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SADB phosphorylation of gamma-tubulin regulates centrosome duplication.

Alvarado-Kristensson, Maria LU ; Rodríguez, María Josefa; Silió, Virginia; Valpuesta, José M and Carrera, Ana C (2009) In Nature Cell Biology 11(9). p.86-1081
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... (More)
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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Nature Cell Biology
volume
11
issue
9
pages
86 - 1081
publisher
Nature Publishing Group
external identifiers
  • WOS:000269482500009
  • PMID:19648910
  • Scopus:69949187550
ISSN
1465-7392
DOI
10.1038/ncb1921
language
English
LU publication?
yes
id
3fb8e0e2-7f9d-4c61-9f3d-2c73e84a3875 (old id 1470148)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/19648910?dopt=Abstract
date added to LUP
2009-09-04 11:17:41
date last changed
2016-12-04 04:38:47
@misc{3fb8e0e2-7f9d-4c61-9f3d-2c73e84a3875,
  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.},
  author       = {Alvarado-Kristensson, Maria and Rodríguez, María Josefa and Silió, Virginia and Valpuesta, José M and Carrera, Ana C},
  issn         = {1465-7392},
  language     = {eng},
  number       = {9},
  pages        = {86--1081},
  publisher    = {ARRAY(0x8a1ede0)},
  series       = {Nature Cell Biology},
  title        = {SADB phosphorylation of gamma-tubulin regulates centrosome duplication.},
  url          = {http://dx.doi.org/10.1038/ncb1921},
  volume       = {11},
  year         = {2009},
}