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Jennifer A Benanti PhD

TitleAssociate Professor
InstitutionUMass Chan Medical School
DepartmentMolecular, Cell and Cancer Biology
AddressUMass Chan Medical School
364 Plantation Street LRB-525
Worcester MA 01605
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    Other Positions
    InstitutionT.H. Chan School of Medicine
    DepartmentBiochemistry and Molecular Biotechnology

    InstitutionT.H. Chan School of Medicine
    DepartmentMolecular, Cell and Cancer Biology

    InstitutionT.H. Chan School of Medicine
    DepartmentProgram in Molecular Medicine

    InstitutionT.H. Chan School of Medicine
    DepartmentSystems Biology

    InstitutionMorningside Graduate School of Biomedical Sciences
    DepartmentCancer Biology

    InstitutionMorningside Graduate School of Biomedical Sciences
    DepartmentInterdisciplinary Graduate Program

    InstitutionMorningside Graduate School of Biomedical Sciences
    DepartmentMD/PhD Program

    InstitutionMorningside Graduate School of Biomedical Sciences
    DepartmentMillennium MD/PhD Program

    InstitutionMorningside Graduate School of Biomedical Sciences
    DepartmentPostbaccalaureate Research Education Program

    Collapse Biography 
    Collapse education and training
    University of California, San Diego, San Diego, CA, United StatesBSBiochemistry & Cell Biology
    University of Washington, Seattle, WA, United StatesPHDMolecular & Cellular Biology

    Collapse Overview 
    Collapse overview

    Academic Background    

    Jennifer Benanti received her B.S. from the University of California, San Diego in 1996, and her Ph.D. from the University of Washington and the Fred Hutchinson Cancer Research Center in 2003. She did her postdoctoral work at the University of California, San Francisco from 2004-2010, where she was supported by a Damon Runyon Cancer Research Foundation Fellowship and a Pathway to Independence Award from the NIH. Dr. Benanti joined the Program in Gene Function and Expression at the University of Massachusetts Medical School in spring 2010. She is a recipeint of the 2011 Smith Family Award for Excellence in Biomedical Research.


    Regulation of Cell Growth and Division

    The Benanti laboratory is interested in the molecular mechanisms that control cell growth and proliferation, and in understanding how these mechanisms are disrupted in cancer cells. The lab is studying how transcription, phosphorylation and protein degradation contribute to the regulatory network that controls the cell cycle. To do this, they use genetics, biochemistry, and cell biology, in both yeast and human cells, with the goal of understanding properties of cell cycle control networks that are conserved in diverse systems.


    Transcriptional control of the cell cycle

    Cell proliferation is controlled by a tightly-regulated transcriptional program, which ensures that cells only proceed through the cell division cycle when they receive the appropriate signals. This program is established by a network of conserved transcription factors, many of which are mutated or misregulated in cancer cells. The Benanti lab uses yeast as a model system to study the connections between cell cycle-regulatory transcription factors, and to determine how phosphorylation and ubiquitination coordinate their activities. These studies are complemented by work in human cells aimed at understanding the regulation of oncogenic transcription factors that are core components of the cell-cycle network.

    Figure 1. The cell cycle-regulatory transcription factor network in yeast.


    Cell cycle-regulation of chromosome strucure

    Chromosome conformation is cell cycle-regulated so that chromosomes are tightly compacted during mitosis to facilitate their segregation, and decondensed during interphase to facilitate DNA-dependent processes such as replication and transcription. Understanding how chromosomes transition between these different states is important in order to understand how cells maintain a stable genome. The Benanti lab is investigating how cell cycle-regulation of chromatin proteins functions to coordinate chromosome strucutre with the cell cycle, and aims to understand the consequences of disrupting this regulation.

    Figure 2. Interphase and mitotic chromosome strucutre.


    Control of the cell cycle by the ubiquitin-proteasome system

    Protein degradation via the ubiquitin-proteasome system is essential for cells to grow and divide. Consistent with this role, numerous ubiquitin ligases (E3s) that promote protein degradation, as well as deubiquitinating enzymes (DUBs) that antagonize E3 function, are mutated in cancer cells. However, the targets of most of these enzymes remain unknown. The Benanti Lab is using yeast as a model system to determine how conserved E3s and DUBs recognize and select their substrates, and to develop proteome-wide approaches to identify targets of these critical enzymes.



