Abstract
THERE is currently much interest in the mechanism which controls the timing of cell division. Certain features of the control have been found to be common to a variety of eukaryotes. In particular, the importance of cell size as a parameter affecting cell cycle progress has been reported for mammalian cells1,2 and for several single-celled eukaryotes3–6. Another feature common to several systems is that growth conditions have a direct effect on the timing of division cycle events7–9, and on cell size9,10. In the fission yeast Schizosaccharomyces pombe, both cell size6 and nutritional conditions9 have been shown to affect cycle kinetics. The organism has been used extensively as a model eukaryotic system, largely because of the ease of measuring cell size and because division occurs by binary fission11. More recently, its genetic tractability has led to the isolation of cell division cycle (cdc) mutants12, and also of wee mutants altered in the control coordinating growth with the division cycle13–15. The existence of such control mutants allows a more direct approach to the investigation of the molecular basis of division control, in contrast to the indirect methods used in other systems4,16–18. wee mutants are so far unique to S. pombe. The most conspicuous property of wee mutants is their reduced cell size13,14. Analysis of these mutants15,19 and other evidence9 has shown that control over cell division timing normally acts at entry to mitosis. As the function of a number of cdc genes is specifically required for mitosis12, interactions between wee and cdc mutants which affect mitosis might be expected. I report here that the mitotic defect caused by a defective cdc25 allele is suppressed in wee mutants. Suppression by wee1 mutants is almost complete, while the wee2.1 mutation is a less effective suppressor. The significance of these findings for genetic models of the control of mitosis is considered.
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FANTES, P. Epistatic gene interactions in the control of division in fission yeast. Nature 279, 428–430 (1979). https://doi.org/10.1038/279428a0
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DOI: https://doi.org/10.1038/279428a0
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