模拟氮沉降对长白山岳桦林下草本植物和土壤肥力的短期影响

选取长白山岳桦林中的岳桦-蟹甲草群落（Comm.Betula ermanii-Parasenecio forrestii）、岳桦-藜芦群落（Comm.Betula ermanii-Veratrum nigrum）和岳桦-小叶章群落（Comm.Betula ermanii-Deyeuxia purpurea）开展野外模拟氮沉降实验,采用野外原位模拟实验方法,设置对照（0 kg·hm^-2·a^-1）、低氮（30 kg·hm^-2·a^-1）、中氮（50 kg·hm^-2·a^-1）和高氮（100 kg·hm^-2·a^-1）4个氮处理水平,测定草本植物生长状况和土壤肥力,研究岳桦林下草本层植物和土壤肥力对氮沉降的短期响应。结果显示：（1）岳桦林下草本植物随氮沉降量的增加而加速生长,小叶章对氮沉降的响应较为敏感,藜芦次之,蟹甲草最弱;（2）氮添加造成林下土壤肥力发生变化,有机质含量下降,特别是岳桦-小叶章群落下的土壤有机质含量下降最明显;土壤总氮和速效氮含量增大,岳桦-蟹甲草群落下的土壤总氮和速效氮增加最多;土壤总磷和速效磷含量减小,岳桦-小叶章群落下的土壤总磷和速效磷含量的减少最多。本研究结果表明氮添加在短期内会促进长白山岳桦林下草本植物生长,尤其是小叶章的生长,加快土壤有机质的分解和磷的释放,逐步改变土壤肥力并反馈给植物,促使其进一步变化。     

Suppression of Extensive Neurofilament Phosphorylation Rescues α-Internexin/Peripherin-Overexpressing PC12 Cells from Neuronal Cell Death

Intermediate filament (IF) overproduction induces abnormal accumulation of neuronal IF, which is a pathological indicator of some neurodegenerative disorders. In our study, α-Internexin- and peripherin-overexpressing PC12 cells (pINT-EGFP and pEGFP-peripherin) were used as models to study neuropathological pathways responsible for neurodegenerative diseases. Microarray data revealed that Cdk5-related genes were downregulated and Cdk5 regulatory subunit-associated protein 3 (GSK-3α and GSK-3β) were upregulated in pINT-EGFP cells. Increased expression of phosphorylated neurofilament and aberrant activation of Cdk5 and GSK-3β were detected in both pEGFP-peripherin and pINT-EGFP cells by Western blotting. In addition, pharmacological approaches to retaining viability of pINT-EGFP and pEGFP-peripherin cells were examined. Treatment with Cdk5 inhibitor and GSK-3β inhibitor significantly suppressed neuronal death. Dynamic changes of disaggregation of EGFP-peripherin and decrease in green fluorescence intensity were observed in pEGFP-peripherin and pINT-EGFP cells by confocal microscopy after GSK-3β inhibitor treatment. We conclude that inhibition of Cdk5 and GSK-3β suppresses neurofilament phosphorylation, slows down the accumulation of neuronal IF in the cytoplasm, and subsequently avoids damages to cell organelles. The results suggest that suppression of extensive neurofilament phosphorylation may be a potential strategy for ameliorating neuron death. The suppression of hyperphosphorylation of neuronal cytoskeletons with kinase inhibitors could be one of potential therapeutic treatments for neurodegenerative diseases.     

肿瘤抑制因子Hamartin和Tuberin信号调控机制

结节硬化复合症由tscl、tsc2基因突变引起,这2个基因分别编码hamartin和tuberin,它们均为肿瘤抑制因子,在细胞生长和增殖过程中起关键性的调节作用。生长因子刺激的PI3K／Akt信号通路通过磷酸化tuberin,调控下游效应因子功能,最终影响细胞的生长和增殖。现对hamartin和tuberin信号调控机制的最新进展进行综述,并展望其发展趋势。     

大鼠胫骨近端骨骺损伤后骨桥形成分子机制的研究

利用胫骨近端干骺端骨骺损伤的大鼠动物模型,研究骨桥形成的分子病理机制.通过Alcian blue染色观察损伤模型的建立、损伤愈合过程以及骨桥形成情况.采用Tunel试剂盒原位细胞凋亡检测,了解损伤区及周围细胞凋亡情况.利用免疫组织化学及原位杂交实验,观察损伤区周围软骨细胞改变,检测损伤区是否有软骨细胞生成,检测刀Ihh以及Ptch1表达阳性细胞.发现骨骺损伤骨桥形成过程中,完全损伤区中心没有软骨细胞特异的因子Col2al和ColX以及删Ihh和Ptch1的表达,但是完全损伤区和周围正常软骨交界间存在次损伤软骨区,存在软骨细胞凋亡,有Col X的表达,vimentin检测发现,在此区和周围正常软骨间有正常肥大区软骨细胞异常分化而来的成纤维样细胞并形成软骨外膜样结构,次损伤区和软骨外膜结构逐渐被骨桥替代,在此过程中软骨外膜样结构存在Collal、Ptch1和Ihh的表达,提示Ihh可能参与骨桥形成过程.提出骨桥形成过程中损伤中心区域存在膜内化骨,边缘区域存在软骨化骨作用机制.     

