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1.
植物化石气孔参数分析是目前恢复古大气二氧化碳浓度较为精准的方法之一,银杏类和松柏类等是恢复古大气CO_2浓度常用的化石类群。本文利用新疆准噶尔盆地下侏罗统三工河组的松柏类掌鳞杉科Brachyphyllum(Hirmeriella?)sp.化石对早侏罗世大气CO_2浓度进行了重建,获得早侏罗世大气CO_2浓度为~1200ppm,丰富了早侏罗世大气CO_2浓度信息,进一步说明掌鳞杉科植物通过气孔比率法在重建侏罗纪大气CO_2浓度方面的可靠性。掌鳞杉科植物的旱生构造和较高的大气CO_2浓度表明早侏罗世Toarcian期大洋缺氧事件在陆地生态系统内可能产生了一定的响应。  相似文献   

2.
陆生植物气孔参数与大气CO2浓度变化   总被引:2,自引:0,他引:2  
陆生植物的起源与演化与全球气候和环境的变化密不可分,利用植物气孔参数(气孔密度和气孔指数)来指示或重建古大气CO2浓度变化是近年来全球变化研究的热点之一。就陆生植物气孔参数的研究进行了概述,对研究中存在的问题及其前景作了简要探讨,并对植物生物学方法在定量研究古气候和古环境变化的趋势进行了分析。  相似文献   

3.
陆生植物气孔参数与大气CO_2浓度变化   总被引:1,自引:0,他引:1  
陆生植物的起源与演化与全球气候和环境的变化密不可分,利用植物气孔参数(气孔密度和气孔指数)来指示或重建古大气CO2浓度变化是近年来全球变化研究的热点之一。就陆生植物气孔参数的研究进行了概述,对研究中存在的问题及其前景作了简要探讨,并对植物生物学方法在定量研究古气候和古环境变化的趋势进行了分析。  相似文献   

4.
气孔导度对CO_2浓度变化的模拟及其生理机制   总被引:2,自引:0,他引:2  
王建林  温学发 《生态学报》2010,30(17):4815-4820
基于气孔运动的生理生化机制重点进行了气孔导度(gs)对CO2浓度变化的响应机制分析,并推导得到气孔导度(gs)对CO2浓度变化响应模型,并以9种植物进行了模型验证。结果表明:随着CO2浓度的升高,气孔导度会逐渐降低,且下降的幅度会随着CO2浓度的升高而逐渐减弱。气孔导度对CO2浓度(Cs)变化的响应模型可以表达为gs=gmax/(1+Cs/Cs0),其中式中gmax是最大气孔导度和Cs0是实验常数。该模型较好地模拟了气孔导度随CO2浓度变化的规律,模型参数具有明确的生理意义,与Jarvis模型和Ball-Berry模型相比,该模型如何实现多种环境因子的耦合有待进一步突破。另外,模型是在短期改变叶片CO2浓度的条件下得出的,在CO2浓度长期胁迫下的适用性也有待进一步确认。  相似文献   

5.
CO2倍增对不同氮水平下小麦幼苗根系及叶片NR活性的影响   总被引:2,自引:0,他引:2  
以小麦品种'小偃22'幼苗为材料,采用开顶式气室和水培实验研究了不同供氮水平(2.5、5.0、10.0和 15.0 mmol·L-1)下小麦幼苗植株生长量、根系形态、有机碳分泌速率和硝酸还原酶(NR)活性对大气CO2浓度升高的响应.结果显示,大气CO2浓度倍增均增加了小麦幼苗各生长阶段根冠生物量以及根系长度、面积、有机碳分泌速率和叶片NR活性.随供氮水平的提高,各生长阶段幼苗根冠生物量、根长和面积以及叶片NR活性呈上升趋势,而有机碳分泌速率呈下降趋势;根冠比变化不同阶段表现不一致,一叶一心期呈下降趋势,二叶一心期和三叶一心期分别以15.0和10.0 mmol·L-1氮水平较高.研究表明,大气CO2浓度升高可促进小麦幼苗根系生长和有机碳分泌速率,提高其氮素同化能力;增加介质供氮有利于高CO2浓度条件下小麦幼苗根冠生长和氮素同化,提高根冠比,减少根系有机碳过度分泌引起的碳损耗.  相似文献   

