THESIS
2005
xviii, 223 leaves : ill. (chiefly col.) ; 30 cm
Abstract
Cell walls are not static, they are dynamic and play a central role during plant cell growth and differentiation. Unlike higher plants, cellulosic deposition in alveolar vesicles forms the "internal cell wall' in thecated dinoflagellates. Cell size increase can be interpreted as cell surface increase, and regulation of cell surface area might be important in coordinating cell growth and cell wall synthesis. The possible roles of both cellulose synthesis (CS) and degradation in the dinoflagellate cell cycle,
especially cell cycle control, were investigated. A cell cycle delay in G
1, but not G
2/M was observed following inhibition of CS. A cell cycle inhibitor of G
1/S, but not
G
2/M, was able to delay cell cycle progression with a corresponding reduction of CS.
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Cell walls are not static, they are dynamic and play a central role during plant cell growth and differentiation. Unlike higher plants, cellulosic deposition in alveolar vesicles forms the "internal cell wall' in thecated dinoflagellates. Cell size increase can be interpreted as cell surface increase, and regulation of cell surface area might be important in coordinating cell growth and cell wall synthesis. The possible roles of both cellulose synthesis (CS) and degradation in the dinoflagellate cell cycle,
especially cell cycle control, were investigated. A cell cycle delay in G
1, but not G
2/M was observed following inhibition of CS. A cell cycle inhibitor of G
1/S, but not
G
2/M, was able to delay cell cycle progression with a corresponding reduction of CS.
The increase of cellulose content in the cell cycle corresponded well to the expected increase of surface area. No differences were observed in the cellulose to surface area ratio between normal and fast-growing G
1 cells, implicating the significance of
surface area in linking CS to the coupling of cell growth with cell cycle progression. The coupling of CS to G
1 implicates a novel link between CS and cell cycle control and we postulate that the coupling mechanism might integrate cell wall integrity to the cell size checkpoint.
Inhibition of fatty acid synthesis (FAS) up-regulated CS and resulted in an increase in cellulosic contents, while an inhibition of CS had no effects on FAS. FAS and CS are apparently coupled to the cell cycle via independent pathways. Antibodies raised against a putative dinoflagellate cellulase recognized a cell cortex-localized protein, with associated cellulase activity in immunoprecipitation. Addition of cellulase inhibitors resulted in a cell cycle delay at both early and very late G
2/M, suggesting a role of cellulase activities in modulating the cell cycle progression at G
2/M.
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