genetic analyses indicate that this process is regulated by Fnr controlling the expression of lpxO .
Biochemical analyses indicate that this process is regulated by Fnr controlling the expression of lpxO .
Thus , the oxygen-dependent regulation of lpxO expression is lost when fnr is deleted , indicating that Fnr is a negative regulator of lpxO expression under anaerobic conditions .
Thus , the oxygen-dependent regulation of lpxO expression is lost when fnr is deleted , indicating that Fnr is a negative regulator of lpxO expression under anaerobic conditions .
These results indicate that Fnr regulate lpxO expression through direct binding to its promoter region .
In addition , we also demonstrate that global regulators Fnr control the oxygen-dependent lipid-A hydroxylation by directly regulating the expression of lpxO .
Our results also showed that both Fnr are able to bind in-vitro to the promoter regions of lpxO , strongly suggesting a direct role for these regulators in the control of lpxO transcription .
Our results also showed that both Fnr are able to bind in-vitro to the promoter regions of lpxO , strongly suggesting a direct role for these regulators in the control of lpxO transcription .
a model in which Fnr control the expression of lpxO in S. Enteritidis to achieve a fine-tuning of lipid-A hydroxylation levels