Your browser doesn't support javascript.
loading
Spindle rotation in human cells is reliant on a MARK2-mediated equatorial spindle-centering mechanism.
Zulkipli, Ihsan; Clark, Joanna; Hart, Madeleine; Shrestha, Roshan L; Gul, Parveen; Dang, David; Kasichiwin, Tami; Kujawiak, Izabela; Sastry, Nishanth; Draviam, Viji M.
Afiliación
  • Zulkipli I; Department of Genetics, University of Cambridge, Cambridge, England, UK.
  • Clark J; Department of Genetics, University of Cambridge, Cambridge, England, UK.
  • Hart M; School of Biological and Chemical Sciences, Queen Mary University of London, London, England, UK.
  • Shrestha RL; Department of Genetics, University of Cambridge, Cambridge, England, UK.
  • Gul P; School of Biological and Chemical Sciences, Queen Mary University of London, London, England, UK.
  • Dang D; School of Biological and Chemical Sciences, Queen Mary University of London, London, England, UK.
  • Kasichiwin T; Department of Informatics, King's College, London, England, UK.
  • Kujawiak I; School of Biological and Chemical Sciences, Queen Mary University of London, London, England, UK.
  • Sastry N; Department of Genetics, University of Cambridge, Cambridge, England, UK.
  • Draviam VM; Department of Informatics, King's College, London, England, UK.
J Cell Biol ; 217(9): 3057-3070, 2018 09 03.
Article en En | MEDLINE | ID: mdl-29941476
The plane of cell division is defined by the final position of the mitotic spindle. The spindle is pulled and rotated to the correct position by cortical dynein. However, it is unclear how the spindle's rotational center is maintained and what the consequences of an equatorially off centered spindle are in human cells. We analyzed spindle movements in 100s of cells exposed to protein depletions or drug treatments and uncovered a novel role for MARK2 in maintaining the spindle at the cell's geometric center. Following MARK2 depletion, spindles glide along the cell cortex, leading to a failure in identifying the correct division plane. Surprisingly, spindle off centering in MARK2-depleted cells is not caused by excessive pull by dynein. We show that MARK2 modulates mitotic microtubule growth and length and that codepleting mitotic centromere-associated protein (MCAK), a microtubule destabilizer, rescues spindle off centering in MARK2-depleted cells. Thus, we provide the first insight into a spindle-centering mechanism needed for proper spindle rotation and, in turn, the correct division plane in human cells.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Proteínas Serina-Treonina Quinasas / Mitosis / Huso Acromático Límite: Humans Idioma: En Revista: J Cell Biol Año: 2018 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Proteínas Serina-Treonina Quinasas / Mitosis / Huso Acromático Límite: Humans Idioma: En Revista: J Cell Biol Año: 2018 Tipo del documento: Article Pais de publicación: Estados Unidos