6.
气孔参数与大气CO2浓度的相关性及其影响因素   总被引:5,自引:0,他引:5  
通常认为气孔参数(气孔密度和气孔指数)和大气CO2浓度有负相关关系,但不是每种植物的气孔参数都与CO2浓度的变化有负相关关系,气孔参数对大气CO2浓度的显著反应也只在一定的CO2浓度范围内发生。大气CO2浓度是影响气孔参数变化的主要因素,同时温度、水分的供应和光照条件等其它环境因素也影响气孔参数。CO2浓度和光照条件主要影响气孔发生,而其它环境因素主要影响叶片表皮细胞的大小。气孔指数部分消除了表皮细胞大小带来的影响,用气孔指数指示大气CO2浓度比用气孔密度指示更为可靠。  相似文献   

7.
重点描述云南腾冲晚第三纪两种被子植物化石Betula mioluminifera Hu et Chaney,Carpinus subcordata Nathorst的角质层构造,并分析它们的现存最近亲缘种B.luminifera Winkler和C.cordata B1.var.mollis Cheng et Chen的表皮特征。实验分析证明:化石叶片的气孔参数可以推测地质历史时期大气CO2的浓度,并进而分析古环境的变化。C.subcordata Nathorst叶片能作为大气CO2浓度的生物指标。  相似文献   

8.
氮素对高大气CO_2浓度下小麦叶片光合作用的影响   总被引:2,自引:0,他引:2  
通过测定小麦拔节期叶片的光合气体交换参数和光强-光合速率(Pn)响应曲线,研究了氮素对长期高大气CO2浓度(760μmol.mol-1)下小麦叶片光合作用的影响.结果表明:在长期高大气CO2浓度下,增施氮肥能提高小麦叶片Pn、蒸腾速率(Tr)和瞬时水分利用效率(WUEi);与正常大气CO2浓度相比,高大气CO2浓度下小麦叶片的Pn和WUEi增加,气孔导度(Gs)和胞间CO2浓度(Ci)降低.随光合有效辐射的增强,高大气CO2浓度下小麦叶片的Pn和WUEi均高于正常大气CO2浓度处理,Gs则较低,而Ci和Tr无显著变化.高氮水平下小麦叶片Gs与Pn、Tr、WUEi呈线性正相关,Gs与Ci在正常大气CO2浓度下呈线性负相关,但高大气CO2浓度下二者无相关性;低氮水平下小麦叶片的Gs与Pn、WUEi无相关性,而与Ci和Tr呈线性正相关,表明高大气CO2浓度下低氮水平的小麦叶片Pn由非气孔因素限制.  相似文献   

9.
大气CO2浓度升高对植物根系的影响   总被引:3,自引:0,他引:3  
植物长期生长在CO2浓度不断升高的环境中,其结构和功能都将受到影响,这种影响不仅表现在植物的地上部分,同时也表现在植物的地下部分(根系),尤其是细根的长度、直径、产量、周转以及根与枝的分配模式等方面。植物根系结构和功能的改变影响植物地上部分和生态系统物质循环中的碳动态及土壤中碳库的变化。目前有关大气CO2浓度升高对根系动态影响的研究报道主要包括大气CO2浓度升高对根系结构(直径、分枝、长度、数量等)和根系生理(周转率、产量、碳分配模式等)的影响2个方面。目前,该领域研究还存在一些不足,例如在CO2浓度升高条件下,对植物根系内部的调控机制,以及由其引起的物质循环和能量流动的动态变化的了解较少;至今没有令人信服的证据说明大气CO2浓度升高使根系周转升高还是降低。今后应加强研究在CO2浓度升高条件下根系的周转变化和光合产物分配模式变化,CO2浓度升高和外界环境因素的共同作用对根系的影响,以及采用不同研究方法和研究对象在不同立地条件下开展升高CO2浓度对根系影响的对比研究等。  相似文献   

