Bio


Christine Jacobs-Wagner is a Dennis Cunningham Professor in the Department of Biology and the ChEM-H Institute at Stanford University. She is interested in understanding the fundamental mechanisms and principles by which cells, and, in particular, bacterial cells, are able to multiple. She received her PhD in Biochemistry in 1996 from the University of Liège, Belgium where she unraveled a molecular mechanism by which some bacterial pathogens sense and respond to antibiotics attack to achieve resistance. For this work, she received multiple awards including the 1997 GE & Science Prize for Young Life Scientists. During her postdoctoral work at Stanford Medical School, she demonstrated that bacteria can localize regulatory proteins to specific intracellular regions to control signal transduction and the cell cycle, uncovering a new, unsuspected level of bacterial regulation.

She started her own lab at Yale University in 2001. Over the years, her group made major contributions in the emerging field of bacterial cell biology and provided key molecular insights into the temporal and spatial mechanisms involved in cell morphogenesis, cell polarization, chromosome segregation and cell cycle control. For her distinguished work, she received the Pew Scholars award from the Pew Charitable Trust, the Woman in Cell Biology Junior award from the American Society of Cell Biology and the Eli Lilly award from the American Society of Microbiology. She held the Maxine F. Singer and William H. Fleming professor chairs at Yale. She was elected to the Connecticut academy of Science, the American Academy of Microbiology and the National Academy of Sciences. She has been an investigator of the Howard Hughes Medical Institute since 2008.

Her lab moved to Stanford in 2019. Current research examines the general principles and spatiotemporal mechanisms by which bacterial cells replicate, using Caulobacter crescentus and Escherichia coli as models. Recently, the Jacobs-Wagner lab expanded their interests to the Lyme disease agent Borrelia burgdorferi, revealing unsuspected ways by which this pathogen grows and causes disease

Academic Appointments


Administrative Appointments


  • Investigator, Howard Hughes Medical Institute (2008 - Present)

Honors & Awards


  • Gabilan Fellowship, Stanford University (2019)
  • Ely Lilly Award, American Society of Microbiology (2011)
  • Finalist, Blavatnik Award for Young Scientists, New York Academy of Sciences (2008)
  • Women in Cell Biology Junior Award, American Society of Cell Biology (2007)
  • E. Van Beneden Prize, University of Liège, Belgium (2001)
  • Wetrems Prize in Natural Sciences, Royal Academy of Sciences, Literature and Arts, Belgium (1998)
  • Outstanding Young Person Award in Medical Innovations, Young Economic Chamber of Belgium (1998)
  • Grand Prize Winner, GE & Science Prize for Young Life (1997)

Boards, Advisory Committees, Professional Organizations


  • Member, National academy of Sciences (2015 - Present)
  • Member, the American Academy of Microbiology (2017 - Present)
  • Member, Connecticut Academy of Science and Engineering (2016 - Present)
  • Member, Pew Scholars National Advisory Committee (2015 - Present)
  • Member, Temporary Nominating Group for the National Academy of Sciences (2017 - Present)
  • Board Member, Belgian American Educational Foundation (2008 - Present)
  • Member, Scientific Advisory Board of Global Institute of Health, EPFL, Switzerland (2017 - Present)

Professional Education


  • Postdoc, Stanford Medical School, Developmental Biology
  • PhD, University of Liège, Belgium (1996)
  • BS/MS, University of Liège, Belgium (1991)

2019-20 Courses


Stanford Advisees


All Publications


  • Long-Distance Cooperative and Antagonistic RNA Polymerase Dynamics via DNA Supercoiling CELL Kim, S., Beltran, B., Irnov, I., Jacobs-Wagner, C. 2019; 179 (1): 106-+

    Abstract

    Genes are often transcribed by multiple RNA polymerases (RNAPs) at densities that can vary widely across genes and environmental conditions. Here, we provide in vitro and in vivo evidence for a built-in mechanism by which co-transcribing RNAPs display either collaborative or antagonistic dynamics over long distances (>2 kb) through transcription-induced DNA supercoiling. In Escherichia coli, when the promoter is active, co-transcribing RNAPs translocate faster than a single RNAP, but their average speed is not altered by large variations in promoter strength and thus RNAP density. Environmentally induced promoter repression reduces the elongation efficiency of already-loaded RNAPs, causing premature termination and quick synthesis arrest of no-longer-needed proteins. This negative effect appears independent of RNAP convoy formation and is abrogated by topoisomerase I activity. Antagonistic dynamics can also occur between RNAPs from divergently transcribed gene pairs. Our findings may be broadly applicable given that transcription on topologically constrained DNA is the norm across organisms.

    View details for DOI 10.1016/j.cell.2019.08.033

    View details for Web of Science ID 000486618500017

    View details for PubMedID 31539491

  • Osmolality-Dependent Relocation of Penicillin-Binding Protein PBP2 to the Division Site in Caulobacter crescentus JOURNAL OF BACTERIOLOGY Hocking, J., Priyadarshini, R., Takacs, C. N., Costa, T., Dye, N. A., Shapiro, L., Vollmer, W., Jacobs-Wagner, C. 2012; 194 (12): 3116-3127

    Abstract

    The synthesis of the peptidoglycan cell wall is carefully regulated in time and space. In nature, this essential process occurs in cells that live in fluctuating environments. Here we show that the spatial distributions of specific cell wall proteins in Caulobacter crescentus are sensitive to small external osmotic upshifts. The penicillin-binding protein PBP2, which is commonly branded as an essential cell elongation-specific transpeptidase, switches its localization from a dispersed, patchy pattern to an accumulation at the FtsZ ring location in response to osmotic upshifts as low as 40 mosmol/kg. This osmolality-dependent relocation to the division apparatus is initiated within less than a minute, while restoration to the patchy localization pattern is dependent on cell growth and takes 1 to 2 generations. Cell wall morphogenetic protein RodA and penicillin-binding protein PBP1a also change their spatial distribution by accumulating at the division site in response to external osmotic upshifts. Consistent with its ecological distribution, C. crescentus displays a narrow range of osmotolerance, with an upper limit of 225 mosmol/kg in minimal medium. Collectively, our findings reveal an unsuspected level of environmental regulation of cell wall protein behavior that is likely linked to an ecological adaptation.

    View details for DOI 10.1128/JB.00260-12

    View details for Web of Science ID 000304978400010

    View details for PubMedID 22505677

    View details for PubMedCentralID PMC3370875