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Postembryonic Development

Naadiya Hopkins Datoya Brown Quincy Petterson Taques e Phillips Shannon Harris Brandon

Amphibian Metamorphosis
By: Naadiya Hopkins

Amphibian Metamorphosis
Thyroid Gland Thyroxine (T4) Tri-iodothyronine (T3)





Ex: Tadpole & Frog Ex: Tadpole & Frog

Concept Map Summary

It was discovered in 1912 by Gudernatsch that the metamorphosis of certain organisms were controlled by the thyroid hormone. There are two major hormones that play a significant role in amphibian metamorphosis. They are the thyroxine hormone (T4) and the triiodothyronine hormone (T4). There are 4 major roles that these two hormones aid in, which are the growth of cells, the death of cells, the remodeling of cells and the biochemical respecification of cells. An example that is widely used when talking about this kind of metamorphosis is the tadpole and the frog. The developmental stage is the frog are brought about by the secretion of T4 into the blood by the thyroid glans, the conversion of T4 into the more active T3 hormone by the target tissues and the degradation of T3 in the target tissues. T3 is highly important in metamorphosis because it is able to bind with the thyroid hormone receptors with a much higher affinity which causes the receptors to become activators for gene expression. Although T3 cannot fully function without the concentration of T4 in the blood stream.

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 Brown, Donald D., Cai, Liquan. (2007), Amphibian Metamorphosis.

Regeneration in the Salamander Limb

Shannon Harris

Regeneration in the Salmandar Limb

Regeneration in the Salamander Limb

The regeneration of salamander limbs are accomplished by epimorphic regeneration. Epimorphosis in some species can undergo dedifferentiation to form a relatively undifferentiated mass of cells that then redifferentiates to form the new structure. Salamander limbs can only regenerate a new limb from the point of amputation. This is done by the salamander forming a regeneration blastema- an aggregation of relatively dedifferentiated cells derived from the originally differentiated tissue-which then proliferates and redifferentiates into the new limb parts. Upon amputation of the salamander limb, the wound is covered by the wound epidermis (epidermal cells covering the wound surface) and the nerves innervating the limb degenerate. In about 4 days the wound epidermis thickens to form the apical epidermal cap ( AEC ) which works with the nerves to stimulate the growth of the blastema. The blastema is a heterogeneous assortment of restricted progenitor cells, meaning that the blastema is not a collection of unspecified multipotential progenitor cells rather the blastema cells retain their specification. The AEC secretes Fgf8 to stimulate the growth of the blastema but it will not grow if the nerves are not present. The newt anterior gradient protein ( nAG) is a protein that can cause blastema cells to proliferate,and it permits normal regeneration in limbs that have been denervated. If activated nAG genes are present the limbs are able to regenerate, if nAG is not administered, the limbs remain as stumps.

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 2) Salamander cells remember their origins in limb regeneration. Nature. Laursen, Lucas. 2009 . ml 3) Salamanders, Regenerative Wonders, Heal Like Mammals, People. Science Daily. 2009.

Aging: The Biology of Senescence

Datoya Brown

Multicellular Organism (s)

Deterioration succeeds over synthesis

Necessary physiological functions



Possible prevention 2 major aspects

DNA repair

Life span

Results from

DNA synthesis

Species dependent

Old age

(Vijg, 2008)

Genes Growth & reproduction Life span (Gilbert, 2010)

Results in

Somatic maintenance

Somatic damage


Signal suppression
Life extension factor

As result of

Age-related cellular degeneration and disease

Sirtuin genes IGF-1 p53 Growth factor

Aids in

Aids in

Timely gene expression

Regulation of cell division(s)

(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.

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