Laboratory of Biotechnology, Chulabhorn Research Institute, Bangkok, Thailand.
FEMS Microbiol Lett. 2012 Apr;329(1):87-92. doi: 10.1111/j.1574-6968.2012.02509.x. Epub 2012 Feb 13.
An Agrobacterium tumefaciens membrane-bound ferritin (mbfA) mutant was generated to assess the physiological functions of mbfA in response to iron and hydrogen peroxide (H(2) O(2) ) stresses. Wild-type and the mbfA mutant strains showed similar growth under high- and low-iron conditions. The mbfA mutant was more sensitive to H(2) O(2) than wild-type strain. Expression of a functional mbfA gene could complement the H(2) O(2) -hypersensitive phenotype of the mbfA mutant and a rhizobial iron regulator (rirA) mutant, suggesting that MbfA protects cells from H(2) O(2) toxicity by sequestering intracellular free iron, thus preventing the Fenton reaction. The expression of mbfA could be induced in response to iron and to H(2) O(2) treatment. The iron response regulator (irr) also acted as a repressor of mbfA expression. An irr mutant had high constitutive expression of mbfA, which partly contributed to the H(2) O(2) -hyperresistant phenotype of the irr mutant. The data reported here demonstrate an important role of A. tumefaciens MbfA in the cellular defence against iron and H(2) O(2) stresses.
为了评估 mbfA 在应对铁和过氧化氢 (H(2)O(2)) 应激中的生理功能,生成了一个根癌农杆菌膜结合铁蛋白 (mbfA) 突变体。野生型和 mbfA 突变菌株在高、低铁条件下表现出相似的生长。mbfA 突变体比野生型菌株对 H(2)O(2) 更敏感。功能性 mbfA 基因的表达可以互补 mbfA 突变体和根瘤菌铁调节因子 (rirA) 突变体的 H(2)O(2) 超敏表型,表明 MbfA 通过螯合细胞内游离铁来保护细胞免受 H(2)O(2) 毒性,从而防止 Fenton 反应。mbfA 的表达可以响应铁和 H(2)O(2) 处理而诱导。铁反应调节剂 (irr) 也作为 mbfA 表达的抑制剂。irr 突变体具有 mbfA 的高组成型表达,这在一定程度上导致了 irr 突变体对 H(2)O(2) 的超抗性表型。这里报告的数据表明,A. tumefaciens MbfA 在细胞防御铁和 H(2)O(2) 应激中起着重要作用。