The design of immunoglobulin-like domains from scratch has been a long-standing challenge. We have identified…
The work, a collaboration between the group of Joan Roig at IBMB and that of Isabelle Vernos at CRG, describes how the Nek9 protein kinase controls the initial phases of cell division and has been published in Current Biology. Incorrect cell division is a frequent cause of aneuploidy (alteration in chromosome number) that can in turn can result in abortions, mental retardation or cancer.
Nek9 is activated around the centrosome, a cellular organelle that is crucial for the organization of the mitotic spindle, the molecular machine in charge of separating the chromosomes among the two daughter cells during mitosis, the division of the cell nucleus.
When Nek9 levels are low, centrosome separation in early mitosis is disrupted. The cell has several redundant systems to ensure that the centrosomes separate to form the mitotic spindle, but the results suggest that Nek9 is key for correct separation and interfering with the enzyme frequently results in abnormal cell division.
In the published work, the researchers show that Nek9 controls the kinesin Eg5, a molecular motor in charge of separating the centrosomes, and TPX2, a protein initially identified and studied by Isabelle Vernos that is frequently altered in human cancers. Nek9 regulates TPX2 localization and binding to Eg5, allowing this motor to exert the forces needed to separate centrosomes during early mitosis.
Alterations in centrosome separation can result in abnormal chromosome segregation and aneuploidy and thus result in abortions, mental retardation, cancer and other pathologies. In addition cancer cells frecuently show alterations in centrosome structure and number.
Artículo de referencia:
Nek9 Phosphorylation Defines a New Role for TPX2 in Eg5-Dependent Centrosome Separation before Nuclear Envelope Breakdown. Susana Eibes, Núria Gallisà-Suñé, Miquel Rosas-Salvans, Paula Martínez-Delgado, Isabelle Vernos, Joan Roig. DOI: http://dx.doi.org/10.1016/j.cub.2017.11.046