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== Research ==
== Research ==
Freudenreich’s lab studies [[genome instability]] in yeast, with the aim of uncovering mechanisms of genetic disease and [[cancer]]. In particular, much of her research has focused on conserved trinucleotide repeat sequences, specifically CAG/CTG, and their contributions to genome fragility and instability.<ref name=":2">{{Cite web |title=Research Overview {{!}} Department of Biology |url=https://as.tufts.edu/biology/freudenreich-lab/research-teaching |access-date=2024-06-18 |website=as.tufts.edu}}</ref><ref name=":3">{{Cite journal |last1=Lahiri |first1=Mayurika |last2=Gustafson |first2=Tanya L |last3=Majors |first3=Elizabeth R |last4=Freudenreich |first4=Catherine H |date=2004-07-23 |title=Expanded CAG Repeats Activate the DNA Damage Checkpoint Pathway |url=https://doi.org/10.1016/j.molcel.2004.06.034 |journal=Molecular Cell |volume=15 |issue=2 |pages=287–293 |doi=10.1016/j.molcel.2004.06.034 |pmid=15260979 |issn=1097-2765}}</ref> Recently, Freudenreich’s group looked at CAG/CTG repeats in [[Huntington's disease|Huntington’s disease]], finding that the cells’ attempts to repair CAG sequences often lead to large, deleterious deletions.<ref>{{Cite web |date=2023-05-10 |title=How DNA Repair Can Go Wrong and Lead to Disease {{!}} Tufts Now |url=https://now.tufts.edu/2023/05/10/how-dna-repair-can-go-wrong-and-lead-disease |access-date=2024-06-18 |website=now.tufts.edu |language=en}}</ref><ref name=":4">{{Cite journal |last1=Polleys |first1=Erica J. |last2=Del Priore |first2=Isabella |last3=Haber |first3=James E. |last4=Freudenreich |first4=Catherine H. |date=2023-04-29 |title=Structure-forming CAG/CTG repeats interfere with gap repair to cause repeat expansions and chromosome breaks |url=https://www.nature.com/articles/s41467-023-37901-2 |journal=Nature Communications |language=en |volume=14 |issue=1 |pages=2469 |doi=10.1038/s41467-023-37901-2 |pmid=37120647 |bibcode=2023NatCo..14.2469P |issn=2041-1723}}</ref>
Freudenreich’s lab studies [[genome instability]] in yeast, with the aim of uncovering mechanisms of genetic disease and [[cancer]]. In particular, much of her research has focused on conserved trinucleotide repeat sequences, specifically CAG/CTG, and their contributions to genome fragility and instability.<ref name=":2">{{Cite web |title=Research Overview {{!}} Department of Biology |url=https://as.tufts.edu/biology/freudenreich-lab/research-teaching |access-date=2024-06-18 |website=as.tufts.edu}}</ref><ref name=":3">{{Cite journal |last1=Lahiri |first1=Mayurika |last2=Gustafson |first2=Tanya L |last3=Majors |first3=Elizabeth R |last4=Freudenreich |first4=Catherine H |date=2004-07-23 |title=Expanded CAG Repeats Activate the DNA Damage Checkpoint Pathway |url=https://doi.org/10.1016/j.molcel.2004.06.034 |journal=Molecular Cell |volume=15 |issue=2 |pages=287–293 |doi=10.1016/j.molcel.2004.06.034 |pmid=15260979 |issn=1097-2765}}</ref> Recently, Freudenreich’s group looked at CAG/CTG repeats in [[Huntington's disease|Huntington’s disease]], finding that the cells’ attempts to repair CAG sequences often lead to large, deleterious deletions.<ref>{{Cite web |date=2023-05-10 |title=How DNA Repair Can Go Wrong and Lead to Disease {{!}} Tufts Now |url=https://now.tufts.edu/2023/05/10/how-dna-repair-can-go-wrong-and-lead-disease |access-date=2024-06-18 |website=now.tufts.edu |language=en}}</ref><ref name=":4">{{Cite journal |last1=Polleys |first1=Erica J. |last2=Del Priore |first2=Isabella |last3=Haber |first3=James E. |last4=Freudenreich |first4=Catherine H. |date=2023-04-29 |title=Structure-forming CAG/CTG repeats interfere with gap repair to cause repeat expansions and chromosome breaks |url=https://www.nature.com/articles/s41467-023-37901-2 |journal=Nature Communications |language=en |volume=14 |issue=1 |pages=2469 |doi=10.1038/s41467-023-37901-2 |pmid=37120647 |bibcode=2023NatCo..14.2469P |issn=2041-1723}}</ref><ref>{{Cite web |title=Understanding the Link Between DNA Mutations & Repair Dysfunction {{!}} Genetics And Genomics |url=https://www.labroots.com/trending/genetics-and-genomics/25263/understanding-link-dna-mutations-repair-dysfunction |access-date=2024-06-24 |website=Labroots}}</ref>


