Transcriptomic and physiological analysis of common duckweed Lemna minor responses to NH(4)(+) toxicity

BACKGROUND: Plants can suffer ammonium (NH(4)(+)) toxicity, particularly when NH(4)(+) is supplied as the sole nitrogen source. However, our knowledge about the underlying mechanisms of NH(4)(+) toxicity is still largely unknown. Lemna minor, a model duckweed species, can grow well in high NH(4)(+) environment but to some extent can also suffer toxic effects. The transcriptomic and physiological analysis of L. minor responding to high NH(4)(+) may provide us some interesting and useful information not only in toxic processes, but also in tolerance mechanisms. RESULTS: The L. minor cultured in the Hoagland solution were used as the control (NC), and in two NH(4)(+) concentrations (NH(4)(+) was the sole nitrogen source), 84 mg/L (A84) and 840 mg/L (A840) were used as stress treatments. The NH(4)(+) toxicity could inhibit the growth of L. minor. Reactive oxygen species (ROS) and cell death were studied using stained fronds under toxic levels of NH(4)(+). The malondialdehyde content and the activities of superoxide dismutase and peroxidase increased from NC to A840, rather than catalase and ascorbate peroxidase. A total of 6.62G nucleotides were generated from the three distinct libraries. A total of 14,207 differentially expressed genes (DEGs) among 70,728 unigenes were obtained. All the DEGs could be clustered into 7 profiles. Most DEGs were down-regulated under NH(4)(+) toxicity. The genes required for lignin biosynthesis in phenylpropanoid biosynthesis pathway were up-regulated. ROS oxidative-related genes and programmed cell death (PCD)-related genes were also analyzed and indicated oxidative damage and PCD occurring under NH(4)(+) toxicity. CONCLUSIONS: The first large transcriptome study in L. minor responses to NH(4)(+) toxicity was reported in this work. NH(4)(+) toxicity could induce ROS accumulation that causes oxidative damage and thus induce cell death in L. minor. The antioxidant enzyme system was activated under NH(4)(+) toxicity for ROS scavenging. The phenylpropanoid pathway was stimulated under NH(4)(+) toxicity. The increased lignin biosynthesis might play an important role in NH(4)(+) toxicity resistance. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12870-016-0774-8) contains supplementary material, which is available to authorized users.