Abstract
Mean cell size at division is generally constant for specific conditions and cell types, but the mechanisms coupling cell growth and cell cycle control with cell size regulation are poorly understood in intact tissues. Here we show that the continuously dividing fields of cells within the shoot apical meristem of Arabidopsis show dynamic regulation of mean cell size dependent on developmental stage, genotype and environmental signals. We show cell size at division and cell cycle length is effectively predicted using a two-stage cell cycle model linking cell growth and two sequential cyclin dependent kinase (CDK) activities, and experimental results concur in showing that progression through both G1/S and G2/M is size dependent. This work shows that cell-autonomous co-ordination of cell growth and cell division previously observed in unicellular organisms also exists in intact plant tissues, and that cell size may be an emergent rather than directly determined property of cells.
Highlights
Mean cell size at division is generally constant for specific conditions and cell types, but the mechanisms coupling cell growth and cell cycle control with cell size regulation are poorly understood in intact tissues
Since it has been demonstrated that non-linearly growing cells must have cell size control to prevent differences in size from being amplified over generations[1], we agree with previous studies[35] in concluding that a cell size control mechanism must be operating in the shoot apical meristem (SAM)
Since loss of either G1/S regulation or G2/M regulation both resulted in increased cell size, our results indicate that both transitions may be important in regulating cell size in plants
Summary
Mean cell size at division is generally constant for specific conditions and cell types, but the mechanisms coupling cell growth and cell cycle control with cell size regulation are poorly understood in intact tissues. Size-dependent production of the positive G1/S regulator cyclin Cln[3] has been proposed as such a size-control mechanism[21], but more recently dilution of the negative cell cycle regulator Whi[5] through cell growth has been suggested as a more likely mechanism[19] In both fission yeast[12,13] and budding yeast[14], the critical size for division is set according to nutrient availability via the conserved TOR signaling pathway which feeds into the activity of key cell cycle regulators. Studies using mammalian cell cultures have produced conflicting results[25,26,27,28,29,30], but recent technical advances suggest that cell growth is not linear[28,29,30] and active control of cell size is required, the mechanism is not yet clear
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