Subcellular cadmium distribution and antioxidant enzymatic activities in the leaves of four Hylotelephium spectabile populations exhibit differences in phytoextraction potential

Hylotelephium spectabile with high tolerance to cadmium (Cd) might be a potential candidate for phytoremediation. However, the mechanisms for Cd accumulation and tolerance in H. spectabile are poorly understood. Four H. spectabile populations, namely HB1, HB2, JS, and LN, were selected to investigate their Cd extraction potential and the underlying mechanism of Cd accumulation, focusing on subcellular distribution and antioxidant enzymes. The Cd concentration, bioconcentration factor and transfer factor of the LN was significantly higher than other populations, particularly with increasing Cd exposure, and no obvious growth inhibition observed. Segregation of excessive Cd to Cd-rich granule in LN was much higher than other populations which reveal one possible mechanism of Cd accumulation. A significant increase in superoxide dismutase (SOD) and catalase (CAT) activities with increasing Cd stress suggested SOD and CAT contribute to the Cd tolerance of H. spectabile. LN displayed significantly higher and constant peroxidase (POD) activities than other populations, which indicated that an effective mechanism existed in the LN to cope with Cd stress. Therefore, the subcellular distribution and antioxidant enzymes might play important roles in Cd accumulation and tolerance of H. spectabile. LN possessed high Cd extraction potential, and further studies under field conditions are warranted.     

ACOT12-Dependent Alteration of Acetyl-CoA Drives Hepatocellular Carcinoma Metastasis by Epigenetic Induction of Epithelial-Mesenchymal Transition

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Down-regulated expression of LINC00518 prevents epithelial cell growth and metastasis in breast cancer through the inhibition of CDX2 methylation and the Wnt signaling pathway

Breast cancer (BC)-related mortality is associated with the potential metastatic properties of the primary breast tumors. The following study was conducted with the main focus on the effect of LINC00518 on the growth and metastasis of BC epithelial cells via the Wnt signaling pathway through regulation of the methylation of CDX2 gene. Initially, differentially expressed long intergenic non-protein coding RNAs (lincRNAs) related to BC were screened out in the Cancer Genome Atlas (TCGA) database, after which we detected the LINC00518 expression and localization in BC tissues and cells. Then the CDX2 positive expression and methylation level were identified. The targeting relationship of LINC00518 and CDX2, and binding methyltransferase in the promoter region were examined. BC epithelial cell proliferation, colony formation ability, invasion, migration and apoptosis were further evaluated. The lincRNA expression data related to BC downloaded from the TCGA database revealed that there was a high expression of LINC00518 in BC, and a negative correlation between LINC00518 and CDX2. In addition, LINC00518 promotes CDX2 methylation by recruiting DNA methyltransferase through activating the Wnt signaling pathway. The down-regulation of LINC00518 inhibited proliferation, invasion, migration, and EMT of BC epithelial cells while enhancing apoptosis. The inhibitory effects of LINC00518 down-regulation was reversed by CDX2 down-regulation. In conclusion, our findings revealed that down-regulation of LINC00518 might have the ability to suppress BC progression by up-regulating CDX2 expression through the reduction of methylation and blockade of the Wnt signaling pathway, resulting in the inhibition of proliferation and promotion of apoptosis of BC epithelial cells.     

Transgenic maize phosphoenolpyruvate carboxylase alters leaf–atmosphere CO2 and 13CO2 exchanges in Oryza sativa

Photosynthesis Research - The engineering process of C4 photosynthesis into C3 plants requires an increased activity of phosphoenolpyruvate carboxylase (PEPC) in the cytosol of leaf mesophyll...     

Impacts of Catastrophic Earthquakes on the Insect Communities in Estuarine Mangroves, Northern Taiwan

As a catastrophic earthquake is unpredictable and occurs only occasionally, impacts on biotic communities are seldom known. Monthly changes in insect communities in the mangroves along the Danshui Estuary were monitored for more than 3 years from before and after two catastrophic earthquakes in Taiwan the Chi–Chi earthquake (M_L = 7.3) of September 21, 1999 and the 3–31 earthquake (M_L = 6.8) of March 31, 2002. Here we show that the Chi–Chi earthquake not only caused large declines in total individual number but also total species number of insects. It also resulted in greater variability among samples, and shifts in insect communities. Non-biting midges and rove beetles, whose immatures inhabited the riparian underground or aquatic sediments, were most severely affected. By 7 months after the Chi–Chi earthquake, the insect communities had recovered to a level comparable to that before the earthquake. However, the influence of the 3–31 earthquake on the insect communities was less severe. It is concluded that the more-severe impacts of the Chi–Chi earthquake than the 3–31 earthquake can be attributable to differences in ground shaking, occurrence time, biodiversity, and growing conditions of insects at those times.     

Regulation of mitochondrial NAD pool via NAD+ transporter 2 is essential for matrix NADH homeostasis and ROS production in Arabidopsis

Reactive oxygen species(ROS) play a crucial role in numerous biological processes in plants, including development, responses to environmental stimuli, and programmed cell death(PCD). Deficiency in MOSAIC DEATH 1(MOD1), a plastid-localized enoyl-ACP reductase essential for de novo fatty acid biosynthesis in Arabidopsis thaliana, leads to the increased malate export from chloroplasts to mitochondria, and the subsequent accumulation of mitochondria-generated ROS and PCD. In this study, we report the identification and characterization of a mod1 suppressor, som592. SOM592 encodes mitochondrion-localized NAD~+ transporter 2(NDT2). We show that the mitochondrial NAD pool is elevated in the mod1 mutant. The som592 mutation fully suppressed mitochondrial NADH hyper-accumulation, ROS production, and PCD in the mod1 mutant, indicating a causal relationship between mitochondrial NAD accumulation and ROS/PCD phenotypes. We also show that in wild-type plants, the mitochondrial NAD+uptake is involved in the regulation of ROS production in response to continuous photoperiod. Elevation of the alternative respiration pathway can suppress ROS accumulation and PCD in mod1, but leads to growth restriction. These findings uncover a regulatory mechanism for mitochondrial ROS production via NADH homeostasis in Arabidopsis thaliana that is likely important for growth regulation in response to altered photoperiod.