Also, the role for flagella in dispersal is controversial. The hypothesis [23] that ompR expression may be highest during irreversible Selleck Entospletinib attachment was built upon the fact that phospho-OmpR was a negative regulator of flhD expression [24] and a positive regulator of curli [28, 35]. Our Evofosfamide cell line temporal expression profile of ompR is in agreement with this hypothesis. The peak for ompR was at 34 h, where flhD

expression was minimal (Figure 2). The production of curli has previously been recognized as a control mechanism for biofilm formation [36], an adherence tool to human uroepithelical cells [37], and part of the motility-to-biofilm transition. CsgD contributes to this transition by activating the expression of curli and inhibiting flagella biosynthesis [38]. The expression peak of the positive curli regulator, OmpR, at 34 h could be our marker for irreversible attachment. Maturation of a biofilm typically requires the synthesis of an exopolysaccharide capsule that serves as a ‘glue’ to keep the microcolony together and contributes to adherence to the

surface. This capsule can consist of many different substances, among them the K-capsule polysaccharide that is a contributor to the intracellular lifestyle of uropathogenic E. coli[1] OSI-906 price and colanic acid, which has been recognized early as an important factor in forming the three dimensional structures that constitute the biofilm [39]. The phosphorelay system RcsCDB is an activator of colanic acid production [40], while also activating the synthesis of type I fimbriae [25]. These multiple functions of RcsB may explain the slow and steady increase of rcsB expression during biofilm formation

(Figure 2) that cannot be correlated with a single phase of biofilm development. With the exception of the late increase in flhD expression, our temporal expression profiles are in agreement with our hypothesis from the review article [23], as well as current literature. Regulation of flhD by multiple response regulators offers ample opportunity to control biofilm amounts and cell division Since the goal of Chloroambucil our research was to modulate signal transduction pathways and reduce biofilm amounts, the next step after the identification of FlhD/FlhC as our first target would be the attempt to increase flhD expression levels, ultimately causing a reduction in biofilm amounts. The expression of flhD is regulated by many environmental and genetic factors. Environmental factors include temperature [41], osmolarity [24], and the nutritional state of the cell [42]. Genetic factors are similarly diverse and include the Catabolite Repressor Protein CRP and the nucleoid associated protein H-NS [43], the transcriptional regulator LrhA [44], the LysR family protein HdfR [33], and the insertion of IS elements into the flhD promoter [45–47]. Post transcriptional regulation involves the carbon storage regulator CsrA [48] and a negative regulator of cell motility, YdiV [49].