Anhydrobiosis: plant desiccation gene found in a nematode

When subjected to drought conditions, some organisms enter a state of suspended animation known as anhydrobiosis, surviving for indefinite periods until rehydration allows them to resume normal metabolism. We have identified a gene in the anhydrobiotic nematode Aphelenchus avenae that is upregulated in response to desiccation stress and whose encoded protein shares sequence similarity with a late-embryonic gene that is induced in many plants when they are deprived of water. This finding suggests that animals and plants that undergo anhydrobiosis may use common protective strategies against dehydration, and provides a unifying insight into the mechanism of anhydrobiosis.     

盐胁迫下植物质膜H+-ATPase研究进展

质膜H -ATPase在植物细胞的跨膜物质转运、胞内pH值调节以及植物对环境胁迫的响应等诸多方面具有重要作用,是植物生命活动过程的主宰酶.盐胁迫是影响植物生长发育的主要环境因子,植物质膜H -ATPase活性的调节是植物适应盐环境、提高耐盐性的重要细胞机理.综述了植物质膜H -ATPase活性变化及其调节机理对盐胁迫响应的研究状况,对质膜H -ATPase活性调节机理研究中仍未解决的问题进行了展望.     

螺旋藻抗氧化酶系统对干燥胁迫的响应

对极大螺旋藻(Spirulina maxima)进行常温脱水处理,研究干燥胁迫对螺旋藻抗氧化酶活性的影响.结果表明:螺旋藻超氧化物歧化酶(SOD)对细胞脱水反应不敏感,脱水过程中其活性保持不变,过氧化氢酶(CAT)和抗坏血酸过氧化物酶(APX)能很快对干燥胁迫作出响应,两者活性均上升1倍左右,而过氧化物酶(POD)活性呈下降趋势.干燥胁迫30 h后各抗氧化酶活性均下降,其中POD失活.丙二醛(MDA)质量摩尔浓度在整个胁迫过程中波动较小,脱水过程中略有下降,干燥胁迫30 h后又有所上升.螺旋藻的抗氧化酶系统能抵御细胞脱水所引起的氧化伤害,其中CAT和APX的活性变化幅度可作为检验螺旋藻脱水耐受力的敏感性指标.     

Haemodynamic shear stress activates a K+ current in vascular endothelial cells

The endothelial lining of blood vessels is subjected to a wide range of haemodynamically-generated shear-stress forces throughout the vascular system. In vivo and in vitro, endothelial cells change their morphology and biochemistry in response to shear stress in a force- and time-dependent way, or when a critical threshold is exceeded. The initial stimulus-response coupling mechanisms have not been identified, however. Recently, Lansman et al. described stretch-activated ion channels in endothelial cells and suggested that they could be involved in the response to mechanical forces generated by blood flow. The channels were relatively nonselective and were opened by membrane stretching induced by suction. Here we report whole-cell patch-clamp recordings of single arterial endothelial cells exposed to controlled levels of laminar shear stress in capillary flow tubes. A K+ selective, shear-stress-activated ionic current (designated Ik.s) was identified which is unlike previously described stretch-activated currents. Ik.s varies in magnitude and duration as a function of shear stress (half-maximal effect at 0.70 dyn cm-2), desensitizes slowly and recovers rapidly and fully on cessation of flow. Ik.s activity represents the earliest and fastest stimulus-response coupling of haemodynamic forces to endothelial cells yet found. We suggest that localized flow-activated hyperpolarization of endothelium involving Ik.s may participate in the regulation of vascular tone.     

木本植物响应干旱胁迫的研究现状

为深入了解木本植物响应干旱胁迫的分子机理，本文系统的从木本植物对干旱信号的感知、信号转导到转录调控、生理生化反应以及表型变化等方面总结了木本植物对干旱胁迫可能的响应过程.认为木本植物由于其固着根生的特点，不得不进化出相应的机制来应对不断变化的环境.当遭受干旱胁迫时，木本植物根系细胞膜上的感受器首先感知到土壤水分状态的变化，细胞内的蛋白质和激素调控系统触发相应的干旱适应反应.干旱信号通过细胞间的信号传导路径传递到植物体内的各个部位，主要的信号传导途径包括Ca²⁺信号、激素信号和转录因子调控等.一些关键基因和信号通路，如脱落酸(ABA)信号通路、DREB蛋白家族等也参与调控植物的干旱适应性.木本植物也会发生形态和解剖上的变化来减少水分蒸发和增强根系的吸水能力.本文可为抗旱型木本植物选育提供见解.     

