J.P. Brockes

The urodele (tailed) amphibians such as the newts and salamanders are the champions of regeneration among adult vertebrates. An adult newt can regenerate its limbs and tail, upper and lower jaws, ocular tissues such as the lens and retina, as well as large sections of the heart. We tend to regard these animals as exceptional or exotic in respect of this property, but regenerative ability on this scale is widespread throughout metazoan phylogeny and it is usual to regard it as a basic attribute which is lost for reasons which are unclear. In all contexts it is common to find closely related species which have lost the ability, and it is not understood how regeneration plays as an evolutionary variable. The biomedical implications of understanding this issue in a vertebrate context could be quite significant - it is hard to envisage any other single attribute which could have a more profound impact on our prospects.

How do adult newts regenerate so many different structures? Why does this not occur in mammals, and for that matter related urodeles which do not regenerate? What are the prospects for promoting the urodele type of regeneration in a mammal?

Urodele regeneration appears to depend on the local activation of plasticity in residual differentiated cells, for example in cardiomyocytes, pigmented epithelial cells of the iris, and skeletal myofibres. In this sense it presents something of an alternative to the current agendas for mammalian regeneration based on stem cells. In my lecture I will try to address the three questions above from the base of our current understanding of urodele regeneration.

ref; Plasticity and reprogramming of differentiated cells in amphibian regeneration. JP Brockes & A Kumar, Nature Revs. Mol. Cell Biol. 3, 566-574 (2002)

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