森林草莓SUN基因家族的鉴定及其对逆境的响应

SUN基因是调控植物生长发育的关键基因。本研究鉴定了二倍体森林草莓(Fragaria vesca)的SUN基因家族,并对各成员的理化性质、基因结构、系统进化以及基因表达进行了分析。结果表明,森林草莓有31个FvSUN基因,其编码蛋白可聚类为7个组,同一组内成员具有高度相似的基因结构与编码蛋白保守域;FvSUNs蛋白的亚细胞定位主要在细胞核中。共线性分析表明森林草莓FvSUNs基因家族主要通过染色体片段复制产生,拟南芥与森林草莓存在23对直系同源基因。利用森林草莓的转录组数据,对FvSUNs基因的组织表达特征进行分析,发现主要可归为3类：各组织均表达、组织中几乎不表达、组织特异性表达,并通过实时荧光定量PCR (quantitative real-time polymerase chain reaction, qRT-PCR)进一步验证结果。此外,还对森林草莓进行不同的逆境胁迫处理,qRT-PCR分析了31个FvSUNs基因的表达情况,发现大部分基因均在不同程度上受低温、高盐或干旱胁迫的诱导表达。这些研究结果为深入揭示草莓SUN基因的生物学功能及其分子机制奠定了基础。     

化龙山七筋姑种内二倍体与四倍体表型分化分析

七筋姑(Clintonia udensis Trautv. et Mey.)属百合科(Liliaceae)七筋姑属(Clintonia Raf.),多年生草本,具有二倍体(2n=14)和四倍体(4n=28)两种倍性。在陕西化龙山地区,二倍体主要分布在南坡海拔2 450 m处,四倍体主要生长在北坡海拔1 900 m左右,成为研究种内多倍体分化的理想材料。该研究从七筋姑营养和繁殖系统出发,研究其不同倍性的表型分化,揭示不同倍性的生态适应特征,为阐明七筋姑种内多倍体的演化提供线索。研究表明：(1)在根、茎、叶、花、果实、种子的11个性状中,二倍体的果实体积性状最为稳定(CV=0.02),叶长性状遗传多样性最高(CV=0.85);四倍体中果实体积性状也最为稳定(CV=0.06),而花数量性状多样性最高(CV=0.42)。(2)四倍体的果实体积平均值明显高于二倍体,但种子数量平均值显著少于二倍体,果实体积和种子体积性状在不同倍性间的分化占比最高(V_st=0.69)。(3)四倍体营养器官表型性状的遗传变异丰富度低于二倍体,其平均变异系数(CV=0.16)小于二倍体的变异系数(CV=0.44);在繁殖系统表型性状中,四倍体的遗传变异丰富度高于二倍体,平均变异系数(CV=0.30)大于二倍体(CV=0.26)。(4)显著性分析表明,二倍体与四倍体表型性状差异显著(P<0.05),而繁殖系统性状在不同倍性间无显著差异(P>0.05);PCA分析同样显示二倍体与四倍体间存在明显差异。四倍体显著的表型差异是对低海拔环境长期适应的结果。     

Immune modulation of effector CD4+ and regulatory T cell function by sorafenib in patients with hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is a difficult to treat cancer characterized by poor tumor immunity with only one approved systemic drug, sorafenib. If novel combination treatments are to be developed with immunological agents, the effects of sorafenib on tumor immunity are important to understand. In this study, we investigate the impact of sorafenib on the CD4+CD25? effector T cells (Teff) and CD4+CD25+ regulatory T cells (Tregs) from patients with HCC. We isolated Teff and Treg from peripheral mononuclear cells of HCC patients to determine immune reactivity by thymidine incorporation, ELISA and flow cytometry. Teff cultured alone or with Treg were supplemented with different concentrations of sorafenib. The effects of sorafenib on Teff responses were dose-dependent. Pharmacologic doses of sorafenib decreased Teff activation by down regulating CD25 surface expression. In contrast, sub-pharmacologic concentrations of sorafenib resulted in Teff activation. These low doses of sorafenib in the Teff cultures led to a significant increase in Teff proliferation, IL2 secretion and up-regulation of CD25 expression on the cell surface. In addition, low doses of sorafenib in the suppression Teff/Treg cocultures restored Teff responses by eliminating Treg suppression. The loss of Treg suppressive function correlated with an increase in IL2 and IL6 secretion. Our findings show that sub-pharmacologic doses of sorafenib impact subsets of T cells differently, selectively increasing Teff activation while blocking Treg function. In conclusion, this study describes novel immune activating properties of low doses of sorafenib by promoting immune responsiveness in patients with HCC.     

