SADB phosphorylation of gamma-tubulin regulates centrosome duplication.

Maria Alvarado-Kristensson, María Josefa Rodríguez, Virginia Silió, José M Valpuesta, Ana C Carrera

Research output: Contribution to journalArticlepeer-review

61 Citations (SciVal)

Abstract

Symmetrical cell division requires duplication of DNA and protein content to generate two daughter cells. Centrosomes also duplicate during cell division, but the mechanism controlling this process is incompletely understood. We describe an alternative splice form of SadB encoding a short SADB Ser/Thr kinase whose activity fluctuates during the cell cycle, localizes to centrosomes, and controls centrosome duplication. Reduction of endogenous SADB levels diminished centrosome numbers, whereas enhanced SADB expression induced centrosome amplification. SADB exerted this action through phosphorylation of gamma-tubulin on Ser 131, as expression of a phosphomimetic Ser 131-to-Asp gamma-tubulin mutant alone increased centrosome numbers, whereas non-phosphorylatable Ala 131-gamma-tubulin impaired centrosome duplication. We propose that SADB kinase activity controls centrosome homeostasis by regulating phosphorylation of gamma-tubulin.
Original languageEnglish
Pages (from-to)1081-U86
JournalNature Cell Biology
Volume11
Issue number9
DOIs
Publication statusPublished - 2009

Subject classification (UKÄ)

  • Cancer and Oncology

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