Lipid phase structure in the regulation of lipid composition in Acholeplasma laidlawii membranes

In Acholeplasma laidlawii membranes the ratio between the dominating lipids, monoglucosyldiglyceride (MGDG) and diglucosyldiglyceride (DGDG), depends on temperature, configuration of incorporated fatty acids, and membrane cholesterol content, which affect the molecular geometry of the lipids. MGDG and DGDG have wedge- and rod-like molecular shapes, respectively, that are modifiable. The packing constraints of lipids in amphiphilic aggregates, i.e., the area of the hydrocarbon-water interface and the volume and length of the hydrocarbon chains, are important in determining the aggregate structure. Pure MGDG forms a reversed hexagonal- (HII) phase structure with different acyl chain contents, while DGDG forms a lamellar phase. Depending on the unsaturated acyl chain content in the lipids, an in vitro mixture of MGDG and DGDG forms lamellar or cubic phases at physiologic temperatures. A high degree of cis-unsaturation, large amounts of MGDG and high temperatures favor formation of the cubic phase. Addition of cholesterol corresponding to the maximal amount incorporable into A. laidlawii induces a transition from a lamellar or a cubic phase to a reversed hexagonal phase. Lipid mixtures containing only unsaturated acyl chains are more sensitive to the bilayer-destabilizing effect of cholesterol than are mixtures with equal amounts of saturated and unsaturated acyl chains. The lamellar phase is the only one compatible with a functional biological membrane. Consequently, the balance between lipids that form lamellar and other mesophase structures must keep within certain limits. The cubic and reversed hexagonal structures were discovered under conditions not existing in the living Acholeplasma cell. Thus, the response of A. laidlawii lipid metabolism to external and internal stimuli can be predicted on the basis of molecular shapes and is necessary to the maintenance of optimal membranes stability. The reduced capacity of Acholeplasma membranes to incorporate cholesterol is a consequence of this regulation.