土壤氮磷添加下豆科草本植物生物固氮与磷获取策略的权衡机制

豆科草本植物固氮是陆地生态系统重要的自然氮输入方式, 影响着草地生产的经济性和可持续性。为探讨氮磷交互作用影响豆科草本植物生物固氮率的潜在生理生态机制, 该研究选取8种豆科草本植物分别种植在对照、氮肥添加、磷肥添加和氮磷耦合添加处理的土壤中, 进行野外盆栽实验。测定了初花期植物生物量和营养含量、根部碳水化合物含量、根际pH、根际柠檬酸含量、根际有效磷含量、植物根瘤生物量、磷含量及其生物固氮率。主要结果: 依赖于豆科物种, 氮添加显著促进了豆科草本植物根际磷的活化, 降低了根生物量分配以及根系非结构性碳水化合物含量。在两种磷添加处理下, 氮添加导致8种豆科草本植物根瘤生物量平均下降27%-36%, 生物固氮率平均下降20%-33%。磷添加降低了根际的磷活化, 但促进了豆科草本植物根系发育和非结构性碳水化合物的积累。在施氮和不施氮条件下, 磷添加分别使8种豆科草本植物的生物固氮率提高了45%-69%和0-47%。氮添加降低豆科草本植物生物固氮率, 其原因是氮添加提高了植物磷需求, 为活化更多磷, 豆科草本植物降低根系生物量和根系非结构性碳水化合物的含量, 导致根瘤发育受到限制。在氮添加的同时进行磷添加, 能够改善土壤氮磷平衡, 促进根系生长和非结构性碳水化合物积累, 缓解了增氮对生物固氮的抑制作用。     

Critical roles of reactive oxygen species in mitochondrial permeability transition in mediating evodiamine-induced human melanoma A375-S2 cell apoptosis

Previous studies have shown that evodiamine could trigger apoptosis in human malignant melanoma A375-S2 cells within 24 h. To further investigate the biochemical basis of this activity, the roles of reactive oxygen species (ROS) and mitochondrial permeability transition (MPT) were evaluated. Exposure to evodiamine led to a rapid increase in intracellular ROS followed by an onset of mitochondrial depolarization. ROS scavenger rescued the ΔΨm dissipation and cell death induced by evodiamine, whilst MPT inhibitor blocked the second-time ROS formation as well as cell death. Expressions of key proteins in Fas- and mitochondria-mediated pathways were furthermore examined. Both pathways were activated and regulated by ROS and MPT and were converged to a final common pathway involving the activation of caspase-3. These data suggested that a phenomenon termed ROS-induced ROS release (RIRR) was involved in evodiamine-treated A375-S2 cells and greatly contributed to the apoptotic process through both extrinsic and intrinsic pathways.     

A rapid double-staining technique to improve seed viability testing in terrestrial orchids

Abstract

The need to optimize seed banking efforts has stimulated research for rapid methods to estimate quality in seed-lots. For terrestrial orchids, viability testing using tetrazolium (TTC) staining requires chemical scarification, as seeds have an impermeable testa. Different seed-coat permeability may affect TTC staining, thus affecting the results. The aim of this study was to perform a permeability test to assess the effectiveness of the used scarification method and its usefulness to correct TTC viability results. Mature seeds of Anacamptis laxiflora were subjected to eight scarification treatments with sodium hypochlorite solutions with different concentration and duration. Viability tests were performed using the basic TTC methodology, followed by a permeability test performed by means of trypan blue dye. The different scarification methods resulted in estimated TTC viability ranging from 0% and 94% for the same seed lot of A. laxiflora seeds. Our results proved that the used scarification protocol significantly affects both seed coat permeability and subsequent TTC staining (two-way ANOVA, p?< 0.0001). We describe a new rapid protocol that can be used to test terrestrial orchid seed viability. This double-staining method, providing rapid information on seed coat permeability, can be useful to avoid under-estimation of TTC results.     

Determinants of serum levels of surfactant proteins A and B and Clara cell protein CC16

Increased leakage of surfactant proteins A and B (SP-A and SP-B) and Clara cell secretory protein (CC16) from the air spaces into the circulation occurs in a range of respiratory conditions. However, circulating levels depend not only on the rate of entry into the circulation, but also on the rate of clearance. In order to clarify the role of the kidney in the clearance of these proteins, serum levels were related to markers of glomerular filtration in 54 non-smoking patients with varying degrees of renal dysfunction, none of whom had respiratory disease or were receiving dialysis at the time of sampling. Serum SP-A was related to SP-B (r=0.53, p<0.001) and to CC16 (r=0.33, p<0.02). Similarly, SP-B was related to CC16 (r=0.39, p<0.004). Stepwise multiple linear regression analysis suggested that serum SP-A and SP-B are influenced by age (～20 and ～25% of variance, respectively), whereas CC16 is determined by renal function and, to a lesser extent, by body weight (～63% of variance in total). We conclude that CC16 is cleared from blood by the renal route, whereas SP-A and SP-B are not. Serum SP-A and SP-B are influenced by age, which we speculate reflects increased damage to the alveolocapillary barrier.     