Freudenreich has also notably studied how DNA repeat sequences contribute to DNA structures that can cause DNA breaks, and how the cell protects against genomic damage from these mechanisms. <ref name=":2" /><ref>{{Cite journal |last=Pennisi |first=Elizabeth |date=2006-06-09 |title=DNA's Molecular Gymnastics |url=https://www.science.org/doi/10.1126/science.312.5779.1467 |journal=Science |language=en |volume=312 |issue=5779 |pages=1467–1468 |doi=10.1126/science.312.5779.1467 |pmid=16763129 |issn=0036-8075}}</ref><ref name=":5">{{Cite journal |last1=Zhang |first1=Haihua |last2=Freudenreich |first2=Catherine H. |date=2007-08-03 |title=An AT-Rich Sequence in Human Common Fragile Site FRA16D Causes Fork Stalling and Chromosome Breakage in S. cerevisiae |url=https://doi.org/10.1016/j.molcel.2007.06.012 |journal=Molecular Cell |volume=27 |issue=3 |pages=367–379 |doi=10.1016/j.molcel.2007.06.012 |issn=1097-2765 |pmc=2144737 |pmid=17679088}}</ref><ref>{{Cite web |date=2019-08-01 |title=Mapping the Kinks in Faulty DNA {{!}} Tufts Now |url=https://now.tufts.edu/2019/08/01/mapping-kinks-faulty-dna |access-date=2024-06-18 |website=now.tufts.edu |language=en}}</ref>
Freudenreich has also notably studied how DNA repeat sequences contribute to DNA structures that can cause DNA breaks, and how the cell protects against genomic damage from these mechanisms. <ref name=":2" /><ref>{{Cite journal |last=Pennisi |first=Elizabeth |date=2006-06-09 |title=DNA's Molecular Gymnastics |url=https://www.science.org/doi/10.1126/science.312.5779.1467 |journal=Science |language=en |volume=312 |issue=5779 |pages=1467–1468 |doi=10.1126/science.312.5779.1467 |pmid=16763129 |issn=0036-8075}}</ref><ref name=":5">{{Cite journal |last1=Zhang |first1=Haihua |last2=Freudenreich |first2=Catherine H. |date=2007-08-03 |title=An AT-Rich Sequence in Human Common Fragile Site FRA16D Causes Fork Stalling and Chromosome Breakage in S. cerevisiae |url=https://doi.org/10.1016/j.molcel.2007.06.012 |journal=Molecular Cell |volume=27 |issue=3 |pages=367–379 |doi=10.1016/j.molcel.2007.06.012 |issn=1097-2765 |pmc=2144737 |pmid=17679088}}</ref><ref>{{Cite web |date=2019-08-01 |title=Mapping the Kinks in Faulty DNA {{!}} Tufts Now |url=https://now.tufts.edu/2019/08/01/mapping-kinks-faulty-dna |access-date=2024-06-18 |website=now.tufts.edu |language=en}}</ref>

Revision as of 03:24, 24 June 2024

Catherine H. Freudenreich
Alma materRice University (BA) Duke University (PhD)
Scientific career
FieldsMolecular biology
InstitutionsTufts University
Doctoral advisorKenneth Kreuzer
Other academic advisorsVirginia Zakian (postdoctoral)
Websitehttps://as.tufts.edu/biology/freudenreich-lab

Catherine Freudenreich is an American molecular biologist at Tufts University. Since 2019, Freudenreich has served as chair of the Department of Biology.[1]

