盐碱胁迫下西伯利亚蓼体内无机离子的变化

研究了碳酸氢钠溶液处理后西伯利亚蓼营养器官内部无机离子含量的变化。实验结果表明碳酸氢钠溶液处理前西伯利亚蓼茎部认为是“K+库”;碳酸氢钠溶液处理过程中“K+库”转变成为“Na+库”,以维持叶部的正常生理功能,并且“Na+库”具有一定的限度;碳酸氢钠溶液处理后,西伯利亚蓼不同部位对外界盐碱胁迫的反应存在多样性。植株在“Na+库”达到限度之前进行旺盛的光合作用,在有限的时间内向地下组织输送更多的有机养分,用以繁殖后代。     

Nutritional imbalance in wheat (Triticum aestivum L.) genotypes grown at soil water stress

An experiment was conducted to determine the effect of water stress on nutritional changes in tolerant (DS-4 and Chakwal-86) and susceptible (DS-17 and Pavon) genotypes in lysimeters. The stress was imposed at different growth stages (pre-anthesis, post-anthesis, terminal drought). The biomass (dry weight) and Ca, Mg and P concentration decreased with water stress in all the wheat genotypes. However, the tolerant genotypes had less reduction than susceptible at all the treatments. Potassium increased in all wheat genotypes due to water stress and was higher in tolerant than susceptible genotypes. Sodium content was not affected by water stress.     

Adaptation of signature-tagged mutagenesis to Escherichia coli K1 and the infant-rat model of invasive disease

With the exception of the polysialic acid capsule (K1 antigen), little is known about other virulence factors needed for systemic infection by Escherichia coli K1, the leading cause of Gram-negative neonatal meningitis in humans. In this work, the functional genomics method of signature-tagged mutagenesis (STM) was adapted to E. coli K1 and the infant-rat model to identify non-capsule virulence genes. Validation of the method was demonstrated by the failure to recover a reconstructed acapsular mutant from bacterial pools used to systemically infect 5-day-old rats. Three new genes required for systemic disease were identified from a total of 192 mutants screened by STM (1.56% hit rate). Gut colonization, Southern blot hybridization, mixed-challenge infection, and DNA sequence analyses showed that the attenuating defects in the mutants were associated with transposon insertions in rfaL (O antigen ligase), dsbA (thiol:disulfide oxidoreductase), and a new gene, puvA (previously unidentified virulence gene A), with no known homologues. The results indicate the ability of STM to identify novel systemic virulence factors in E. coli K1.     

Millennial musings on molecular motors

In a universe that is dominated by increasing entropy, living organisms are a curious anomaly. The organization that distinguishes living organisms from their inanimate surroundings relies upon their ability to execute vectorial processes, such as directed movements and the assembly of macromolecules and organelle systems. Many of these phenomena are executed by molecular motors that harness chemical potential energy to perform mechanical work and unidirectional motion. This article explores how these remarkable protein machines might have evolved and what roles they could play in biological and medical research in the coming decades.     

PLS3 predicts poor prognosis in pancreatic cancer and promotes cancer cell proliferation via PI3K/AKT signaling

Plastin-3 plays a key role in cancer cell proliferation and invasion, but its prognostic value in pancreatic cancer (PACA) remains poorly defined. In this study, we show that PLS3 messenger RNA is overexpressed in PACA tissue compared with normal tissue. We accumulated 207 cases of PACA specimens to perform immunohistochemical analysis and demonstrated that PLS3 levels correlate with T-classification (p < .001) and pathology (p < .001). Furthermore, overall survival rates (p < .001) in tumors with high PLS3 expression were poor, as assessed through Kaplan–Meier survival analysis. PLS3 was found to be an independent prognostic factor for PACA through multivariate Cox regression analysis. Moreover, we found that PLS3 enhances the proliferation and invasion of tumor cells as assessed through Cell Counting Kit-8, wounding healing assays, and Transwell assays. The upregulation of PLS3 also led to enhanced phosphatidylinositol-3 kinase/protein kinase B signaling in PACA cells. These data suggest that PLS3 is a biomarker to estimate PACA progression and represents a molecular target for PACA therapy.     