    Collapse Post Docs

    Postdoctoral Positions

    A postdoctoral position is available in the Benanti laboratory to study molecular mechanisms that regulate cell growth and division. Candidates must be highly motivated and technically accomplished, and should have a recent Ph.D. in cell biology, molecular biology, genetics or related area of study. To apply, please send a letter (via email) describing your current research activities and future research interests, a CV, and contact information for three references to Jennifer Benanti (jennifer.benanti@umassmed.edu).

    Collapse Bibliographic 
    Collapse selected publications
    Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.
    Newest   |   Oldest   |   Most Cited   |   Most Discussed   |   Timeline   |   Field Summary   |   Plain Text
    PMC Citations indicate the number of times the publication was cited by articles in PubMed Central, and the Altmetric score represents citations in news articles and social media. (Note that publications are often cited in additional ways that are not shown here.) Fields are based on how the National Library of Medicine (NLM) classifies the publication's journal and might not represent the specific topic of the publication. Translation tags are based on the publication type and the MeSH terms NLM assigns to the publication. Some publications (especially newer ones and publications not in PubMed) might not yet be assigned Field or Translation tags.) Click a Field or Translation tag to filter the publications.
    1. Conti MM, Li R, Narv?ez Ramos MA, Zhu LJ, Fazzio TG, Benanti JA. Phosphosite Scanning reveals a complex phosphorylation code underlying CDK-dependent activation of Hcm1. Nat Commun. 2023 01 19; 14(1):310. PMID: 36658165.
      Citations:    Fields:    Translation:AnimalsCells
    2. Arsenault HE, Benanti JA. Identification of Deubiquitinase Substrates in Saccharomyces cerevisiae by Systematic Overexpression. Methods Mol Biol. 2023; 2591:237-253. PMID: 36350552.
      Citations:    Fields:    Translation:Animals
    3. Conti MM, Ghizzoni JM, Gil-Bona A, Wang W, Costanzo M, Li R, Flynn MJ, Zhu LJ, Myers CL, Boone C, Andrews BJ, Benanti JA. Repression of essential cell cycle genes increases cellular fitness. PLoS Genet. 2022 08; 18(8):e1010349. PMID: 36037231.
      Citations: 1     Fields:    Translation:AnimalsCells
    4. Flynn MJ, Benanti JA. Cip1 tunes cell cycle arrest duration upon calcineurin activation. Proc Natl Acad Sci U S A. 2022 06 07; 119(23):e2202469119. PMID: 35653562.
      Citations:    Fields:    Translation:Animals
    5. Arsenault HE, Ghizzoni JM, Leech CM, Diers AR, Gesta S, Vishnudas VK, Narain NR, Sarangarajan R, Benanti JA. Ubc1 turnover contributes to the spindle assembly checkpoint in Saccharomyces cerevisiae. G3 (Bethesda). 2021 12 08; 11(12). PMID: 34586382.
      Citations:    Fields:    Translation:AnimalsCells
    6. Leech CM, Flynn MJ, Arsenault HE, Ou J, Liu H, Zhu LJ, Benanti JA. The coordinate actions of calcineurin and Hog1 mediate the stress response through multiple nodes of the cell cycle network. PLoS Genet. 2020 04; 16(4):e1008600. PMID: 32343701.
      Citations: 6     Fields:    Translation:AnimalsCells
    7. Marceau AH, Brison CM, Nerli S, Arsenault HE, McShan AC, Chen E, Lee HW, Benanti JA, Sgourakis NG, Rubin SM. An order-to-disorder structural switch activates the FoxM1 transcription factor. Elife. 2019 05 28; 8. PMID: 31134895.
      Citations: 15     Fields:    Translation:Cells
    8. Mapa CE, Arsenault HE, Conti MM, Poti KE, Benanti JA. A balance of deubiquitinating enzymes controls cell cycle entry. Mol Biol Cell. 2018 11 15; 29(23):2821-2834. PMID: 30207830.
      Citations: 9     Fields:    Translation:AnimalsCells
