  Ongoing sub-cellular oscillation of Min proteins is required to block
minicelling in E. coli. Experimentally, Min oscillations are seen in newly
divided cells and no minicells are produced. In model Min systems many daughter
cells do not oscillate following septation because of unequal partitioning of
Min proteins between the daughter cells. Using the 3D model of Huang et al., we
investigate the septation process in detail to determine the cause of the
asymmetric partitioning of Min proteins between daughter cells. We find that
this partitioning problem arises at certain phases of the MinD and MinE
oscillations with respect to septal closure and it persists independently of
parameter variation. At most 85% of the daughter cells exhibit Min oscillation
following septation. Enhanced MinD binding at the static polar and dynamic
septal regions, consistent with cardiolipin domains, does not substantially
increase this fraction of oscillating daughters. We believe that this problem
will be shared among all existing Min models and discuss possible biological
mechanisms that may minimize partitioning errors of Min proteins following
septation.