10.
俄有浩  霍治国  赵花荣  马玉平 《生态学报》2020,40(18):6613-6620
旨在了解农田CO2浓度长期动态变化特征、趋势、浓度增量分布模式等,收集了2007—2018年中国气象局固城生态与农业气象试验站开路式涡相关CO2浓度观测数据。研究了华北平原农田CO2浓度的年际、年内、昼夜和CO2通量等动态变化特征,对比分析了华北平原农田CO2浓度与城市站和大气本底站CO2浓度变化趋势及差异。结果表明,近十多年来华北平原农田CO2年平均浓度显著升高31.0 μmol/mol(r=0.263, P<0.01),年均增幅(2.58 μmol/mol)与全球和瓦里关本底站大气CO2浓度增幅接近,但农田CO2浓度年际和年内季节变化波动巨大,日平均浓度和逐时平均浓度标准差分别为33.7和33.5 μmol/mol。夜间CO2平均浓度395.8 μmol/mol,比白天高36.2 μmol/mol(10.1%),8月最高差值达到74.4 μmol/mol(20.6%)。在作物生长季节,5月和8—9月白天CO2浓度出现的两个谷值准确地对应了CO2通量动态变化的两个峰值,表明4—9月昼间CO2浓度和通量动态变化很好地反映了华北平原冬小麦和夏玉米生长过程、农事活动和农田碳交换的关系。农田CO2浓度动态变化与城市、湿地和大气本底站的变化特征不同,表明其动态变化的形成机制有差异。农田CO2浓度昼夜及季节变化特征为研究和评估CO2浓度升高影响作物生长和产量提供指导依据。  相似文献   

11.
A system was developed to control arterial O2 and CO2 partial pressure (Pao2, and Paco2) simultaneously and independently of each other. The system makes changes in inspired fractional concentration of O2 and CO2 based on values for end-tidal O2 and CO2 partial pressure. The system was applied in 23 normal subjects. In attempts to maintain a Pao2 of 90 Torr and a Paco2 of 40 Torr, arterial blood gases were 91.1 +/- 6.5 (SD) Torr for Pao2 and 41.2 +/- 3.2 Torr for Paco2. In attempts to maintain a Pao2 of 40 Torr and a Paco2 of 40 Torr, arterial blood gases were 40.4 +/- 3.9 Torr for Pao2 and 38.9 +/- 2.5 Torr for Paco2. In attempts to maintain a Pao2 of 90 Torr and a Paco2 of 55 Torr, arterial blood gases were 98.1 +/- 11.5 Torr for Pao2 and 52.8 +/- 3.4 Torr for Paco2. Coefficients of variations ranged from 7.1 to 11.7% for Pao2 and 6.4 to 7.8% for Paco2.  相似文献   

12.
eIF2B is a multisubunit protein that is critical for protein synthesis initiation and its control. It is a guanine nucleotide exchange factor (GEF) for its GTP-binding protein partner eIF2. eIF2 binds initiator tRNA to ribosomes and promotes mRNA AUG codon recognition. eIF2B is critical for regulation of protein synthesis via a conserved mechanism of phosphorylation of eIF2, which converts eIF2 from a substrate to an inhibitor of eIF2B GEF. In addition, inherited mutations affecting eIF2B subunits cause the fatal disorder leukoencephalopathy with Vanishing White Matter (VWM), also called Childhood Ataxia with Central nervous system Hypomyelination (CACH). Here we review findings which reveal that eIF2B is a decameric protein and also define a new function for the eIF2B. Our results demonstrate that the eIF2Bγ subunit is required for eIF2B to gain access to eIF2•GDP. Specifically it displaces a third translation factor eIF5 (a dual function GAP and GDI) from eIF2•GDP/eIF5 complexes. Thus eIF2B is a GDI displacement factor (or GDF) in addition to its role as a GEF, prompting the redrawing of the eIF2 cycling pathway to incorporate the new steps. In structural studies using mass spectrometry and cross-linking it is shown that eIF2B is a dimer of pentamers and so is twice as large as previously thought. A binding site for GTP on eIF2B was also found, raising further questions concerning the mechanism of nucleotide exchange. The implications of these findings for eIF2B function and for VWM/CACH disease are discussed.  相似文献   

13.
Acidovorax sp. strain JS42 is able to utilize 2-nitrotoluene (2NT) as its sole carbon, nitrogen, and energy source. We report here that strain JS42 is chemotactic to 2NT and that the response is increased when cells are grown on compounds such as 2NT that are known to induce the first step of 2NT degradation. Assays with JS42 mutants unable to oxidize 2NT showed that the first step of 2NT metabolism was required for the induced response, but not for a portion of the constitutive response, indicating that 2NT itself is an attractant. The 2NT metabolite nitrite was shown to be a strong attractant for strain JS42, and sufficient nitrite was produced during the taxis assay to account for a large part of the induced response. A mutant with an inactivated ntdY gene, which is located adjacent to the 2NT degradation genes and codes for a putative methyl-accepting chemotaxis protein, showed a defect in taxis toward 2NT that may involve a reduced response to nitrite. Responses of a mutant defective for the energy-taxis receptor, Aer, indicated that a functional aer gene is required for a substantial part of the wild-type induced response to 2NT. In summary, strain JS42 utilizes three types of taxis to sense and respond to 2NT: constitutive 2NT-specific chemotaxis to directly sense 2NT, metabolism-dependent nitrite-specific chemotaxis that may be mediated by NtdY, and energy taxis mediated by Aer.  相似文献   

