12.2 Sensing Temperature Stress
KEY CONCEPTS
By the end of this section, you will be able to do the following:
- Apply your understanding of cell signalling pathways (Chapter 5.6) to explain two examples of signal reception and transduction involved in detecting temperature stress.
- Evaluate why receptor proteins (e.g., TRP channels) and changes in membrane fluidity can be good early indicators of temperature stress.
- Explain why macromolecule damage is an indicator of extreme temperature stress.
Cells can sense temperature stress through various pathways. Temperature-sensitive transient receptor potential channels and membrane fluidity are both used to detect mild temperatures stress. During more extreme temperature stress, cellular damage, such as protein denaturation and aggregation can often trigger signalling pathways. Note that this section does not consider freezing temperatures; freezing stress is discussed in Chapter 13. In this section, we will investigate the pathways involved in sensing temperature stress.
TRP Channels can Detect Mild Temperature Stress
Mild increases or decreases in temperature can cause receptor proteins to change shape, initiating cell signalling. For example, temperature-sensitive TRP (transient receptor potential) channels found in the plasma membrane of sensory neurons can be used by some animals to detect specific temperatures. TRP channels are a family of proteins, all of which are multipass integral membrane ion channels that will open or close in response to a specific stimulus (Figure 12.7). [1]Some TRPs respond to temperature, while others respond to different stimuli. TRP channels are found in almost all types of eukaryotic cells, including those which are excitable (e.g., animal muscle cells and neurons) and non-excitable. Most TRP channels are in the plasma membrane, however they can be present in all cellular membranes, except for the nuclear envelope and the mitochondrial membrane.
When a temperature-sensitive TRP channel in the plasma membrane of a neuron is stimulated, this activates neuron signalling (action potential; Figure 12.8) that is then interpreted by the brain as “hot” or “cold,” depending on the type of TRP channel. For example, if you take a sip of hot tea, the high temperature will likely cause a conformational change in the structure of a TRPV1 protein channel in the plasma membrane of sensory neurons in your mouth. The change in structure of TRPV1 allows its ion channel to open, allowing positively charged ions to enter the neuron. The influx of these causes the cytoplasm to be positively charged relative to the outside of the cell – a local depolarization. If the depolarization reaches the neuron’s threshold, it will initiate an action potential, which sends an electrical signal through the neuron (Figure 12.8). The electrical signal can be transmitted to the brain of the animal, allowing the animal to detect the change in temperature then respond accordingly.
In addition to being stimulated by changes in temperature, many TRP channels can be stimulated by a variety of chemicals from natural substances (Figure 12.9). If a certain chemical binds to a TRP channel, the channel undergoes a similar conformational change to the one induced by its activating temperature. This means that some substances can act as a false temperature stimulus, deceiving the cell or organism of a change in temperature. For example, chili peppers contain capsaicin, a chemical which stimulates TRPV1 channels in mammals, causing their brain to interpret the chili pepper as “hot” (Figure 12.9).
Membrane Fluidity is an Indicator of Mild Temperature Stress
The cyanobacterium, Synechocystis sp., provides an example of how temperature-induced changes in membrane fluidity can initiate cell signalling that “tells” the cell about mild temperature stress. These organisms contain a membrane protein, transmembrane histidine kinase 33 (HiK33) (Figure 12.10), which changes shape when membrane fluidity decreases. [2]Researchers have shown that this change in HiK33 shape is driven by membrane fluidity rather than direct impacts of temperature on HiK33 structure. When HiK33 changes shape due to decreased membrane fluidity, this protein initiate signalling pathways in the cell that help the cell adjust to the low temperatures. As a kinase, HiK33 primarily initiates signal transduction pathways by phosphorylating target protein(s) within the cell.
Cellular Damage is an Indicator of Extreme Temperature Stress
Cellular damage, such as protein aggregation caused by extreme temperature stress, can also initiate signaling pathways within a cell. While it is beneficial for cells to detect and respond to temperature stress at earlier stages (before this type of damage occurs), these pathways to detect damage are important for initiating cellular responses that repair more extreme damage. These specific cell signaling pathways will be explored in Chapter 14.
- Nilius, B., and Owsianik, G. 2011. The transient receptor potential family of ion channels. Genome Biology 12(3): 218. doi:10.1186/gb-2011-12-3-218. ↵
- Los, D.A., and Murata, N. 2000. Regulation of Enzymatic Activity and Gene Expression by Membrane Fluidity. Science’s STKE 2000(62): pe1–pe1. American Association for the Advancement of Science. doi:10.1126/stke.2000.62.pe1. ↵