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J Biol Chem, Vol. 273, Issue 10, 5431-5434, March 6, 1998
From the Department of Biochemistry and Biophysics and the Center
for Gene Research and Biotechnology, Oregon State University,
Corvallis, Oregon 97331
The prevalence of p53 gene mutations
in many human tumors implies that p53 protein plays an important role
in preventing cancers. Central among the activities ascribed to p53 is
its ability to stimulate transcription of other genes that inhibit
cells from entering S phase with damaged DNA. Human p53 can be studied
in yeast where genetic tools can be used to identify proteins that affect its ability to stimulate transcription. Although p53 strongly stimulated reporter gene expression in wild type yeast, it only weakly
stimulated reporter gene expression in 
trr1 yeast that lacked the gene encoding thioredoxin reductase. Furthermore, ectoptic expression of TRR1 in trr1 yeast restored
p53-dependent reporter gene activity to high levels.
Immunoblot assays established that the trr1 mutation
affected the activity and not the level of p53 protein. The results
suggest that p53 can form disulfides and that these disulfides must be
reduced in order for the protein to function as a transcription
factor.
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