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 2ⁿ G₁-cell size and divide n number of times to resume the G₁ 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...[ Read more ]

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 2ⁿ G₁-cell size and divide n number of times to resume the G₁ 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 G₁ phase and resulted in an increase in the frequency of MF. A significant induction of MF could only be observed when elevation of Ca²⁺_i was induced at late G₁ phase. Positive correlations between cell growth, elevation of Ca²⁺_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-Ca²⁺ pathway may provide a link between cellular metabolism and cell cycle progression.