Department of Oceanography, Texas A&M University, College Station, TX 77843, USA.
Proc Natl Acad Sci U S A. 2011 Jun 28;108(26):10597-601. doi: 10.1073/pnas.1104247108. Epub 2011 Jun 13.
With the increase in frequency of harmful algal blooms (HABs) worldwide, a better understanding of the mechanisms that influence toxin production is needed. Karenia brevis, the major HAB dinoflagellate in the Gulf of Mexico, produces potent neurotoxins, known as brevetoxins. Human health is directly impacted by blooms of K. brevis through consumption of shellfish contaminated by accumulated brevetoxins (neurotoxic shellfish poisoning) or from aerosolized brevetoxins in sea spray (reduced respiratory function); however, the reason for brevetoxin production has remained a mystery. Here we show that brevetoxin production increased dramatically in response to osmotic stress in three of the four K. brevis clones examined. By rapidly changing salinity to simulate a shift from oceanic conditions to a decreased salinity typical of coastal conditions, brevetoxin production was triggered. As a result, brevetoxin cell quota increased by >14-fold, while growth rate remained unchanged. Live images of K. brevis cells were also examined to assess changes in cell volume. In the K. brevis Wilson clone, cells responded quickly to hypoosmotic stress by increasing their brevetoxin cell quota from ∼10 to 160 pg of brevetoxin per cell, while cell volume remained stable. In contrast, the K. brevis SP1 clone, which has a consistently low brevetoxin cell quota (<1 pg per cell), was unable to balance the hypoosmotic stress, and although brevetoxin production remained low, average cell volume increased. Our findings close a critical gap in knowledge regarding mechanisms for toxin production in K. brevis by providing an explanation for toxin production in this harmful dinoflagellate.
随着世界范围内有害藻华（HAB）的频率增加，需要更好地了解影响毒素产生的机制。墨西哥湾的主要 HAB 甲藻凯伦藻产生强效神经毒素，称为短裸甲藻毒素。人类健康直接受到凯伦藻赤潮的影响，通过食用贝类而受到积累的短裸甲藻毒素（神经毒性贝类中毒）或通过海雾中的气溶胶化短裸甲藻毒素（降低呼吸功能）而受到影响；然而，产生短裸甲藻毒素的原因仍然是个谜。在这里，我们表明，在我们检查的四个凯伦藻克隆中的三个中，短裸甲藻毒素的产生在渗透压胁迫下急剧增加。通过快速改变盐度来模拟从海洋条件到沿海条件下降低的盐度的转变，引发了短裸甲藻毒素的产生。结果，短裸甲藻毒素的细胞配额增加了 14 倍以上，而生长速率保持不变。还检查了凯伦藻细胞的实时图像，以评估细胞体积的变化。在凯伦藻威尔逊克隆中，细胞对低渗透压胁迫的快速反应是通过将其短裸甲藻毒素细胞配额从约 10 增加到 160 pg 短裸甲藻毒素/细胞来实现的，而细胞体积保持稳定。相比之下，凯伦藻 SP1 克隆的短裸甲藻毒素细胞配额一直较低（<1 pg/细胞），无法平衡低渗透压胁迫，尽管短裸甲藻毒素的产生仍然较低，但平均细胞体积增加。我们的研究结果通过为这种有害甲藻的毒素产生提供解释，填补了关于凯伦藻毒素产生机制的知识中的一个关键空白。
