We show for soil bacterium LF7 that the possession of anndole-3-cetic acid atabolic () gene cluster is causatively linked to the ability to utilize the plant hormone indole-3-acetic acid (IAA) as a carbon and energy source. Genome-wide transcriptional profiling by mRNA sequencing revealed that these genes, chromosomally arranged as and coding for the transformation of IAA to catechol, were the most highly induced (>29-fold) among the relatively few (<1%) differentially expressed genes in response to IAA. Also highly induced and immediately downstream of the cluster were genes for a major facilitator superfamily protein () and enzymes of the β-ketoadipate pathway (), which channels catechol into central metabolism. This entire gene set was constitutively expressed in an deletion mutant, confirming the role of , annotated as coding for a MarR-type regulator and located upstream of, as a repressor of gene expression. In LF7 carrying the DNA region upstream of fused to a promoterless gene, green fluorescence accumulated in response to IAA at concentrations as low as 1.6 μM. The promoter region also responded to chlorinated IAA, but not other aromatics tested, indicating a narrow substrate specificity. In an deletion mutant, expression from the promoter region was constitutive, consistent with the predicted role of as a repressor. A deletion analysis revealed putative -35/-10 promoter sequences upstream of, as well as a possible binding site for the IacR repressor. Bacterial genes code for the enzymatic conversion of the plant hormone indole-3-acetic acid (IAA) to catechol. Here, we demonstrate that the genes of soil bacterium LF7 enable growth on IAA by coarrangement and coexpression with a set of and genes that code for complete conversion of catechol to central metabolites. This work contributes in a number of novel and significant ways to our understanding of gene biology in bacteria from (non-)plant environments. More specifically, we show that LF7's response to IAA involves derepression of the MarR-type transcriptional regulator IacR, which is quite fast (less than 25 min upon IAA exposure), highly specific (only in response to IAA and chlorinated IAA, and with few genes other than, , and induced), relatively sensitive (low micromolar range), and seemingly tailored to exploit IAA as a source of carbon and energy.