植物SWEET蛋白的结构与分类及功能研究进展

植物SWEET蛋白是一类重要的转运蛋白,研究其生理生化功能,有助于分子辅助育种,缩短育种年限。本文基于文献资料,梳理归纳了近年来国内外的植物SWEET蛋白的结构、分类、转运底物和功能方面的相关研究进展,阐述表明SWEET蛋白是植物中广泛存在的一类糖转运体,既能转运单糖又能转运蔗糖,属于Mt N3家族。不同植物间的SWEET蛋白具有一定的保守性,根据亲缘关系SWEET家族可以分为四类。植物SWEET蛋白是位于膜系统上,参与糖分的跨膜转运,在植物生长发育及逆境胁迫中均有不同程度的调控作用,如调控花蜜的分泌、花粉的营养、灌浆期种子的发育、果实发育、植物抗逆性和抗病性等。然而不同植物的SWEET蛋白转运底物和调控功能不同,目前仅在拟南芥等少数植物中研究较为深入。     

副猪嗜血杆菌间接ELISA抗体检测试剂盒的研制与应用

【背景】副猪嗜血杆菌（Haemophilus parasuis,HPS）是猪的上呼吸道病原菌,引起格拉瑟氏病,主要引起断奶前后和保育阶段的猪发病,通常见于5—8周龄的青年猪,发病率一般为10%—15%。该菌有15种血清型,目前主要养猪国家流行的血清型为4型、5型、12型和13型,是严重危害养猪业发展的主要细菌性病原之一。目前国内还没有检测该菌抗体的商品化试剂盒。【目的】研制一种针对副猪嗜血杆菌的快速、敏感和特异性强的抗体检测试剂盒,为格拉瑟氏病的有效防控提供技术支持。【方法】表达并纯化OppA、DppA、HbpA 3种不同的副猪嗜血杆菌ABC转运体周质底物结合蛋白,使用副猪嗜血杆菌阴、阳性参考血清筛选以上3种蛋白中免疫反应性和反应特异性好的蛋白。以筛选的蛋白为包被抗原,建立检测HPS抗体的间接ELISA方法,优化间接ELISA反应条件,并组装试剂盒。在此基础上,确定该试剂盒的敏感性、特异性;通过对不同时间、不同猪场采集的2 000份临床猪血清样本进行检测,评价该试剂盒的实用性;在以上临床血清样本中随机选取200份,分别以研制的试剂盒、间接血凝试验以及进口商品化试剂盒进行检测,比较检测结...     

硫化氢提高水稻磷吸收转运的生理和分子机制

目的 低磷胁迫是限制水稻产量的主要因素之一。水稻淹水条件下产生H₂S,然而,H₂S作为信号分子是否参与调节水稻响应缺磷胁迫还未可知。方法 在正常磷和低磷条件下测定水稻H₂S含量,揭示H₂S在水稻响应缺磷胁迫中的作用。用2 μmol/L H₂S前体物质NaHS预处理水稻1 d,然后在加磷和低磷条件下培养6 d,测定水稻体内总磷含量、酸性磷酸酶活性、抗氧化酶活性、木质部汁液磷含量、磷转运子基因表达以及根系构型变化,从而探究H₂S参与调节水稻响应缺磷胁迫的生理和分子机制。结论 低磷胁迫下,水稻根系和地上部H₂S含量显著增加。NaHS预处理水稻显著增加低磷条件下水稻体内有效磷和总磷含量,提高根系酸性磷酸酶活性,提高抗氧化酶活性、木质部汁液磷含量和磷转运子基因表达水平,同时还改变水稻根系构型,增加总根长、总根表面积、总根体积和总根尖数,从而促进低磷条件下水稻对外界磷的吸收和转运,最终缓解缺磷胁迫。     

不同形态氮肥对紫花苜蓿生长、硝酸盐转运蛋白基因MtNRT1.3表达及氮吸收的影响

为了探讨豆科牧草对不同形态氮素的吸收,以紫花苜蓿（Medicago sativa L.）为试验材料,通过盆栽试验探究不同形态氮肥对紫花苜蓿生长、硝酸盐转运蛋白基因MtNRT1.3表达和氮吸收的影响。试验设有4个处理,分别为不施氮处理（对照组,Con）、施铵态氮（NH₄Cl—T1）、硝态氮（NaNO₃—T2）和混合氮（铵态氮、硝态氮1：1混合—T3）,各形态氮肥施加总量为按纯氮250 mg（每1 kg土）。试验结果表明,施氮处理提高了紫花苜蓿中的氮含量,施加各种氮肥均提高了紫花苜蓿根中MtNRT1.3基因的表达量,且该基因的表达量与土壤铵态氮和硝态氮呈正相关性（P<0.01）。相比于铵态氮肥,施加硝态氮肥不但可增加植株中硝态氮含量,而且能提高植株铵态氮含量;相比于单施硝态氮和铵态氮肥,混合氮肥对提高植株氮含量效果最好;施加硝态氮肥更有利于紫花苜蓿地上部分生物量的累积。因此,对紫花苜蓿施加氮肥应重视铵态氮和硝态氮的比例,增加硝态氮的比例更有利于紫花苜蓿的生长和对氮素的吸收。     

