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Published online ahead of print on 30 April 2009 as doi:10.1099/mic.0.027060-0
Microbiology 2009;155:2420.

Microbiology (2009), DOI 10.1099/mic.0.027060-0
© 2009 Society for General Microbiology

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Microbiology 0 (2009), mic.0.027060; DOI  10.1099/mic.0.027060-0
© 2009 Society for General Microbiology


Intracellular 2-keto-3-deoxy-6-phosphogluconate is the signal for carbon catabolite repression of phenylacetic acid metabolism in Pseudomonas putida KT2440

Juhyun Kim1, Jinki Yeom1, Che Ok Jeon2 and Woojun Park1,3

1 Korea University;
2 Chung-Ang University

ABSTRACT

The growth pattern of Pseudomonas putida KT2440 in the presence of glucose and phenylacetic acid (PAA) with the sugar being used before the aromatic compound suggests that there is a carbon catabolite repression (CCR) of PAA metabolism by glucose or gluconate. However, this CCR phenomenon does not occur in PAA-amended minimal medium containing fructose, pyruvate, or succinate. We previously identified 2-keto-3-deoxy-6-phosphogluconate (KDPG) as the inducer of glucose metabolism, which led to this investigation into the role of KDPG as a signal compound for this CCR event. Both the edd mutant (non-KDPG producer) and eda mutant (KDPG overproducer) grew in the presence of PAA but not in the presence of glucose. The edd mutant utilized PAA even in the presence of glucose, indicating that CCR was abolished. Unlike the edd mutant, the eda mutant did not grow in the presence of glucose and PAA. Interestingly, there was no uptake and/ or the metabolism of PAA in the eda mutant cells under the same condition and the accumulated intracellular KDPG did not affect cell viability. Targeted disruption of PaaX, a repressor of the PAA operon, showed the CCR of PAA metabolism in the presence of glucose, which suggested that there is another repression system associated with the KDPG signal. This is the first study to demonstrate that KDPG is the true catabolite-repression signal of PAA metabolism in P. putida KT2440.

3 E-mail: wpark{at}korea.ac.kr







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Copyright © 2009 Society for General Microbiology.