Genomic deletions and point mutations induced in Saccharomyces cerevisiae by the trinucleotide repeats (GAA*TTC) associated with Friedreich's ataxia

Expansion of certain trinucleotide repeats causes several types of human diseases, and such tracts are associated with the formation of deletions and other types of genetic rearrangements in Escherichia coli, yeast, and mammalian cells. Below, we show that long (230 repeats) tracts of the trinucleotide associated with Friedreich's ataxia (GAA-TTC) stimulate both large (>50bp) deletions and point mutations in a reporter gene located more than 1kb from the repetitive tract.