Correction: Noncanonical DNA Motifs as Transactivation Targets by Wild Type and Mutant p53

Jennifer J Jordan,Douglas Bell,Daniel Menendez,Michael A Resnick,Alberto Inga,Maher Nourredine,Orna Cohen-Fix

doi:10.1371/annotation/f7fc9c28-14ae-480d-a69e-ee9cc4fba9a7

Abstract

The fourth and fifth authors' names were incorrectly listed. The correct names are: Maher Noureddine and Douglas A. Bell. The correct citation is: Jordan JJ, Menendez D, Inga A, Noureddine M, Bell DA, et al. (2008) Noncanonical DNA Motifs as Transactivation Targets by Wild Type and Mutant p53. PLoS Genet 4(6): e1000104. doi:10.1371/journal.pgen.1000104

Highlights

The tumor suppressor p53 (OMIM no. 191170) is a sequencespecific master regulatory gene that controls an extensive transcriptional network providing for genome integrity in response to cellular and environmental stresses or damage [1,2,3]. p53 differentially regulates the expression of target genes, as well as microRNAs associated with cell cycle control, apoptosis, DNA repair, angiogenesis, senescence and carbon metabolism [4,5]
A consensus p53 DNA binding sequence has been derived comprising a motif of two decamers RRRCWWGYYY (n) RRRCWWGYYY, where each decamer is composed of two adjacent p53 monomer binding sites in inverted orientation [16,17,18]. p53 binds cooperatively to the consensus response elements (REs) as a dimer of dimers, where a tetramer is the accepted functional unit required for full transcriptional activity [19,20,21,22,23,24,25,26]
While many factors may determine p53 transactivation of individual genes in human cells including stress stimuli, post-translational modifications, and transcriptional cofactors, the yeast system addresses the potential for wild type and mutant p53 to bind and transactivate from various REs derived from human genes when placed in a constant chromatin environment

Summary

Introduction

The tumor suppressor p53 (OMIM no. 191170) is a sequencespecific master regulatory gene that controls an extensive transcriptional network providing for genome integrity in response to cellular and environmental stresses or damage [1,2,3]. p53 differentially regulates the expression of target genes, as well as microRNAs associated with cell cycle control, apoptosis, DNA repair, angiogenesis, senescence and carbon metabolism [4,5]. Paramount to p53 transcriptional function is the direct interaction between p53 and its targeted DNA sequence The nature of this interaction could per se determine transactivation capacity, as well as influence p53-mediated biological processes [9]. Such activities are often altered during human cancer development as highlighted by the frequent appearance of p53 missense mutations in its sequencespecific DNA binding domain [10,11] which can abrogate or alter p53 transactivational activity that result in changes in biological responses, such as the balance between apoptosis and survival in response to DNA damage. Most functional response elements (REs) identified in association with p53 target genes depart from this consensus, where base changes are tolerated at each position with the exception of the C and G at positions 4 and 7 in each half-site [27,28]

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Conclusion