4.A.1.1.1
Glucose porter (PtsG; GlcA; Umg) (transports D-glucose and α-methyl-D-glucopyranoside).  The IIC domain has been crystallized, and x-ray data to 4.5 Å resolution have been described (Zurbriggen et al. 2010).  The system has been manipulated to engineer increased production of aromatic metabolites (Carmona et al. 2015, Vargas-Tah et al. 2015). The presence or absence of D-glucose reflects the transporter before and after release of the transported glucose into the cytoplasm. The transition associated with substrate release appears to require a subtle structural rearrangement in the region that includes hairpin 1 (Kalbermatter et al. 2017).  Mlc (for makes large colonies) represses transcription of the genes encoding enzyme I, HPr, EIIBC^Glc and EIIABCD^Man in defined media that lack PTS substrates. When glucose is present, the unphosphorylated form of EIIBC^Glc sequesters Mlc to the cell membrane, preventing its interaction with DNA (Plumbridge 2002, Joyet et al. 2013). The Vibrio Mlc functions similarly (Pickering et al. 2014). A small (43 aa) protein, SgrT, acts in tandem with a well-characterized small RNA during metabolic stress, due to the accumulation of cytoplasmic sugar-Ps to help bacterial cells maintain balanced metabolism and continue growing. SgrT acts on the glucose transport system, inhibiting its activity under stress conditions in order to allow cells to utilize alternative carbon sources (Lloyd et al. 2017). ptsG mRNA localization to the inner membrane, coupled with the membrane insertion of nascent peptide, mediates Hfq/SgrS-dependent ptsG mRNA destabilization, presumably by reducing second rounds of translation (Kawamoto et al. 2005). SgrT is a small protein of 43 aas that allosterically inhibits IICB^Glc. while SgrS is a small RNA coompementary to ptsG mRNA that influences its expression.  The sgrST operon is regulated by SgrR, a glucose-6-P-dependent transcriptional activator (Jeckelmann and Erni 2020).