Regulation and Death of Cells

Cell Cycle Control System

Internal regulation system consisting of a group of regulatory proteins produced within the cell to repair mutations or stop the cell cycle

G1 Checkpoint

Occurs towards the end of G1 in interphase and is known as the restriction point. Checks:

• There are adequate resources for the cell to divide, such as enough nucleotides and energy supply to copy the DNA

• The cell is large enough to divide

• The DNA in nucleus have not been damaged

G2 Checkpoint

Occurs towards the end of G2 in interphase. Checks:

• There are adequate resources required for mitosis

• Size of the cell

• DNA and chromosomes have been replicated without mistakes or damage (most important check)

M Checkpoint

• Occurs towards the end of metaphase in mitosis, also known as the spindle checkpoint

• Determines if all of the spindle fibres have correctly attached to the chromosomes, and that they are directly aligned in the middle (equator) of the cell

Apoptosis

Also known as programmed cell death, is a series of changes in a cell that results in the death of the cell, and is driven by biochemical changes

• Highly regulated

• Plasma membrane buds into apoptopic bodies and are then eaten by phagocytic cells

Repair of cells

Enzymes that detect and repair damage by running along strands of DNA like a ‘zip’, checking that DNA is intact and have been replicated properly

Apoptopic bodies

Formed from the plasma membrane during apoptosis and contain the remnants of the cytoplasm, organelles and DNA and protein fragments

Phagocytic cells

Cells specialised to engulf and break down cellular debris

Apoptosis process

1. activation of apoptopic enzymes (capases)

2. digestion of cell content

3. cell shrinkage

4. cell blebbing and breakage

5. removal of fragments my phagocytic cells

Capases

Apoptopic enzymes that digest specific proteins which leads to the degradation of all organelles.

The membrane forms blebs, detaches from the cell, can causes the cell to break up into vesicles (apoptopic bodies), which are digested by phagocytes

Mitochondrial pathway

• Is triggered when cell components (e.g. DNA) are damaged

• Intracellular signalling proteins then act directly on the mitochondria, which leads to the release of cytochrome c into the cytosol

• release of cytochrome c leads to the formation of an apoptosome and starts a series of reactions that result in the activation of capases

Death Receptor pathway

• Extracellular signals can be recognised by the death receptor molecule on the surface of cells that are under stress from factors such as: growth factors, hypoxia, DNA damage, viral infection, ultraviolet radiation

• Leads to the initiation of a cascade of reactions, which result in capase enzyme activation

Necrosis

Accidental cell death which can occur via:

• physical damage

• toxins

• pathogens

• a lack of oxygen

Tends to affect a large number of cells

Necrosis process

1. Plasma membrane becomes damaged

2. Water and ions enter the cell and swelling occurs

3. Cell contents are released in an uncontrollable manner, resulting in inflammation and damage to surrounding cells

Limited mitotic divisions

Cells from most multicellular organisms do not live indefinitely but die after a certain number of divisions,

A small amount of DNA is lost from their telomeres at each division, and after about 50 divisions, the tips are lost and the cell either stops dividing or enters apoptosis

Neoplasm

Abnormal growth of tissues that usually, but not always, forms a mass due to uncontrolled cell division in organisms

Benign neoplasm

Form localised masses but do not turn into cancer

Potentially malignant neoplasm

Form localised masses that will eventually invade other tissues and transform into cancer

Malignant neoplasm

Form masses that invade other tissues and transform into cancer

Cancer cells

Abnormal group of diseases that commonly involve unregulated and abnormal cell growth and division.

Can be caused by genetic mutations in the cells that either increase the rate of cell division and/or result in the suppression of apoptosis

Characteristics of cancer cells

• Divide at a faster rate. Some divide very rapidly, others more slowly

• Not affected by the normal signals that control the cell cycle (e.g. contact inhibition)

• Look different and may become less specialised

• Can continue dividing endlessly