14.
We isolated and characterized a cDNA for the N-terminal half of the eukaryotic initiation of translation factor 2 (cIF2) during a screen of chicken osteoblast cDNAs. The apparent size of the message for this protein, approximately 5.6 kb, is slightly larger in size than that for human IF2 (hIF2). There is a high degree of sequence similarity between the human and chicken N-terminal portions of the protein that extends to the encoding nucleotide sequence. The tissue specific expression pattern for cIF2 and hIF2 are similar, being moderately abundant in brain, liver, and skeletal muscle, and detectable in kidney, chondrocytes, and freshly isolated osteoblasts. The ratio of message for cIF2 to that of beta-actin was 0.10 and 0.18 for liver and brain. Message levels peak in osteoblasts between 8 and 12 days of culture, coinciding with high levels of matrix protein synthesis. At peak expression, the ratio of cIF2:beta-actin for 8 day osteoblasts was 0.76. Treatment of osteoblast cultures with cycloheximide markedly reduces the level of cIF2 message indicating that novel protein synthesis is required for its expression. Hybridization of RNA samples from either chicken osteoblasts or a human osteoblast cell line with a probe for a subunit of human eukaryotic initiation of translation factor 2 (eIF2alpha), the housekeeping initiation factor, indicates that levels of eIF2 remain low. With hIF2, cIF2 represents the only other vertebrate homolog of IF2 for which a major portion of the coding sequence has been identified. This is the first report of regulated expression for a eukaryotic IF2 and is the first demonstration of its abundance in osteoblasts.  相似文献   

15.
We identified the mitotic kinesin-like protein 2 (MKlp2), a kinesin required for chromosome passenger complex (CPC)-mediated cytokinesis, as a target of the mitotic checkpoint protein Mad2. MKlp2 possesses a consensus Mad2-binding motif required for Mad2 binding. Mad2 prevents MKlp2 from loading onto the mitotic spindle, a prerequisite step for its function as a mitotic kinesin. Furthermore, Mad2 inhibits the ability of MKlp2 to relocate the CPC from centromeres, an essential step to promote cytokinesis. An MKlp2 mutant that is refractory to Mad2-mediated inhibition prematurely translocates to the mitotic spindle and mislocalizes the CPC component Aurora B from the midbody of dividing cells. This correlates with an increased incidence of cytokinesis failure. Together, these findings reveal that MKlp2 is a novel mitotic target of Mad2 necessary for proper mitotic progression and cytokinesis.  相似文献   

16.
The present investigation was designed to develop an assay suitable for pharmacokinetic studies of new compounds, i.e. the novel 7,8-methylenedioxy-4H-2,3-benzodiazepin-4-one derivatives (2a and 2b), acting as non-competitive AMPA-receptor antagonists. A reversed-phase high-performance liquid chromatographic method has been developed to determine the time-course of plasma concentrations of derivatives 2a and 2b administered intraperitoneally to Sprague-Dawley rats. The separation of compounds studied and a N-methyl-2,3-benzodiazepin-4-one derivative as internal standard (I.S.) from plasma, were carried out by liquid-liquid extraction using diethyl ether. The samples were injected onto the analytical column (Partisil 10 ODS) eluted with acetonitrile/0.01 M acetate buffer (pH 5.3) at a flow-rate of 2 ml/min and detected at 240 nm. Compounds 2a, 2b and I.S. gave retention times of 8.5, 5.25 and 11.1 min, respectively. The selectivity of the method was satisfactory. The mean recovery from spiked rat plasma ranged from 86.7 to 91.6% for 2a, and from 85.1 to 87.0% for 2b. The procedures were validated with a good reproducibility and linear response from 0.0625 to 2 microg/ml, with a regression coefficient of 0.9932 for 2a and 0.9854 for 2b. The lower limit of quantification (LOQ) was taken as 15 ng/ml for the two compounds. 2a and 2b showed no signs of significant degradation in rat plasma during storage at -20 degrees C and following freeze/thaw cycles. Moreover, plasma levels of the tested compounds have been correlated with their anticonvulsant activity, determined in vivo in genetically epilepsy-prone rats. Due to its sensitivity, the method was suitable for application to pharmacokinetic study.  相似文献   

