亚热带地区竞争型和忍耐型树种叶片可溶性有机质数量及光谱学特征

气候变化下,不同生态策略的树种对环境变化有着不同的响应能力,影响其叶片淋溶产生的DOM(Dissolved organic matter)的数量和质量,进而影响土壤的养分循环。通过探究亚热带地区不同生态策略树种叶片DOM数量及光谱学特征的差异,评估不同数量和结构特征DOM输入到土壤对养分循环的影响。本研究选取6种树种鲜叶进行浸提,其中竞争型(Competitive,C)和忍耐型(Stress-tolerant,S)各3种(树参(Dendropanax dentiger),黄绒润楠(Machilus grijsii),黄牛奶树(Symplocos cochinchinensis(Lour.)),细柄阿丁枫(Altingia gracilipes),丝栗栲(Castanopsis fargesii)和罗浮栲(Castanopsis faberi))。通过溶解性有机碳(Dissolved organic carbon,DOC)、溶解性有机氮(Dissolved organic nitrogen,DON)表征DOM的数量特征,通过紫外吸收值(Special Ultraviolet-Visible Absorption,SUVA),腐殖化指标(Humification index,HIX)和傅里叶红外光谱(Fouriertransform infrared,FTIR)等光谱指标表征DOM质量特征。结果表明:不同生态策略树种的叶浸提液中可溶性有机碳浓度无显著差异,但是C策略树种浸提液中可溶性有机氮浓度大于S策略的DON浓度。此外,S策略的芳香化指数(Aromatic index,AI)和腐殖化指数(HIX)均高于C策略。C策略树种的发射荧光强度也高于S策略,说明C策略树种DOM腐殖化程度较低,易分解物质含量高;S策略难分解物质多,腐殖化程度较高。傅里叶红外光谱结果表明,各树种叶浸提的DOM存在相似的吸收峰,其中以H键键合的—OH伸缩振动最强且C策略树种结果相对简单,验证了荧光光谱的结果。总体而言,与C策略相比,S策略树种叶片浸提的DOM结构更复杂,养分含量更高。这可能是因为,S策略树种对环境变化具有更高的适应性。由于其DOM结构相对复杂,输入土壤后减缓土壤碳周转速率,在未来气候变化情景下,S策略树种可能有利于土壤碳汇的形成。     

氮沉降对中亚热带米槠天然林微生物生物量及酶活性的影响

氮沉降对土壤微生物的扰动可能会影响土壤的养分循环,然而关于中亚热带天然林土壤微生物及酶活性对氮沉降的响应鲜有报道。通过3 a的氮沉降模拟实验,研究中亚热带米槠天然林土壤的理化性质、土壤微生物量及土壤酶活性的响应。结果表明:氮沉降并未引起土壤的有机碳和总氮显著性变化;高氮(80 kg N hm~(-2)a~(-1))处理下,土壤p H下降,出现酸化现象;低氮(40 kg N hm~(-2)a~(-1))处理促进淋溶层(A层)中土壤纤维素分解酶(β-葡萄糖苷酶和纤维素水解酶)和木质素分解酶(多酚氧化酶和过氧化物酶)活性升高,同时促进土壤微生物生物量碳、氮的积累。冗余分析(RDA)表示,可溶性有机碳(DOC)是驱动A层土壤酶活性的重要环境因子;而在淀积层(B层),这4种酶活性并未发生显著性差异。施氮处理后,A、B层中土壤的酸性磷酸酶活性增加(P0.05)。研究表明:低水平氮沉降增加了土壤微生物生物量碳氮含量以及土壤有机碳分解相关酶活性,从而加速了土壤碳周转;这为未来氮沉降增长背景下,探索中亚热带天然林土壤碳源汇问题提供了依据。     

Over-expression of a <Emphasis Type="Italic">LEA</Emphasis> gene in rice improves drought resistance under the field conditions

