations at the hip locus of Escherichia coli K-12. The nucleotide sequence of DNA fragments which complement these mutations revealed an operon consisting of a possible regulatory region, including sequences with modest homology to an E. coli promoter, and two open reading frames which are translated both in vitro and in vivo. The stop codon of a 264-bp open reading frame, hipB, and the start codon of a 1,320-bp open reading frame, hipA, share an adenine residue. Assays of promoter strength, the location of the probable promoter with respect to the start of transcription, and codon usage all indicate that hipB and hipA are weakly expressed genes. The activity of the promoter is impaired by an adjacent downstream sequence which includes the coding region of hipB. The impairment is partially relieved by insertion of a premature translation termination signal within the coding region of hipB, suggesting involvement of the HipB protein in the regulation of this promoter. The arrangement of hipB and hipA within the operon and the toxicity of hipA for strains defective in or lacking hipB suggest an important interaction between the products of these genes.