putida indicating that these targets may also be regulated by directly by Crc [34]. Besides the role that CRC plays in the bioremediation activities of P. putida, little else is known about the control that CRC imposes on the ecological functions of Pseudomonads other than for virulence-associated functions in Pseudomonas aeruginosa. A crc mutant of P. aeruginosa PA14 was defective in biofilm

formation and type IV pilus-mediated twitching motility [36]. and a crc mutant of P. aeruginosa PAO1 displayed increased susceptibility to some antibiotics as well as defects in type III secretion, motility and expression of quorum sensing-regulated virulence factors [27]. Given the range of ecological functions that Pseudomonas may perform there is great scope for Crc to be Proteases inhibitor a significant regulator beyond JNK inhibitor mouse the realm

of primary metabolism. For instance, glucose metabolism is subject to CRC and gluconate is a product of glucose metabolism. Gluconate itself is linked to phosphate solubilisation [9] and biocontrol [37] and there is a link between the ability to produce gluconate and the levels of antimicrobial compounds produced such as 2,4-diacetylphloroglucinol and pyoluteorin [38]. Additionally, recent evidence indicates that there is a link between primary metabolism and secondary metabolism controlled by the GacS/Rsm system [39]. This suggests that there is great potential for

CRC to interact with other regulatory networks, at least indirectly, and it is therefore a high priority to better understand the Crc regulon. Based on the size of the Crc product and the proposed mechanism of action, it is thought that Crc binding must occur within -70 to +16 bp relative to the origin of translation [18]. There remain, however, very few known direct targets of Crc: only benR [33], alkS [18], xylR and xylB [34] mRNAs from P. putida and amiE mRNA [17] (product of the amidase gene amiE), in P. aeruginosa have been demonstrated to bind Crc. To extend the number of direct targets known, we carried out a bioinformatic analysis using genome information from sequenced Pseudomonas strains. By identifying the specific targets from in pathways that are known to be regulated by CRC, it will be possible to determine precisely how different Pseudomonads control nutrient uptake and utilisation. Furthermore, the analysis is expected to identify new pathways and processes, not previously known to be CRC-regulated. A better understanding of how Pseudomonas species use CRC will enhance knowledge of the ecology of these bacteria and will facilitate efforts to exploit the metabolic capacity of these bacteria in industrial and environmental microbiology.