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Amphibian Metamorphosis
By: Naadiya Hopkins
Amphibian Metamorphosis
Thyroid Gland Thyroxine (T4) Tri-iodothyronine (T3)
Remodeling
Growth
Death
Respecification
Apoptosis
Ex: Tadpole & Frog Ex: Tadpole & Frog
References
Gilbert, S.F. (2010). Developmental Biology. 9th ed. Sunderland, MA: Sinauer Associates, Inc. WEBSITE 15.1 The molecular biology of wing formation. Ishizuya-Oka, A. (2011), Amphibian organ remodeling during metamorphosis: Insight into thyroid hormone-induced apoptosis. Development, Growth & Differentiation, 53: 202212. doi: 10.1111/j.1440-169X.2010.01222.x http://onlinelibrary.wiley.com/doi/10.1111/j.1440169X.2010.01222.x/full Brown, Donald D., Cai, Liquan. (2007), Amphibian Metamorphosis. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1945045/
1) The Polar Coordinate Model of The Polar Coordinate Model of Positional Information in the Developing and Regenerating Limb. DevBio. Gilbert, Scott. 9th ed. 2010 http://9e.devbio.com/article.php?ch=15&id=184 2) Salamander cells remember their origins in limb regeneration. Nature. Laursen, Lucas. 2009 . http://www.nature.com/news/2009/090701/full/news.2009.614.ht ml 3) Salamanders, Regenerative Wonders, Heal Like Mammals, People. Science Daily. 2009. http://www.sciencedaily.com/releases/2009/07/090701131314.htm
Aging
Necessary physiological functions
Fertility
Survival
Mutations
Process
Possible prevention 2 major aspects
DNA repair
Life span
Maximum
Senescence
Results from
DNA synthesis
Species dependent
Old age
(Vijg, 2008)
Somatic maintenance
Somatic damage
Prevents
Signal suppression
Life extension factor
As result of
Aids in
(Campisi, 2011)
Cellular Senescence
Senescence is the biological process of age-related deterioration in function (Vijg, 2008). It manifests as dozens of changes in cells, tissues, and organs during aging. Human life is supported by a complex network of biochemical substances and reactions which affect the physical state and vitality of the body and mind. Senescent changes can be seen in the rate and outcome of many of these reaction. Such changes range from those affecting its cells and their function to that of the whole organism. Characteristics of this process include repair and recycling mechanisms slowing down. A minority of deteriorating cells release chemicals which harm other, healthy cells. The neuro-endocrine and immune systems seem to follow a developmental program of decline, which may cause them to send chemical signals of differentiation and death to various tissues. Cells are lost by apoptosis and necrosis, especially among non-dividing cells of the heart, skeletal muscle, and brain. Organs and tissues deteriorate over time when cells are lost faster than they are replaced and stem cells stop dividing and no longer replace essential cells or regenerate tissues. Aging is species specific. It is not the failure of individual cells that causes aging, but a breakdown in communication and response processes between cells so that the system is no longer controlled. The tumor-suppressor protein p53 accumulates when DNA is damaged due to a chain of biochemical factors. Part of this pathway includes alpha-interferon and betainterferon, which induce transcription of the p53 gene and result in the increase of p53 protein level and enhancement of cancer cell-apoptosis.p53 prevents the cell from replicating by stopping the cell cycle at G1, or interphase, to give the cell time to repair, however it will induce apoptosis if damage is extensive and repair efforts fail. Any disruption to the regulation of the p53 or interferon genes will result in impaired apoptosis and the possible formation of tumors (Campisi, 2011). Side-effects of intracellular molecular signals from the insulin receptors affect the lifespan of the nematode worm, C. elegans (Gilbert, 2010). It is hypothesized that they may affect human health and lifespan as well.
References
J. Campisi et al. Seminars in Cancer Biology 21 (2011) 354359. Gilbert, S.F. Developmental Biology. 9th edition. Sunderland (MA): Sinauer Associates; 2010. Aging: The Biology of Senescence. Vijg, J. and Campisi, J. 2008. Puzzles, promises and a cure for ageing. Nature 454: 1065-1071