Late embryogenesis abundant (LEA) proteins have been implicated in many stress responses of plants. In this report, a LEA protein gene OsLEA3-1 was identified and over-expressed in rice to test the drought resistance of transgenic lines under the field conditions. OsLEA3-1 is induced by drought, salt and abscisic acid (ABA), but not by cold stress. The promoter of OsLEA3-1 isolated from the upland rice IRAT109 exhibits strong activity under drought- and salt-stress conditions. Three expression constructs consisting of the full-length cDNA driven by the drought-inducible promoter of OsLEA3-1 (OsLEA3-H), the CaMV 35S promoter (OsLEA3-S), and the rice Actin1 promoter (OsLEA3-A) were transformed into the drought-sensitive japonica rice Zhonghua 11. Drought resistance pre-screening of T₁ families at anthesis stage revealed that the over-expressing families with OsLEA3-S and OsLEA3-H constructs had significantly higher relative yield (yield under drought stress treatment/yield under normal growth conditions) than the wild type under drought stress conditions, although a yield penalty existed in T₁ families under normal growth conditions. Nine homozygous families, exhibiting over-expression of a single-copy of the transgene and relatively low yield penalty in the T₁ generation, were tested in the field for drought resistance in the T₂ and T₃ generations and in the PVC pipes for drought tolerance in the T₂ generation. Except for two families (transformed with OsLEA3-A), all the other families (transformed with OsLEA3-S and OsLEA3-H constructs) had higher grain yield than the wild type under drought stress in both the field and the PVC pipes conditions. No significant yield penalty was detected for these T₂ and T₃ families. These results indicate that transgenic rice with significantly enhanced drought resistance and without yield penalty can be generated by over-expressing OsLEA3-1 gene with appropriate promoters and following a bipartite (stress and non-stress) in-field screening protocol.     

C型利钠利尿肽对犬冠脉循环的作用

Ｃ型利钠利尿肽（ＣＮＰ）是新近发现的一种由内皮细胞分泌的利钠利尿肽,本研究采用冠脉内给药方法对比观察了ＣＮＰ、心房利钠尿肽（ＡＮＰ）对犬正常及心肌缺血后冠脉循环的作用,并应用常规离体血管灌流的方法测定了离体冠脉对ＣＮＰ、ＡＮＰ的舒张反应。结果显示：（１）对正常犬,ＣＮＰ、ＡＮＰ均可降低平均动脉压（ＭＡＰ）、远端小冠脉压和大、小冠脉阻力,增加冠脉流量,而不影响心率;（２）心肌缺血后,ＣＮＰ的上述作用依然存在,但ＡＮＰ降低ＭＡＰ的作用基本消失。（３）离体心外膜冠状动脉对ＣＮＰ、ＡＮＰ均呈剂量依赖性舒张反应。结果提示ＣＮＰ、ＡＮＰ均可舒张冠状动脉而改善冠脉循环,并可能对急性心肌缺血的治疗有益     

喀斯特峰丛洼地石漠化治理自然地域分区

峰丛洼地是我国西南地区面积最大的喀斯特地貌类型区,水热资源相对较好,由于其较高的景观异质性,该区面临着石漠化治理投入与分区粗放、治理技术与模式区域针对性不强等问题,亟需开展面向石漠化治理的喀斯特峰丛洼地自然地域分区。基于修正的地质图将峰丛洼地区划分成碎屑岩为主的非喀斯特区和碳酸盐岩为主的喀斯特区,依据气候分异特征将喀斯特区划分为滇东南桂西南西南季风非典型峰丛洼地区和东亚季风典型峰丛洼地区,进一步依据大地貌部位及微地貌特征将东亚季风典型峰丛洼地区细分为黔西南高原面浅碟型锥峰洼地区、黔南桂北大斜坡北部漏斗型锥峰洼地区、桂中大斜坡南部漏斗型锥塔峰洼地区和桂南丘陵浅碟型锥塔峰洼谷区等亚区。分区结果表明各分区自然地域特征鲜明:碎屑岩为主的非喀斯特区坡缓土厚,人口压力相对舒缓;西南季风非典型峰丛洼地区受气候影响显著,地貌形态以常态山为主;桂中大斜坡南部漏斗型锥塔峰洼地区重度、极重度石漠化问题突出,但削减快、治理成效显著;黔西南高原面浅碟型锥峰洼地区人地矛盾最为尖锐,石漠化问题严重;黔南桂北大斜坡北部漏斗型锥峰洼地区石漠化比例相对较低、喀斯特景观资源丰富;桂南丘陵浅碟型锥塔峰洼谷地区水热资源最为充沛...     

