Inactivation of cytochrome o XXXX oxidase relieves catabolic repression of the @entity15250 GPo1 alkane degradation pathway.

@entity15401 @entity4588 @entity19765 @entity15250 @entity880 @entity505
Expression of the alkane degradation pathway encoded by the OCT plasmid of @entity15250 GPo1 is regulated by two control systems. One relies on the transcriptional regulator AlkS, which activates expression of the pathway in the presence of @entity19765 . The other, which is a dominant global regulation control, represses the expression of the pathway genes when a preferred @entity505 source is present in the growth medium in addition to @entity19765 . This catabolite repression control occurs through a poorly characterized mechanism that ultimately regulates transcription from the two AlkS-activated promoters of the pathway. To identify the factors involved, a screening method was developed to isolate mutants without this control. Several isolates were obtained, all of which contained mutations that mapped to genes encoding cytochrome o @entity15401 oxidase, the main terminal oxidase of the electron transport chain under highly aerobic conditions. Elimination of this terminal oxidase led to a decrease in the catabolic repression observed both in rich Luria-Bertani medium and in a defined medium containing @entity880 or @entity4588 as the @entity505 source. This suggests that catabolic repression could monitor the physiological or metabolic status by using information from the electron transport chain or from the redox state of the cell. Since inactivation of the crc gene also reduces catabolic repression in rich medium (although not that observed in a defined medium), a strain was generated lacking both the Crc function and the cytochrome o terminal oxidase. The two mutations had an additive effect in relieving catabolic repression in rich medium. This suggests that crc and cyo belong to different regulation pathways, both contributing to catabolic repression.
