Proposed model for PG biosynthesis and maintenance in pathogenic <i>Chlamydia</i>.

<p><b>(a)</b> Upon invading a host cell, MreB facilitates mid-cell PG (green) ring formation 8 hpi and the first cell division occurs. Inhibition of MreB (red) prior to EB-RB transition prevents this first division and results in accumulation of intracellular ‘EB-like’ particles in the host cytosol. Once RBs form, PG is constantly synthesized and incorporated into the ring non-uniformly by dynamic MreB patches. If MreB polymerization is inhibited, the PG ring dissociates, resulting in slightly enlarged, static, PG-less aberrant bodies. Inhibition of PG crosslinking by β-lactams does not affect transglycosylase activity and MreB localization, but instead results in unchecked enlargement of the RB. Bottom, upon cell division, the new division planes form immediately and perpendicular to the previous division plane. During transition to non-replicative EBs, MreB and PG biosynthesis enzymes are downregulated [<a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1005590#ppat.1005590.ref058" target="_blank">58</a>], resulting in the complete disassembly of the PG ring. <b>(b)</b> Chlamydial PG biosynthesis and degradation mechanisms overlap and are active throughout the cell cycle. MreB (red) moves along the ring plane (black arrows), initiating the non-uniform synthesis of new PG (green) and influencing the action of an unknown degradation mechanism that continuously removes older material (white arrows). PG degradation enzymes (amidases and lytic transglycosylases) are visualized as blue pacmen.