ExpG activates EPS II biosynthesis under phosphate-limiting conditions and in the presence of extra expG copies . Its activity is modulated by:
Phosphate Regulation: PhoB binds PHO box-like sequences in exp promoters, synergizing with ExpG under phosphate starvation .
MucR Mutation: Deletion of mucR (a repressor) elevates exp transcription, further enhanced by phosphate limitation .
Self-Induction: Extra expG copies upregulate all exp complementation groups .
ExpG binds to conserved promoter regions upstream of expA1, expG/expD1, and expE1 . Key findings include:
Binding Site: A 28-bp palindromic sequence with two flanking motifs .
Binding Kinetics: Atomic force microscopy (AFM) revealed unbinding forces of 50–165 pN and dissociation rates of ~1.2 × 10⁻³ s⁻¹ .
Promoter Regulation: ExpG activates proximal promoters of expA, expD, and expE operons, while MucR represses distal promoters .
EPS II production is critical for root colonization and symbiosis with legumes like alfalfa . ExpG’s role includes:
Symbiotic Efficiency: EPS II promotes nodule formation and nitrogen fixation .
Stress Resistance: EPS II protects against osmotic and oxidative stress .
Regulatory Cross-Talk: ExpG and PhoB integrate phosphate signaling with symbiotic requirements .
Recombinant ExpG: While not explicitly studied, recombinant ExpG could enable heterologous EPS II production in industrial microbes or biofilm engineering .
Therapeutic Potential: ExpG’s regulatory mechanisms may inspire novel biotechnological strategies for controlling polysaccharide biosynthesis .
KEGG: sme:SM_b21317