Which factor is responsible for phase transitions in phospholipid bilayers?
Lipid phase behavior reflects cooperative melting of hydrocarbon lattice from ordered gel to disordered liquid crystalline phases. Transition temperature Tm defines midpoint where fifty percent of chains contain gauche kinks and lateral expansion occurs, measured by differential scanning calorimetry as sharp endothermic peak representing enthalpy change. Tm rises with longer saturated acyl length because more CH2 groups increase van der Waals energy and with high sphingolipid content forming hydrogen bonding network at amide and hydroxyl groups. Cis unsaturation introduces permanent thirty degree kink disrupting packing lowering Tm by thirty to fifty degrees per double bond. Cholesterol abolishes sharp transition by forming liquid ordered phase intermediate with broadened endotherm. Glycoproteins, integral proteins, ATP levels modulate fluidity via picket fencing and phosphorylation cascades but do not set intrinsic lipid Tm. Cells sense packing defects through Mga2 ubiquitin dependent processing and SREBP pathway regulating desaturases OLE1. Linking Tm to permeability for liposomal drug delivery, cryopreservation, and cold adaptation explains why phase transitions are central to membrane biophysics strongly tested in GATE and NET.
Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 10: Phase transitions Tm and calorimetry.