Department of Biotechnology, College of Life Sciences, Ritsumeikan University, Kusatsu, Shiga 525-8577, Japan.
Int J Mol Sci. 2018 Mar 11;19(3):809. doi: 10.3390/ijms19030809.
The gene in encodes a putative outer membrane channel porin, which resides within a cluster of genes. This cluster is highly conserved across the and includes multiple putative -type cytochromes. In silico analyses of the ExtI sequence, together with Western blot analysis and proteinase protection assays, showed that it is an outer membrane protein. The expression level of ExtI did not respond to changes in osmolality and phosphate starvation. An -deficient mutant did not show any significant impact on fumarate or Fe(III) citrate reduction or sensitivity to β-lactam antibiotics, as compared with those of the wild-type strain. However, deficiency resulted in a decreased ability to reduce selenite and tellurite. Heme staining analysis revealed that deficiency affects certain heme-containing proteins in the outer and inner membranes, which may cause a decrease in the ability to reduce selenite and tellurite. Based on these observations, we discuss possible roles for ExtI in selenite and tellurite reduction in .
该基因编码一种假定的外膜通道孔蛋白，位于一组基因中。该基因簇在 中高度保守，包括多个假定的 -型细胞色素。ExtI 序列的计算机分析，以及 Western blot 分析和蛋白酶保护试验表明，它是一种外膜蛋白。ExtI 的表达水平不会响应渗透压和磷酸盐饥饿的变化。与野生型菌株相比，-缺陷突变体在延胡索酸盐或 Fe(III)柠檬酸盐还原或对β-内酰胺类抗生素的敏感性方面没有显示出任何显著影响。然而， 缺陷导致还原亚硒酸盐和碲酸盐的能力下降。血红素染色分析表明， 缺陷影响外膜和内膜中某些含血红素的蛋白质，这可能导致还原亚硒酸盐和碲酸盐的能力下降。基于这些观察结果，我们讨论了 ExtI 在 中还原亚硒酸盐和碲酸盐中的可能作用。
