Chapter 14 Summary

Chapter 14.1

• Stress may cause damage to cells and their components. For the cell to survive, damaged components must be repaired or replaced.
• Cells unable to repair damaged components are likely to die.
• DNA can be damaged by oxidative stress, along with other stressors, resulting in single nucleotide changes, single-strand breaks, or double-strand breaks.
• Lipids and membranes can be damaged as a result of oxidative stress, temperature stress, and freezing.
• Protein damage can result from by oxidative stress, osmotic stress, extreme temperature stress, and freezing.

Chapter 14.2

• Some damage to cellular components can be repaired, especially if the cell only experiences mild stress.
• Mild DNA damage can be repaired by base excision repair.
• Mild lipid and membrane damage can be repaired by removing or replacing damaged membrane, or by reversing lipid oxidation with enzymes.
• Protein damage can be repaired by refolding using molecular chaperones, or by reversing amino acid oxidation with enzymes.

Chapter 14.3

• When macromolecules and organelles are damaged beyond repair, the cell uses processes to degrade them and synthesize new ones, as long as it is possible to replace the damaged cellular components and the cell has sufficient resources to do so.
• Proteasomal degradation degrades unfolded/damaged proteins into small peptide fragments.
• Autophagy is another process cells can use to degrade proteins as well as damaged organelles, via either macroautophagy or microautophagy.
• Protein and lipid synthesis are two important processes required for the synthesis of new macromolecules and organelles.

Chapter 14.4

• The cellular stress response (CSR) is a conserved eukaryotic cell response that activates several mechanisms to mitigate damage associated with stress.
• The unfolded protein response (UPR) is a major component of CSR that is initiated by unfolded proteins in the endoplasmic reticulum (ER) and coordinates the mechanisms below.
• As part of the UPR, most protein synthesis is shut down, except for those required for the stress response.
• Damaged proteins in the ER are degraded by proteasomes via the ER-associated degradation (ERAD) pathway.
• In cases of severe damage, the UPR may activate autophagy and/or apoptosis.

Chapter 14.5

• Cell death is a natural and essential process that occurs in multicellular organisms, and there are different types of cell death, including necrosis, autophagic cell death, and apoptosis.
• Apoptosis, also known as programmed cell death, is a regulated process that eliminates unnecessary or damaged cells in multicellular organisms, and it can be triggered by internal or external signals.
• Caspases are a family of protease enzymes that play a crucial role in the process of apoptosis, as they are responsible for the proteolytic cleavage of many key cellular proteins.
• Apoptosis can be initiated by two distinct signaling pathways: intrinsic and extrinsic. The intrinsic pathway is initiated from within the cell, in response to various internal stress signals, while the extrinsic pathway is initiated by signals from outside the cell.