Abstract
A critical aspect of mitosis is the interaction of the kinetochore with spindle microtubules. Fission yeast Mal3 is a member of the EB1 family of microtubule plus-end binding proteins, which have been implicated in this process. However, the Mal3 interaction partner at the kinetochore had not been identified. Here, we show that the mal3 mutant phenotype can be suppressed by the presence of extra Spc7, an essential kinetochore protein associated with the central centromere region. Mal3 and Spc7 interact physically as both proteins can be coimmunoprecipitated. Overexpression of a Spc7 variant severely compromises kinetochore-microtubule interaction, indicating that the Spc7 protein plays a role in this process. Spc7 function seems to be conserved because, Spc105, a Saccharomyces cerevisiae homolog of Spc7, identified by mass spectrometry as a component of the conserved Ndc80 complex, can rescue mal3 mutant strains.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Centromere / chemistry
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Centromere / metabolism
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Chromosomal Proteins, Non-Histone / genetics
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Chromosomal Proteins, Non-Histone / metabolism*
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Gene Expression
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Immunoprecipitation
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Kinetochores / chemistry
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Kinetochores / metabolism*
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Microtubule-Associated Proteins / genetics
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Microtubule-Associated Proteins / metabolism*
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Microtubules / metabolism
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Mitosis
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Mutation / genetics
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Phenotype
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Protein Binding
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Schizosaccharomyces / cytology*
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Schizosaccharomyces / genetics
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Schizosaccharomyces / metabolism*
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Schizosaccharomyces pombe Proteins / genetics
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Schizosaccharomyces pombe Proteins / metabolism*
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Spindle Apparatus / metabolism*
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ran GTP-Binding Protein / genetics
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ran GTP-Binding Protein / metabolism
Substances
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Chromosomal Proteins, Non-Histone
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Mal3 protein, S pombe
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Microtubule-Associated Proteins
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Schizosaccharomyces pombe Proteins
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Spc7 protein, S pombe
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ran GTP-Binding Protein