褪黑素参与植物抗逆功能研究进展

褪黑素(N-乙酰基-5-甲氧基色胺)是一种生命必需的小分子吲哚胺类物质,广泛存在于动植物体内,对动植物的生长发育起至关重要的作用。随着植物褪黑素研究的逐渐深入,褪黑素在植物体内的合成途径及作用也更加明确。研究表明,褪黑素在提高植物抵抗非生物和生物胁迫能力等方面具有调控作用。该文对近年来有关植物褪黑素参与非生物和生物胁迫的研究进展进行总结,旨在为阐明褪黑素影响植物抵御逆境胁迫的调控机理提供参考。     

植物褪黑素研究进展

褪黑素最初是在动物中发现的一种吲哚类小分子,具有昼夜节律调节、清除自由基等多种生理功能,还具有改善睡眠的保健作用。后来在植物中也检测到了褪黑素,这表明植物也能合成褪黑素。随着对植物褪黑素的深入研究,发现褪黑素在调控植物生长发育、耐受干旱、高温、低温、高盐、重金属等非生物胁迫、抵御细菌和真菌病害方面具有重要作用。从植物褪黑素合成途径、生长发育调控和胁迫应答反应方面的研究进展进行了综述,以期为植物褪黑素研究提供参考。     

干旱、盐、温度对植物体NADP-苹果酸酶的影响与机理

NADP-苹果酸酶是植物体代谢的重要酶之一,参与了多个代谢过程,在植物体内广泛存在,与各种环境胁迫关系密切。目前,胁迫条件下的植物体NADP-苹果酸酶基因的表达情况以及酶活性的变化是关注的重点,同时,NADP-苹果酸酶在抗胁迫方面的机理研究也在逐渐的展开。综述了干旱、盐、高温和低温胁迫条件下NADP-苹果酸酶活性及该酶基因表达变化的特点,揭示了其在对植物体抵御各种胁迫带来的危害时所发挥的作用以及作用机理。     

植物microRNA与逆境响应研究进展

MieroRNA(miRNA)是一类在生物体内普遍存在的非编码、长度约16～29 nt的小分子RNA,由内源基因编码,于转录后水平通过介导靶mRNA降解或翻译抑制调控基因表达,是真核细胞基因表达的重要调控因子.随着生物信息学与研究技术的发展,越来越多的植物miRNA得到预测和验证.逆境胁迫下,植物体诱导或下调相关miRNA表达,参与植物逆境生理调节与适应.文章综述了植物miRNA生物合成、与靶基因的作用方式,生物功能以及逆境胁迫响应miRNA,概要介绍了目前常用的miRNA研究方法.     

植物小分子RNA研究进展

植物体内存在多种不同类型的小分子RNA(small RNA,sRNA),在调节植物生长发育、抑制转座子活性和抵御逆境等过程中发挥着重要的作用。近年来,人们在sRNA的产生机制、效应复合物的形成和对靶基因的调控方式及其生物学功能等方面的研究取得了很大进展。该文对这些进展作简要介绍。     

植物甾醇在植物逆境胁迫中的研究进展

植物甾醇是一类重要的生理活性物质,对植物的生长发育具有重要作用,对响应植物逆境胁迫也具有重要功能.植物甾醇是细胞膜和脂质筏的重要组分,与膜的稳定性密切相关,主要通过甾醇含量的相对变化维持膜的稳定性及影响脂质筏的生物功能响应逆境胁迫.植物甾醇作为信号分子参与逆境胁迫中的信号传导,油菜素内酯类(BRs)是植物甾醇合成途径的重要产物,作为一种重要的信号分子调控植物甾醇合成酶基因的表达以响应逆境胁迫.     

