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Jennifer A Benanti PhD

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

    InstitutionMorningside Graduate School of Biomedical Sciences
    DepartmentSystems Computational and Quantitative Biology

    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 UMass Chan Medical School in spring 2010. She is a recipeint of the 2011 Smith Family Award for Excellence in Biomedical Research.

    Research Summary

    Misregulation of the cell division cycle is one of the hallmarks that defines all cancer cells. The cell cycle is regulated at three levels–transcription, protein degradation, and phosphorylation–all of which are important to control cell-cycle events. Our goal is to understand how these different modes of regulation are integrated to generate a robust control network. A better understanding of this network will enable us to identify regulatory steps that can be targeted to inhibit proliferation and develop more effective cancer therapies.

    Phosphoregulation of the cell cycle

    Cyclin-dependent kinases (CDKs) phosphorylate a wide array of proteins to coordinate diverse cellular processes with cell division. Although hundreds of CDK substrates have been identified, for most substrates it is not known how phosphorylation regulates protein function. Our lab studies how CDK phosphorylation controls the activity of cell cycle-regulatory proteins (Landry et al, EMBO J, 2014; Marceau et al, eLife, 2019). We utilize systems-level genetic approaches to determine how CDK phosphorylation of substrates impacts cellular physiology (Conti, Ghizzoni, et al, PLoS Genetics, 2022), and have developed high-throughput methods to decode multisite phosphorylated domains to identify the critical phosphorylation sites that impact protein function (Conti et al, Nat Commun, 2023).

    Rewiring the cell cycle in response to environmental stress

    When cells are exposed to an environmental stressor, the cell cycle is delayed until they adapt to their new environment. Our lab is interested in understanding how stress response pathways interface with the cell cycle-regulatory network to pause the cell cycle as cells adapt. We study how conserved stress response pathways inactivate cell-cycle regulatory transcription factors to downregulate gene expression in response to stress (Arsenault, Roy et al, Mol Biol Cell, 2015; Leech, Flynn, et al PLoS Genet, 2020). We are also interested in understanding how stress response pathways cooperate to arrest the cell cycle (Flynn & Benanti, PNAS, 2022), and in the importance of crosstalk between these pathways for survival in stressful environments.

    Cell cycle regulation by the ubiquitin-proteasome system

    Protein degradation via the ubiquitin-proteasome system (UPS) is essential for cells to grow and divide. Consistent with this role, numerous ubiquitin ligases (E3s) that target proteins to the proteasome for 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. We use budding 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 (Benanti et al, Nat Cell Biol, 2007; Mapa et al, Mol Biol Cell, 2018). We are also interested in understanding the cell-cycle regulatory roles of other UPS proteins that are misregulated in cancer cells (Arsenault et al, G3, 2021).

    For more information, visit our lab website.


    Collapse Rotation Projects

    Rotation Projects

    Several rotation projects are available for current Morningside Graduate School of Biomedical Sciences students. Contact Jennifer Benanti to discuss potential projects.

    Collapse Post Docs

    Postdoctoral Positions

    Candidates should have a recent Ph.D. in cell biology, molecular biology, genetics or related area. To apply, send a letter describing your current research activities and future research interests, a CV, and contact information for three references to Jennifer Benanti.

    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. Flynn MJ, Harper NW, Li R, Zhu LJ, Lee MJ, Benanti JA. Calcineurin promotes adaptation to chronic stress through two distinct mechanisms. bioRxiv. 2024 Mar 20. PMID: 38562881.
    2. 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: 2     Fields:    Translation:AnimalsCells
    3. 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
    4. 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
    5. 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
    6. 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
    7. 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: 7     Fields:    Translation:AnimalsCells
    8. 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: 18     Fields:    Translation:Cells
    9. 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
    10. 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
    11. 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
    12. 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: 12     Fields:    Translation:AnimalsCells
    13. 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
    14. 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
    15. 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: 31     Fields:    Translation:AnimalsCells
    16. 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
    17. 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
    18. 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
    19. 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: 24     Fields:    Translation:HumansCells
    20. 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: 51     Fields:    Translation:Cells
    21. 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
    22. 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
    23. 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
    24. 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.
      Citations: 21     Fields:    Translation:HumansAnimalsCells
    25. 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: 32     Fields:    Translation:HumansAnimalsCells
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