Human RASSF7 regulates the microtubule cytoskeleton and is required for spindle formation, Aurora B activation and chromosomal congression during mitosis

Asha Recino, Victoria Sherwood, Amy Flaxman, Wendy N. Cooper, Farida Latif, Andrew Ward, Andrew D. Chalmers (Lead / Corresponding author)

    Research output: Contribution to journalArticlepeer-review

    21 Citations (Scopus)

    Abstract

    RASSF7, a member of the N-terminal Ras association domain family, has increased expression in various cancers and, on the basis of our previous work in Xenopus embryos, may be a regulator of mitosis. In the present study, we address, for the first time, the role of human RASSF7 in mitosis. We demonstrate that RASSF7 is expressed in a broad range of different cell types and that this expression could be enhanced following exposure to hypoxia. Knocking down RASSF7 in human cell lines inhibited cell growth and induced defects in mitosis, including aberrant spindle formation and a failure in chromosomal congression. In order to understand the molecular basis of the defects in more detail, we analysed the activity of mitotic signalling proteins and found that activation of Aurora B did not occur in cells in which RASSF7 was knocked down. We also show that endogenous RASSF7 protein localizes to the centrosome and demonstrate using microtubule-regrowth assays that RASSF7 is an important regulator of microtubule dynamics. On the basis of these observations, we propose that, owing to its key role in regulating the microtubule cytoskeleton, RASSF7 is required for mitosis in human cells.

    Original languageEnglish
    Pages (from-to)207-213
    Number of pages7
    JournalBiochemical Journal
    Volume430
    Issue number2
    DOIs
    Publication statusPublished - 1 Sep 2010

    Keywords

    • Animals
    • Aurora kinase B
    • Aurora kinases
    • Cell line
    • Centrosome
    • Chromosome segregation
    • HeLa cells
    • Humans
    • Mice
    • Microtubules
    • Mitosis
    • Protein transport
    • Protein-Serine-Threonine Kinases
    • Spindle apparatus
    • Transcription factors

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