亚热带不同海拔黄山松林土壤磷组分及微生物特征

磷是亚热带地区植物生长必需的养分元素之一,海拔梯度可能会改变土壤-植物-微生物系统并影响土壤磷形态及有效性。了解不同海拔土壤磷组分状况,对维持山地森林生态系统可持续发展具有重要的意义。以戴云山地区不同海拔梯度(1300m和1600 m)黄山松林为研究对象,分析了土壤磷组分、微生物群落特征和磷酸酶活性。结果显示:海拔显著影响黄山松林土壤磷组分,与海拔1300 m相比,海拔1600 m处土壤总磷含量减少了48.4%—49.8%,且各磷组分(易分解态磷、中等易分解态磷和难分解态磷)含量也显著降低,淋溶层(A层)土壤的降低程度分别为45.7%、58.6%和38.7%,淀积层(B层)为82.6%、59.9%和31.1%。海拔对土壤微生物群落特征和酶活性亦有显著影响,各类微生物群落和总微生物磷脂脂肪酸含量(PLFAs),以及磷酸双酯酶(PD)活性均表现为海拔1600 m 1300 m,但酸性磷酸单酯酶(ACP)活性呈相反的趋势。冗余分析(RDA)表明,土壤磷组分主要受有机碳(SOC)调控,且SOC与有机磷组分(Na HCO3-Po和Na OH-Po)呈显著正相关;磷酸酶和外生菌根真菌(EMF)也是影响土壤磷组分变化的重要因素。研究表明,土壤有机质含量和微生物群落结构及功能的变化可能是不同海拔黄山松林土壤磷有效性的关键调控因素。     

TMEM16 Proteins Produce Volume-regulated Chloride Currents That Are Reduced in Mice Lacking TMEM16A

All vertebrate cells regulate their cell volume by activating chloride channels of unknown molecular identity, thereby activating regulatory volume decrease. We show that the Ca²⁺-activated Cl⁻ channel TMEM16A together with other TMEM16 proteins are activated by cell swelling through an autocrine mechanism that involves ATP release and binding to purinergic P2Y₂ receptors. TMEM16A channels are activated by ATP through an increase in intracellular Ca²⁺ and a Ca²⁺-independent mechanism engaging extracellular-regulated protein kinases (ERK1/2). The ability of epithelial cells to activate a Cl⁻ conductance upon cell swelling, and to decrease their cell volume (regulatory volume decrease) was dependent on TMEM16 proteins. Activation of I_Cl,swell was reduced in the colonic epithelium and in salivary acinar cells from mice lacking expression of TMEM16A. Thus TMEM16 proteins appear to be a crucial component of epithelial volume-regulated Cl⁻ channels and may also have a function during proliferation and apoptotic cell death.Regulation of cell volume is fundamental to all cells, particularly during cell growth and division. External hypotonicity leads to cell swelling and subsequent activation of volume-regulated chloride and potassium channels, to release intracellular ions and to re-shrink the cells, a process termed regulatory volume decrease (RVD)³ (1). Volume-regulated chloride currents (I_Cl,swell) have dual functions during cell proliferation as well as apoptotic volume decrease (AVD), preceding apoptotic cell death (2). Although I_Cl,swell is activated in swollen cells to induce RVD, AVD takes place under normotonic conditions to shrink cells (3, 4). Early work suggested intracellular Ca²⁺ as an important mediator for activation of I_Cl,swell and volume-regulated K⁺ channels (5), whereas subsequent studies only found a permissive role of Ca²⁺ for activation of I_Cl,swell (6), reviewed in Ref. 1. In addition, a plethora of factors and signaling pathways have been implicated in activation of I_Cl,swell, making cell volume regulation an extremely complex process (reviewed in Refs. 1, 3, and 7). These factors include intracellular ATP, the cytoskeleton, phospholipase A2-dependent pathways, and protein kinases such as extracellular-regulated kinase ERK1/2 (reviewed in Refs. 1 and 7). Previous approaches in identifying swelling-activated Cl⁻ channels have been unsuccessful or have produced controversial data. Thus none of the previous candidates such as pI_Cln, the multidrug resistance protein, or ClC-3 are generally accepted to operate as volume-regulated Cl⁻ channels (reviewed in Refs. 8 and 9). Notably, the cystic fibrosis transmembrane conductance regulator (CFTR) had been shown in earlier studies to influence I_Cl,swell and volume regulation (10–12). The variable properties of I_Cl,swell suggest that several gene products may affect I_Cl,swell in different cell types.The TMEM16 transmembrane protein family consists of 10 different proteins with numerous splice variants that contain 8–9 transmembrane domains and have predicted intracellular N- and C-terminal tails (13, 16–18). TMEM16A (also called ANO1) is required for normal development of the murine trachea (14) and is associated with different types of tumors, dysplasia, and nonsyndromic hearing impairment (13, 15). TMEM16A has been identified as a subunit of Ca²⁺-activated Cl⁻ channels that are expressed in epithelial and non-epithelial tissues (16–18). Interestingly, members of the TMEM16 family have been suggested to play a role in osmotolerance in Saccharomyces cerevisiae (19). Here we show that TMEM16 proteins also contribute to I_Cl,swell and regulatory volume decrease.     

