putida grows in nutrient-rich LB medium [53]. For instance, the inactivation of the crc gene resulted in three times higher abundance of OprB1 in LB-grown cells [53]. Interestingly, it was recently reported

that Crc is not important for the growth of P. putida DOT-T1E on glucose as single PU-H71 price carbon source and this was explained by dispensability of Crc in the medium lacking nutrients MM-102 concentration alternative to glucose [52]. However, our data demonstrate that Crc can actually affect the usage of glucose as the sole carbon source because the abundance of OprB1 was shown to be elevated in the crc mutant. Yet, the effect of Crc on the amount of OprB1 was observed only in glucose-rich but not in glucose-limiting conditions (Figure 7D) suggesting that the Crc-mediated repression of OprB1 is probably completely absent in hungry bacteria allowing a full expression of OprB1. Thus, in addition to regulating the hierarchical use of carbon sources in complete medium, Crc is also involved in fine tuning

single carbon source assimilation. The up-regulation of the glucose-scavenging OprB1 this website is the most appropriate behavior of P. putida at glucose limitation. However, “”there is no free lunch in nature.”" Data of this study suggest that hunger response is costly and if not regulated properly, it might be even deadly as judged by the requirement of ColRS signaling. Interestingly, a largely Miconazole similar cell death phenomenon was recently characterized in E. coli where constitutive expression of the maltoporin LamB resulted in cell lysis in the absence of a functional response regulator OmpR [59, 60]. The authors proposed that cell death resulted from envelope stress involving an imbalance in the lipopolysaccharide/porin composition of the outer membrane

and an increased requirement for inorganic phosphate [60]. Analogous scenario can be considered for the colR mutant, as recent studies conducted in P. fluorescens and Xanthomonas citri have indicated that ColRS system is involved in LPS production and/or modification [20, 61]. Our current study describes not only the participation of ColRS system in hunger response of P. putida, but also provides clues to better understand the role of this system in root colonization. It is notable that the colonization defect observed for P. fluorescens ColRS system mutant became evident only under the condition of competition with the wild-type strain [19]. This indicates that the colonization ability per se is not impaired but rather some other population-related trait is hampered in the absence of ColRS signaling. Our results suggest that hunger-induced lysis of a subpopulation may be responsible for the reduced fitness of the colR mutant under competition conditions. Nutrient concentration in the rhizosphere is low [62] and thereby rhizosphere colonization takes place under condition of hunger [63].