Comparative study for the effects of variable nutrient conditions on the biodegradation of microcystin-LR and concurrent dynamics in microcystin-degrading gene abundance

Comparative study for the effects of variable nutrient conditions on the biodegradation of microcystin-LR and concurrent dynamics in microcystin-degrading gene abundance
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DOI:
10.1016/j.biortech.2011.07.112
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发表时间:
2011-10-01
影响因子:
11.4
通讯作者:
Sugiura, Norio
Sugiura, Norio
中科院分区:
工程技术1区
文献类型:
--
作者:
Li, Jieming;Shimizu, Kazuya;Sugiura, Norio

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研究了在添加和不添加营养盐(硝酸盐、铵、蛋白胨和葡萄糖)的情况下,微囊藻毒素LR(Mcl-LR)在100和1000 mg L(-1)浓度下的生物膜降解能力。除低浓度葡萄糖对MCLR降解无明显影响外,硝酸盐对MCLR降解有促进作用,其它营养物质对MCLR降解有抑制作用。随着相应营养物质浓度的增加,刺激和抑制作用均增强。定量聚合酶链反应(qPCR)表明,增强生物降解抑制相关的功能基因(mlrA)丰度的抑制增加,营养浓度的增加。低硝酸盐浓度下的刺激生物降解可能是由于mlrA基因丰度的更快增加。这些表明,MCLR的降解在很大程度上取决于负责的细菌种群,根据16 S rDNA靶向qPCR,生物膜中的其他细菌的种群影响。然而,抑制mlrA基因丰度暗示,在高硝酸盐浓度下的刺激生物降解可能参与机制无关的MCLRDB人口。(C)2011爱思唯尔有限公司保留所有权利。
Microcystin-LR (MCLR) degradation capability of biofilm was investigated with and without additional nutrients (nitrate, ammonium, peptone and glucose) at concentrations of 100 and 1000 mg L(-1). The MCLR-degradation was stimulated with nitrate and inhibited with other nutrients, except for that glucose of low concentration had no obvious effect. Both stimulatory and inhibitory effects enhanced with increasing concentration of corresponding nutrient. Quantitative polymerase chain reaction (qPCR) indicated that enhanced inhibition in biodegradation correlated to increased inhibition in functional gene (mlrA) abundance, as nutrient concentration increased. Stimulated biodegradation under low nitrate concentration may result from more rapid increase in mlrA gene abundance. These suggested that MCLR-degradation largely depended upon responsible bacterial population, which was affected by population of other bacteria in biofilm according to 16S rDNA-targeting qPCR. However, inhibited mlrA gene abundance implied that the stimulated biodegradation under high nitrate concentration might be involved in the mechanisms not related to MCLRDB population. (C) 2011 Elsevier Ltd. All rights reserved.