Abstract

Microtubules play important roles in organelle transport, the maintenance of cell polarity and chromosome segregation and generally form bundles during these processes. The fission yeast gene scp3 + was identified as a multicopy suppressor of the cps3-81 mutant, which is hypersensitive to isopropyl N-3-chlorophenylcarbamate (CIPC), a poison that induces abnormal multipolar spindle formation in higher eukaryotes. In this study, we investigated the function of Scp3 along with the effect of CIPC in the fission yeast Schizosaccharomyces pombe. Microscopic observation revealed that treatment with CIPC, cps3-81 mutation and scp3 + gene deletion disturbed the orientation of microtubules in interphase cells. Overexpression of scp3 + suppressed the abnormal orientation of microtubules by promoting bundling. Functional analysis suggested that Scp3 functions independently from Ase1, a protein largely required for the bundling of the mitotic spindle. A strain lacking the ase1 + gene was more sensitive to CIPC, with the drug affecting the integrity of the mitotic spindle, indicating that CIPC has a mitotic target that has a role redundant with Ase1. These results suggested that multiple systems are independently involved to ensure microtubule orientation by bundling in fission yeast.

Highlights

  • Microtubules are polymers formed by the association of α- and β-tubulin dimers, and they have different roles in each phase of the cell cycle [1,2,3,4]

  • We further showed that Scp3 and Ase1 function independently in the maintenance of microtubule bundling in interphase and that Ase1, but not Scp3, plays an important role in mitotic spindle organization

  • It was previously reported that isopropyl N-3-chlorophenylcarbamate (CIPC) induces abnormal multipolar spindle formation in higher eukaryotes [31]

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Summary

Introduction

Microtubules are polymers formed by the association of α- and β-tubulin dimers, and they have different roles in each phase of the cell cycle [1,2,3,4]. The cps3–81 mutant, which is hypersensitive to CIPC, and a strain lacking the scp3+ gene, a multicopy suppressor of the cps3–81 mutant, exhibited abnormal microtubule morphology indicative of the loss of bundling.

Results
Conclusion
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