中国西藏种子植物区系新资料

本文报道了采自西藏喜马拉雅南坡的8个中国种子植物新记录种以及1个西藏新记录属。前者分别是吉隆牛奶菜(Marsdenia roylei)、塔基棕榈(Trachycarpus takil)、喀西蜂斗草(Sonerila khasiana)、旋花锡生藤(Cissampelos convolvulacea)、吉隆角盘兰(Herminium edgeworthii)、尼泊尔西番莲(Passiflora napalensis)、椭穗姜花(Hedychium ellipticum)和藏南象牙参(Roscoea brandisii); 1个西藏新记录属为箭药藤属(Belostemma) (箭药藤 Belostemma hirsutum)。凭证标本存放于中国科学院西双版纳热带植物园标本馆(HITBC)和西藏自治区高原生物研究所标本室(XZ)。     

中国三瘤蝉属一新种(同翅目：蝉科)

中国三瘤蝉属一新种（同翅目：蝉科）雷仲仁,李莉（西北农业大学昆虫研究所陕西杨陵７１２１００）作者在进行中国蝉科较系统的分类研究时,发现三瘤蝉属一新种。模式标本保存在西北农业大学昆虫博物馆（正模）和中国科学院动物研究所（副模）。长度单位为ｍｍ。穹三瘤蝉...     

不同光照强度对兴安落叶松几种主要防御蛋白活力的影响

林木组成抗性对抵御害虫危害发挥着重要作用。为了研究环境因子对其组成抗虫性的影响,以兴安落叶松幼苗为试验材料,通过搭建遮阳棚设置3个光照强度(自然光照作为对照、50%和25%自然光照强度),模拟森林幼苗生长的林缘、林窗和林下3种不同的光环境,分析不同光照强度对其针叶内与植物抗虫性有关的几种主要防御蛋白活力的影响。研究结果表明,不同光照强度对针叶内主要防御蛋白活力有显著影响(P<0.05)。50%和25%光照强度下,POD、SOD、PAL、PPO和CI的活性显著高于自然光照下的(P<0.05),POD和CI的活性在50%光照强度下最高,SOD、PAL和PPO的活性在25%光照强度下最高;自然光照条件下CAT的活性显著高于50%和25%光照强度下的(P<0.05);遮荫处理对TI的活性有显著影响(P<0.05),但在不同月份中波动较大,规律性不明显。相同的光照强度条件下,主要防御蛋白活力在3个月中也有显著变化(P<0.05)。7月和8月份保护性酶POD和CAT的活性显著高于6月(P<0.05);防御性酶PAL、PPO以及蛋白酶抑制剂CI的活性在6月份最高。综合以上研究结果,光照可影响兴安落叶松针叶中几种主要防御蛋白活力,这也说明在较荫蔽的光照环境下,兴安落叶松有较强的抗性。其中SOD、CAT、PAL、PPO和POD是植物次生物质生成过程中的关键酶,其活性的改变在一定程度上表征着植物防御体系在变化。研究环境因子与植物防御之间的关系具有重要的理论和实际应用价值。     

非生物胁迫因子对棘孢木霉嗜铁素及钙调磷酸酶基因表达的影响

木霉菌(Trichoderma spp.)嗜铁素具有吸收、贮存和胞内运输铁的功能,对菌体自身的生长发育有重要作用,也是重要的生防促生因子,但嗜铁素的产量会受到环境中多种胁迫因子的影响。真菌的钙调磷酸酶基因能够调控外源离子的胁迫反应,但钙调磷酸酶信号通路与嗜铁素合成之间的关系并不明确。以棘孢木霉菌(Trichoderma asperellum)T6为材料,研究了NaCl、CaCl_2及pH对棘孢木霉菌T6嗜铁素产量以及嗜铁素合成关键基因(SidA)与钙调磷酸酶催化亚基基因(CnA)表达量的影响。结果表明,高浓度NaCl和CaCl_2以及高pH均能抑制嗜铁素的产生。利用半定量PCR分析得知,CnA基因与SidA基因之间存在一定的负调控关系,该结果与钙调磷酸酶专性抑制剂环孢菌素A能够提高嗜铁素产量的结果相一致。     

肠道微生物菌群分型的研究进展

人体肠道内存在着处于动态平衡中的复杂微生物群体,包含1000多种细菌和古生菌等共生微生物。它们广泛参与人体的营养、代谢和免疫等生理过程,是影响健康最重要的因素之一。同一个体不同胃肠道部位的微生物群落组成显著不同,而在不同个体的肠道微生物群落组成也存在很大差异。肠道微生物群落结构受到饮食习惯、药物干预以及生活环境等因素影响,形成了不同个体间菌群组成的差异。通过菌群测序分析和群体分型,可以将不同个体的肠道微生物群落组成分为拟杆菌、普氏菌和瘤胃球菌三种肠型。确定肠道微生物群落结构的分型,将复杂的肠道微生物系统模式化,有利于对大样本肠道微生物菌群进行分析,更好地指导相关疾病的诊断和治疗。本文综述了肠道微生物的分型和相关影响因素的进展。     

