Analysis of Biological Development (K. Kalthoff)

Updates to Topic 28: Organismic Growth and Oncogenes

Answers to Questions in Text

Intrinsic Growth Properties of Limb Buds (p. 747/748)

  1. In the experiments by Harrison described here, the growth of limb grafts was analyzed through comparison with the control limb on the opposite side of the host. This control limb belonged to a different species and therefore had a different set of intrinsic growth factors, whereas the extrinsic factors were the same for both the transplant and the host control. However, comparisons were also made between the grafted limb and its nontransplanted counterpart in the donor. What conclusions could be drawn from this comparison? Answer: Since the donor's control limb belonged to the same individual, it shared the same intrinsic factors, but the extrinsic factors, such as hormones and nutritional state, were different. For instance, a diet of beef and liver favored the growth of A. tigrinum over A. punctatum, whereas a diet of small crustacea and worms had the reverse effect.
  2. Harrison considered the growth of the A. tigrinum graft in the A. punctatum host to be of particular interest. What could have been the reason? Answer: Under these conditions, the grafted limb grows to a larger size than its host control limb even though both limbs are supplied with the same nutrients, hormones, and other systemic factors of the host. It must be concluded that the grafted limb, because of its intrinsic properties, utilizes the host environment more efficiently than the host control limb.


Clarifications and Corrections

New Review Articles

Anderson G.R., Stoler D.L., and Brenner B.M. (2001) Cancer: the evolved consequence of a destabilized genome. Bioessays 23: 1037-1046

Bromberg J..F. (2001) Activation of STAT proteins and growth control. BioEssays 23: 161-169

Day S.J. and Lawrence P.A. (2002) Measuring dimensions: the regulation of size and shape. Development 127: 2977-2987

Gibbs W.W. (2003) Untangling the roots of cancer. Scient.Amer. July 2003: 56-65

Johnston L.A. and Gallant P. (2002) Control of growth and organ size in Drosophila. Bioessays 24: 54-64

Levens D.L. (2003) Reconstructing MYC. Genes & Dev. 17: 1071-1077

Sharpless N.E. and DePinho R.A. (2002) p53: good cop/bad cop. Cell 110: 9-12

Tyler D. and Baker N.E. (2002) Size is not everything. BioEssays 25: 5-8

New Research Articles

Tyner SD, Venkatachalam S, Choi J, Jones S, Ghebranious N, Igelmann H, Lu X, Soron G, Cooper B, Brayton C, Hee Park S, Thompson T, Karsenty G, Bradley A, Donehower LA. (2002) p53 mutant mice that display early ageing-associated phenotypes. Nature 415: 45-53

Abstract: The p53 tumour suppressor is activated by numerous stressors to induce apoptosis, cell cycle arrest, or senescence. To study the biological effects of altered p53 function, we generated mice with a deletion mutation in the first six exons of the p53 gene that express a truncated RNA capable of encoding a carboxy-terminal p53 fragment. This mutation confers phenotypes consistent with activated p53 rather than inactivated p53. Mutant (p53+/m) mice exhibit enhanced resistance to spontaneous tumours compared with wild-type (p53+/+) littermates. As p53+/m mice age, they display an early onset of phenotypes associated with ageing. These include reduced longevity, osteoporosis, generalized organ atrophy and a diminished stress tolerance. A second line of transgenic mice containing a temperature-sensitive mutant allele of p53 also exhibits early ageing phenotypes. These data suggest that p53 has a role in regulating organismal ageing.

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