    9. Doughty TW, Arsenault HE, Benanti JA. Levels of Ycg1 Limit Condensin Function during the Cell Cycle. PLoS Genet. 2016 07; 12(7):e1006216. PMID: 27463097.
      Citations: 10     Fields:    Translation:AnimalsCells
    10. Benanti JA. Create, activate, destroy, repeat: Cdk1 controls proliferation by limiting transcription factor activity. Curr Genet. 2016 May; 62(2):271-6. PMID: 26590602.
      Citations: 14     Fields:    Translation:HumansAnimalsCells
    11. Arsenault HE, Roy J, Mapa CE, Cyert MS, Benanti JA. Hcm1 integrates signals from Cdk1 and calcineurin to control cell proliferation. Mol Biol Cell. 2015 Oct 15; 26(20):3570-7. PMID: 26269584.
      Citations: 11     Fields:    Translation:AnimalsCells
    12. Landry BD, Mapa CE, Arsenault HE, Poti KE, Benanti JA. Regulation of a transcription factor network by Cdk1 coordinates late cell cycle gene expression. EMBO J. 2014 May 02; 33(9):1044-60. PMID: 24714560.
      Citations: 25     Fields:    Translation:AnimalsCells
    13. Edenberg ER, Vashisht A, Benanti JA, Wohlschlegel J, Toczyski DP. Rad53 downregulates mitotic gene transcription by inhibiting the transcriptional activator Ndd1. Mol Cell Biol. 2014 Feb; 34(4):725-38. PMID: 24324011.
      Citations: 11     Fields:    Translation:HumansAnimalsCells
    14. Landry BD, Doyle JP, Toczyski DP, Benanti JA. F-box protein specificity for g1 cyclins is dictated by subcellular localization. PLoS Genet. 2012; 8(7):e1002851. PMID: 22844257.
      Citations: 30     Fields:    Translation:AnimalsCells
    15. Benanti JA. Coordination of cell growth and division by the ubiquitin-proteasome system. Semin Cell Dev Biol. 2012 Jul; 23(5):492-8. PMID: 22542766.
      Citations: 22     Fields:    Translation:HumansAnimals
    16. Benanti JA, Matyskiela ME, Morgan DO, Toczyski DP. Functionally distinct isoforms of Cik1 are differentially regulated by APC/C-mediated proteolysis. Mol Cell. 2009 Mar 13; 33(5):581-90. PMID: 19285942.
      Citations: 24     Fields:    Translation:AnimalsCells
    17. Benanti JA, Toczyski DP. Cdc20, an activator at last. Mol Cell. 2008 Nov 21; 32(4):460-1. PMID: 19026776.
      Citations: 3     Fields:    Translation:AnimalsCells
    18. Benanti JA, Wang ML, Myers HE, Robinson KL, Grandori C, Galloway DA. Epigenetic down-regulation of ARF expression is a selection step in immortalization of human fibroblasts by c-Myc. Mol Cancer Res. 2007 Nov; 5(11):1181-9. PMID: 17982115.
      Citations: 22     Fields:    Translation:HumansCells
    19. Benanti JA, Cheung SK, Brady MC, Toczyski DP. A proteomic screen reveals SCFGrr1 targets that regulate the glycolytic-gluconeogenic switch. Nat Cell Biol. 2007 Oct; 9(10):1184-91. PMID: 17828247.
      Citations: 49     Fields:    Translation:Cells
    20. Vega LR, Phillips JA, Thornton BR, Benanti JA, Onigbanjo MT, Toczyski DP, Zakian VA. Sensitivity of yeast strains with long G-tails to levels of telomere-bound telomerase. PLoS Genet. 2007 Jun; 3(6):e105. PMID: 17590086.
      Citations: 34     Fields:    Translation:AnimalsCells
    21. Benanti JA, Galloway DA. The normal response to RAS: senescence or transformation? Cell Cycle. 2004 Jun; 3(6):715-7. PMID: 15153805.
      Citations: 15     Fields:    Translation:HumansAnimalsCells
    22. Benanti JA, Galloway DA. Normal human fibroblasts are resistant to RAS-induced senescence. Mol Cell Biol. 2004 Apr; 24(7):2842-52. PMID: 15024073.
      Citations: 42     Fields:    Translation:HumansAnimalsCells
    23. Passalaris TM, Benanti JA, Gewin L, Kiyono T, Galloway DA. The G(2) checkpoint is maintained by redundant pathways. Mol Cell Biol. 1999 Sep; 19(9):5872-81. PMID: 10454534.
      Citations: 31     Fields:    Translation:HumansAnimalsCells
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