Bachok Marine Research Station, Institute of Ocean and Earth Sciences, University of Malaya, Bachok 16310, Kelantan, Malaysia.
Bachok Marine Research Station, Institute of Ocean and Earth Sciences, University of Malaya, Bachok 16310, Kelantan, Malaysia.
Gene. 2019 Aug 30;711:143950. doi: 10.1016/j.gene.2019.143950. Epub 2019 Jun 28.
The marine dinoflagellate Alexandrium minutum is known to produce saxitoxins that cause paralytic shellfish poisoning in human worldwide through consumption of the contaminated shellfish mollusks. Despite numerous studies on the growth physiology and saxitoxin production of this species, the knowledge on the molecular basis of nutrient uptakes in relation to toxin production in this species is limited. In this study, relative expressions of the high-affinity transporter genes of nitrate, ammonium, and phosphate (AmNrt2, AmAmt1 and AmPiPT1) and the assimilation genes, nitrate reductase (AmNas), glutamine synthase (AmGSIII) and carbamoyl phosphate synthase (AmCPSII) from A. minutum were studied in batch clonal culture condition with two nitrogen sources (nitrate: NO or ammonium: NH) under different N:P ratios (high-P: N:P of 14 and 16, and low-P: N:P of 155). The expression of AmAmt1 was suppressed in excess NH-grown condition but was not observed in AmNrt2 and AmNas. Expressions of AmAmt1, AmNrt2, AmNas, AmGSIII, AmCPSII, and AmPiPT1 were high in P-deficient condition, showing that A. minutum is likely to take up nutrients for growth under P-stress condition. Conversely, relative expression of AmCPSII was incongruent with cell growth, but was well correlated with toxin quota, suggesting that the gene might involve in arginine metabolism and related toxin production pathway. The expression of AmGSIII is found coincided with higher toxin production and is believed to involve in mechanism to detoxify the cells from excess ammonium stress. The gene regulation observed in this study has provided better insights into the ecophysiology of A. minutum in relation to its adaptive strategies in unfavorable environments.
海洋甲藻亚历山大藻被认为会产生石房蛤毒素，人类通过食用受污染的贝类而导致麻痹性贝类中毒。尽管已经对该物种的生长生理学和石房蛤毒素的产生进行了大量研究，但对其与毒素产生相关的营养物质吸收的分子基础的了解是有限的。在这项研究中，研究了在两种氮源（硝酸盐：NO 或铵盐：NH）下，不同氮磷比（高磷：N:P 为 14 和 16，低磷：N:P 为 155）的分批克隆培养条件下，亚历山大藻的硝酸盐、铵盐和磷酸盐高亲和力转运体基因（AmNrt2、AmAmt1 和 AmPiPT1）和同化基因（硝酸还原酶（AmNas）、谷氨酰胺合成酶（AmGSIII）和氨基甲酰磷酸合成酶（AmCPSII）的相对表达。在过量 NH 生长条件下，AmAmt1 的表达受到抑制，但在 AmNrt2 和 AmNas 中未观察到。在 P 缺乏条件下，AmAmt1、AmNrt2、AmNas、AmGSIII、AmCPSII 和 AmPiPT1 的表达均较高，表明在 P 胁迫条件下，亚历山大藻可能会吸收营养物质进行生长。相反，AmCPSII 的相对表达与细胞生长不一致，但与毒素配额很好地相关，表明该基因可能涉及精氨酸代谢和相关的毒素产生途径。AmGSIII 的表达与更高的毒素产量一致，据信涉及细胞从过量铵胁迫中解毒的机制。本研究中观察到的基因调控为了解亚历山大藻在不利环境中的生态生理学及其适应策略提供了更好的认识。
