We are looking for a highly motivated and team oriented postdoctoral candidate to work on the role and the regulation of the Polo-like kinase during mitotic entry using the early C. elegans embryo as model system. The Polo-like kinase Plk1 is an evolutionarily conserved serine-threonine kinase that plays a critical role during mitosis. Plk1 regulates mitotic entry, centrosomes maturation, spindle assembly, chromosomes segregation and cytokinesis. Plk1 activity must be tightly regulated, in space and time, as defect in Plk1 regulation has drastic consequences. Plk1 is overexpressed in numerous cancer types and this overexpression is associated with a poor prognosis for the patients. Despite considerable progress, how Plk1 activation is regulated remains only partially elucidated. Our objectives are i) to identify the mechanism regulating Plk1 activity in space and time, ii) define its role in mitosis and iii) develop novel Plk1 pathway inhibitors with anti-cancer properties. In this context, the candidate will focus on the role of Plk1 in nuclear envelope breakdown.

Our group is part of the Institut Jacques Monod (https://www.ijm.fr) which is housed in a new building of 1800 square meters, located on the new campus of the Paris left bank urban project. The Institute Jacques Monod is one of the main public centers for fundamental research in biology in the Paris area and offers a state-of-the-art research environment.

Financing is available for 12 months with the possibility for renewal but the candidate is expected to apply for its own funding with the support of the laboratory. The candidate is expected to hold a PhD, with no or max. 2 years of postdoctoral experience and with a solid background in Cell Biology/Molecular Biology and/or Biochemistry with at least one first author publication in a peer-reviewed journal from his/her PhD work.

lnterested candidates should send their CV including research interests and contact details of two referees in a single pdf file to lionel.pintard@ijm.fr. Priority will be given to applications received before June 15th, but the position will remain open until a suitable candidate has been found.



  • Martino, L., Morchoisne-Bolhy, S., Cheerambathur, D. K., Van Hove, L., Dumont, J., Joly, N., Desai, A., Doye, V., and Pintard, L. (2017). Channel Nucleoporins Recruit PLK-1 to Nuclear Pore Complexes to Direct Nuclear Envelope Breakdown in C. elegans. Dev Cell 43, 157-171.e7.
  • Thomas, Y., Cirillo, L., Panbianco, C., Martino, L., Tavernier, N., Schwager, F., Van Hove, L., Joly, N., Santamaria, A., Pintard, L., and Gotta, M. (2016). Cdk1 Phosphorylates SPAT-1/Bora to Promote Plk1 Activation in C. elegans and Human Cells. Cell Rep 15, 510-518.
  • Cirillo, L., Thomas, Y., Pintard, L., and Gotta, M. (2016). BORA-dependent PLK1 regulation: A new weapon for cancer therapy. Mol Cell Oncol 3, e1199265.
  • Parrilla, A., Cirillo, L., Thomas, Y., Gotta, M., Pintard, L., and Santamaria, A. (2016). Mitotic entry: The interplay between Cdk1, Plk1 and Bora. Cell Cycle 15, 3177-3182.
  • Tavernier, N., Noatynska, A., Panbianco, C., Martino, L., Van Hove, L., Schwager, F., Léger, T., Gotta, M., and Pintard, L. (2015). Cdk1 phosphorylates SPAT-1/Bora to trigger PLK-1 activation and drive mitotic entry in C. elegans embryos. J Cell Biol 208, 661-669.
  • Tavernier, N., Panbianco, C., Gotta, M., and Pintard, L. (2015). Cdk1 plays matchmaker for the Polo-like kinase and its activator SPAT-1/Bora. Cell Cycle 1-5.