SADB phosphorylation of gamma-tubulin regulates centrosome duplication.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1470148
- author
- Alvarado-Kristensson, Maria LU ; Rodríguez, María Josefa ; Silió, Virginia ; Valpuesta, José M and Carrera, Ana C
- organization
- publishing date
- 2009
- 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
- 2016-04-04 09:18:35
- date last changed
- 2022-05-01 08:54:26
@article{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 = {{Nature Publishing Group}},
series = {{Nature Cell Biology}},
title = {{SADB phosphorylation of gamma-tubulin regulates centrosome duplication.}},
url = {{http://dx.doi.org/10.1038/ncb1921}},
doi = {{10.1038/ncb1921}},
volume = {{11}},
year = {{2009}},
}