cell membrane fluid

Question

the assess the transition temperature of membrane composed of the following phospholipid molecular select the two have the most transition temperature

Answer 1

Bacteria can encounter a wide range of environments and must adapt to new conditions in order to survive. As the selective barrier between living cells and their environment, the plasma membrane plays a key role in cell viability. The barrier function of the cytoplasmic membrane is known to depend critically on the physical state of lipid bilayers (17), making it susceptible to changes in environmental temperature. In fact, it has been established that normal cell function requires membrane lipid bilayers that are largely fluid; indeed, the bilayers of most organisms are entirely or mostly fluid at physiological temperatures. However, at lower temperatures, membrane lipid bilayers undergo a reversible change of state from a fluid (disordered) to a nonfluid (ordered) array of the fatty acyl chains (21, 56). The temperature at the midpoint of this transition is called the transition temperature, and the change of state accompanying an increase in temperature is called the lipid phase transition, the gel-liquid crystalline transition, or most properly, the order-disorder transition. The transition temperature is a function of the membrane lipid composition and, in organisms deficient in cholesterol, mainly depends on the fatty acid composition of the membrane lipids (21, 56). The (overly simplified) rule of thumb is that phospholipids that contain unsaturated fatty acids (UFAs) have much lower transition temperatures than those lipids made of saturated fatty acids (SFAs). The effect is due to different packing of the two types of phospholipid acyl chains. SFA acyl chains can pack tightly, but the steric hindrance imparted by the rigid kink of the cis double bond results in much poorer chain packing of UFAs, even below the phase transition temperature (16, 17).

From these considerations, it seems clear that bacteria and most (if not all) poikilothermic organisms must regulate their phase transition in response to temperature. Without regulation, an organism shifted from a high to a low temperature would have membrane lipids with suboptimal fluidity, resulting in subnormal membrane function. The mechanism of regulation in all of the cases examined seems to occur via the incorporation of proportionally more UFAs (or fatty acids of analogous properties) as the temperature decreases. This regulatory mechanism system, called thermal control of fatty acid synthesis, seems to be a universally conserved adaptation response allowing cells to maintain the appropriate fluidity of membrane lipids regardless of the ambient temperature. This means that cells must process temperature signals to adjust enzyme activities or to activate unique genes necessary to adapt the membranes to the new temperature. The question arises, how do cells sense a change in temperature and adjust the fluidity of the membrane lipid bilayer accordingly?

Here, we discuss the basic features of thermal regulation of membrane lipid fluidity in Escherichia coli and Bacillus subtilis, in which the proposed mechanisms are firmly based on both genetic and biochemical evidence. Although the physiological consequences of this regulation are the same in both organisms, the mechanisms involved are entirely different.

TEMPERATURE-DEPENDENT CHANGES IN THE CONTENT OF UFAS OF GLYCEROPHOSPHOLIPIDS IN E. COLI

The molecular mechanism of regulation of UFA synthesis by growth temperature in E. coli was elucidated more than 20 years ago and has been discussed in a number of reviews (18, 19, 21). Here, we will briefly review this paradigmatic mechanism with the purpose of contrasting it with recent progress in the elucidation of the pathway controlling the synthesis of UFAs in B. subtilis.

E. coli has one of the simplest membrane bilayer phospholipid compositions found in nature, consisting of three phospholipids having only three different fatty acyl chains (19). The three fatty acids are an SFA, palmitic (hexadecanoic) acid, and two UFAs, palmitoleic (cis-9-hexadecenoic) acid and cis-vaccenic (cis-11-octadecenoic) acid. Marr and Ingraham first noted that E. coli adjusts its fatty acid composition in response to a decrease in temperature by increasing the amount of cis-vaccenic acid and reducing the amount of palmitic acid incorporated into membrane phospholipids (47). Lower growth temperatures result in an increase in the number of diunsaturated phospholipids in the membrane. At 37°C, palmitic acid occupies position 1 of the phospholipid backbone, whereas palmitoleic acid is found only at position 2. As the growth temperature is lowered, cis-vaccenic acid competes with palmitic acid for position 1 of the newly synthesized phospholipids (7, 16). This mechanism is thought to allow an organism to regulate the membrane fluidity to optimize its function at various growth temperatures. In E. coli, synthesis of the normal UFA content requires three enzymes, the products of the fabA, fabB, and fabF genes (Fig.