World Library  
Flag as Inappropriate
Email this Article

Phenoptosis

Article Id: WHEBN0005818925
Reproduction Date:

Title: Phenoptosis  
Author: World Heritage Encyclopedia
Language: English
Subject: Senescence, Evolution of ageing, Programmed cell death, Salmon
Collection: Programmed Cell Death, Senescence
Publisher: World Heritage Encyclopedia
Publication
Date:
 

Phenoptosis

Phenoptosis

(pheno - showing or demonstrating, ptosis - programmed death), designated by V.P. Skulachev in 1999, signifies the phenomenon of programmed

See also

  1. ^ Skulachev, V.P. (November 1997). "Organism’s Aging is a Special Biological Function Rather than a Result of Breakdown of a Complex Biological System: Biochemical Support of Weismann’s Hypothesis". Biokhimiya 62 (12): 1191–1195.  
  2. ^ a b c Weismann, A (1889). Essays upon Heredity and Kindred Bio_. Oxford: Clarendon Press. p. 23.  
  3. ^ a b c Skulachev, VP (Apr 2002). "Programmed death phenomena: from organelle to organism.". Ann N Y Acad Sci 959: 214–237.  
  4. ^ Skulachev, VP (November 2011). "Aging as a particular case of phenoptosis, the programmed death of an organism (A response to Kirkwood and Melov "On the programmed/non-programmed nature of ageing within the life history")". Aging 3 (11): 1120–1123.  
  5. ^ a b c Skulachev, VP (December 1999). "Phenoptosis: programmed death of an organism.". Biokhimiya 64 (12): 1418–1426.  
  6. ^ a b c Severin, FF; Skulachev, VP (2011). "Programmed Cell Death as a Target to Interrupt the Aging Program". ADVANCES IN GERONTOLOGY 1 (1): 16–27.  
  7. ^ Thompson, CR; Kay, RR (November 2000). "Cell-FateChoice in Dictyostelium: Intrinsic Biases Modulate Sensitivity to DIF Signaling". Developmental Biology 277 (1): 56–64.  
  8. ^ Pestov, NB; Shakhparonov, M.; Korneenko, T. (Sep–Oct 2011). "Matricide in Caenorhabditis elegans as an example of programmed death of an animal organism: The role of mitochondrial oxidative stress". Russian Journal of Bioorganic Chemistry 37 (5): 705–710.  
  9. ^ Dawkins, R (1976). The Selfish Gene. Oxford: Oxford Univ.Press.  
  10. ^ Nesis, K (1997). "A Cruel Love of Squids". The Russian Science:To Withstand and Resurrect: 358–365. 
  11. ^ Kirkwood, TB; Cremer T (1982). "Cytogerontology since 1881: a reappraisal of August Weismann and a review of modern progress.". Hum Genet 60 (2): 101–121.  
  12. ^ Yun, A; Lee, P.; Doux, J. (2006). "Osteoarthritis: An example of phenoptosis through autonomic dysfunction?". Medical Hypotheses 67 (5): 1079–1085.  
  13. ^ Liu, X; Jiang, N.; Bigras, E.; Shoubridge, E.; Hekimi, S. (15 Oct 2005). "Evolutionary conservation of the clk-1-dependent mechanism of longevity: loss of mclk1 increases cellular fitness and lifespan in mice.". Genes Dev 19 (20): 2424–34.  
  14. ^ Holley, CL; Michael R. Olson; Daniel A. Colón-Ramos; Sally Kornbluth (June 2002). "Reaper eliminates IAP proteins through stimulated IAP degradation and generalized translational inhibition". Nat Cell Biol 4 (6): 439–444.  

References

"The bizarre thing is that this sequence... not only occurs in five species of salmon, but also among a dozen species of Australian marsupial mice... Pacific salmon and marsupial mice are not close relatives. At least twice in evolutionary history, completely independently, two very different sets of species have come up with the identical trick: if you want to degenerate very fast, secrete a ton of glucocorticoids."
"If you catch salmon right after they spawn... you find they have huge adrenal glands, peptic ulcers, and kidney lesions, their immune systems have collapsed... [and they] have stupendously high glucocorticoid concentrations in their bloodstreams. When salmon spawn, regulation of their glucocortocoid secretion breaks down... But is the glucocorticoid excess really responsible for their death? Yup. Take a salmon right after spawning, remove its adrenals, and it will live for a year afterward.

Robert Sapolsky discusses phenoptosis in his book Why Zebras Don't Get Ulcers, 3rd Ed., p.245-247. He states that:

Other examples

Glucocorticoid regulation - A common route for phenoptosis is breakdown of glucocorticoid regulation and inhibition, leading to massive excess of these corticosteroids in the body. [3]

EF2 kinase – Blocks phosphorylation of elongation factor 2 thus blocking protein synthesis. [14]

Clk1 gene – the gene thought to be responsible to aging due to mitochondrial ROS. [13]

Mitochondrial ROS – The production of ROS by the mitochondria. This causes oxidative damage to the inner compartment of the mitochondria and destruction of the mitochondria.[5]

Proposed mechanisms

Vascular disease, menopause, cancer, and osteoarthritis[12] are thought to be means of human phenoptosis. Phenoptosis has recently been heavily studied in the hopes of increasing human longevity. By understanding the mechanisms of slow phenoptosis we may be able to halt or even reverse the processes that cause our aging and eventual deaths.

Examples in humans

[5]

Salmon – Die soon after spawning.[11]

marsupial mice – Males die 2 weeks after reproducing from an overabundance of their own pheromones.[6]

Squid – Some male squid die immediately after mating. This provides an abundant food source for those predators that would prey on the eggs. [10]

Mite Adactylidium – The initial food source of Adactylidium mitelarvae is the body tissues of their mother resulting in her death.[6]

Praying mantis – The male praying mantis ejaculates only after being decapitated by the female.[9]

Mayfly – Adult mayflies have no functional mouth and die from malnutrition.[2]

Nematode Caenorhabditis elegans – Under normal conditions Caenorhabditis elegans display a normal aging life cycle. However, if there is increased stress after breeding they undergo phenoptosis, like in yeast, induced by the mitochondria.[8]

Amoeba Dictyostelium – Under stress amoeba form multicellular fruiting bodies. The better nourished cells differentiate into spores. The less healthy cells differentiate into the stalks of the fruiting body. After maturation of the spores, the stalk cells undergo phenoptosis.[7]

Saccharomyces cerevisiae – Under stress the yeast mitochondria produce reactive oxygen species ROS, leading to loss of membrane potential within the mitochondria and death of the cell.[6]

E. coli – programmed death is initiated by infection by phage. This prevents further spread of phage to the remaining population.[5]

Examples in nature

An example made by V. P. Skulachev provides that of two hares, one faster and one smarter, the faster hare may have a selective advantage in youth but as aging occurs and muscles deteriorate it is the smarter hare that now has the selective advantage. [4] It has also been proposed that age provides a selective advantage to brains over brawn.[3] Inside of our bodies, worn-out, ineffective cells are dismantled and recycled for the greater good of the whole organism. This is a process called

Evolutionary significance

Contents

  • Evolutionary significance 1
  • Examples in nature 2
  • Examples in humans 3
  • Proposed mechanisms 4
  • Other examples 5
  • References 6
  • See also 7

, whose ramifications for humans is still being explored. species Phenoptosis is a common feature of living [1]

This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and USA.gov, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for USA.gov and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
 
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
 
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.
 


Copyright © World Library Foundation. All rights reserved. eBooks from Project Gutenberg are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.