Interleukin-8 Regulates Endothelial Permeability by Down-regulation of Tight Junction but not Dependent on Integrins Induced Focal Adhesions

Interleukin-8 (IL-8) is a common inflammatory factor, which involves in various non-specific pathological processes of inflammation. It has been found that increased endothelial permeability accompanied with high expression of IL-8 at site of injured endothelium and atherosclerotic plaque at early stages, suggesting that IL-8 participated in regulating endothelial permeability in the developing processes of vascular disease. The purpose of this study is to investigate the regulation effects of IL-8 on the vascular endothelial permeability, and the mRNA and protein expression of tight junction components (i.e., ZO-1, Claudin-5 and Occludin). Endothelial cells were stimulated by IL-8 with the dose of 50, 100 and 200 ng/mL, and duration of 2, 4, 6, 8h, respectively. The mRNA and protein expression level of tight junction components with IL-8 under different concentration and duration was examined by RT-PCR and Western blot, respectively. Meanwhile, the integrins induced focal adhesions event with IL-8 stimulation was also investigated. The results showed that IL-8 regulated the permeability of endothelium by down-regulation of tight junction in a dose- and time-dependence manner, but was not by integrins induced focal adhesions. This finding reveals the molecular mechanism in the increase of endothelial cell permeability induced by IL-8, which is expected to provide a new idea as a therapeutic target in vascular diseases.     

Induction of localized auxin response during spontaneous nodule development in Lotus japonicus

In leguminous plants, rhizobial infection of the epidermis triggers proliferation of cortical cells to form a nodule primordium. Recent studies have demonstrated that two classic phytohormones, cytokinin and auxin, have important functions in nodulation. The identification of these functions in Lotus japonicus was facilitated by use of the spontaneous nodule formation 2 (snf2) mutation of the putative cytokinin receptor LOTUS HISTIDINE KINASE 1 (LHK1). Analyses using snf2 demonstrated that constitutive activation of cytokinin signaling causes formation of spontaneous nodule-like structures in the absence of rhizobia and that auxin responses are induced in proliferating cortical cells during such spontaneous nodule development. Thus, cytokinin signaling positively regulates the auxin response. In the present study, we further investigated the induction of the auxin response using a gain-of-function mutation of Ca²⁺/calmodulin-dependent protein kinase (CCaMK) that causes spontaneous nodule formation. We demonstrate that CCaMK^T265D-mediated spontaneous nodule development is accompanied by a localized auxin response. Thus, a localized auxin response at the site of an incipient nodule primordium is essential for nodule organogenesis.     

植物根中质外体屏障结构和生理功能研究进展

综述了近10年来植物根中质外体屏障结构和功能的研究进展。质外体屏障指根中内、外皮层初生壁的凯氏带,或次生壁栓质化和木质化,以及植物体表角质层组成的保护组织,能隔绝水、离子和氧气不能自由进出植物体的屏障结构,具有保护植物体的生理功能。根中凯氏带的分子发育机理研究表明根内皮层类似哺乳动物上皮组织的保护作用。植物根中质外体保证内部各种生理代谢在稳定的内部环境中进行,是植物适应各种逆境的重要屏障结构。根中质外体屏障在植物适应干旱、洪涝灾害、离子胁迫和病虫害的侵袭等方面具有重要作用,在探索适应并修复极端生态环境的植物资源中有广阔的应用前景。     

Mitochondria could be a potential key mediator linking the intestinal microbiota to depression

The intestinal microbiota has been reported to affect depression, a common mental condition with severe health-related consequences. However, what mediates the effect of the intestinal microbiota on depression has not been well elucidated. We summarize the roles of the mitochondria in eliciting beneficial effects on the gut microbiota to ameliorate symptoms of depression. It is well known that mitochondria play a key role in depression. An important pathogenic factor, namely inflammatory response, may adversely impact mitochondrial functionality to maintain cellular homeostasis. Dysfunction of mitochondria not only affects neuronal function but also reduces neuron cell numbers. We posit that the intestinal microbiota could affect neuronal mitochondrial function through short-chain fatty acids such as butyrate. Brain inflammatory processes could also be affected through the modulation of gut permeability and blood lipopolysaccharide levels. Aberrant mitochondria functionality coupled to adverse cellular homeostasis could be a key mediator for the effect of the intestinal microbiota on the progression of depression.