Université de Strasbourg

Manuel Mendoza


Institute of Genetics and Molecular and Cellular Biology (IGBMC), University of Strasbourg, CNRS and Inserm

Manuel Mendoza, USIAS Fellow 2019

Manuel Mendoza obtained a master's degree in biological sciences in the University of Rome Tor Vergata, Italy in 1997 and a PhD in biochemistry in 2002 from the University of Vienna, Austria. His doctoral work was carried out in the laboratory of Dr. Michael Glotzer at the Research Institute of Molecular Pathology on the mechanism of cytokinesis. From 2002 to 2008, he worked in the polarity of fission yeast in the European Molecular Biology Laboratory (EMBL), Heidelberg, Germany with Dr. Damian Brunner, and in cell division in budding yeast at the Swiss Federal Institute of Technology (ETH Zurich) with Professor Yves Barral. Dr. Mendoza established his laboratory at the Centre for Genomic Regulation (CRG) in Barcelona, Spain in 2008, working on chromosome segregation and cytokinesis using budding yeast and human cultured cells as model systems. Dr. Mendoza was awarded a Starting Grant from the European Research Council in 2011. Since 2017, he is an investigator at the French National Institute of Health and Medical Research (Inserm) and Group Leader at the Institute of Genetics and Molecular and Cellular Biology (IGBMC) in Illkirch, Strasbourg.

Manuel Mendoza’s main research findings include the discovery and characterisation of the NoCut abscission checkpoint, a signalling pathway that coordinates cytokinesis with the completion of chromosome segregation to maintain genomic stability. Furthermore, the Mendoza laboratory discovered that cell-specific nuclear pore acetylation regulates cell cycle progression and nuclear organization during asymmetric divisions in budding yeast. Current research in the Mendoza group aims to understand fundamental mechanisms of nuclear and cellular division.

Project - The role of nuclear pore complex acetylation in differentiation of stem cells

01/10/2019 - 31/03/2022

Nuclear pores are large protein complexes that form channels in the envelope that separates the nucleus (which contains genetic information) from the rest of the cell. Nuclear pores therefore act like small doors that allow movement of molecules in and out the nucleus. They can also interact with genes inside the nucleus to regulate their activation. Nuclear pores were thought to have similar properties in all the cells in our bodies, but reality may be different. Indeed, recent work in budding yeast cells revealed that distinct types of nuclear pores are present in different cell types.

Budding yeast is a unicellular organism that divides asymmetrically to generate a large mother and a smaller daughter cell. Studies in yeast have revealed fundamental principles of cell division that are also found in human cells. The Mendoza laboratory identified a protein that specifically associates with the nuclear pores of yeast daughter cells, and removes a chemical modification on these pores, called acetylation. Differences in nuclear pore acetylation between mother and daughter cells cause differences in the transport of molecules into the nucleus, and in the interaction of genes with nuclear pores, which ultimately lead to different cell division times in mothers and daughters.

Acetylation of nuclear pores has been previously observed in human cells, but the function of this modification is unknown. Thus, results from the Mendoza lab opened the possibility that nuclear pore deacetylation may be a mechanism to regulate the functions of nuclear pores and the determination of cell fate also in human cells that divide asymmetrically, such as stem cells. USIAS will support studies in this direction in the Mendoza lab, using mouse embryonic stem cells to investigate the potential roles of nuclear pore acetylation in their differentiation into different cell types. These studies may reveal novel principles of how human stem cells and tissues are maintained, and of pathologies associated with defects in these processes, such as developmental disorders and cancer.

Post-doc biography - Faezeh Forouzanfar

Institute of Genetics and Molecular and Cellular Biology (IGBMC), University of Strasbourg, CNRS & Inserm

Faezeh ForouzanfarFaezeh Forouzanfar obtained her PhD in cell and molecular biology from the University of Strasbourg in 2016, under the supervision of Professor Olivier Rohr. Her work focused on the molecular control of HIV-1 latency and the interactions between viral and host factors that control viral reactivation.

In 2017, Dr. Forouzanfar moved to the laboratory of Professor T. Dianne Langford at Temple University’s Lewis Katz School of Medicine, Department of Neuroscience and Neurovirology (Philadelphia, USA), to work on the mechanism of Tau-mediated neurodegeneration as a postdoctoral fellow. In 2018, she joined the team of Dr. Marcel Méchali at the Institute of Human Genetics (IGH) of the University of Montpellier/French National Centre for Scientific Research (CNRS), where she investigated the role of the Polycomb complex in the control of DNA replication. Since January 2020, she works as a post-doc researcher in Dr. Manuel Mendoza’s laboratory at the Institute of Genetics and Molecular and Cellular Biology (IGBMC). She investigates the role of nuclear pore complex acetylation during differentiation in mouse stem cells.


  • Article in Nature Cell Biology: Kumar A, Sharma P, Gomar-Alba M, Shcheprova Z, Daulny A, Sanmartin T, Matucci I, Funaya C, Beato M, Mendoza M (2018). Daughter-cell-specific modulation of nuclear pore complexes controls cell cycle entry during asymmetric division. Nature Cell Biology 20, 432-442 (First version posted to bioRxiv)

  • Article in Nature Cell Biology: Amaral, A., Vendrell, A., Funaya, C … and Mendoza, M. (2016). The Aurora B dependent NoCut checkpoint prevents damage of anaphase bridges after DNA replication stress. Nature Cell Biology, 18, 516-526

  • Article in Science: Neurohr, G., Naegeli, A., Titos, I. …Mendoza, M.* and Barral, Y.* (2011). A midzone-based ruler adjusts chromosome compaction to anaphase spindle length. Science, 332, 465-468 (*, co-corresponding authors)

  • Article in Cell: Norden, C.*, Mendoza, M.*, Dobbelaere, J., Kotwaliwale, C.V., Biggins, S., and Barral, Y. (2006). The NoCut pathway links completion of cytokinesis to spindle midzone function to prevent chromosome breakage. Cell 125, 85-98 (*, co-first authors)

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