NDLI: Functional mutants of the sequence-specific transcription factor p53 and implications for master genes of diversity.

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Functional mutants of the sequence-specific transcription factor p53 and implications for master genes of diversity.

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Functional mutants of the sequence-specific transcription factor p53 and implications for master genes of diversity.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Resnick, Michael A. Inga, Alberto
Description	Author Affiliation: Resnick MA ( Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. resnick@niehs.nih.gov);
Abstract	There are many sources of genetic diversity, ranging from programmed mutagenesis in antibody genes to random mutagenesis during species evolution or development of cancer. We propose that mutations in DNA sequence-specific transcription factors that target response elements (REs) in many genes can also provide for rapid and broad phenotypic diversity, if the mutations lead to altered binding affinities at individual REs. To test this concept, we examined the in vivo transactivation capacity of wild-type human and murine p53 and 25 partial function mutants. The p53s were expressed in yeast from a rheostatable promoter, and the transactivation capacities toward >15 promoter REs upstream of a reporter gene were measured. Surprisingly, there was wide variation in transactivation by the mutant p53s toward the various REs. This is the first study to address directly the impact of mutations in a sequence-specific transcription factor on transactivation from a wide array of REs. We propose a master gene hypothesis for phenotypic diversity where the master gene is a single transcriptional activator (or repressor) that regulates many genes through different REs. Mutations of the master gene can lead to a variety of simultaneous changes in both the selection of targets and the extent of transcriptional modulation at the individual targets, resulting in a vast number of potential phenotypes that can be created with minimal mutational changes without altering existing protein-protein interactions.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	17
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Genes, P53 Genetic Variation Models, Genetic Mutation Amino Acid Substitution Animals DNA Genetics Evolution, Molecular Genes, Reporter Mice Phenotype Promoter Regions, Genetic Saccharomyces Cerevisiae Transcription Factors Metabolism Transcriptional Activation Tumor Suppressor Protein P53 Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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