氮磷肥配施对冬小麦灌浆期光合参数及产量的影响

在西北绿洲生态条件下, 实验设4个处理, 即165(N₁)和225 kg·hm^-2(N₂)2个氮素(纯氮)水平及105(P₁)和165 kg·hm^-2(P₂)2个磷素(P₂O₅)水平, 研究了氮磷肥配施对冬小麦(Triticum aestivum)品种临抗2号光合特性及产量的影响。结果表明, 低氮(165 kg·hm^-2)处理组的净光合速率(P_n)、气孔导度(G_s)及蒸腾速率(T_r)日变化均呈双峰曲线, 有光合“午休”现象; 高氮(225 kg·hm^-2)处理可减弱甚至使光合“午休”现象消失; 高磷(165 kg·hm^-2)和低磷(105 kg·hm^-2)处理对光合特性的影响差异不显著。N₂P₂具有最高的群体叶面积指数(LAI)、群体光合速率(CAP)、穗粒数、亩穗数、千粒重及产量, 且与N₁P₁和N₁P₂的差异均达显著水平, 与N₂P₁则无显著差异。但N₂P₂水分利用效率(WUE)低于N₂P₁, 显著高于N₁P₁和N₁P₂ (N₁P₁高于N₁P₂, 但无显著差异)。氮肥对光合“午休”的影响大于磷肥, 二者互作效应差异不显著。该实验条件下, 当N、P分别为225和105 kg·hm^-2时有利于提高冬小麦的光合速率及产量。     

Perforin and Fas cytolytic pathways coordinately shape the selection and diversity of CD8+-T-cell escape variants of influenza virus

Antigenic variation is a viral strategy exploited to promote survival in the face of the host immune response and represents a major challenge for efficient vaccine development. Influenza viruses are pathogens with high transmissibility and mutation rates, enabling viral escape from immunity induced by prior infection or vaccination. Intense selection from neutralizing antibody drives antigenic changes in the surface glycoproteins, resulting in emergence of new strains able to reinfect hosts immune to previously circulating viruses. CD8+ cytotoxic T cells (CTLs) also provide protective immunity from influenza virus infection and may contribute to the antigenic evolution of influenza viruses. Utilizing mice transgenic for an influenza virus NP366-374 peptide-specific T-cell receptor, we demonstrated that the respiratory tract is a suitable site for generation of escape variants of influenza virus selected by CTL in vivo. In this report the contributions of the perforin and Fas pathways utilized by influenza virus-specific CTLs in viral clearance and selection of CTL escape variants have been evaluated. While transgenic CTLs deficient in either perforin- or Fas-mediated pathways are efficient in initial pulmonary viral control, variant virus emergence was observed in all the mice studied, although the spectrum of viral CTL escape variants selected varied profoundly. Thus, a less-restricted repertoire of escape variants was observed in mice with an intact perforin cytotoxic pathway compared with a limited variant diversity in perforin pathway-deficient mice, although maximal variant diversity was observed in mice having both Fas and perforin pathways intact. We conclude that selection of viral CTL escape variants reflects coordinate action between the tightly controlled perforin/granzyme pathway and the more promiscuous Fas/FasL pathway.     

NIRF, a novel ubiquitin ligase, interacts with hepatitis B virus core protein and promotes its degradation

Hepatitis B virus (HBV) core protein (HBc) is a major component of viral nucleocapsid and a multifunctional protein involved in viral maturation and release. It is unstable and present in cells at low level because of K96 lysine residue, which is a ubiquitin acceptor site. Np95/ICBP90-like RING finger protein (NIRF) has auto-ubiquitination activity which is the hallmark of a ubiquitin ligase. In the present study, ubiquitin ligase, NIRF, binds to HBc and leads to the proteasome-mediated degradation of HBc in vivo. NIRF down-regulates HBc protein level, resulting in the decrease of the amount of HBV particles in supernatant of HepG2.2.15 cells. However knockdown of NIRF significantly increases endogenous HBc protein level, leading to HBV release. The results reveal that NIRF interacts with HBc and promotes the degradation of HBc in vivo. The pathway of NIRF-mediated ubiquitin–proteasome affects the release of HBV particles by controlling the amounts of HBc. It indicates that NIRF may participate in the maturation of HBV.     

Heregulin targets gamma-catenin to the nucleolus by a mechanism dependent on the DF3/MUC1 oncoprotein

The DF3/MUC1 transmembrane oncoprotein is aberrantly overexpressed in most human breast carcinomas and interacts with the Wnt effector gamma-catenin. Here, we demonstrate that MUC1 associates constitutively with ErbB2 in human breast cancer cells and that treatment with heregulin/neuregulin-1 (HRG) increases the formation of MUC1-ErbB2 complexes. The importance of the MUC1-ErbB2 interaction is supported by the demonstration that HRG induces binding of MUC1 and gamma-catenin and targeting of the MUC1-gamma-catenin complex to the nucleolus. Significantly, nucleolar localization of gamma-catenin in response to HRG is dependent on MUC1 expression. Moreover, mutation of a RRK motif in the MUC1 cytoplasmic domain abrogates HRG-induced nucleolar localization of MUC1 and gamma-catenin. In concert with these results, we show nucleolar localization of MUC1 and gamma-catenin in human breast carcinomas but not in normal mammary ductal epithelium. These findings demonstrate that MUC1 functions in cross talk between ErbB2 and Wnt pathways by acting as a shuttle for HRG-induced nucleolar targeting of gamma-catenin.