Model of the consequences of inc overexpression. In wild-type Chlamydia, inc expression is temporal, which results in an inclusion membrane that can expand with the growing number of organisms and optimal host-Chlamydia interactions that maximizes the amount of infectious progeny produced. When certain Incs, like IncF and CT813, are produced at high amounts, they are type III secreted and inserted in the inclusion membrane. It is unknown at this point if these exogenous Incs “flood” the type III secretion system at the expense of endogenous Incs, which causes a decrease in endogenous inc transcripts. The ultimate result is a disorganized inclusion membrane that has altered interactions with the host cell (e.g., loss of SNX6 recruitment) and, thus, altered chlamydial development. These data indicate that inclusion membrane dynamics, which includes inclusion membrane organization and the resulting Inc-host interactions, contributes to optimal chlamydial development.