Disease relevance of pcaI

• PcaU was expressed in Escherichia coli and shown to bind to a portion of the pcaI-pcaU intergenic region containing a sequence identical in 16 of 19 nucleotide residues to a segment of the pob operator [1].

High impact information on pcaI

• The increase of the pcaU gene copy number leads to a decrease of the basal expression at pcaIp, indicating that the occupancy of the PcaU binding site is well balanced and depends on the concentration of PcaU in the cell [2].
• It is shown that both activities of the IclR-type regulator protein PcaU at the structural gene promoter pcaIp, namely protocatechuate-dependent activation of pca-qui operon expression as well as repression in the absence of protocatechuate, can be observed in a different cellular background (Escherichia coli) and therefore are intrinsic to PcaU [2].
• Luciferase is used as a reporter to demonstrate strong repression of pcaIp when benzoate, a substrate of the catechol branch of the pathway, is present in addition to substrates of the protocatechuate branch (cross-regulation) [2].
• Northern blot analysis allowed the identification of a 12-kb transcript spanning pcaI to quiX [3].
• The 2.4-kb transcript makes up about 25% of the total transcript abundance of quiA, and thus the majority of transcription of the last gene of the area is also driven by pcaIp [3].

Biological context of pcaI

• The binding site in the pcaU-pcaI intergenic region is located between the two divergent promoters covering 45 bp, which includes three perfect 10-bp repetitions [4].

Other interactions of pcaI

• PcaU was shown to bind to DNA containing this segment as well as to the DNA in the pcaU-pcaI intergenic region [1].

References