Reversible inactivation of K+ channels of Vicia stomatal guard cells following the photolysis of caged inositol 1,4,5-trisphosphate

RECENT investigations suggest that cytoplasmic D-myo-inositol 1,4,5-trisphosphate (InsP3) functions as a second messenger in plants, as in animals, coupling environmental and other stimuli to intracellular Ca2+ release. Cytoplasmic levels of InsP3 and the turnover of several probable precursors in plants are affected by physiological stimuli--including light, osmotic stress and the phytohormone indoleacetic acid--and InsP3 activates Ca2+ channels and Ca2+ flux across plant vacuolar and microsomal membranes. Complementary data also link changes in cytoplasmic free Ca2+ to several physiological responses, notably in guard cells which regulate gas exchange through the stomatal pores of higher plant leaves. Recent evidence indicates that guard cell K+ channels and, hence, K+ flux for stomatal movements may be controlled by cytoplasmic Ca2+. So far, however, direct evidence of a role for InsP3 in signalling in plants has remained elusive. Here we report that InsP3 released from an inactive, photolabile precursor, the P5-1-(2-nitrophenyl)ethyl ester of InsP3 (caged InsP3) reversibly inactivates K+ channels thought to mediate K+ uptake by guard cells from Vicia faba L. while simultaneously activating an apparently time-independent, inward current to depolarize the membrane potential and promote K+ efflux through a second class of K+ channels. The data are consistent with a transient rise in cytoplasmic free Ca2+ and demonstrate that intact guard cells are competent to use InsP3 in signal cascades controlling ion flux through K+ channels.     

植物抗菌肽研究进展

植物抗菌肽是一类对细菌,真菌等微生物有抑制或杀灭作用的小分子多肽,它能被细菌,真菌或物理的,化学的刺激所诱导,有些抗菌肽甚至在植物体内能组成性的表达,从化学结构来看,植物抗菌肽要包括硫堇,植物防卫素,脂转移蛋白和橡胶素类等,它们抗菌能力强,有较好的耐热性,抗菌机理独特,在农业,医药及食品等领域有着广泛的应用前景。作者总结了国内外植物抗菌肽研究进展,对其应用研究的基因工程等方面作了阐述,并对进一步研     

盐胁迫对植物的影响及植物耐盐机理研究进展

盐分是影响植物生长发育的一个重要环境因素,盐胁迫对植物的整个生命进程产生影响,盐分通过渗透胁迫、离子毒害,使植物细胞膜透性改变,造成氧化胁迫、代谢紊乱及蛋白质合成受阻等现象,植物的耐盐性主要体现在离子的选择性吸收和区域化作用、渗透调节、光合作用途径的改变以及活性氧清除机制。     

植物体内的多功能蛋白酶——谷胱甘肽转移酶

谷胱甘肽转移酶(Glutathione S-transferases,GSTs)在植物体内普遍存在,是由一个大的多基因家族编码的多功能蛋白酶。GSTs的表达受多种环境因子的诱导,在植物的生长发育、次生代谢和耐逆中有重要作用。本文简要介绍了GST的研究概况,重点讨论了其生理功能。     

干旱与半干旱区一年生植物水势对模拟降水变化的响应

植物水势可以反映和度量植物水分状况.通过测量叶片水势,可以掌握植物受水分胁迫程度,以及植物对水分的敏感程度.以内蒙古干旱与半干旱区2种藜科一年生猪毛菜类植物:猪毛菜(Salsola collina)、雾冰藜(Bassia dasyphylla)和2种禾本科一年生小禾草类植物:虎尾草(Chloris virgata)、冠芒草(Pappophorum boreale)为研究对象,模拟5 mm、20mm、70 mm和150 mm四种降水量水平,通过监测叶片水势来研究一年生植物水势对降水量变化的响应.研究表明,一年生猪毛菜类植物比一年生小禾草类植物对降水更敏感,一年生小禾草类植物比一年生猪毛菜类植物更抗旱.一年生猪毛菜类植物表现出以相对较高的水势来延迟脱水的干旱适应方式,一年生小禾草类则表现出更多以较低的水势来忍耐脱水的干旱适应方式.     

通过反常研究Reissner-Nordstrφm -de Sitter黑洞的霍金辐射

用Robinson and Wilczek提出的反常取消法,研究了Reissner-Nordstrφm-de Sitter黑洞事件视界和宇宙视界处的霍金辐射.结果表明在事件视界和宇宙视界处的规范和能动张量补偿流都精确的等于具有霍金温度的1+1维的黑体辐射流.     

