Involved in the control of the switch from cell motility to adhesion via regulation of cellular levels of cyclic-di-GMP (c-di-GMP) (PubMed:18765794). Part of a signaling cascade that regulates curli biosynthesis. The cascade is composed of two c-di-GMP control modules, in which c-di-GMP controlled by the DgcE/PdeH pair (module I) regulates the activity of the DgcM/PdeR pair (module II), which in turn regulates activity of the transcription factor MlrA and expression of the master biofilm regulator csgD (PubMed:23708798). Effect on flagella is controlled via the c-di-GMP-binding flagellar brake protein YcgR (PubMed:18765794). cyclic di-3',5'-guanylate + H2O = 5'-phosphoguanylyl(3'->5')guanosine + H(+) A class 3 flagellar gene, it is dependent on the master transcriptional regulators FlhC and FlhD, and then FliA for expression. Induced in early post-exponential phase at both 28 and 37 degrees Celsius, it shuts down later than class 1 and class 2 operon genes. Expression has to be shut down for adhesive curli fimbriae to be induced, i.e. on solid medium where biofilms form. Repressed by RpoS. Disruption leads to increased expression of adhesive curli fimbriae genes (PubMed:18765794), including CsgD (PubMed:19332833). Also leads to a severe reduction in swarm size and swimming velocity, and 80% reduced concentrations of c-di-GMP. Disruption of ycgR, or concomitant disruption of dosC, dgcE, dgcQ and dgcN completely restores motility, suggesting these 4 genes, together with this c-di-GMP phosphodiesterase, form a network that regulates cell motility by altering levels of c-di-GMP (PubMed:20303158). Overlapping but different results were seen by another group, where disruption of dgcJ, another probable diguanylate cyclase, partially suppresses the pdeH disruption, full suppression requires concomitant disruption of dgcJ, dgcQ and dgcE (PubMed:18765794).