Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

The mitotic arrest in response to hypoxia and of polar bodies during early embryogenesis requires Drosophila Mps1

Fischer, MG ; Heeger, S ; Häcker, Udo LU and Lehner, CF (2004) In Current Biology 14(22). p.2019-2024
Abstract
Mps1 kinase plays an evolutionary conserved role in the mitotic spindle checkpoint [1-8]. This system precludes anaphase onset until all chromosomes have successfully attached to spindle microtubules via their kinetochores [9]. Mps1 overexpression in budding yeast is sufficient to trigger a mitotic arrest, which is dependent on the other mitotic. checkpoint components, Bub1, Bub3, Mad1, Mad2, and Mad3 [3]. Therefore, Mps1 might act at the top of the mitotic checkpoint cascade. Moreover, in contrast to the other mitotic checkpoint components, Mps1 is essential for spindle pole body duplication in budding yeast [10]. Centrosome duplication in mammalian cells might also be controlled by Mps1 [6,11], but the fission yeast homolog is not... (More)
Mps1 kinase plays an evolutionary conserved role in the mitotic spindle checkpoint [1-8]. This system precludes anaphase onset until all chromosomes have successfully attached to spindle microtubules via their kinetochores [9]. Mps1 overexpression in budding yeast is sufficient to trigger a mitotic arrest, which is dependent on the other mitotic. checkpoint components, Bub1, Bub3, Mad1, Mad2, and Mad3 [3]. Therefore, Mps1 might act at the top of the mitotic checkpoint cascade. Moreover, in contrast to the other mitotic checkpoint components, Mps1 is essential for spindle pole body duplication in budding yeast [10]. Centrosome duplication in mammalian cells might also be controlled by Mps1 [6,11], but the fission yeast homolog is not required for spindle pole body duplication [4]. Our phenotypic characterizations of Mps1 mutant embryos in Drosophila do not reveal an involvement in centrosome duplication, while the mitotic spindle checkpoint is defective in these mutants. In addition, our analyses reveal novel functions. We demonstrate that Mps1 is also required for the arrest of cell cycle progression in response to hypoxia. Finally, we show that Mps1 and the mitotic spindle checkpoint are responsible for the developmental cell cycle arrest of the three haploid products of female meiosis that are not used as the female pronucleus. (Less)
Please use this url to cite or link to this publication:
author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Current Biology
volume
14
issue
22
pages
2019 - 2024
publisher
Elsevier
external identifiers
  • wos:000225352800022
  • pmid:15556864
  • scopus:9244221681
ISSN
1879-0445
DOI
10.1016/j.cub.2004.11.008
language
English
LU publication?
yes
id
e7b39ea1-d3ec-482e-a3a0-c57e1bd67a33 (old id 260336)
date added to LUP
2016-04-01 11:40:25
date last changed
2022-01-26 08:33:44
@article{e7b39ea1-d3ec-482e-a3a0-c57e1bd67a33,
  abstract     = {{Mps1 kinase plays an evolutionary conserved role in the mitotic spindle checkpoint [1-8]. This system precludes anaphase onset until all chromosomes have successfully attached to spindle microtubules via their kinetochores [9]. Mps1 overexpression in budding yeast is sufficient to trigger a mitotic arrest, which is dependent on the other mitotic. checkpoint components, Bub1, Bub3, Mad1, Mad2, and Mad3 [3]. Therefore, Mps1 might act at the top of the mitotic checkpoint cascade. Moreover, in contrast to the other mitotic checkpoint components, Mps1 is essential for spindle pole body duplication in budding yeast [10]. Centrosome duplication in mammalian cells might also be controlled by Mps1 [6,11], but the fission yeast homolog is not required for spindle pole body duplication [4]. Our phenotypic characterizations of Mps1 mutant embryos in Drosophila do not reveal an involvement in centrosome duplication, while the mitotic spindle checkpoint is defective in these mutants. In addition, our analyses reveal novel functions. We demonstrate that Mps1 is also required for the arrest of cell cycle progression in response to hypoxia. Finally, we show that Mps1 and the mitotic spindle checkpoint are responsible for the developmental cell cycle arrest of the three haploid products of female meiosis that are not used as the female pronucleus.}},
  author       = {{Fischer, MG and Heeger, S and Häcker, Udo and Lehner, CF}},
  issn         = {{1879-0445}},
  language     = {{eng}},
  number       = {{22}},
  pages        = {{2019--2024}},
  publisher    = {{Elsevier}},
  series       = {{Current Biology}},
  title        = {{The mitotic arrest in response to hypoxia and of polar bodies during early embryogenesis requires Drosophila Mps1}},
  url          = {{http://dx.doi.org/10.1016/j.cub.2004.11.008}},
  doi          = {{10.1016/j.cub.2004.11.008}},
  volume       = {{14}},
  year         = {{2004}},
}