Fig. 10.

Models for the regulation of cell division by KhpA and KhpB in S. pneumoniae D39. A. The absence of KhpA or/and KhpB increases cellular FtsA amount, which bypasses the requirement for essential bPBP2b, MreCD, and RodA. FtsA overproduction by itself partly contributes to the reduced cell size and induction of the WalRK regulon caused by ΔkhpA/B mutants. In addition, KhpA and KhpB regulate genes other than ftsA such that ΔkhpA/B mutants bypass the requirement for essential RodZ and GpsB. See text for details. B. Three models for how the KhpA/B RNA binding protein could post-transcriptionally regulate FtsA amount via the ftsA 5′-UTR leader region. Model 1 and 2 propose direct and indirect models of negative regulation of the ftsA 5′-UTR leader, whereas Model 3 is an indirect model wherein KhpA/B negatively regulates the expression or function of an unknown sRNA or protein that positively regulates FtsA production. The mutant analysis in this paper favors Model 3 (✓) as discussed in the text, although Models 1 and 2 (?) cannot be ruled out at this point.