机械损伤对9种水生植物叶片的影响

水生植物叶片的功能性状特征与陆生植物有所不同,同时叶脉类型也显著影响叶片的功能性状。本研究选取9种具有不同叶脉类型的水生植物,通过对叶脉进行直接损伤,分析叶片性状(形态、色素含量和叶绿素荧光指标)在叶脉受损后的变化程度与叶脉类型的关系。结果显示:具有平行脉的3种水生植物对叶脉损伤具有较强的耐受性;具羽状脉的4种植物主脉受损后显著抑制叶片生长,而侧脉受损的影响在不同物种间有所不同,具有物种特异性。本研究可为大型湖泊水生植物修复的水生物种筛选提供参考。     

Nitrogen fertilizer application affects lodging resistance by altering secondary cell wall synthesis in japonica rice (<Emphasis Type="Italic">Oryza sativa</Emphasis>)

Stem mechanical strength is an important agricultural quantitative trait that is closely related to lodging resistance in rice, which is known to be reduced by fertilizer with higher levels of nitrogen. To understand the mechanism that regulates stem mechanical strength in response to nitrogen, we analysed stem morphology, anatomy, mechanical properties, cell wall components, and expression of cell wall-related genes, in two varieties of japonica rice, namely, Wuyunjing23 (lodging-resistant variety) and W3668 (lodging-susceptible variety). The results showed that higher nitrogen fertilizer increased the lodging index in both varieties due to a reduction in breaking strength and bending stress, and these changes were larger in W3668. Cellulose content decreased slightly under higher nitrogen fertilizer, whereas lignin content reduced remarkably. Histochemical staining revealed that high nitrogen application decreased lignin deposition in the secondary cell wall of the sclerenchyma cells and vascular bundle cells compared with the low nitrogen treatments, while it did not alter the pattern of cellulose deposition in these cells in both Wuyunjing23 and W3668. In addition, the expression of the genes involved in lignin biosynthesis, OsPAL, OsCoMT, Os4CL3, OsCCR, OsCAD2, OsCAD7, OsCesA4, and OsCesA7, were also down-regulated under higher nitrogen conditions at the early stage of culm growth. These results suggest that the genes involved in lignin biosynthesis are down-regulated by higher nitrogen fertilizer, which causes lignin deficiency in the secondary cell walls and the weakening of mechanical tissue structure. Subsequently, this results in these internodes with reduced mechanical strength and poor lodging resistance.     

蜈蚣肠道共生菌来源的吩嗪类化合物分离与鉴定

动植物共生菌是药物发现的重要来源之一。为了获取结构新颖且具有良好生物活性的微生物次生代谢产物,本文利用划线分离方法从蜈蚣肠道中分离获得一株共生菌WG4(未鉴定),经土豆液体发酵培养,发酵液经乙酸乙酯萃取、浓缩,获得次级代谢产物浸膏。浸膏经硅胶柱层析、高效液相色谱等分离方法反复纯化,获得3个化合物。通过核磁共振谱和低分辨质谱测试,3个化合物分别鉴定为1-羟基吩嗪(1)、吩嗪-1-甲酰胺(2)和吩嗪-1-羧酸(3)。据文献报道,吩嗪化合物具有抗菌、抗虫、抗病毒、抗肿瘤等生物活性,本实验证实了动植物来源的共生菌具有生产药源化合物的潜力。     

Exosome cofactor hMTR4 competes with export adaptor ALYREF to ensure balanced nuclear RNA pools for degradation and export

The exosome is a key RNA machine that functions in the degradation of unwanted RNAs. Here, we found that significant fractions of precursors and mature forms of mRNAs and long noncoding RNAs are degraded by the nuclear exosome in normal human cells. Exosome‐mediated degradation of these RNAs requires its cofactor hMTR4. Significantly, hMTR4 plays a key role in specifically recruiting the exosome to its targets. Furthermore, we provide several lines of evidence indicating that hMTR4 executes this role by directly competing with the mRNA export adaptor ALYREF for associating with ARS2, a component of the cap‐binding complex (CBC), and this competition is critical for determining whether an RNA is degraded or exported to the cytoplasm. Together, our results indicate that the competition between hMTR4 and ALYREF determines exosome recruitment and functions in creating balanced nuclear RNA pools for degradation and export.     

