“…glycerolkinase) and non-PTS transporters such as the lactose permease LacY and the maltose uptake system MalFGK 2 E (Dean et al, 1990;Hurley et al, 1993;Osumi & Saier, 1982). By this means, disruption of the PTS phosphorelay by deletion of ptsI or ptsH leads to the inhibition of maltose uptake in E. coli and S. enterica serovar Typhimurium and, thus, exclusion of the inducer (Bao & Duong, 2013;Blüschke et al, 2006;Chen et al, 2013;Saier & Roseman, 1976a, b;Simoni et al, 1976). Furthermore, PTS components are also directly involved, by protein-protein interactions, in the control of chemotaxis (unphosphorylated EI inhibits CheA autophosphorylation), glycogen metabolism (dephosphorylated HPr binds and activates the glycogen phosphorylase) and s 70 -dependent transcription (in stationary-phase cells HPr forms a tight complex with the anti-s factor Rsd and thereby inhibits complex formation between Rsd and s 70 ) (Lux et al, 1995;Park et al, 2013;Seok et al, 1997).…”