The Mitotic Arrest in Response to Hypoxia and of Polar Bodies during Early Embryogenesis Requires Drosophila Mps1

• Published in: Current biology Vol. 14; no. 22; pp. 2019 - 2024
• Main Authors: Fischer, Matthias G., Heeger, Sebastian, Häcker, Udo, Lehner, Christian F.
• Format: Journal Article
• Language: English
• Published: England Elsevier Inc 23.11.2004
• Subjects: Animals; Biologi; Biological Sciences; Cell Cycle - physiology; Cyclin B - metabolism; Developmental Biology; DNA Primers; Drosophila; Drosophila - embryology; Drosophila - metabolism; Drosophila Proteins; Fluorescent Antibody Technique; Gene Components; Mitosis - physiology; Mutation; Natural Sciences; Naturvetenskap; Oxygen - metabolism; Protein-Serine-Threonine Kinases - genetics; Protein-Serine-Threonine Kinases - metabolism; Protein-Serine-Threonine Kinases - physiology; Reverse Transcriptase Polymerase Chain Reaction; Spindle Apparatus - metabolism; Utvecklingsbiologi
• ISSN: 0960-9822; 1879-0445; 1879-0445
• DOI: 10.1016/j.cub.2004.11.008

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.