Nek2A specifies the centrosomal localization of Erk2

Nek2A is a cell-cycle-regulated protein kinase that localizes to the centrosome and kinetochore. Our recent studies provide a link between Nek2A and spindle checkpoint signaling [J. Biol. Chem. 279 (2004) 20049]. Extracellular signal-regulated kinase 2 (Erk2) is an important kinase, which belongs to mitogen activating protein (MAP) kinase family. Here we demonstrated that Nek2A binds specifically to Erk2. Erk2 interacts with Nek2A via a conserved Erk2 docking site located to the C-terminus of Nek2A. Our studies indicate this docking site is essential and sufficient for a direct Nek2A-Erk2 interaction. In addition, our immunocytochemical studies show that Nek2A and Erk2 are co-localized to centrosome. Significantly, elimination of Nek2A by RNA interference delocalized Erk2 from its centrosomal location, while inhibition of Erk2 kinase activity did not affect the localization of Nek2A in centrosome. We propose that Erk2 links extracellular signaling to centrosome dynamics by Nek2A.     

DNA barcoding and species delimitation of butterflies (Lepidoptera) from Nigeria

Molecular Biology Reports - Accurate identification of species is a prerequisite for successful biodiversity management and further genetic studies. Species identification techniques often require...     

Seeds of Locally Aligned Motion and Stress Coordinate a Collective Cell Migration

We find how collective migration emerges from mechanical information transfer between cells. Local alignment of cell velocity and mechanical stress orientation—a phenomenon dubbed “plithotaxis”—plays a crucial role in inducing coordinated migration. Leader cells at the monolayer edge better align velocity and stress to migrate faster toward the open space. Local seeds of enhanced motion then generate stress on neighboring cells to guide their migration. Stress-induced motion propagates into the monolayer as well as along the monolayer boundary to generate increasingly larger clusters of coordinately migrating cells that move faster with enhanced alignment of velocity and stress. Together, our analysis provides a model of long-range mechanical communication between cells, in which plithotaxis translates local mechanical fluctuations into globally collective migration of entire tissues.     

小泛素相关修饰物SUMO研究进展

蛋白质翻译后修饰对改变蛋白功能、活性或定位都起着非常重要的作用,泛素及其相似蛋白的修饰是其中一种重要形式。与其他诸如磷酸化、乙酰化、糖基化等不同的是,泛素及其相似蛋白的修饰基团本身即是一个小的多肽,通过异肽键与靶蛋白Lys侧链ε-NH2相连,其中小泛素相关修饰物(small ubiquitin—related modifier,SUMO)与蛋白的共价连接是一种新的广泛存在的翻译后修饰形式。SUMO是广泛存在于真核生物中高度保守的蛋白家族,在脊椎动物中有三个SUMO基因,称为SUMO-1,-2,-3,与泛素在二级结构上极其相似,且催化修饰过程的酶体系也具有很高的同源性。然而,与泛素化介导的蛋白酶降解途径不同,SUMO化修饰发挥着更为广泛的功能,如核质转运、细胞周期调控、信号转导、转录活性调控等。     

臭椿不同发育阶段叶片表面结构特征

利用光学显微镜和扫描电子显微镜技术,对臭椿(Ailanthus altissima(Mill.)Swingle)叶片从叶芽到成熟叶4个发育阶段(叶芽、幼叶、近成熟叶和成熟叶)的4种叶表面结构(表皮毛、气孔器、角质层、腺体)进行了详细地观察和比较。结果显示:叶片上、下表面具单细胞非腺毛和头状腺毛两种表皮毛,其密度在叶芽阶段最大,之后随着叶片的生长和展开表皮毛密度逐渐降低;气孔器主要分布于下表面,叶片近成熟时气孔器密度最大;角质层具有条纹状结构,其隆起程度在近成熟叶阶段达到最大;叶片基部两侧具锯齿状突起,每个突起上有一个腺体,腺体发育成熟后可分泌透明黏液。说明叶片表面各结构特征是臭椿对环境长期适应的结果。