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Catherine H. Freudenreich
Tufts University
51Publications
23H-index
1,875Citations
Publications 50
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#1Erica J. Polleys (Tufts University)H-Index: 3
#2Catherine H. Freudenreich (Tufts University)H-Index: 23
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#1Simran Kaushal (Tufts University)H-Index: 2
#2Charles E. Wollmuth (Tufts University)H-Index: 1
Last.Catherine H. Freudenreich (Tufts University)H-Index: 23
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Summary Common fragile sites (CFSs) are genomic regions that display gaps and breaks in human metaphase chromosomes under replication stress and are often deleted in cancer cells. We studied an ∼300-bp subregion (Flex1) of human CFS FRA16D in yeast and found that it recapitulates characteristics of CFS fragility in human cells. Flex1 fragility is dependent on the ability of a variable-length AT repeat to form a cruciform structure that stalls replication. Fragility at Flex1 is initiated by struc...
2 CitationsSource
#1Lionel Gellon (Tufts University)H-Index: 2
#2Simran Kaushal (Tufts University)H-Index: 2
Last.Catherine H. Freudenreich (Tufts University)H-Index: 23
view all 6 authors...
1 CitationsSource
#1Hannah L. KleinH-Index: 36
Last.Anna MalkovaH-Index: 28
view all 48 authors...
5 CitationsSource
#1Simran Kaushal (Tufts University)H-Index: 2
#2Catherine H. Freudenreich (Tufts University)H-Index: 23
7 CitationsSource
R-loops form when transcribed RNA remains bound to its DNA template to form a stable RNA:DNA hybrid. Stable R-loops form when the RNA is purine-rich, and are further stabilized by DNA secondary structures on the non-template strand. Interestingly, many expandable and disease-causing repeat sequences form stable R-loops, and R-loops can contribute to repeat instability. Repeat expansions are responsible for multiple neurodegenerative diseases, including Huntington’s disease, myotonic dystrophy, a...
14 CitationsSource
#1Nealia C.M. House (Harvard University)H-Index: 5
#2Erica J. Polleys (Tufts University)H-Index: 3
Last.Catherine H. Freudenreich (Tufts University)H-Index: 23
view all 9 authors...
DNA are sites of genomic instability. Long CAG/CTG repeats form hairpin structures, are fragile, and can expand during DNA repair. The chromatin response to DNA damage can influence repair fidelity, but the knowledge of chromatin modifications involved in maintaining repair fidelity within repetitive DNA is limited. In a screen for CAG repeat fragility in Saccharomyces cerevisiae, histone 2A copy 1 (H2A.1) was identified to protect the repeat from increased rates of breakage. To address the role...
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#1Melissa R. Koch (Tufts University)H-Index: 2
#2Nealia C.M. House (Tufts University)H-Index: 5
Last.Catherine H. Freudenreich (Tufts University)H-Index: 23
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CAG/CTG trinucleotide repeats are unstable sequences that are difficult to replicate, repair, and transcribe due to their structure-forming nature. CAG repeats strongly position nucleosomes; however, little is known about the chromatin remodeling needed to prevent repeat instability. In a Saccharomyces cerevisiae model system with CAG repeats carried on a YAC, we discovered that the chromatin remodeler Isw1 is required to prevent CAG repeat expansions during transcription. CAG repeat expansions ...
5 CitationsSource
#1Erica J. Polleys (Tufts University)H-Index: 3
#2Catherine H. Freudenreich (Tufts University)H-Index: 23
4 CitationsSource
#1Junhua Zhao (University of Texas at Austin)H-Index: 6
#2Guliang Wang (University of Texas at Austin)H-Index: 18
Last.Karen M. Vasquez (University of Texas at Austin)H-Index: 39
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Summary Sequences with the capacity to adopt alternative DNA structures have been implicated in cancer etiology; however, the mechanisms are unclear. For example, H-DNA-forming sequences within oncogenes have been shown to stimulate genetic instability in mammals. Here, we report that H-DNA-forming sequences are enriched at translocation breakpoints in human cancer genomes, further implicating them in cancer etiology. H-DNA-induced mutations were suppressed in human cells deficient in the nucleo...
6 CitationsSource
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