Lateral hypothalamic Orexin‐A‐ergic projections to the arcuate nucleus modulate gastric function in vivo

It has been well‐known that hypothalamic orexigenic neuropeptides, orexin‐A, and melanin‐concentrating hormone (MCH), play important roles in regulation of gastric function. However, what neural pathway mediated by the two neuropeptides affects the gastric function remains unknown. In this study, by way of nucleic stimulation and extracellular recording of single unit electrophysiological properties, we found that electrically stimulating the lateral hypothalamic area (LH) or microinjection of orexin‐A into the arcuate nucleus (ARC) excited most gastric distension‐responsive neurons in the nuclei and enhanced the gastric function including motility, emptying, and acid secretion of conscious rats. The results indicated that LH‐ARC orexin‐A‐ergic projections may exist and the orexin‐A in the ARC affected afferent and efferent signal transmission between ARC and stomach. As expected, combination of retrograde tracing and immunohistochemistry showed that some orexin‐A‐ergic neurons projected from the LH to the ARC. In addition, microinjection of MCH and its receptor antagonist PMC‐3881‐PI into the ARC affected the role of orexin‐A in the ARC, indicating a possible involvement of the MCH pathway in the orexin‐A role. Our findings suggest that there was an orexin‐A‐ergic pathway between LH and ARC which participated in transmitting information between the central nuclei and the gastrointestinal tract and in regulating the gastric function of rats.

     

Molecular cloning and expression analysis of two <Emphasis Type="Italic">FAD2</Emphasis> genes from chia (<Emphasis Type="Italic">Salvia hispanica</Emphasis>)

FATTY ACID DESATURASE 2 (FAD2, EC 1.3.1.35), also known as delta-12 oleate desaturase, is a key enzyme for linoleic acid and α-linolenic acid biosynthesis. Chia (Salvia hispanica) seeds contain the highest known proportion of α-linolenic acid in any plant sources. In this study, two full-length FAD2 genes, named as ShFAD2-1 and ShFAD2-2, were isolated from S. hispanica based on RACE method. Both ShFAD2-1 and ShFAD2-2 proteins possess strong transmembrane helices, three histidine motifs and a C-terminal ER-located signal (YNNKL). Phylogenetic analysis showed that both ShFAD2-1 and ShFAD2-2 are grouped with constitutive plant FAD2s. Heterologous expression in Saccharomyces cerevisiae indicated that ShFAD2-1 and ShFAD2-2 genes both encode a bio-functional delta-12 oleate desaturase. ShFAD2-2 was mainly expressed in flowers and early-stage seeds while ShFAD2-1 expression was almost constitutive in different organs. qRT-PCR results demonstrated that ShFAD2-1 and ShFAD2-2 show a cold-induced and heat-repressed expression pattern, whereas they also were differentially up-regulated or repressed by other abiotic stresses. This is the first cloning and function characterization of FAD2 from S. hispanica, which can provide insights into molecular mechanism of high ALA traits of S. hispanica and enrich our understanding of the roles of FAD2 genes in various abiotic stresses.     

藜蒿提取物抑菌作用的初步研究

采用榨汁、水提、醇提等 3种不同的方法 ,提取藜蒿中的抗菌有效成分。测定了各种提取物对 14种食品腐败菌的最低抑菌浓度 ( MIC) ,结果表明 :1.藜蒿汁的 MIC:痢疾杆菌为 2 5% ,大肠杆菌为 2 5% ,巨大芽孢杆菌为 50 % ,面包酵母为 5% ;2 .藜蒿水提物的 MIC:痢疾杆菌为 2 .5% ,大肠杆菌为 5% ,巨大芽孢杆菌为 5% ,面包酵母为 10 % ;3.黎蒿醇提物的 MIC:痢疾杆菌、巨大芽孢杆菌、大肠杆菌均为 5% ,蜡状芽孢杆菌、金黄色葡萄球菌、面包酵母、黄曲霉均为 10 % ,产朊酵母、裂殖酵母、异常汉逊酵母、白地霉、桔青霉、镰刀霉均为 2 0 %     

Discordant effects of glucosamine on insulin-stimulated glucose metabolism and phosphatidylinositol 3-kinase activity.

