Apoptosis

programmed cell death in multicellular organisms

Apoptosis is the controlled death of a cell.[1] It is an important part of tissue development. For example, during limb development in a foetus, apoptosis allows digits (fingers and toes) to separate from each other. The process is quite common until puberty begins. Apoptosis is a regulated and controlled process which works throughout an organism's life cycle. The rate of apoptosis is balanced by the rate of cell production by mitosis.[2]

Discovery change

The phenomenon of programmed cell death was first described by Carl Vogt in 1842. In 1885, anatomist Walther Flemming gave a more precise description of the process.

The average adult human loses between 50 and 70 billion cells each day due to apoptosis. The average human adult has more than 13 trillion cells of which at most only 70 billion die each day. That is, about 5 out of every 1,000 cells (0.5%) die each day due to apoptosis. For an average human child between the ages of 8 and 14, approximately 20–30 billion cells die per day.[3]

Sequence of events in apoptosis change

When a cell dies by apoptosis, surrounding tissue is not harmed.
1. Enzymes break down the cytoskeleton of the cell.
2. Cytoplasm becomes dense, with organelles tightly packed.
3. Cell surface membrane forms "blebs".
4. Chromatin condenses and the nuclear envelope breaks. DNA breaks into fragments.
5. The cell breaks down into vesicles, taken up by phagocytosis.[4]

Controlling the cell cycle change

Apoptosis is the normal end of a cell's life. At any point in time, there may be too many cells in one area, and the DNA coding for apoptosis will activate in some of those cells and they will die safely. This is important to the overall functioning of the organism. If, for example, the making of liver cells were to speed up and they never died, the liver would no longer function properly. The liver cells would eventually take over the organism's body. Apoptosis takes place by the help of lysosomes. Lysosomes rupture when the cell is old or damaged, this lets out digestive enzymes all over the cell and digests it, therefore killing the cell.[1]

Cancer change

Cancerous cells do not undergo apoptosis, which is why they are such a problem. They continuously multiply until the host organ or the organism's body cannot function anymore. This occurs because the apoptosis coding has mutated and so has other coding. This causes rapid mitotic division of the unwanted cells. This is a cancerous growth.

Nobel Prize change

The Nobel Prize in Physiology or Medicine 2002 was awarded jointly to Sydney Brenner, H. Robert Horvitz and John E. Sulston "for their discoveries concerning genetic regulation of organ development and programmed cell death'."[5] Sydney Brenner, Sir John Sulston and Robert Horvitz received the Nobel Prize for their work on the genome and cells of the roundworm Caenorhabditis elegans. C. elegans was the first animal to have its complete genome sequenced.[6]

References change

  1. 1.0 1.1 Fullick, Ann (2008). Edexcel AS Biology Students' Book. Pearson Education. pp. 143. ISBN 978-1-4058-9632-0.
  2. Jiang, Lijing 2012. History of Apoptosis Research. eLS. doi:10.1002/9780470015902.a0023954. ISBN 978-0470016176
  3. Karam JA (2009). Apoptosis in Carcinogenesis and Chemotherapy. Netherlands: Springer. ISBN 978-1-4020-9597-9.
  4. Kerr JF, Wyllie AH, Currie AR 1972. Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics. Br J Cancer. 26 (4): 239–57. doi:10.1038/bjc.1972.33. PMC 2008650. PMID 4561027
  5. The Nobel Prize in Physiology or Medicine 2002. NobelPrize.org. Nobel Media AB 2020. Sun. 1 Nov 2020. https://www.nobelprize.org/prizes/medicine/2002/summary
  6. Sulston, John & Ferry, Georgina 2002. The common thread: a story of science, politics, ethics, and the human genome. Washington D.C. Joseph Henry Press.

Related pages change