Career

Freudenreich attended Rice University, where she graduated in 1988 with a B.A in biology. She received her PhD in 1994 from Duke University, where she studied inhibitor binding sites of Type II topoisomerases in the lab of Kenneth Kreuzer, and continued to do so as a postdoctoral researcher in the same lab.[2] Freudenreich then undertook further postdoctoral research at Princeton University with Virginia Zakian, studying CTG repeats in yeast.[3][1]

After her postdoctoral studies, Freudenreich was appointed to an assistant professor position in the Department of Biology at Tufts University in 1999, where she is currently professor and department chair. [1]

Research

Freudenreich’s lab studies genome instability in yeast, with the aim of uncovering mechanisms of genetic disease and cancer. In particular, much of her research has focused on conserved trinucleotide repeat sequences, specifically CAG/CTG, and their contributions to genome fragility and instability.[4][5] Recently, Freudenreich’s group looked at CAG/CTG repeats in Huntington’s disease, finding that the cells’ attempts to repair CAG sequences often lead to large, deleterious deletions.[6][7][8]

Freudenreich has also notably studied how DNA repeat sequences contribute to DNA structures that can cause DNA breaks, and how the cell protects against genomic damage from these mechanisms. [4][9][10][11]

Notable publications

  1. Freudenreich, Catherine H.; Kantrow, Sara M.; Zakian, Virginia A. (1998-02-06). "Expansion and Length-Dependent Fragility of CTG Repeats in Yeast". Science. 279 (5352): 853–856. doi:10.1126/science.279.5352.853. ISSN 0036-8075.[3]
  2. Lahiri, Mayurika; Gustafson, Tanya L; Majors, Elizabeth R; Freudenreich, Catherine H (2004-07-23). "Expanded CAG Repeats Activate the DNA Damage Checkpoint Pathway". Molecular Cell. 15 (2): 287–293. doi:10.1016/j.molcel.2004.06.034. ISSN 1097-2765.[5]
  3. Polleys, Erica J.; Del Priore, Isabella; Haber, James E.; Freudenreich, Catherine H. (2023-04-29). "Structure-forming CAG/CTG repeats interfere with gap repair to cause repeat expansions and chromosome breaks". Nature Communications. 14 (1): 2469. doi:10.1038/s41467-023-37901-2. ISSN 2041-1723.[7]
  4. Zhang, Haihua; Freudenreich, Catherine H. (2007-08). "An AT-Rich Sequence in Human Common Fragile Site FRA16D Causes Fork Stalling and Chromosome Breakage in S. cerevisiae". Molecular Cell. 27 (3): 367–379. doi:10.1016/j.molcel.2007.06.012. ISSN 1097-2765. PMC 2144737. PMID 17679088.[10]
  5. Kerrest, Alix; Anand, Ranjith P.; Sundararajan, Rangapriya; Bermejo, Rodrigo; Liberi, Giordano; Dujon, Bernard; Freudenreich, Catherine H.; Richard, Guy-Franck (2009-01-11). "SRS2 and SGS1 prevent chromosomal breaks and stabilize triplet repeats by restraining recombination". Nature Structural & Molecular Biology. 16 (2): 159–167. doi:10.1038/nsmb.1544. ISSN 1545-9985.[12]
  6. House, Nealia C.M.; Yang, Jiahui H.; Walsh, Stephen C.; Moy, Jonathan M.; Freudenreich, Catherine H. (2014-09-18). "NuA4 Initiates Dynamic Histone H4 Acetylation to Promote High-Fidelity Sister Chromatid Recombination at Postreplication Gaps". Molecular Cell. 55 (6): 818–828. doi:10.1016/j.molcel.2014.07.007. ISSN 1097-2765. PMC 4169719. PMID 25132173.[13]
  7. Su, Xiaofeng A.; Freudenreich, Catherine H. (2017-10-03). "Cytosine deamination and base excision repair cause R-loop–induced CAG repeat fragility and instability in Saccharomyces cerevisiae". Proceedings of the National Academy of Sciences. 114 (40). doi:10.1073/pnas.1711283114. ISSN 0027-8424. PMC 5635916. PMID 28923949.[14]

