The Membrane as a Transporter, Ion Channels and Membrane Pumps - Membrane Biophysics, Biological and Medical Physics, Biomedical Engineering - page 51

proteins simply act as a passive pore, where molecules randomly move through the
opening via diffusion. This requires no energy, and molecules move from an area of
high concentration to an area of low concentration. Symports also use the process
of diffusion. In this case, a molecule that is moving naturally into the cell through
diffusion is used to drag another molecule into the cell. For example, glucose hitches
a ride with sodium.
Marker proteins extend across the cell membrane and serve to identify the cell.
The immune system uses these proteins to tell own cells from foreign invaders.
The cell membrane can also engulf structures that are much too large to fit through
the pores in the membrane proteins. This process is known as endocytosis, and in it
the membrane wraps itself around the particle and pinches off a vesicle inside the cell.
The opposite of endocytosis is exocytosis. Large molecules that are manufactured
in the cell are released through the cell membrane. A prominent example of this
process is the exocytosis of neurotransmitter molecules into the synapse region of a
nerve cell.
The primary function of bilayer-spanning proteins is to catalyze the selec-
tive transfer of materials and information across biological membranes. In this
process, MPs undergo conformational changes, e.g., the opening/closing transi-
tions in ion channels [ 38 , 39 , 54 ], the shift in substrate binding site accessibility
in conformational carriers and ATP-driven pumps [ 53 ], etc. To the extent that these
protein conformational changes involve the protein/bilayer interface, where the pro-
tein is coupled to the bilayer through hydrophobic interactions, they will perturb the
bilayer immediately adjacent to the protein [ 1 , 16 , 25 , 28 , 42 ]. That is, protein con-
formational changes involve not only rearrangements within the protein, but more
importantly, also interactions with the environment, particularly with the host bilayer.
Some of these phenomena have been schematically illustrated in Fig. 4.1 , in light of
the investigations on the gating mechanisms observed in mechanosensitive channels
in model membranes [ 39 ]. Here, the mechanosensitive channels are predicted to act
as membrane-embedded mechano-electrical switches. The switches induce opening
of large water-filled pores that hydrophobically couple with lipid bilayers. This pore
bilayer coupling (or binding) forces the bilayer to deform near the pore opening to
adjust the mismatch between pore length and the bilayer's resting thickness. The
elastic properties of a bilayer [ 27 ] ensure that due to a possible continuous bending
in the lipid monolayers near both longitudinal edges of the pore, the bilayer does not
disintegrate. A structural change in the channel-forming agents is also a prediction
made in the qualitative model (see Fig. 4.1 ). We have made this prediction mainly
as a result of the observed structural rearrangements in the mechanosensitive chan-
nels during the back-and-forth transitions between the channel's closed and open
states [ 39 ]. These structural changes may be due to rotation, bending, translation,
etc. Behind the structural changes within both pore and lipid monolayers, near the
pore, there exists a driving force. This driving force causes the coupling between
pores/channels and a bilayer by creating structural changes in both lipid layers and
the channels. We have recently discovered the origin of this driving force to be the
coupling energy, originating from the interactions primarily due to the localized elec-
trical properties of channel-forming agents (MPs, AMPs, etc.) and lipids within the