Answers are grounded in this paper and cite their sources.
Mutants defective in the Fnr transcriptional activator protein lack formate hydrogenlyase activity (Fhl) for at least two reasons. First, the Fnr protein is required to activate expression of pyruvate formate lyase which catalyses the formation of formate, the inducer of Fhl activity, from pyruvate. Secondly, Fnr is required for expression of the hydC gene which is essential for the normal transport or processing of Ni2+. The Fhl− phenotype of fnr mutants can be reversed phenotypically by adding both formate and high concentrations of Ni2+ ions to the growth medium. Addition of Ni2+ alone is partially effective, but formate alone is ineffective. There is no evidence that the fnr region of the Escherichia coli chromosome codes for more than one regulatory protein. Furthermore, the role of the Fnr protein is clearly not restricted to anaerobic respiratory processes.
No takes yet. Share an insight, caveat, or question.
Jeffrey A. Cole (1988) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: