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Jennifer A Benanti PhD

TitleAssociate Professor
InstitutionUniversity of Massachusetts Medical School
DepartmentMolecular, Cell and Cancer Biology
AddressUniversity of Massachusetts Medical School
364 Plantation Street, LRB-525
Worcester MA 01605
Phone508-856-1773
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    Other Positions
    InstitutionUMMS - School of Medicine
    DepartmentMolecular, Cell and Cancer Biology

    InstitutionUMMS - School of Medicine
    DepartmentProgram in Molecular Medicine

    InstitutionUMMS - Graduate School of Biomedical Sciences
    DepartmentCancer Biology

    InstitutionUMMS - Graduate School of Biomedical Sciences
    DepartmentInterdisciplinary Graduate Program


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    University of California, San Diego, San Diego, CA, United StatesBSBiochemistry & Cell Biology
    University of Washington, Seattle, WA, United StatesPHDMolecular & Cellular Biology

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    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.



     



     









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    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).




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    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.
    List All   |   Timeline
    1. Doughty TW, Arsenault HE, Benanti JA. Levels of Ycg1 Limit Condensin Function during the Cell Cycle. PLoS Genet. 2016 Jul; 12(7):e1006216. PMID: 27463097.
      View in: PubMed
    2. Benanti JA. Create, activate, destroy, repeat: Cdk1 controls proliferation by limiting transcription factor activity. Curr Genet. 2016 May; 62(2):271-6. PMID: 26590602.
      View in: PubMed
    3. 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.
      View in: PubMed
    4. 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 2; 33(9):1044-60. PMID: 24714560.
      View in: PubMed
    5. 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.
      View in: PubMed
    6. 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.
      View in: PubMed
    7. 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.
      View in: PubMed
    8. 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.
      View in: PubMed
    9. Benanti JA, Toczyski DP. Cdc20, an activator at last. Mol Cell. 2008 Nov 21; 32(4):460-1. PMID: 19026776.
      View in: PubMed
    10. 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.
      View in: PubMed
    11. 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.
      View in: PubMed
    12. 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.
      View in: PubMed
    13. Benanti JA, Galloway DA. The normal response to RAS: senescence or transformation? Cell Cycle. 2004 Jun; 3(6):715-7. PMID: 15153805.
      View in: PubMed
    14. Benanti JA, Galloway DA. Normal human fibroblasts are resistant to RAS-induced senescence. Mol Cell Biol. 2004 Apr; 24(7):2842-52. PMID: 15024073.
      View in: PubMed
    15. Benanti JA, Williams DK, Robinson KL, Ozer HL, Galloway DA. Induction of extracellular matrix-remodeling genes by the senescence-associated protein APA-1. Mol Cell Biol. 2002 Nov; 22(21):7385-97. PMID: 12370286.
      View in: PubMed
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