The interspecific competition presents greater nutrient facilitation compared with intraspecific competition through AM fungi interacting with litter for two host plants in karst soil

AM 真菌和枯落物互作下两种喀斯特植物种间竞争较种内竞争更能促进植物养分利用 枯落物是植物养分获取和土壤养分转化的关键载体。丛枝菌根(Arbuscular mycorrhizae, AM)对植物养分摄取的影响已被广泛认知。然而，在养分亏缺的喀斯特生境中，不同竞争方式的植物如何通过AM真菌和枯落物利用养分尚不清楚。本研究对两种喀斯特适生植物构树(Broussonetia papyrifera)和云贵鹅耳枥(Carpinus pubescens)进行种内竞争和种  间竞争种植处理，并通过幼套球 囊霉(Glomus etunicatum)接种或不接种处理，以及土壤中添加或不添加两物种叶片混合枯落物处理，测定了植物生物量以及氮、磷、钾浓度等指标，研究植物的生长和养分利用。研究结果表明，AM真菌对两种植物养分摄取影响不同，AM真菌显著提高了种内和种间竞争下构树的养分摄取量，但降低了云贵鹅耳枥的养分摄取量。种间竞争下接种AM真菌，枯落物添加促进了云贵鹅耳枥对氮的摄取，抑制了构树对氮的摄取。接种AM真菌和添加枯落物条件下，种间竞争的构树对氮、磷和钾的摄取量及云贵鹅耳枥对氮的摄取量均高于种内竞争；种间竞争下两物种养分竞争力呈现明显差异，即构树对磷和钾养分竞争力显著提高，对氮则不显著；云贵鹅耳枥仅对钾的养分竞争力显著降低，对氮和磷则无显著影响。这些结果说明，在AM真菌与枯落物相互作用下，两种喀斯特植物种间竞争较种内竞争更能促进植物养分利用。     

Phosphatidylinositol Phosphate 5-Kinase Iγi2 in Association with Src Controls Anchorage-independent Growth of Tumor Cells

A fundamental property of tumor cells is to defy anoikis, cell death caused by a lack of cell-matrix interaction, and grow in an anchorage-independent manner. How tumor cells organize signaling molecules at the plasma membrane to sustain oncogenic signals in the absence of cell-matrix interactions remains poorly understood. Here, we describe a role for phosphatidylinositol 4-phosphate 5-kinase (PIPK) Iγi2 in controlling anchorage-independent growth of tumor cells in coordination with the proto-oncogene Src. PIPKIγi2 regulated Src activation downstream of growth factor receptors and integrins. PIPKIγi2 directly interacted with the C-terminal tail of Src and regulated its subcellular localization in concert with talin, a cytoskeletal protein targeted to focal adhesions. Co-expression of PIPKIγi2 and Src synergistically induced the anchorage-independent growth of nonmalignant cells. This study uncovers a novel mechanism where a phosphoinositide-synthesizing enzyme, PIPKIγi2, functions with the proto-oncogene Src, to regulate oncogenic signaling.     

Reversible Control by Vitamin D of Granulocytes and Bacteria in the Lungs of Mice: An Ovalbumin-Induced Model of Allergic Airway Disease

Vitamin D may be essential for restricting the development and severity of allergic diseases and asthma, but a direct causal link between vitamin D deficiency and asthma has yet to be established. We have developed a ‘low dose’ model of allergic airway disease induced by intraperitoneal injection with ovalbumin (1 µg) and aluminium hydroxide (0.2 mg) in which characteristics of atopic asthma are recapitulated, including airway hyperresponsiveness, antigen-specific immunoglobulin type-E and lung inflammation. We assessed the effects of vitamin D deficiency throughout life (from conception until adulthood) on the severity of ovalbumin-induced allergic airway disease in vitamin D-replete and -deficient BALB/c mice using this model. Vitamin D had protective effects such that deficiency significantly enhanced eosinophil and neutrophil numbers in the bronchoalveolar lavage fluid of male but not female mice. Vitamin D also suppressed the proliferation and T helper cell type-2 cytokine-secreting capacity of airway-draining lymph node cells from both male and female mice. Supplementation of initially vitamin D-deficient mice with vitamin D for four weeks returned serum 25-hydroxyvitamin D to levels observed in initially vitamin D-replete mice, and also suppressed eosinophil and neutrophil numbers in the bronchoalveolar lavage fluid of male mice. Using generic 16 S rRNA primers, increased bacterial levels were detected in the lungs of initially vitamin D-deficient male mice, which were also reduced by vitamin D supplementation. These results indicate that vitamin D controls granulocyte levels in the bronchoalveolar lavage fluid in an allergen-sensitive manner, and may contribute towards the severity of asthma in a gender-specific fashion through regulation of respiratory bacteria.     

Role of methyl groups in dynamics and evolution of biomolecules

Recent studies have discovered strong differences between the dynamics of nucleic acids (RNA and DNA) and proteins, especially at low hydration and low temperatures. This difference is caused primarily by dynamics of methyl groups that are abundant in proteins, but are absent or very rare in RNA and DNA. In this paper, we present a hypothesis regarding the role of methyl groups as intrinsic plasticizers in proteins and their evolutionary selection to facilitate protein dynamics and activity. We demonstrate the profound effect methyl groups have on protein dynamics relative to nucleic acid dynamics, and note the apparent correlation of methyl group content in protein classes and their need for molecular flexibility. Moreover, we note the fastest methyl groups of some enzymes appear around dynamical centers such as hinges or active sites. Methyl groups are also of tremendous importance from a hydrophobicity/folding/entropy perspective. These significant roles, however, complement our hypothesis rather than preclude the recognition of methyl groups in the dynamics and evolution of biomolecules.     

