Apoptosis and Animal Development

Study Notes

Apoptosis is a programmed cell death process, characterized by a series of cellular changes leading to the cell's death.
Apoptosis is a normal and controlled part of an organism's growth and development.
Cells undergoing apoptosis are actively destroyed by the body, removing unneeded or abnormal cells.
The term apoptosis is derived from the Greek word for the falling of leaves from a tree or petals from a flower.
Apoptosis is distinct from accidental cell death (necrosis), which is caused by injury or inflammation.

Animal development begins with rapid proliferation of embryonic cells, which differentiate into specialized cell types, tissues, and organs.
Humans have approximately 10¹⁴ cells and more than 200 differentiated cell types.
Cell death and cell proliferation are balanced throughout the life of multicellular organisms.
Cell renewal is essential; in adult organisms, stem cells replace lost cells in most tissues.
The ability of stem cells to differentiate into diverse cell types is crucial for replacing damaged tissues.

Programmed cell death (apoptosis) is crucial in embryonic development.
Worn-out red blood cells (RBCs) undergo apoptosis in the spleen.
Old white blood cells (WBCs) and platelets also undergo apoptosis.
Virus-infected cells undergo apoptosis to prevent the spread of the virus.
DNA damage can also induce apoptosis to eliminate cells with mutations that may lead to cancer.
Development of the mammalian nervous system involves the elimination of excess neurons through apoptosis.

Apoptosis is an active process, while necrosis is a passive process resulting from injury.
Apoptosis typically affects single cells, while necrosis affects groups of cells.
Apoptotic cells are removed efficiently by macrophages and neighboring cells, while necrotic cells trigger an inflammatory response.

Two main pathways lead to apoptosis: the intrinsic and extrinsic pathways.
The intrinsic pathway is activated by internal surveillance mechanisms or signals and includes signals like DNA damage and exposure to chemicals.
The extrinsic pathway is activated by signals from other cells, such as Cytotoxic T lymphocytes (CTLs) through Fas ligand.
In both pathways, caspases play a central role in the cell death cascade.
Central regulators of apoptosis are the Bcl-2 family proteins (some promote apoptosis others inhibit apoptosis).

Apoptosis is crucial for maintaining constant cell numbers in tissues undergoing cell turnover.
Apoptosis is also a defense mechanism, eliminating damaged or potentially dangerous cells.
Cell survival depends on growth factors, contacts with neighboring cells, and the extracellular matrix.

There are different stages of apoptosis (pre-apoptotic, early apoptotic, and late apoptotic cell).
The cell shrinks and breaks down into membrane-enclosed apoptotic bodies.
Neighboring cells and macrophages efficiently remove apoptotic bodies to prevent inflammation.

Apoptosis is followed by the phagocytosis of cellular remnants to prevent inflammatory response.
Apoptotic cells and cell fragments are efficiently recognized and phagocytosed by macrophages and neighboring cells.
Apoptotic cells are signaled to be removed by the expression of "eat me" signals, like phosphatidylserine, on their surface.

The intrinsic pathway involves the mitochondria releasing cytochrome c, which then triggers caspase activation to induce apoptosis.
The extrinsic pathway involves extracellular signals binding to death receptors, leading to initiator caspase activation, and then to a cascade of caspase activation.
Specific protein families (e.g., the Bcl-2 family) regulate these crucial steps in both pathways.