DYNAMICS AND PHYSIOLOGY OF SAXITOXIN PRODUCTION BY THE DINOFLAGELLATES ALEXANDRIUM SPP
DYNAMICS AND PHYSIOLOGY OF SAXITOXIN PRODUCTION BY THE DINOFLAGELLATES ALEXANDRIUM SPP
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DOI：
10.1007/bf01314358
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发表时间：
1990-01-01
期刊：
影响因子：
2.4
通讯作者：
LEE, C
中科院分区：
文献类型：
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作者：
ANDERSON, DM;KULIS, DM;LEE, C
对分批培养的亚历山大藻、塔玛亚历山大藻和亚历山大藻的毒素含量(fmolcell-1)和一系列元素和大分子变量进行了测定。来自美国新英格兰南部地区。半连续培养提供了一个不同的视角，它揭示了细胞对N和P限制的持续、稳定的生理适应。研究了两种类型的变异性。在分批培养中，养分有效性随时间的变化导致了毒素含量在生长阶段的变化，通常在指数生长中期达到顶峰。第二种类型的变异性可以叠加在生长阶段的差异上，最好的例证是在次优温度下生长的细胞含量很高。对这些不同培养处理和模式的净产毒率(Rtox；fmolcell-1d-1)的计算使得将毒素产生的动力学与细胞分裂分开是可能的。在广泛的生长速度范围内，细胞产生毒素的速度接近于在分裂过程中弥补子细胞“损失”所需的速度。这种直接比例的例外是磷限制，这与毒素产生率的急剧增加有关，因为在批培养中，由于营养限制，细胞停止分裂。因此，分批培养的生长阶段变异性反映了毒素产生和细胞分裂的特定速率之间的微小不平衡(通常在两倍之内)。氮限制和二氧化碳耗竭都会在细胞分裂所需的毒素合成途径之前影响到参与合成的途径；而限制磷的剂量则相反。毒素的积累模式与主要细胞代谢物或元素池相同。毒素产量最高的原因似乎是细胞内精氨酸(Arg)的可用性增加，这要么是因为参与细胞分裂的途径缺乏对这种氨基酸的竞争，要么是因为从头合成的增加。无论是在高盐度下驯化生长，还是在盐度短期升高或降低的情况下，毒素含量都没有显著变化。这些结果表明，毒素的产生是一个复杂的过程，在某些条件下，与生长速度密切耦合，在另一些条件下，这些过程是完全解耦的。对观察到的差异的解释可能与重要代谢物的池大小以及关键生化反应对这些池大小和环境条件的不同反应有关。
Toxin content (fmol cell-1) and a suite of elemental and macromolecular variables were measured in batch cultures of the dinoflagellates Alexandrium fundyense, A. tamarense and Alexandrium sp. from the southern New England region, USA. A different perspective was provided by semicontinuous cultures which revealed sustained, steady-state physiological adaptations by cells to N and P limitation. Two types of variability were investigated. In batch cultures, changes in nutrient availability with time caused growth stage variability in toxin content, which often peaked in mid-exponential growth. A second type of variability that could be superimposed on growth stage differences is best exemplified by the high content of cells grown at suboptimal temperatures. Calculations of the net rate of toxin production (Rtox; fmol cell-1 d-1) for these different culture treatments and modes made it possible to separate the dynamics of toxin production from cell division. Over a wide range of growth rates, cells produced toxin at rates approximating those needed to replace "losses" to daughter cells during division. The exception to this direct proportionality was with P limitation, which was associated with a dramatic increase in the rate of toxin production as cells stopped dividing due to nutrient limitation in batch culture. Growth stage variability in batch culture thus reflects small imbalances (generally within a factor of two) between the specific rates of toxin production and cell division. N limitation and CO2 depletion both affect pathways involved in toxin synthesis before those needed for cell division; P limitation doses the opposite. The pattern of toxin accumulation were the same as for major cellular metabolites or elemental pools. The highest rates of toxin production appear to result from in increased availability of arginine (Arg) within the cell, due to either a lack of competition for this amino acid from pathways involved in cell division or to increased de novo synthesis. There were no significant changes in toxin content with either acclimated growth at elevated salinity, or with short term increases or decreases of salinity. These results demonstrate that toxin production is a complex process which, under some conditions, is closely coupled to growth rate; under other conditions, these processes are completely uncoupled. Explanations for the observed variability probably relate to pool sizes of important metabolites and to the differential response of key biochemical reactions to these pool sizes and to environmental conditions.