Transport of cadmium from soil to grain in cereal crops: A review

Due to rapid urbanization and industrialization, many soils for crop production are contaminated by cadmium(Cd), a heavy metal highly toxic to many organisms. Cereal crops such as rice, wheat, maize, and barley are the primary dietary source of Cd for humans, and reducing Cd transfer from soil to their grains is therefore an important issue for food safety. During the last decade, great progress has been made in elucidating the molecular mechanisms of Cd transport, particularly in rice. Inter-and intraspecific variations in Cd accumulation have been observed in cereal crops. Transporters for Cd have been identified in rice and other cereal crops using genotypic differences in Cd accumulation and mutant approaches. These transporters belong to different transporter families and are involved in the uptake, vacuolar sequestration, root-to-shoot translocation, and distribution of Cd. Attempts have been made to reduce Cd accumulation in grains by manipulating these transporters through overexpression or knockout of the transporter genes, as well as through marker-assisted selection breeding based on genotypic differences in Cd accumulation in the grains. In this review, we describe recent progress on molecular mechanisms of Cd accumulation in cereal crops and compare different molecular strategies for minimizing Cd accumulation in grains.     

Modulation of plant root traits by nitrogen and phosphate: transporters,long-distance signaling proteins and peptides,and potential artificial traps

As sessile organisms, plants rely on their roots for anchorage and uptake of water and nutrients. Plant root is an organ showing extensive morphological and metabolic plasticity in response to diverse environmental stimuli including nitrogen (N) and phosphorus (P) nutrition/stresses. N and P are two essential macronutrients serving as not only cell structural components but also local and systemic signals triggering root acclimatory responses. Here, we mainly focused on the current advances on root responses to N and P nutrition/stresses regarding transporters as well as long-distance mobile proteins and peptides, which largely represent local and systemic regulators, respectively. Moreover, we exemplified some of the potential pitfalls in experimental design, which has been routinely adopted for decades. These commonly accepted methods may help researchers gain fundamental mechanistic insights into plant intrinsic responses, yet the output might lack strong relevance to the real situation in the context of natural and agricultural ecosystems. On this basis, we further discuss the established—and yet to be validated—improvements in experimental design, aiming at interpreting the data obtained under laboratory conditions in a more practical view.     

MCT1抑制剂p-CMB对乙酰胆碱诱导的大鼠胰液分泌的影响

采用在体试验方法研究单羧酸转运蛋白第1亚型（monocarboxylate transporter 1,MCT1）抑制剂（p-chloromercuribenzene sulfonate,p-CMB）对乙酰胆碱（acetylcholine,Ach）诱导的大鼠胰液分泌的影响。Spra-gue-Dwley（SD）雄性大鼠,体重180g-210g,分6组,每组5只,试验前禁食24h,自由饮水。动物麻醉后经外科手术后,每隔10min收集一次胰液,采用Lowry法测定胰液蛋白量,Bernfeld法测定胰酶。结果对照组（-p-CMB）和实验组（＋p-CMB）,在注射1、5、10μg／kg的Ach后对胰液分泌量、胰蛋白分泌量以及胰淀粉酶分泌量都呈现增加作用,注射后1h内达到峰值,之后逐渐降低。然而,试验组的胰液分泌各项指标比对照组的显著减少（P〈0．01）。表明MCT1抑制剂p-CMB减弱了Ach增加大鼠胰液分泌的作用。     

Relationship between zinc and zinc transporter expression in breast cancer MCF-7 cells

AIM: To study the changes of zinc transporter gene expression in MCF-7 cell line exposed to ZnCl₂ and TPEN. METHODS: Human breast cancer cell line MCF-7 was exposed to different concentrations of ZnCl₂ (0, 50, 100, 150, 200 μmol/L) and TPEN (0, 5, 10, 15 μmol/L), respectively. Twelve hours later, the cell viability was measured by MTT and levels of zinc transporter mRNA by RT-PCR. Zinquin was used to estimate the intracellular zinc concentrations. RESULTS: MCF-7 cells viability rate was significantly decreased when exposed to ZnCl₂ (with 150 μmol/L and 200 μmol/L) and TPEN. The intracellular zinc concentration was significantly increased when exposed to ZnCl₂ and decreased when exposed to TPEN. ZnT-1 mRNA level was increased along with the increasing concentration of ZnCl₂ but decreased when exposed to TPEN. The expressions of ZIP2 and ZIP10 were increased along with the increasing concentration of TPEN. CONCLUSION: ZnT-1 gene expression is induced by zinc supplement and repressed by zinc deficiency. ZIP2 and ZIP10 gene expressions are induced by zinc deficiency.