Thomas D. Petes

TL;DR: It is suggested that the mechanism of GAA/TTC‐induced chromosomal aberrations defined in yeast can also operate in human carriers with expanded tracts and is shown that fragility is mediated by mismatch repair machinery and requires the MutSβ and endonuclease activity of MutLα.

TL;DR: It is concluded that the chromosomal sequence or structure has a dramatic effect on meiotic recombination.

TL;DR: Using a PCR assay, it is demonstrated that mec1 tel1 strains also have telomere–telomere fusions (T-TFs), which argue that many of these deletions reflect a cycle of T-TF formation (resulting in dicentric chromosomes), followed by chromosome breakage.

TL;DR: It is shown that strains with the rad50, but not the rad52, mutation are defective in heteroduplex formation, and it is demonstrated that, although cruciform structures can be formed in vivo as a consequence of heterod uplex formation between DNA strands that contain different palindromic insertions, small palINDromic sequences in homodupLex DNA are rarely extruded into the cruciform conformation.

TL;DR: When the yeast Saccharomyces cerevisiae was transformed with DNA that shares no homology to the genome, three classes of transformants were obtained; the final class involved the in vivo ligation of transforming DNA with nucleus-localized linear fragments of mitochondrial DNA.