The impact of increased GlcN availability on insulin-stimulated p85/p110 phosphatidylinositol 3-kinase (PI3K) activity in skeletal muscle was examined in relation to GlcN-induced defects in peripheral insulin action. Primed continuous GlcN infusion (750 micromol/kg bolus; 30 micromol/kg.min) in conscious rats limited both maximal stimulation of muscle PI3K by acute insulin (I) (1 unit/kg) bolus (I + GlcN = 1.9-fold versus saline = 3.3-fold above fasting levels; p < 0.01) and chronic activation of PI3K following 3-h euglycemic, hyperinsulinemic (18 milliunits/kg.min) clamp studies (I + GlcN = 1.2-fold versus saline = 2.6-fold stimulation; p < 0.01). To determine the time course of GlcN-induced defects in insulin-stimulated PI3K activity and peripheral insulin action, GlcN was administered for 30, 60, 90, or 120 min during 2-h euglycemic, hyperinsulinemic clamp studies. Activation of muscle PI3K by insulin was attenuated following only 30 min of GlcN infusion (GlcN 30 min = 1.5-fold versus saline = 2.5-fold stimulation; p < 0.05). In contrast, the first impairment in insulin-mediated glucose uptake (Rd) developed following 110 min of GlcN infusion (110 min = 39.9 +/- 1.8 versus 30 min = 42.8 +/- 1.4 mg/kg.min, p < 0.05). However, the ability of insulin to stimulate phosphatidylinositol 3,4, 5-trisphosphate production and to activate glycogen synthase in skeletal muscle was preserved following up to 180 min of GlcN infusion. Thus, increased GlcN availability induced (a) profound and early inhibition of proximal insulin signaling at the level of PI3K and (b) delayed effects on insulin-mediated glucose uptake, yet (c) complete sparing of insulin-mediated glycogen synthase activation. The pattern and time sequence of GlcN-induced defects suggest that the etiology of peripheral insulin resistance may be distinct from the rapid and marked impairment in insulin signaling.     

Phosphorylation of Atg31 is required for autophagy

Autophagy is an evolutionarily conserved cellular process which degrades intracellular contents. The Atg17- Atg31-Atg29 complex plays a key role in autophagy induction by various stimuli. In yeast, autophagy occurs with autophagosome formation at a special site near the vacuole named the pre-autophagosomal structure (PAS). The Atg17-Atg31-Atg29 complex forms a scaffold for PAS organization, and recruits other autophagy-related (Atg) proteins to the PAS. Here, we show that Atg31 is a phosphorylated protein. The phosphorylation sites on Atg31 were identified by mass spectrometry. Analysis of mutants in which the phosphorylated amino acids were replaced by alanine, either individually or in various combinations, identified S174 as the functional phosphorylation site. An S174A mutant showed a similar degree of autophagy impairment as an Atg31 deletion mutant. S174 phosphorylation is required for autophagy induced by various autophagy stimuli such as nitrogen starvation and rapamycin treatment. Mass spectrometry analysis showed that S174 is phosphorylated constitutively, and expression of a phosphorylation-mimic mutant (S174D) in the Atg31 deletion strain restores autophagy. In the S174A mutant, Atg9-positive vesicles accumulate at the PAS. Thus, S174 phosphorylation is required for formation of autophagosomes, possibly by facilitating the recycling of Atg9 from the PAS. Our data demonstrate the role of phosphorylation of Atg31 in autophagy.     

Structural basis for differential recognition of brassinolide by its receptors

Brassinosteroids, a group of plant steroid hormones, regulate many aspects of plant growth and development. We and other have previously solved the crystal structures of BRI1(LRR) in complex with brassinolide, the most active brassinosteroid identifi ed thus far. Although these studies provide a structural basis for the recognition of brassinolide by its receptor BRI1, it still remains poorly understood how the hormone differentiates among its conserved receptors. Here we present the crystal structure of the BRI1 homolog BRL1 in complex with brassinolide. The structure shows that subtle differences around the brassinolide binding site can generate a striking effect on its recognition by the BRI1 family of receptors. Structural comparison of BRL1 and BRI1 in their brassinolide-bound forms reveals the molecular basis for differential binding of brassinolide to its different receptors, which can be used for more effi cient design of plant growth regulators for agricultural practice. On the basis of our structural studies and others’ data, we also suggest possible mechanisms for the activation of BRI1 family receptors.