Study on different potato continuous cropping ways on rhizosphere soil nutrients and enzyme activities

To address the problem of food security, China produced potatoes as a staple food in 2015.However, there are increasing problems with continuous cropping production methods, potato continuous cropping has been inevitable.So it is necessary to research under the different potato continuous cropping ways, potato rhizosphere soil nutrients and enzyme activities which can direct potato fertilizer and ease potato continuous cropping obstacle. A two-growing season investigation was carried out during the spring and autumn of 2014 and 2015 to determine the different ways of potato continuous cropping on the overall growth of potatoes, soil nutrients, and enzyme activities. During continuous cropping nitrogen (N) content of rhizosphere soil was reduced; available potassium (Kav) was significantly reduced(p≤5%), especially in spring and autumn continuous cropping; and total phosphorus (Ptot) was reduced during the growth stage. However, the total potassium (Ktot), available phosphorus(Pav), and organic carbon (Ctot) increased before they decreased. For rhizosphere soil enzyme activities, urease initially increased and then decreased, and was lower in continuous cropping than multiple continuous cropping; in spring of 2015, invertase was the highest with continuous cropping. Catalase and polyphenol oxidase decreased initially before increasing. Continuous cropping in spring and autumn consumed more nutrients, especially potassium (K) than in spring. Therefore, potatoes planted in both spring and autumn enhanced the problems of continuous cropping. However, multiple continuous cropping that eased rhizosphere soil nutrient absorption and effectively improves soil nutrients and enzyme activities could provide an effective method for managing the negative impacts associated with continuous cropping

Transcriptional Regulation of PP2A-Aα Is Mediated by Multiple Factors Including AP-2α, CREB, ETS-1, and SP-1

Protein phosphatases-2A (PP-2A) is a major serine/threonine phosphatase and accounts for more than 50% serine/threonine phosphatase activity in eukaryotes. The holoenzyme of PP-2A consists of the scaffold A subunit, the catalytic C subunit and the regulatory B subunit. The scaffold subunits, PP2A-Aα/β, provide a platform for both C and B subunits to bind, thus playing a crucial role in providing specific PP-2A activity. Mutation of the two genes encoding PP2A-Aα/β leads to carcinogenesis and likely other human diseases. Regulation of these genes by various factors, both extracellular and intracellular, remains largely unknown. In the present study, we have conducted functional dissection of the promoter of the mouse PP2A-Aα gene. Our results demonstrate that the proximal promoter of the mouse PP2A-Aα gene contains numerous cis-elements for the binding of CREB, ETS-1, AP-2α, SP-1 besides the putative TFIIB binding site (BRE) and the downstream promoter element (DPE). Gel mobility shifting assays revealed that CREB, ETS-1, AP-2α, and SP-1 all bind to PP2A-Aα gene promoter. In vitro mutagenesis and reporter gene activity assays reveal that while SP-1 displays negative regulation, CREB, ETS-1 and AP-2Aα all positively regulate the promoter of the PP2A-Aα gene. ChIP assays further confirm that all the above transcription factors participate the regulation of PP2A-Aα gene promoter. Together, our results reveal that multiple transcription factors regulate the PP2A-Aα gene

Dimethyl Sulfoxide Damages Mitochondrial Integrity and Membrane Potential in Cultured Astrocytes

Dimethyl sulfoxide (DMSO) is a polar organic solvent that is used to dissolve neuroprotective or neurotoxic agents in neuroscience research. However, DMSO itself also has pharmacological and pathological effects on the nervous system. Astrocytes play a central role in maintaining brain homeostasis, but the effect and mechanism of DMSO on astrocytes has not been studied. The present study showed that exposure of astrocyte cultures to 1 % DMSO for 24 h did not significantly affect cell survival, but decreased cell viability and glial glutamate transporter expression, and caused mitochondrial swelling, membrane potential impairment and reactive oxygen species production, and subsequent cytochrome c release and caspase-3 activation. DMSO at concentrations of 5 % significantly inhibited cell variability and promoted apoptosis of astrocytes, accompanied with more severe mitochondrial damage. These results suggest that mitochondrial impairment is a primary event in DMSO-induced astrocyte toxicity. The potential cytotoxic effects on astrocytes need to be carefully considered during investigating neuroprotective or neurotoxic effects of hydrophobic agents dissolved by DMSO