Inhibition of Nischarin Expression Promotes Neurite Outgrowth through Regulation of PAK Activity

Nischarin is a cytoplasmic protein expressed in various organs that plays an inhibitory role in cell migration and invasion and the carcinogenesis of breast cancer cells. We previously reported that Nischarin is highly expressed in neuronal cell lines and is differentially expressed in the brain tissue of adult rats. However, the physiological function of Nischarin in neural cells remains unknown. Here, we show that Nischarin is expressed in rat primary cortical neurons but not in astrocytes. Nischarin is localized around the nucleus and dendrites. Using shRNA to knockdown the expression of endogenous Nischarin significantly increases the percentage of neurite-bearing cells, remarkably increases neurite length, and accelerates neurite extension in neuronal cells. Silencing Nischarin expression also promotes dendrite elongation in rat cortical neurons where Nischarin interacts with p21-activated kinase 1/2 (PAK1/2) and negatively regulates phosphorylation of both PAK1 and PAK2. The stimulation of neurite growth observed in cells with decreased levels of Nischarin is partially abolished by IPA3-mediated inhibition of PAK1 activity. Our findings indicate that endogenous Nischarin inhibits neurite outgrowth by blocking PAK1 activation in neurons.     

Significantly reinforced composite fibers electrospun from silk fibroin/carbon nanotube aqueous solutions

Microcomposite fibers of regenerated silk fibroin (RSF) and multiwalled carbon nanotubes (MWNTs) were successfully prepared by an electrospinning process from aqueous solutions. A quiescent blended solution and a three-dimensional Raman image of the composite fibers showed that functionalized MWNTs (F-MWNTs) were well dispersed in the solutions and the RSF fibers, respectively. Raman spectra and wide-angle X-ray diffraction (WAXD) patterns of RSF/F-MWNT electrospun fibers indicated that the composite fibers had higher β-sheet content and crystallinity than the pure RSF electrospun fibers, respectively. The mechanical properties of the RSF electrospun fibers were improved drastically by incorporating F-MWNTs. Compared with the pure RSF electrospun fibers, the composite fibers with 1.0 wt % F-MWNTs exhibited a 2.8-fold increase in breaking strength, a 4.4-fold increase in Young's modulus, and a 2.1-fold increase in breaking energy. Cytotoxicity test preliminarily demonstrated that the electrospun fiber mats have good biocompatibility for tissue engineering scaffolds.     

Nischarin inhibits LIM kinase to regulate cofilin phosphorylation and cell invasion

Nischarin is a novel protein that regulates cell migration by inhibiting p21-activated kinase (PAK). LIM kinase (LIMK) is a downstream effector of PAK, and it is known to play an important role in cell invasion. Here we show that nischarin also associates with LIMK to inhibit LIMK activation, cofilin phosphorylation, and LIMK-mediated invasion of breast cancer cells, suggesting that nischarin regulates cell invasion by negative modulation of the LIMK/cofilin pathway. The amino terminus of nischarin binds to the PDZ and kinase domains of LIMK. Although LIMK activation enhances the interaction with nischarin, only phosphorylation of threonine 508 of LIMK is crucial for the interaction. Inhibition of endogenous nischarin expression by RNA interference stimulates breast cancer cell invasion. Also, nischarin small interfering RNA (siRNA) enhances cofilin phosphorylation. In addition, knock-down of nischarin showed branched projection actin structures. Collectively these data indicate that nischarin siRNA may enhance random migration, resulting in stimulation of invasion.