17.
A high-affinity Mg2+-independent Ca2+-ATPase (Ca2+-ATPase) has been differentiated from the Mg2+-dependent, Ca2+-stimulated ATPase (Ca2+,Mg2+-ATPase) in rat brain synaptosomal membranes. Using ATP as a substrate, the K0.5 of Ca2+ for Ca2+-ATPase was found to be 1.33 microM with a Km for ATP of 19 microM and a Vmax of 33 nmol/mg/min. Using Ca-ATP as a substrate, the Km for Ca-ATP was found to be 0.22 microM. Unlike Ca2+,Mg2+-ATPase, Ca2+-ATPase was not inhibited by N-ethylmaleimide, trifluoperazine, lanthanum, zinc, or vanadate. La3+ and Zn2+, in contrast, stimulated the enzyme activity. Unlike Ca2+, Mg2+-ATPase activity, ATP-dependent Ca2+ uptake was negligible in the absence of added Mg2+, indicating that the Ca2+ transport into synaptosomal endoplasmic reticulum may not be a function of the Ca2+-ATPase described. Ca2+-ATPase activity was not stimulated by the monovalent cations Na+ or K+. Ca2+, Mg2+-ATPase demonstrated a substrate preference for ATP and ADP, but not GTP, whereas Ca2+-ATPase hydrolyzed ATP and GTP, and to a lesser extent ADP. The results presented here suggest the high-affinity Mg2+-independent Ca2+-ATPase may be a separate form from Ca2+,Mg2+-ATPase. The capacity of Mg2+-independent Ca2+-ATPase to hydrolyze GTP suggests this protein may be involved in GTP-dependent activities within the cell.  相似文献   

18.
19.
Matrix metalloproteinase-2 (MMP-2) functions in diverse biological processes through the degradation of extracellular and non-extracellular matrix molecules. Because of its potential for tissue damage, there are several ways to regulate MMP-2 activity, including gene expression, compartmentalization, zymogen activation, and enzyme inactivation by extracellular inhibitors. Enzyme regulation through zymogen activation is important for the regulation of MMP-2 activity. In our previous studies, we showed that thrombin directly cleaved the propeptide of MMP-2 at specific sites for enzyme activation. We also demonstrated that heparan sulfate was required for thrombin-mediated activation of pro-MMP-2 by binding to thrombin, presumably through conformational changes at the active site of the enzyme. This suggests a regulatory mechanism for thrombin-mediated activation of pro-MMP-2. In this study, we found that MMP-2 formed a reduction-sensitive homodimer in a controlled manner and that Ca(2+) ion was essential for homodimerization of MMP-2. Homodimerization was not associated with protein kinase C-mediated phosphorylation of MMP-2. MMP-2 formed a homodimer through an intermolecular disulfide bond between Cys(102) and the neighboring Cys(102). Homodimerization of MMP-2 enhanced thrombin-mediated activation of pro-MMP-2. Moreover, the MMP-2 homodimer could cleave a small peptide substrate without removal of the propeptide. Taken together, our experimental data suggest a novel regulatory mechanism for pro-MMP-2 activation that is modulated through homodimerization of MMP-2.  相似文献   

20.
We report here characterization of calmodulin-stimulated Ca2+ transport activities in synaptic plasma membranes (SPM). The calcium transport activity consists of a Ca2+-stimulated, Mg2+-dependent ATP hydrolysis coupled with ATP-dependent Ca2+ uptake into membraneous sacs on the cytosolic face of the synaptosomal membrane. These transport activities have been found in synaptosomal subfractions to be located primarily in SPM-1 and SPM-2. Both Ca2+-ATPase and ATP-dependent Ca2+ uptake require calmodulin for maximal activity (KCm for ATPase = 60 nM; KCm for uptake = 50 nM). In the reconstituted membrane system, KCa was found to be 0.8 microM for Ca2+-ATPase and 0.4 microM for Ca2+ uptake. These results demonstrate for the first time the calmodulin requirements for the Ca2+ pump in SPM when Ca2+ ATPase and Ca2+ uptake are assayed under functionally coupled conditions. They suggest that calmodulin association with the membrane calcium pump is regulated by the level of free Ca2+ in the cytoplasm. The activation by calmodulin, in turn, regulates the cytosolic Ca2+ levels in a feedback process. These studies expand the calmodulin hypothesis of synaptic transmission to include activation of a high-affinity Ca2+ + Mg2+ ATPase as a regulator for cytosolic Ca2+.  相似文献   

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