Awards and honors

References

  1. ^ a b c "Catherine Freudenreich Faculty Profile". facultyprofiles.tufts.edu. Retrieved 2024-06-18.
  2. ^ Freudenreich, C H; Kreuzer, K N (1994-11-08). "Localization of an aminoacridine antitumor agent in a type II topoisomerase-DNA complex". Proceedings of the National Academy of Sciences. 91 (23): 11007–11011. Bibcode:1994PNAS...9111007F. doi:10.1073/pnas.91.23.11007. ISSN 0027-8424. PMC 45155. PMID 7971998.
  3. ^ a b Freudenreich, Catherine H.; Kantrow, Sara M.; Zakian, Virginia A. (1998-02-06). "Expansion and Length-Dependent Fragility of CTG Repeats in Yeast". Science. 279 (5352): 853–856. Bibcode:1998Sci...279..853F. doi:10.1126/science.279.5352.853. ISSN 0036-8075.
  4. ^ a b "Research Overview | Department of Biology". as.tufts.edu. Retrieved 2024-06-18.
  5. ^ a b Lahiri, Mayurika; Gustafson, Tanya L; Majors, Elizabeth R; Freudenreich, Catherine H (2004-07-23). "Expanded CAG Repeats Activate the DNA Damage Checkpoint Pathway". Molecular Cell. 15 (2): 287–293. doi:10.1016/j.molcel.2004.06.034. ISSN 1097-2765. PMID 15260979.
  6. ^ "How DNA Repair Can Go Wrong and Lead to Disease | Tufts Now". now.tufts.edu. 2023-05-10. Retrieved 2024-06-18.
  7. ^ a b Polleys, Erica J.; Del Priore, Isabella; Haber, James E.; Freudenreich, Catherine H. (2023-04-29). "Structure-forming CAG/CTG repeats interfere with gap repair to cause repeat expansions and chromosome breaks". Nature Communications. 14 (1): 2469. Bibcode:2023NatCo..14.2469P. doi:10.1038/s41467-023-37901-2. ISSN 2041-1723. PMID 37120647.
  8. ^ "Understanding the Link Between DNA Mutations & Repair Dysfunction | Genetics And Genomics". Labroots. Retrieved 2024-06-24.
  9. ^ Pennisi, Elizabeth (2006-06-09). "DNA's Molecular Gymnastics". Science. 312 (5779): 1467–1468. doi:10.1126/science.312.5779.1467. ISSN 0036-8075. PMID 16763129.
  10. ^ a b Zhang, Haihua; Freudenreich, Catherine H. (2007-08-03). "An AT-Rich Sequence in Human Common Fragile Site FRA16D Causes Fork Stalling and Chromosome Breakage in S. cerevisiae". Molecular Cell. 27 (3): 367–379. doi:10.1016/j.molcel.2007.06.012. ISSN 1097-2765. PMC 2144737. PMID 17679088.
  11. ^ "Mapping the Kinks in Faulty DNA | Tufts Now". now.tufts.edu. 2019-08-01. Retrieved 2024-06-18.
  12. ^ Kerrest, Alix; Anand, Ranjith P.; Sundararajan, Rangapriya; Bermejo, Rodrigo; Liberi, Giordano; Dujon, Bernard; Freudenreich, Catherine H.; Richard, Guy-Franck (2009-01-11). "SRS2 and SGS1 prevent chromosomal breaks and stabilize triplet repeats by restraining recombination". Nature Structural & Molecular Biology. 16 (2): 159–167. doi:10.1038/nsmb.1544. ISSN 1545-9985. PMC 4454460. PMID 19136956.
  13. ^ House, Nealia C.M.; Yang, Jiahui H.; Walsh, Stephen C.; Moy, Jonathan M.; Freudenreich, Catherine H. (2014-09-18). "NuA4 Initiates Dynamic Histone H4 Acetylation to Promote High-Fidelity Sister Chromatid Recombination at Postreplication Gaps". Molecular Cell. 55 (6): 818–828. doi:10.1016/j.molcel.2014.07.007. ISSN 1097-2765. PMC 4169719. PMID 25132173.
  14. ^ Su, Xiaofeng A.; Freudenreich, Catherine H. (2017-10-03). "Cytosine deamination and base excision repair cause R-loop–induced CAG repeat fragility and instability in Saccharomyces cerevisiae". Proceedings of the National Academy of Sciences. 114 (40). Bibcode:2017PNAS..114E8392S. doi:10.1073/pnas.1711283114. ISSN 0027-8424. PMC 5635916. PMID 28923949.
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