Chapter 12 Summary

Chapter 12.1

• Temperature stress can be caused by temperatures above (heat stress) or below (cold stress) an organism’s thermal optimal zone, which interfere with cell structure and function.
• Low temperatures decrease flexibility of proteins, while high temperatures increase flexibility of proteins, both which impair protein function, which is often temporary and does not cause permanent damage.
• Extreme low and high temperatures changes pose a more serious risk as they both typically cause protein denaturation.
• Inhibition of protein function can impact metabolism, transmembrane transport, and stability of the cytoskeleton.
• Mild temperature changes cause minor fluctuations around liquid- crystalline phase in membrane fluidity and can cause impairment of cellular transport processes and cellular signalling.
• Extreme temperature changes cause major phase shifts from liquid crystalline phase to fluid phase (high temperatures) or gel phase (low temperatures), which can cause permanent membrane damage and lead to cell death.

Chapter 12.2

• One example of protein receptors that detect changes in temperature is the family of TRP channels, which can alter electrical signalling in some animal neurons in response to a specific range of temperatures.
• Another example of a mechanism to detect changes in temperatures is the direct effect of temperature on membranes, as seen in cyanobacterial cells of the genus Synechocystis.
• Many cells also have signalling pathways to detect damage (see future chapter), which can be used to detect extreme temperature stress.

Chapter 12.3

• Strategies to tolerate mild temperature stress include modifying macromolecule composition and adjusting metabolic processes.
• To modify macromolecule composition, cells can producing heat-adapted or cold-adapted protein isoforms, and change the composition of membranes (cholesterol, types of phospholipids) to maintain optimal fluidity.
• If mild temperature stress causes energy limitation, cells can adjust their metabolism using mechanisms described in Chapter 11.3.
• Under extreme temperature stress, cells respond by repairing macromolecules and preventing further damage using heat shock proteins. They may also undergo programmed cell death and cells may be replaced.