Final answer:
External signals can activate apoptosis through cell-surface receptors known as death receptors, which are integral to preventing uncontrolled cell proliferation and ensuring proper immune function.
Step-by-step explanation:
External signals can stimulate apoptosis by activating a set of cell-surface receptors known as death receptors. Apoptosis, or programmed cell death, is a vital process that allows a cell to die in a controlled manner, which prevents the release of potentially damaging molecules from inside the cell. These specialized cell-surface receptors are part of a complex signaling pathway that can trigger the apoptosis process when certain ligands, such as those from the extracellular matrix or T-cell receptors, bind to them causing the signaling cascade within the cell to promote cell death.
One example of apoptosis being initiated by external signaling includes the interaction between the receptors on normal animal cells and the extracellular matrix. When a cell moves away from the extracellular matrix and the signals cease, apoptosis is induced to prevent cells from proliferating out of control.
Another instance is during T-cell development in the immune system, where if the T-cell receptors bind to self-proteins, they initiate apoptosis to avoid the development of autoimmune diseases. Cell-surface receptors are thus crucial components in maintaining the health and proper function of multicellular organisms.