Nikel Pablo I, de Almeida Alejandra, Pettinari M Julia, Méndez Beatriz S
Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina.
J Bacteriol. 2008 May;190(9):3404-7. doi: 10.1128/JB.00040-08. Epub 2008 Mar 7.
Strains derived from HfrH carrying the arcA2 null mutation exhibit a higher respiratory rate, enhanced glucose consumption, and a more-reduced intracellular redox state than arcA deletion mutants of a different lineage. The phenotype of the arcA2 mutants was due to the presence of a creC constitutive mutation introduced by P1 transduction.
携带arcA2无效突变的源自HfrH的菌株比不同谱系的arcA缺失突变体表现出更高的呼吸速率、增强的葡萄糖消耗和更低的细胞内氧化还原状态。arcA2突变体的表型是由于通过P1转导引入的creC组成型突变的存在。