脱水和复水金发藓酶清除ROS系统响应机制

以生存于变水环境中的金发藓为材料，通过快速脱水和复水的方式，探究金发藓在脱水胁迫时对于活性氧的响应机制，并进一步探究苔藓植物脱水耐性特性.结果显示：（1）随着脱水时间的增长，金发藓内积累大量的活性氧物质，脱水至120 min时·O^-₂、H₂O₂和OH^-等都达到最高水平；（2）抗氧化剂SOD，CAT，APX，ASA，GSH等在脱水复水过程中均上升，复水后下降，但是GSH和ASA在120 min复水后期仍未能恢复到对照水平;（3）金发藓在应对氧化胁迫过程中，通过启动ASA-GSH代谢循环途径以应对氧化胁迫.研究表明，金发藓对于脱水环境导致的氧化胁迫具有很强的应对能力，而且在复水后在极短的时间内能恢复生命活性，金发藓有效的抗氧化代谢机制使金发藓能长期生存于多变水环境中.     

干旱及冻融胁迫对黑麦草抗氧化酶活性和脯氨酸质量比的影响

以冬牧70黑麦草为材料, 用聚乙二醇（PEG 6000）模拟干旱胁迫, 设置5%（D1),10%(D2),15%(D3)三种不同程度干旱（轻度、 中度、 重度）以及对照组（CK）, 温度为10,5,0,-5,0,5,10 ℃, 研究冻融及干旱胁迫对幼苗中抗氧化酶活性和脯氨酸质量比的影响. 结果表明： 单一干旱胁迫下黑麦草幼苗中超氧化物歧化酶（SOD）、 抗氧化物酶 （POD）活性和脯氨酸质量比均 增加; 冻融和复合胁迫下幼苗中SOD活性呈先升高后显著下降趋势, POD活性和脯氨酸质量比呈先升高后缓慢下降趋势, 在-5 ℃出现峰值, 与其他温度下的数值存在显著性差异（P<0.05）; 胁迫伤害下整体呈复合胁迫>单干旱胁迫>单冻融胁迫的趋势, 冻融胁迫下的伤害程度为重度干旱+冻融>轻度干旱+冻融>单一冻融>中度干旱+冻融, 复合胁迫对植物伤害出现叠加效应, 适当的干旱处理可缓解冻融对幼苗的生理损害. 因此植物通过提高抗氧化酶活性和渗透调节物质, 可缓解其遇到胁迫时的伤害.     

干旱及冻融胁迫对黑麦草抗氧化酶活性和脯氨酸质量比的影响

以冬牧70黑麦草为材料, 用聚乙二醇（PEG 6000）模拟干旱胁迫, 设置5%（D1),10%(D2),15%(D3)三种不同程度干旱（轻度、 中度、 重度）以及对照组（CK）, 温度为10,5,0,-5,0,5,10 ℃, 研究冻融及干旱胁迫对幼苗中抗氧化酶活性和脯氨酸质量比的影响. 结果表明： 单一干旱胁迫下黑麦草幼苗中超氧化物歧化酶（SOD）、 抗氧化物酶 （POD）活性和脯氨酸质量比均 增加; 冻融和复合胁迫下幼苗中SOD活性呈先升高后显著下降趋势, POD活性和脯氨酸质量比呈先升高后缓慢下降趋势, 在-5 ℃出现峰值, 与其他温度下的数值存在显著性差异（P<0.05）; 胁迫伤害下整体呈复合胁迫>单干旱胁迫>单冻融胁迫的趋势, 冻融胁迫下的伤害程度为重度干旱+冻融>轻度干旱+冻融>单一冻融>中度干旱+冻融, 复合胁迫对植物伤害出现叠加效应, 适当的干旱处理可缓解冻融对幼苗的生理损害. 因此植物通过提高抗氧化酶活性和渗透调节物质, 可缓解其遇到胁迫时的伤害.     

The p66shc adaptor protein controls oxidative stress response and life span in mammals

Gene mutations in invertebrates have been identified that extend life span and enhance resistance to environmental stresses such as ultraviolet light or reactive oxygen species. In mammals, the mechanisms that regulate stress response are poorly understood and no genes are known to increase individual life span. Here we report that targeted mutation of the mouse p66shc gene induces stress resistance and prolongs life span. p66shc is a splice variant of p52shc/p46shc (ref. 2), a cytoplasmic signal transducer involved in the transmission of mitogenic signals from activated receptors to Ras. We show that: (1) p66shc is serine phosphorylated upon treatment with hydrogen peroxide (H2O2) or irradiation with ultraviolet light; (2) ablation of p66shc enhances cellular resistance to apoptosis induced by H2O2 or ultraviolet light; (3) a serine-phosphorylation defective mutant of p66shc cannot restore the normal stress response in p66shc-/- cells; (4) the p53 and p21 stress response is impaired in p66shc-/- cells; (5) p66shc-/- mice have increased resistance to paraquat and a 30% increase in life span. We propose that p66shc is part of a signal transduction pathway that regulates stress apoptotic responses and life span in mammals.