水稻叶绿素合成缺陷突变体及其生物学研究进展

叶绿素是植物叶绿体内参与光合作用的重要色素,叶绿素合成缺陷突变是一类明显的性状突变,其在理论研究和实际应用方面均具有重要的意义。本文介绍了国内外在水稻叶绿素合成缺陷突变体的发掘、作用机理及其基因定位等方面的研究进展。     

天名精倍半萜内酯化合物

从菊科天名精全草中分得天名精内酯酮,特勒内酯,11（13）－二氢特勒内酯和异埃瓦内酯。其中11（13）－二氢特勒内酯和异埃瓦内酯为新的天然产物。     

小径竹密度对雷公鹅耳枥幼苗早期更新的影响

通过去除法控制竹丛密度,人为设置4种竹丛密度梯度[密度1:(3.83±0.53)株/m~2;密度2:(16±1.80)株/m~2;密度3:(39±1.69)株/m~2;密度4:(69±2.15)株/m~2],测定不同密度竹丛下的微环境(包括土壤温度、湿度、电导率、凋落物厚度),研究竹丛密度及微环境对雷公鹅耳枥(Carpinus viminea Wall.)幼苗数量、存活动态、生长情况的影响。结果显示,竹丛密度对环境有显著影响,随着竹丛密度的增加,竹丛盖度、凋落物厚度、土壤温度升高明显;雷公鹅耳枥幼苗萌生量显著减少,4组密度梯度中幼苗数量分布依次排序为:密度1(28.53±3.14)株/m~2密度2(17.36±1.45)株/m~2密度3(12.36±0.93)株/m~2密度4(8.92±0.93)株/m~2,表明随着小径竹密度增加,其对雷公鹅耳枥幼苗萌发的抑制作用越强;小径竹的密集生长可对雷公鹅耳枥幼苗的存活率产生影响,且对幼苗的生长具有一定抑制作用。研究结果表明小径竹密集生长的环境不仅抑制了雷公鹅耳枥新生幼苗的分布和幼苗生长,还对种群的更新以及森林群落的演替产生一定的负面影响。     

阿拉善干旱荒漠区不同植被类型土壤种子库研究

[1]兰州大学草地农业科技学院,兰州730020 [2]甘肃草原生态研究所,兰州730020 [3]内蒙古阿拉善盟草原站,巴彦浩特750360     

GADD45α mediates arsenite‐induced cell apoptotic effect in human hepatoma cells via JNKs/AP‐1‐dependent pathway

Arsenite (As(III)), an effective chemotherapeutic agent for the acute promyelocytic leukemia (APL) and multiple myeloma (MM), might be also a promise for the therapy of other cancers, including the solid tumors. However, the molecular bases of arsenite‐induced cytotoxicity in the tumor cells have not been fully defined. In this study, we have disclosed that arsenite effectively induces the apoptotic response in the HepG2 human hepatoma cells by triggering GADD45α induction and the subsequent activation of JNKs/AP‐1 cell death pathway. However, signaling events relating to GADD45α/JNKs/AP‐1 pathway activation have not been observed in HL7702 human diploid hepatic cells under the same arsenite exposure condition. Our results thus have illustrated the selective pro‐apoptotic role of arsenite in the hepatoma cells by activating GADD45α‐dependent cell death pathway whereas with little effect on the normal hepatic cells. The approaches to up‐regulate GADD45α levels might be helpful in improving the chemotherapeutic action of arsenite on certain solid tumors including hepatoma. J. Cell. Biochem. 109: 1264–1273, 2010. © 2010 Wiley‐Liss, Inc.     

核糖核酸酶抑制因子对H_2O_2损伤的大鼠神经胶质瘤细胞系C6的影响

核糖核酸酶抑制因子 (ribonucleaseinhibitor,RI)是广泛存在于哺乳动物细胞浆中的一种酸性糖蛋白 .为了进一步了解RI的功能 ,根据RI分子结构富含巯基的特点 ,研究了RI对过氧化氢(H2 O2 )损伤的大鼠神经胶质瘤细胞 (C6 )的影响 .用不同浓度的H2 O2 分别作用于转染有RIcDNA并且RI过表达的C6细胞和正常C6细胞 ,对比损伤前后 2者的细胞存活率、LDH漏出量、细胞内GSH和MDA含量差别 ,以及细胞内抗氧化酶类GPX、CAT和GST活性的差别 .结果表明 ,与正常C6细胞相比 ,RI过表达的C6细胞在H2 O2 作用下存活率高 ,LDH漏出量、MDA含量明显减少 ,而细胞内GSH较多 ;RI过表达的C6细胞在损伤前后均表现出更强的CAT和GST活性 .提示RI具有抗氧化功能 ,能够减轻H2 O2 所致的细胞过氧化损伤 .     

全雌系苦瓜ACC氧化酶基因cDNA克隆及序列分析

为研究1-氨基环丙烷-1-羧酸氧化酶(ACC氧化酶,ACO)基因在苦瓜性别分化中的作用,以全雌系苦瓜‘X-Hei-d-d’花蕾为试材,采用RT-PCR和RACE技术获得了ACC氧化酶基因(Mc-ACO1)的全长cDNA序列。该序列为1 137 bp(GenBank登录号:FJ459813),其完整开放阅读框长1 005 bp,编码334个氨基酸,预测分子量为37.30 kD,肽链N端缺失ACOs家族典型的1个保守区和2个保守二价铁离子/抗坏血酸依赖型双加氧酶氨基酸残基。序列分析表明,植物ACO基因的演化与其来源植物亲缘关系的一致性较高;与其他物种相比,苦瓜Mc-ACO1不同的氨基酸序列主要表现在肽链N端;苦瓜Mc-ACO1应属于黄瓜Cs-ACO2类成员,功能可能与性别分化相关。     

硫丹对黄瓜光合色素及几种有关酶活性的影响

用0.1％-0.6％的硫丹喷施黄瓜幼苗4d后,叶绿素总量、叶绿素a、叶绿素b、原叶绿素、类胡萝卜素含量分别下降21.00％-38．57％、21.27％-38.69％、20.22％-38.24％、6．60％-49.24％和13.54％-68.85％;叶绿素酶活性上升16.51％-72．80％;δ-氨基乙酰丙酸（ALA）合酶和脱水酶活性分别下降14.14％-44.61％和4．38％-40．11％。讨论了硫丹影响叶绿素含量的可能机理。     

The Kv2.1 channels mediate neuronal apoptosis induced by excitotoxicity

Chronic loss of intracellular K⁺ can induce neuronal apoptosis in pathological conditions. However, the mechanism by which the K⁺ channels are regulated in this process remains largely unknown. Here, we report that the increased membrane expression of Kv2.1 proteins in cortical neurons deprived of serum, a condition known to induce K⁺ loss, promotes neuronal apoptosis. The increase in I _K current density and apoptosis in the neurons deprived of serum were inhibited by a dominant negative form of Kv2.1 and MK801, an antagonist to NMDA receptors. The membrane level of Kv2.1 and its interaction with SNAP25 were increased, whereas the Kv2.1 phosphorylation was inhibited in the neurons deprived of serum. Botulinum neurotoxin, an agent known to prevent formation of soluble N -ethylmaleimide-sensitive factor attachment protein receptor complex, suppressed the increase in I _K current density. Together, these results suggest that NMDA receptor-dependent Kv2.1 membrane translocation is regulated by a soluble N -ethylmaleimide-sensitive factor attachment protein receptor-dependent vesicular trafficking mechanism and is responsible for neuronal cell death induced by chronic loss of K⁺.