Nilsson Group – University of Copenhagen

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Mitotic Mechanisms and Regulation 

The Mitotic Mechanisms and Regulation research group is headed by Assoc. Prof. Jakob Nilsson.

First row from the left: Dimitriya Hristoforova Garvanska, Thomas Kruse, Jakob Nilsson, Jamin Hein, Gang Zhang, Emil Peter Thrane Hertz, Maria Sofie Yoo Larsen, Amanda Gammelby Qvesel

The Mitotic Mechanisms and Regulation research group is headed by Assoc. Prof. Jakob Nilsson.

The main focus of the group is to obtain a mechanistic understanding of how key mitotic transitions are regulated to ensure genomic integrity.

Mitosis and segregation of chromosomes:

It is absolutely essential that the duplicated genetic material in the form of chromosomes is segregated equally to the two new daughter cells. Failure in chromosome segregation results in aneuploidy, which is a hallmark of cancer cells and correlates with poor patient prognosis.

Chromosome segregation is achieved by the binding of microtubules of the mitotic spindle to structures on the chromosomes referred to as the kinetochores. It is important that all kinetochores become attached to microtubules before the cell segregates the sister chromatids. The attachment of kinetochores to microtubules is monitored by the Spindle Assembly Checkpoint (SAC) that delays mitotic progression until all kinetochores becomes attached. The SAC acts by inhibiting the large E3 ubiquitin ligase the Anaphase Promoting Complex (APC/C), which prevents the degradation of proteins required for chromosome segregation and mitotic exit. Upon satisfaction of the SAC the APC/C becomes active and in concert with protein phosphatases it coordinates mitotic exit and the generation of the two new daughter cells.

Illustration of how mitosis is regulated by the interplay between the SAC and the APC/C

Our focus areas

We focus on three complementary questions in the group:

  • How does the kinetochore orchestrate SAC signaling?
  • How is the APC/C regulated during the cell cycle?
  • How do protein phosphatases coordinate mitotic events and recognize their substrates?

To understand these questions we employ video microscopy of living cells combined with fluorescent markers, quantitative mass spectrometry and biochemical approaches to reconstitute some of the reactions in vitro. This is achieved through collaboration with other research groups at the center.

For more information:

Visit www.madlab.dk and turn to our recent review:

Lischetti T & Nilsson J (2015), Regulation of Mitotic Progression by the Spindle Assembly Checkpoint Recent publications:

Hein JB & Nilsson J (2016) Interphase APC/C-Cdc20 inhibition by cyclin A2-Cdk2 ensures efficient mitotic entry, Nature Communications 7: 10975

Wild T, Larsen MS, Narita T, Schou J, Nilsson J, Choudhary C, (2016) The Spindle Assembly Checkpoint is not essential for viability of human cells with genetically lowered APC/C activity, Cell Reports 14: 1829-40

Zhang G, Lischetti T, Hayward DG, Nilsson J (2015) Distinct domains in Bub1 localize RZZ and BubR1 to kinetochores to regulate the checkpoint. Nature Communications 6: 7162

Lischetti T, Zhang G, Sedgwick GG, Bolanos-Garcia V, Nilsson J (2014), The internal Cdc20 binding site in BubR1 facilitates both spindle assembly checkpoint signaling and silencing, Nature Communications, 5: 5563


Kruse T, Larsen MS, Sedgwick GG, Sigurdsson JO, Streicher W, Olsen JV, Nilsson J (2014), A direct role of Mad1 in the spindle assembly checkpoint beyond kinetochore recruitment of Mad2, EMBO reports 15: 282-90


Hein JB & Nilsson J (2014), Stable MCC binding to the APC/C is required for a functional spindle assembly checkpoint, EMBO reports 15: 264-72


Zhang G, Lischetti T, Nilsson J (2014), A minimal number of MELT repeats supports all the functions of KNL1 in chromosome segregation, J.Cell. Science 127(4) 871-884