Abstract
ABSTRACTFission yeast cells divide at a similar cell length with little variation about the mean. This is thought to be the result of a control mechanism that senses size and corrects for any deviations by advancing or delaying onset of mitosis. Gene deletions that advance cells into mitosis at a smaller size or delay cells entering mitosis have led to the identification of genes potentially involved in this mechanism. However, the molecular basis of this control is still not understood. In this work, we have screened for genes that when deleted increase the variability in size of dividing cells. The strongest candidate identified in this screen was mga2. The mga2 deletion strain shows a greater variation in cell length at division, with a coefficient of variation (CV) of 15–24%, while the wild-type strain has a CV of 5–8%. Furthermore, unlike wild-type cells, the mga2 deletion cells are unable to correct cell size deviations within one cell cycle. We show that the mga2 gene genetically interacts with nem1 and influences the nuclear membrane and the nuclear–cytoplasmic transport of CDK regulators.
Highlights
Steady-state exponentially growing eukaryotic cells tend to divide with a similar size
The cyclin Cdc13 levels remained similar in all three strains. These results suggest that the increased coefficient of variation (CV) of cell size at division of the mga2Δ mutant is not due to a significant defect in the Tyr15 phosphorylation regulation of cyclin-dependent kinases (CDKs)
We investigated the effect of mga2 mutation on the cellular localization of Cdc13, which controls the localization of CDK
Summary
Steady-state exponentially growing eukaryotic cells tend to divide with a similar size. This is thought to come about by a size control mechanism acting over the progression of the cell cycle, which sets cell size at mitosis and the subsequent cell division (Mitchison, 2003). Such a control implies that cells monitor their size and feed this information into the cyclin-dependent kinases (CDKs) that drive the cell cycle. A range of mechanisms have been proposed as to how cell size might be monitored and fed into the CDK mitotic cell cycle control, there is no agreement as to how the molecular mechanisms operate (Martin, 2009; Rhind, 2018; Schmoller and Skotheim, 2015).
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