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Mutagenesis Advance Access originally published online on October 18, 2007
Mutagenesis 2007 22(6):417-423; doi:10.1093/mutage/gem038
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© The Author 2007. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

Transcriptional properties of feline p53 and its tumour-associated mutants: a yeast-based approach

Umberto Cardellino{dagger}, Yari Ciribilli1,{dagger}, Virginia Andreotti1,{dagger}, Paola Modesto, Paola Menichini1, Gilberto Fronza1, Claudio Pellegrino and Alberto Inga1,*

Istituto Zooprofilattico Sperimentale del Piemonte Liguria e Valle d'Aosta, Genoa, Italy 1Unit of Molecular Mutagenesis, National Institute for Cancer Research, IST, Largo R. Benzi X, 16132 Genoa, Italy

Mutations at the tumour suppressor gene TP53 are associated with nearly half of human cancers, but they appear to be rare (~10%) in feline neoplasms. The reasons for this difference are presently unclear but might be related to evolutionary divergence of p53 functions. To begin exploring this issue, we developed a yeast-based functional assay to measure the transcriptional ability of wild-type (wt) or mutant feline p53 (fe_p53) in comparison with human or murine p53 (hu_p53, mo_p53). fe_p53 cDNA was cloned and expressed in a panel of yeast reporter strains engineered to contain the ADE2 or the luciferase gene under p53 control via different p53 response elements. We established that wt fe_, hu_ and mo_p53 can act as transcription factors in yeast with overlapping DNA sequence specificities. Random mutagenesis and phenotypic evaluation of fe_ and hu_p53 cDNAs was also performed, revealing equal susceptibility to deleterious mutations. Five tumour-associated fe_p53 mutants exhibited a similar impact on the transactivation capacity (partial or complete loss) compared to the corresponding hu_p53 mutants. Given the high conservation of the intrinsic functional properties of fe_p53, further studies will be needed to clarify the role of p53 in feline carcinogenetic pathways.

* To whom correspondence should be addressed. Tel:+39 010 5737225; Fax: +39 010 5737237; Email: alberto.inga{at}istge.it

{dagger} These authors contributed equally to this work.

Received on June 20, 2007; revised on August 28, 2007; accepted on August 28, 2007.


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