Adeno-associated virus serotype 2 mediated transduction and coexpression of the human apoAI and SR-BI gene in HepG2 cells

Cholesterol efflux is the first step in the reverse cholesterol transport (RCT) pathway, removing excess cholesterol from tissues, including the arterial wall, thus preventing the development of atherosclerosis. Adeno-associated virus (rAAV) has demonstrated significant promise as a DNA-delivery vector to treat serious human diseases. In this study, we constructed recombinant adeno-associated viruses coexpressing apoAI and SR-BI successfully, the double gene mRNA and protein were both strongly expressed in transduced HepG2 cells. A novel safe and efficient method of promoting the reverse cholesterol transport (RCT) may be established. These results may provide a new method for gene therapy of Arteriosclerosis.     

Gut microbiota in wild and captive Guizhou snub‐nosed monkeys,Rhinopithecus brelichi

Many colobine species—including the endangered Guizhou snub‐nosed monkey (Rhinopithecus brelichi) are difficult to maintain in captivity and frequently exhibit gastrointestinal (GI) problems. GI problems are commonly linked to alterations in the gut microbiota, which lead us to examine the gut microbial communities of wild and captive R. brelichi. We used high‐throughput sequencing of the 16S rRNA gene to compare the gut microbiota of wild (N = 7) and captive (N = 8) R. brelichi. Wild monkeys exhibited increased gut microbial diversity based on the Chao1 but not Shannon diversity metric and greater relative abundances of bacteria in the Lachnospiraceae and Ruminococcaceae families. Microbes in these families digest complex plant materials and produce butyrate, a short chain fatty acid critical to colonocyte health. Captive monkeys had greater relative abundances of Prevotella and Bacteroides species, which degrade simple sugars and carbohydrates, like those present in fruits and cornmeal, two staples of the captive R. brelichi diet. Captive monkeys also had a greater abundance of Akkermansia species, a microbe that can thrive in the face of host malnutrition. Taken together, these findings suggest that poor health in captive R. brelichi may be linked to diet and an altered gut microbiota.     

Phosphorylation of eIF2α signaling pathway attenuates obesity-induced non-alcoholic fatty liver disease in an ER stress and autophagy-dependent manner

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disorder and frequently exacerbates in postmenopausal women. In NAFLD, the endoplasmic reticulum (ER) plays an important role in lipid metabolism, in which salubrinal is a selective inhibitor of eIF2α de-phosphorylation in response to ER stress. To determine the potential mechanism of obesity-induced NAFLD, we employed salubrinal and evaluated the effect of ER stress and autophagy on lipid metabolism. Ninety-five female C57BL/6 mice were randomly divided into five groups: standard chow diet, high-fat (HF) diet, HF with salubrinal, HF with ovariectomy, and HF with ovariectomy and salubrinal. All mice except for SC were given HF diet. After the 8-week obesity induction, salubrinal was subcutaneously injected for the next 8 weeks. The expression of ER stress and autophagy markers was evaluated in vivo and in vitro. Compared to the normal mice, the serum lipid level and adipose tissue were increased in obese mice, while salubrinal attenuated obesity by blocking lipid disorder. Also, the histological severity of hepatic steatosis and fibrosis in the liver and lipidosis was suppressed in response to salubrinal. Furthermore, salubrinal inhibited ER stress by increasing the expression of p-eIF2α and ATF4 with a decrease in the level of CHOP. It promoted autophagy by increasing LC3II/I and inhibiting p62. Correlation analysis indicated that lipogenesis in the development of NAFLD was associated with ER stress. Collectively, we demonstrated that eIF2α played a key role in obesity-induced NAFLD, and salubrinal alleviated hepatic steatosis and lipid metabolism by altering ER stress and autophagy through eIF2α signaling.Subject terms: Obesity, Metabolic syndrome, Outcomes research     

“绿色革命”新进展:赤霉素与氮营养双重调控的表观修饰助力水稻高产高效育种

以半矮秆育种为代表的“绿色革命”极大地提高了作物产量,但也带来氮营养利用效率降低的严重问题。“绿色革命”主要基于调控赤霉素的代谢和信号转导而实现。前期的研究发现,赤霉素信号转导关键因子DELLA蛋白通过调控GRF4而负调控氮素的吸收利用,为半矮秆品系氮利用效率低的问题提供了解决方案。最近的一项研究进一步揭示了GA信号途径与氮响应交叉互作的新机制。该研究发现水稻(Oryza sativa)NGR5是氮素调控分蘖数目的一个关键基因,其表达受氮诱导。通过招募PRC2,NGR5对D14和OsSPL14等分蘖抑制基因所在位点进行H3K27me3甲基化修饰,从而抑制其表达。而在半矮秆背景下超表达NGR5可以提高低氮水平下的水稻产量。NGR5同时也被发现为赤霉素受体GID1的一个新靶标,受到其负调控。该研究发现了调控赤霉素信号通路的新机制,并对高产高效的新一代“绿色革命”育种实践具有重要启示。     

Effect of iodide on estrogen-induced uterine peroxidase

Iodide administered in the drinking water for 5–7 days increased the activity of estradiol-induced uterine peroxidase in the immature rat. This effect was specific for iodide and could not be mimicked by chloride, bromide, thiocyanate, perchlorate or iodate. Sodium iodide also increased peroxidase activity in the parotid gland but had no effect on glucose-6-phosphate dehydrogenase in the uterus, thyroid or parotid even though estradiol produced a 2-fold increase in the activity of this enzyme in the uterus. ¹²⁵I was taken up more readily by the uterus than by muscle but this process was not influenced by prior treatment of the animals with estrogen. The in vitro effect of sulfhydryl reagents on uterine peroxidase was also investigated and proposals made for possible mechanisms of action of iodide on this enzyme in the intact animal.