The β-ketoadipate pathway of Acinetobacter baylyi undergoes carbon catabolite repression, cross-regulation and vertical regulation, and is affected by Crc

Abstract

The degradation of many structurally diverse aromatic compounds inAcinetobacter baylyiis accomplished by theβ-ketoadipate pathway. In addition to specific induction of expression by certain aromatic compounds, this pathway is regulated by complex mechanisms at multiple levels, which are the topic of this study. Multiple operons feeding into theβ-ketoadipate pathway are controlled by carbon catabolite repression (CCR) caused by succinate plus acetate. The pathways under study enable the catabolism of benzoate (ben), catechol (catA),cis,cis-muconate (catB,C,I,J,F,D), vanillate (van), hydroxycinnamates (hca), dicarboxylates (dca), salicylate (sal), anthranilate (ant) and benzyl esters (are). For analysis of CCR at the transcriptional level a luciferase reporter gene cassette was introduced into the operons. The Crc (cataboliterepressioncontrol) protein is involved in repression of all operons (except forcatA), as demonstrated by the analysis of respectivecrcstrains. In addition, cross-regulation was demonstrated for thevanA,B,hcaanddcaoperons. The presence of protocatechuate caused transcriptional repression of thevanA,B- andhca-encoded funnelling pathways (vertical regulation). Thus the results presented extend the understanding both of CCR and of the effects of Crc for all aromatic degradative pathways ofA. baylyiand increase the number of operons known to be controlled by two additional mechanisms, cross-regulation and vertical regulation.