Platycodin D protects cortical neurons against oxygen-glucose deprivation/reperfusion in neonatal hypoxic-ischemic encephalopathy

Neonatal hypoxic-ischemic encephalopathy is one of the leading causes of death in infants. Increasing evidence indicates that oxidative stress and apoptosis are major contributors to hypoxic-ischemic injury and can be used as particularly promising therapeutic targets. Platycodin D (PLD) is a triterpenoid saponin that exhibits antioxidant properties. The aim of this study was to evaluate the effects of PLD on hypoxic-ischemic injury in primary cortical neurons. We found that oxygen-glucose deprivation/reperfusion (OGD/R) induced inhibition of cell viability and cytotoxicity, which were attenuated by PLD treatment. PLD treatment inhibited oxidative stress induced by OGD/R, which was evidenced by the reduced level of reactive oxygen species and increased activities of catalase, superoxide dismutase, and glutathione peroxidase. Histone-DNA enzyme-linked immunosorbent assay revealed that apoptosis was significantly decreased after PLD treatment in OGD/R-treated cortical neurons. The increased bax expression and decreased bcl-2 expression induced by OGD/R were reversed by PLD treatment. Furthermore, PLD treatment caused the activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway in OGD/R-stimulated cortical neurons. Suppression of this pathway blocked the protective effects of PLD on OGD/R-induced cell injury. These findings suggested that PLD executes its protective effects on OGD/R-induced cell injury via regulating the PI3K/Akt/mTOR pathway in cortical neurons.     

A class II phosphoinositide 3-kinase plays an indispensable role in hepatitis C virus replication

Phosphoinositides function as fundamental signaling molecules and play roles in diverse cellular processes. Certain types of viruses may employ host cell phosphoinositide signaling systems to facilitate their replication cycles. Here we demonstrate that the β isoform of class II PI3K (PI3K-C2β) plays an indispensable role in hepatitis C virus (HCV) propagation in human hepatocellular carcinoma cells. Knockdown of PI3K-C2β abrogated HCV propagation in the cell. Using an HCV replicon system, we found that knockdown of PI3K-C2β substantially repressed the full-genome replication, while showing relatively small reductions in sub-genome replication, in which structural proteins including core protein were deleted. We also found that HCV core protein showed the binding activity towards D4-phosphorylated phosphoinositides and overlapped localization with phosphatidylinositol 3,4-bisphosphate in the cell. These results suggest that the phosphoinositide generated by PI3K-C2β plays an indispensable role in the HCV replication cycle through the binding to HCV core protein.     

The relative impact of lichen symbiotic partners to repeated copper uptake

The relative impact of lichen photobiont and mycobiont was evaluated by submitting nine lichen species with: (i) different photobiont types; (ii) different lichen growth forms; and (iii) different nutrients, pH, humidity preferences; to a range of Cu concentrations (μM) supplied in repeated cycles to simulate the natural process of uptake under field conditions. The physiological performance of the photosystem II photochemical reactions was measured using F_v/F_m and the metabolic activity of the mycobiont was evaluated using ergosterol and intracellular K-loss as indicators. Lichens with higher cation exchange capacity showed higher intracellular Cu uptake and their ecology seemed to be associated with low-nutrient environments. Thus the wall and external matrix, mainly characteristic of the mycobiont partner, cannot be ignored as the first site of interaction of metals with lichens. No common intracellular Cu concentration threshold was found for the physiological impacts observed in the different species. Most physiological effects of Cu uptake in sensitive lichens occurred for intracellular Cu below 200 μg/g dw whereas more tolerant species were able to cope with intracellular Cu at least 3 times higher. Cyanobacterial lichens showed to be more sensitive to Cu uptake than green-algal lichens. Within the Trebouxia lichens, different species showed different sensitivities to Cu uptake, suggesting that the mycobiont may change the microenvironment close to the photobiont partner providing different degrees of protection. Despite the fact that the photobiont is the productive partner, the metabolic activity of the mycobiont of lichen species adapted to environments rich in nutrients, showed to be more sensitive to Cu uptake than the photochemical performance of the photobiont.