Abstract
The Mps1 protein kinase is an intriguing and controversial player in centriole assembly. Originally shown to control duplication of the budding yeast spindle pole body, Mps1 is present in eukaryotes from yeast to humans, the nematode C. elegans being a notable exception, and has also been shown to regulate the spindle checkpoint and an increasing number of cellular functions relating to genomic stability. While its function in the spindle checkpoint appears to be both universally conserved and essential in most organisms, conservation of its originally described function in spindle pole duplication has proven controversial, and it is less clear whether Mps1 is essential for centrosome duplication outside of budding yeast. Recent studies of Mps1 have identified at least two distinct functions for Mps1 in centriole assembly, while simultaneously supporting the notion that Mps1 is dispensable for the process. However, the fact that at least one centrosomal substrate of Mps1 is conserved from yeast to humans down to the phosphorylation site, combined with evidence demonstrating the exquisite control exerted over centrosomal Mps1 levels suggest that the notion of being essential may not be the most important of distinctions.
Highlights
The Mps1 protein kinase is an intriguing and controversial player in centriole assembly
* Correspondence: fisk.13@osu.edu Department of Molecular Genetics, The Ohio State University, 484 W. 12th Avenue, Columbus OH 43210-1292, USA. Worm embryos placed these proteins into an ordered assembly pathway: pro-centriole formation is initiated by the recruitment of SPD-2 to an existing centriole, SPD-2 leads to recruitment of the ZYG-1 protein kinase, which in turn recruits a complex containing SAS-5 and SAS-6 that promotes the formation of a central tube that determines basic centriole structure, followed by SAS-4 that facilitates the assembly of microtubules and mediates pro-centriole elongation [6,7,8,9,10,11]
If Mps1 is dispensable for centrosome duplication in vertebrates, perhaps this is because vertebrates evolved to rely on it for the spindle checkpoint, which presumably becomes increasingly important with increasing genomic complexity, and evolved mechanisms to replace its function in centrosome duplication
Summary
The p53 of the cytoskeleton? Mps is a dual specificity protein kinase conserved from yeast to mammals [48]. Exquisite control over centrosomal Mps levels The G1 to S transition in vertebrate cells marks “the point of no return” in the cell cycle, beyond which the cell is committed to division, and Hogg et al showed a dramatic peak of hMps kinase activity at G1/S with little associated change in total protein levels [64] (Figure 2) This suggests that the function of Mps in centrosome duplication is controlled by a posttranslational mechanism, and the initial mMps study showed that Cdk suppresses the proteasome-mediated degradation of mMps1 [66]. OAZ again acts through the MDS to reduce centrosomal levels and suppress centrosome re-duplication [29,73]
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