Fission 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.

裂殖酵母细胞分裂的细胞长度相似，平均值变化很小。这被认为是控制机制的结果，该机制可以感知大小并通过提前或延迟有丝分裂的开始来纠正任何偏差。使细胞进入更小尺寸的有丝分裂或延迟细胞进入有丝分裂的基因缺失导致了可能参与该机制的基因的鉴定。然而，这种控制的分子基础仍不清楚。在这项工作中，我们筛选了一些基因，这些基因被删除后会增加分裂细胞大小的变异性。在此筛选中确定的最强候选者是mga2 。 mga2缺失菌株在分裂时细胞长度变化较大，变异系数 (CV) 为 15-24%，而野生型菌株的 CV 为 5-8%。此外，与野生型细胞不同， mga2缺失细胞无法在一个细胞周期内纠正细胞大小偏差。我们发现mga2基因与nem1存在遗传相互作用，并影响 CDK 调节因子的核膜和核质转运。