Franz Meitinger

Photo of Professor Meitinger
Franz Meitinger
Assistant Professor
PhD University of Heidelberg, Germany, 2011
Diplom (M.Sc.) University of Regensburg, Germany, 2007

Profile

Franz Meitinger studied biology at the University of Regensburg and pursued a Ph.D. in cell biology at the German Cancer Research Center in Heidelberg. During his doctoral work, he investigated the connection between cell division, polarity, and aging. He conducted his postdoc at the Ludwig Institute for Cancer Research in San Diego, where he discovered novel mechanisms of mitotic quality control and centrosome assembly using genome-wide CRISPR/Cas9 gene-editing screens. Since 2022, he has been running his research group at the Okinawa Institute for Science and Technology. His research interests are centered on the interface between cell and cancer biology with a focus on mechanisms that control cell proliferation and maintain genome stability. In addition, he is interested in how genetic changes in cancer alter cell division, promote cell proliferation, and enable cells to escape protective mechanisms of stress signaling with the goal to create cancer-specific diagnostic and therapeutic opportunities.

Professional Experience

  • Assistant Professor, OIST, Okinawa, Japan, since 2022
  • Postdoctoral fellow, Ludwig Institute for Cancer Research, San Diego, United States, 2014-2022
  • Postdoctoral fellow, German Cancer Research Center, Heidelberg, Germany, 2011-2014

Awards

  • Faculty Excellence in Mentoring Award, OIST, Okinawa, 2024
  • Lloyd Old Award for Collaborative Research Excellence, Ludwig Institute for Cancer Research, San Diego, 2020
  • DFG Research Fellowship, German Science Foundation, 2015-2017

Selected Publications

  • Meitinger, F.#, Belal, H., Davis, R.L., Martinez, M.B., Shiau, A.K., Oegema, K.#, Desai, A.# (2024). Control of cell proliferation by memories of mitosis. Science 383 (6690):1441-1448. # corresponding authors
  • Meitinger, F.*, Kong, D.*, Ohta, M.*, Desai, A., Oegema K., Loncarek, J.  (2021) TRIM37 prevents formation of condensate-organized ectopic spindle poles to ensure mitotic fidelity. Journal of Cell Biology 220. * equal contribution
  • Watanabe, S.*, Meitinger, F.*, Shiau, A.K., Oegema, K.#, Desai, A.#. (2020). Centriole-independent mitotic spindle assembly relies on the PCNT-CDK5RAP2 pericentriolar matrix. Journal of Cell Biology 219. * equal contribution
  • Meitinger, F.#, Ohta, M., Lee, K.Y., Watanabe, S., Davis, R.L., Anzola, J.V., Kabeche, R., Jenkins, J., Shiau, A.K., Desai, A.#, Oegema, K.# (2020). The ubiquitin ligase TRIM37 controls cancer-specific vulnerability to PLK4 inhibition. Nature 585:440-446. # corresponding authors
  • Meitinger, F., Anzola, J.V., Kaulich, M., Richardson, A., Stender, J.D., Benner, C., Glass, C.K., Dowdy, S.F., Desai, A., Shiau, A.K., Oegema, K. (2016). 53BP1 and USP28 mediate p53 activation and G1 arrest after centrosome loss or extended mitotic duration. Journal of Cell Biology 214, 155-166.
  • Meitinger, F., Khmelinskii, A., Morlot, S., Kurtulmus, B., Palani, S., Andres-Pons, A., Hub, B., Knop, M., Charvin, G., and Pereira, G. (2014). A memory system of negative polarity cues prevents replicative aging. Cell 159, 1056-1069.