THESIS
2005
xxiv, 260 leaves : ill. (some col.) ; 30 cm
Abstract
Unicellular organisms are able to adjust their growth and cell cycle in response to nutrient excess and limitation. Coordination between growth and division
is the key for maintaining cell size homeostasis. This study focuses on the study of cell size control in the dinoflagellate Crypthecodinium cohnii, especially on how cell growth is coordinated with multiple fission (MF). Multiple fission cells usually grow
to 2
n G
1-cell size and divide n number of times to resume the G
1 cell size. The underlying mechanisms in which C. cohnii cells decide to undergo MF or not will provide new insights on cell size control. The presence of a commitment point for MF and the requirement of rapid cell growth to MF induction were demonstrated. Richer nutrients and elevation of temperature increased cel...[
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Unicellular organisms are able to adjust their growth and cell cycle in response to nutrient excess and limitation. Coordination between growth and division
is the key for maintaining cell size homeostasis. This study focuses on the study of cell size control in the dinoflagellate Crypthecodinium cohnii, especially on how cell growth is coordinated with multiple fission (MF). Multiple fission cells usually grow
to 2
n G
1-cell size and divide n number of times to resume the G
1 cell size. The underlying mechanisms in which C. cohnii cells decide to undergo MF or not will provide new insights on cell size control. The presence of a commitment point for MF and the requirement of rapid cell growth to MF induction were demonstrated. Richer nutrients and elevation of temperature increased cell growth at early G
1 phase and resulted in an increase in the frequency of MF. A significant induction of MF could only be observed when elevation of Ca
2+i was induced at late G
1 phase.
Positive correlations between cell growth, elevation of Ca
2+i and the induction of MF
were observed. A possible way to couple nutrients availability to cell cycle progression is through the rate of cellular metabolism. We present evidence to
support the cADPR-Ca
2+ pathway may provide a link between cellular metabolism and cell cycle progression.
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