叶脉结构与功能及其对叶片经济谱的影响

叶脉由贯穿于叶肉内部的维管组织及其外围机械组织构成, 多样化的脉序及网络结构使叶脉系统发生变异和功能分化。该文综述了叶脉系统结构与功能的最新研究进展。通过聚焦叶脉分级系统的结构与功能及其在叶片经济谱(LES)中的重要性, 解释叶脉性状与其它叶片功能性状之间的关系及机制。不同等级叶脉在机械支撑与水分运输方面存在功能分化, 其中1-3级粗脉在维持叶片形状和叶表面积以及物理支撑方面发挥重要作用, 有利于维持叶片最大受光面积; 4级及以上细脉具有水分调节功能, 它们与气孔相互协调, 影响叶片水分运输、蒸腾散热和光合作用速率。叶片生长过程与叶脉发育的动态变化模式决定叶脉密度, 并影响叶脉密度与叶片大小之间的关系: 叶面积与粗脉密度呈显著负相关, 与粗脉直径呈显著正相关, 而与细脉密度无关。与叶脉性状相关的叶片经济谱框架模型预测, 叶脉密度较高的叶片寿命短、比叶重较小, 叶片最大碳同化速率、代谢速率以及资源获取策略潜力较高。     

New therapy with XLQ® to suppress chronic prostatitis through its anti-inflammatory and antioxidative activities

Chronic prostatitis is a common urological disease. The etiology of this disease and effective therapy for its treatment are yet to be elucidated. We investigated the functions of XLQ^® in chronic nonbacterial prostatitis using a complete Freund's adjuvant-induced rat model. Prostates and blood samples were collected for further evaluation after oral gavage with XLQ ^® or a vehicle for 4 weeks. The results showed that XLQ ^® significantly decreased the prostate index, ameliorated the histopathologic changes, and reduced CD3+ and CD45+ cell infiltration in the prostate stroma. Further study showed that XLQ ^® suppressed the expression of proinflammatory cytokines, such as interleukin (IL)-1β, IL-2, IL-6, IL-17A, monocyte chemoattractant protein-1, and tumor necrosis factor-α. XLQ ^® showed a strong antioxidant capacity by enhancing the activities of antioxidative enzymes (e.g., total superoxide dismutase, catalase, and glutathione peroxidase) and decreasing the level of lipid peroxidation products (malondialdehyde). Moreover, XLQ ^® can suppress the activation of nuclear factor-κB and P38-mitogen-activated protein kinase signaling pathways. In summary, XLQ ^® has affirmative effects on chronic prostatitis, which could be attributed to its anti-inflammatory and antioxidative capacities. On the basis of these results, XLQ ^® can be developed as an effective and safe therapy for chronic prostatitis.     

植物GLKs生物学功能及分子作用机理研究进展

GLKs (GOLDEN 2-LIKEs)是一类植物特有的转录因子,靶向调控光合作用相关基因的表达,调控叶绿体的发育、分化并维持其机能,并参与调节果实的营养积累、叶片衰老、免疫反应及逆境胁迫应答等。GLKs受多种激素或环境因子的影响,是植物细胞调控网络的关键节点,也是改造作物光合能力的重要基因。基于国内外在植物GLKs研究中取得的众多进展,文中全面阐述了GLKs基因的生物学功能、分子机制及其育种实践,并构建GLKs介导的信号网络模型,为后期GLKs的理论与应用研究提供借鉴。     

Evidence that phosphatidylinositol 3-kinase- and mitogen-activated protein kinase kinase-4/c-Jun NH2-terminal kinase-dependent Pathways cooperate to maintain lung cancer cell survival

Cancer cells in which the PTEN lipid phosphatase gene is deleted have constitutively activated phosphatidylinositol 3-kinase (PI3K)-dependent signaling and require activation of this pathway for survival. In non-small cell lung cancer (NSCLC) cells, PI3K-dependent signaling is typically activated through mechanisms other than PTEN gene loss. The role of PI3K in the survival of cancer cells that express wild-type PTEN has not been defined. Here we provide evidence that H1299 NSCLC cells, which express wild-type PTEN, underwent proliferative arrest following treatment with an inhibitor of all isoforms of class I PI3K catalytic activity (LY294002) or overexpression of the PTEN lipid phosphatase. In contrast, overexpression of a dominant-negative mutant of the p85alpha regulatory subunit of PI3K (Deltap85) induced apoptosis. Whereas PTEN and Delta85 both inhibited activation of AKT/protein kinase B, only Deltap85 inhibited c-Jun NH2-terminal kinase (JNK) activity. Cotransfection of the constitutively active mutant Rac-1 (Val12), an upstream activator of JNK, abrogated Deltap85-induced lung cancer cell death, whereas constitutively active mutant mitogen-activated protein kinase kinase (MKK)-1 (R4F) did not. Furthermore, LY294002 induced apoptosis of MKK4-null but not wild-type mouse embryo fibroblasts. Therefore, we propose that, in the setting of wild-type PTEN, PI3K- and MKK4/JNK-dependent pathways cooperate to maintain cell survival.