水杨酸与植物抗逆性的关系

水杨酸(SA)是植物体内的一种新型激素,它不仅能调节植物的一些生长发育过程,还在植物抗生物胁迫和非生物胁迫中发挥着重要作用。重金属、热、盐等逆境能诱导植物体内SA的合成,缓解逆境对植物造成的伤害,增强植物的抗逆性能力。     

植物铁蛋白与氧化胁迫应激

植物铁蛋白是植物体重要的铁调节蛋白。许多研究表明植物铁蛋白与氧化胁迫抗性之间具有较强关联。植物铁蛋白不仅能抵御高铁产生的氧化毒性,在很多氧化胁迫及环境胁迫抗性中也发挥作用。对植物铁蛋白在氧化及逆境胁迫中的应激加以综述,为铁蛋白在生物工程领域的应用提供理论依据。     

逆境中植物体内特殊物质的合成

植物生长在自然环境中,不可避免地会遭到各种逆境因子的胁迫,如病虫害、干旱、盐渍、寒冷、热、涝、紫外线、重金属离子等。在长期的进化过程中,植物逐渐形成了抵御各种逆境的形态生理结构。除此之外,在遭受逆境因子袭击时,植物体会迅速作出反应,启动相关基因,合成一些具有保护作用的物质,包括各种逆激蛋白、植物激素以及一些小分子有机物。这些物质在正常环境中含量甚微,逆境时则大量合成,使生活在逆境中的植物尽量减少伤害,渡过不良环境。1　植物抗病反应中物质的合成真菌、细菌、病毒、寄生虫等病原物侵染植物后,植物会出现过敏反应,继而…     

盐胁迫盐芥和拟南芥褪黑素含量及合成相关基因表达模式分析

盐生植物盐芥（Eutrema salsugineum）耐盐适应性强且具备模式植物特征,是研究植物逆境适应机理的理想材料。作为一种多功能的激素信号分子,褪黑素在盐芥耐盐性中的作用仍不清楚。本研究以盐芥为主要材料,以拟南芥做对比,主要通过褪黑素酶联免疫以及实时荧光定量PCR分析,比较了二者在不同组织中褪黑素的积累和在响应盐胁迫过程中褪黑素合成、相关基因的表达模式以及外源褪黑素处理对其盐应答表型的影响。结果显示,两种植物的褪黑素合成均在幼叶中最高,盐芥本底褪黑素合成水平显著高于拟南芥,且盐胁迫诱导了两种植物中的褪黑素含量,但不同于盐芥,拟南芥在处理7 d后褪黑素合成明显下降。通过序列比对发现在不同植物中,盐芥和拟南芥褪黑素合成相关基因的亲缘关系较近。盐应答表达分析显示,盐芥SNAT1、ASMT和COMT在盐处理3 d表达上调,而拟南芥中的相关基因在处理1 d和3 d后受盐诱导,7 d后拟南芥中表达下降而盐芥中则无明显变化,表明两种植物相关基因响应盐信号的表达变化存在差异。此外,外源褪黑素处理明显缓解了两种植物在盐逆境下的胁迫表型。综上,褪黑素有效贡献于盐芥抗盐性,参与调节盐芥和拟南芥的耐盐适...     

Role for dopamine in malonate-induced damage in vivo in striatum and in vitro in mesencephalic cultures

Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.     

Scurvy in capybaras bred in captivity in Argentine

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.     

Changes in lactate dehydrogenase activity in chicken tissues in hyperthyreosis in ontogenesis

The lactate dehydrogenase activity in reactions of lactate oxidation and synthesis was studied in subfractions of the chicken brain, heart and liver at the embryonal, early postembryonal and adult stages of development after thyroxine administration. It has been shown that during embryogenesis thyroxine predominantly enhanced the rate of lactate oxidation in the mitochondrial tissues. A marked increase in the lactate synthesis was found in cytoplasm of the adult chicken tissues. Specificity of enzyme activity alterations was detected in the chicken brain during ontogenesis after thyroxine administration.     

SSTR5 ablation in islet results in alterations in glucose homeostasis in mice

Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.