Cyclic di-GMP-dependent Signaling Pathways in the Pathogenic Firmicute Listeria monocytogenes
Figure 4
Inhibition of motility and activation of EPS production in L. monocytogenes by elevated levels of c-di-GMP.
A: Top, Inhibition of swimming of the wild-type L. monocytogenes in semi-solid agar by a heterologous DGC, Slr1143. Bottom, Restoration of swimming in semi-solid agar of the L. monocytogenes ΔpdeB/C/D mutant by a heterologous PDE, YhjH. WT, wild type, EGD-e; A/B/C, ΔpdeB/C/D mutant; pIMK, WT::pIMK2 (vector control); slr, WT::(pIMK2::slr1143); yhjH, WT::(pIMK2::yhjH). B: Congo red staining of EPS in L. monocytogenes. 1, WT, wild type; 2, ΔpdeB/C/D; 3, ΔpdeB/C/D ΔpssE; 4, ΔpdeB/C/D ΔpssC; 5, ΔpdeB/C/D::pIMK2; 6, ΔpdeB/C/D::pIMK2::yhjH; 7, ΔpdeB/C/D::(pIMK2::slr1143); 8, WT::pIMK2; 9, WT::(pIMK2::yhjH); 10, WT::(pIMK2::slr1143). C: Deletion of all three c-di-GMP PDEs drastically inhibits motility of L. monocytogenes in semi-solid agar. WT, wild type strain, B, ΔpdeB; C, ΔpdeC; D, ΔpdeD; B/D, ΔpdeB ΔpdeD; C/D, ΔpdeC ΔpdeD; B/C, ΔpdeB ΔpdeC; B/C/D, ΔpdeB/C/D. D: Rough colony morphology and increased Congo red staining of the L. monocytogenes ΔpdeB/C/D mutant and rescue of the wild-type colony morphology by the ΔpssC mutation (ΔpdeB/C/D ΔpssC). E: Restoration of motility of the ΔpdeB/C/D mutant by the ΔpssC or ΔpssE mutations.