Thelwell C, Robinson N J, Turner-Cavet J S
Department of Biochemistry and Genetics, The Medical School, University of Newcastle, NE2 4HH, United Kingdom.
Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10728-33. doi: 10.1073/pnas.95.18.10728.
ORF slr0798, now designated ziaA, from Synechocystis PCC 6803 encodes a polypeptide with sequence features of heavy metal transporting P-type ATPases. Increased Zn2+ tolerance and reduced 65Zn accumulation was observed in Synechococcus PCC 7942, strain R2-PIM8(smt), containing ziaA and upstream regulatory sequences, compared with control cells. Conversely, reduced Zn2+ tolerance was observed following disruption of ziaA in Synechocystis PCC 6803, and ziaA-mediated restoration of Zn2+ tolerance has subsequently been used as a selectable marker for transformation. Nucleotide sequences upstream of ziaA, fused to a promoterless lacZ gene, conferred Zn2+-dependent beta-galactosidase activity when introduced into R2-PIM8(smt). The product of ORF sll0792, designated ZiaR, is a Zn2+-responsive repressor of ziaA transcription. Reporter gene constructs lacking ziaR conferred elevated Zn2+-independent expression from the ziaA operator-promoter in R2-PIM8(smt). Gel retardation assays detected ZiaR-dependent complexes forming with the zia operator-promoter and ZiaR-DNA binding was enhanced by treatment with a metal-chelator in vitro. Two mutants of ZiaR (C71S/C73S and H116R) bound to, and repressed expression from, the ziaA operator-promoter but were unable to sense Zn2+. Metal coordination to His-imidazole and Cys-thiolate ligands at these residues of ZiaR is thus implicated in Zn2+-perception by Synechocystis PCC 6803.
来自集胞藻PCC 6803的开放阅读框slr0798(现命名为ziaA)编码一种具有重金属转运P型ATP酶序列特征的多肽。与对照细胞相比,在含有ziaA和上游调控序列的聚球藻PCC 7942菌株R2-PIM8(smt)中观察到锌离子耐受性增强和65Zn积累减少。相反,在集胞藻PCC 6803中破坏ziaA后观察到锌离子耐受性降低,随后ziaA介导的锌离子耐受性恢复已被用作转化的选择标记。当将ziaA上游的核苷酸序列与无启动子的lacZ基因融合后导入R2-PIM8(smt)时,可赋予锌离子依赖性β-半乳糖苷酶活性。开放阅读框sll0792的产物命名为ZiaR,是ziaA转录的锌离子反应性阻遏物。缺少ziaR的报告基因构建体在R2-PIM8(smt)中导致ziaA操纵子-启动子的锌离子非依赖性表达升高。凝胶阻滞试验检测到ZiaR依赖性复合物与zia操纵子-启动子形成,并且在体外通过金属螯合剂处理可增强ZiaR与DNA的结合。ZiaR的两个突变体(C71S/C73S和H116R)与ziaA操纵子-启动子结合并抑制其表达,但无法感知锌离子。因此,ZiaR这些残基处与组氨酸-咪唑和半胱氨酸-硫醇盐配体的金属配位与集胞藻PCC 6803对锌离子的感知有关。