晋北典型针叶人工林叶功能性状特征及其与土壤因子的关系

为了解释植物叶片的资源分配特征及其与土壤因子间的适应策略,该研究以黄土高原东北缘山西省大同市新荣区油松、樟子松人工纯林及其柠条混交林为对象,采用样方法采集样木树冠中部生长良好的轮生枝中东西南北4个方向的枝条,并在每个枝条上选择里、中、外3处有代表性的当年生叶和多年生叶;采用 “S”形采样法在每个样方内选取9个取样点,用土钻采集各样点0～20 cm土壤样品;测定分析不同造林模式下油松、樟子松异龄叶功能性状特征、土壤理化性质以及二者的关系,为人工林培育及经营提供理论支撑。结果表明：(1)不同造林模式下油松及樟子松叶功能性状的差异集中在化学计量之间;随着叶龄增长,油松、樟子松均表现出干物质含量上升,氮磷含量下降的特征。(2)土壤全磷、全氮含量分别是油松当年及多年生叶的主要解释因子,土壤全磷与当年生叶碳氮比、有机碳、碳磷比均呈显著正相关关系,与全氮、叶面积及叶干物质含量呈显著负相关关系,土壤全氮与多年生叶全磷含量呈正相关关系,与叶有机碳、碳磷比、碳氮比则呈显著负相关关系。(3)樟子松当年生叶功能性状的关键土壤因子是土壤容重、全磷含量,其与叶碳氮磷的比值、干物质含量、碳含量呈正相关关系,而与氮磷含量呈负相关关系;多年生叶功能性状的关键土壤因子是土壤容重、含水量、pH,其与叶氮磷含量呈正相关关系,与碳含量、干物质含量、比叶面积等呈负相关关系。(4)油松及樟子松纯林的叶功能性状更易向关键土壤因子含量更高的方向偏移,说明与柠条混交可有效分异叶片生长对主要土壤因子的集中需求,但混交造林模式下林木长势有所衰弱;结合研究区资源匮乏现状,林木种植密度较大,竞争加剧了生存压力导致林木生长受限。     

N-Acetyl-d-glucosamine 2-epimerase from Anabaena sp. CH1 contains a novel ATP-binding site required for catalytic activity

ATP is required as a structural activator for the reversible epimerization of N-acetyl-d-glucosamine to N-acetyl-d-mannosamine by N-acetyl-d-glucosamine 2-epimerase (AGE); however, the ATP-binding site on AGE has not been clearly identified. This study aimed to investigate the specific region of Anabaena sp. CH1 AGE (bAGE) that is required for ATP binding. In the absence of ATP, tryptic digest of bAGE resulted in the production of 2 segments of 17 and 26 kDa, while in the presence of 1 mM ATP, the enzyme was resistant to trypsin. ADP also displayed protective effects against trypsin digestion. A trypsin-mediated ATP-footprinting assay identified a deviant ATP-protected region, 156-GKYTK-160, which is located within the flexible loop of bAGE. Site-directed mutagenesis of residues in the loop region was performed, and both K151A and K160A variants greatly decreased the enzymatic activity as well as the ATP-binding ability of bAGE, indicating that residues K151 and K160 may be critical for ATP binding. This study demonstrated that the ATP-binding site (151-KDNPKGKYTK-160) of bAGE was a novel rather than a classical Walker motif A. This is the first ATP-binding site reported for AGEs.     

RhoA inactivation is crucial to manganese-induced astrocyte stellation

Actin depolymerization through Rho GTPases or exogenous mechanical tension has been suggested as a key determinant for the formation of astrocyte stellation. Rho GTPases function as switching molecules to converge both extracellular and intracellular signals in regulation of cytoskeletal organization. Their involvement in manganese-induced astrocyte stellation was assessed. The disruption of cytoskeletal architecture by manganese indicated the decreased activity of RhoA. Pharmacological and biochemical approaches revealed the inactivation of RhoA by manganese. This inactivation was partly through the down-regulation of guanine nucleotide exchange factor phosphorylation. Furthermore, the dephosphorylation of myosin light chain and cofilin through the inactivated RhoA effectors synergistically destabilized actin stress fibers. We conclude that manganese regulates cytoskeletal organization in astrocytes by modulating the activity of p115RhoGEF and RhoA.     

Tracing the origin and evolution of plant TIR-encoding genes

Toll-interleukin-1 receptor (TIR)-encoding proteins represent one of the most important families of disease resistance genes in plants. Studies that have explored the functional details of these genes tended to focus on only a few limited groups; the origin and evolutionary history of these genes were therefore unclear. In this study, focusing on the four principal groups of TIR-encoding genes, we conducted an extensive genome-wide survey of 32 fully sequenced plant genomes and Expressed Sequence Tags (ESTs) from the gymnosperm Pinus taeda and explored the origins and evolution of these genes. Through the identification of the TIR-encoding genes, the analysis of chromosome positions, the identification and analysis of conserved motifs, and sequence alignment and phylogenetic reconstruction, our results showed that the genes of the TIR-X family (TXs) had an earlier origin and a wider distribution than the genes from the other three groups. TIR-encoding genes experienced large-scale gene duplications during evolution. A skeleton motif pattern of the TIR domain was present in all spermatophytes, and the genes with this skeleton pattern exhibited a conserved and independent evolutionary history in all spermatophytes, including monocots, that followed their gymnosperm origin. This study used comparative genomics to explore the origin and evolutionary history of the four main groups of TIR-encoding genes. Additionally, we unraveled the mechanism behind the uneven distribution of TIR-encoding genes in dicots and monocots.     

不同水分胁迫对刺槐生理的影响

本文以二年生刺槐为供试材料,探讨水分胁迫对其生理的影响,为园林绿地中刺槐的灌溉提供理论指导.结果表明,水淹和干旱胁迫明显影响刺槐的生长.水淹11 d后,qP值、ETR值、Fv'/Fm'值和净光合速率的明显下降,qN值上升,19 d后植株死亡.中度干旱胁迫(土壤含水量在8%～15%之间)对植株生长有一定影响,表现为净光合速率的下降和qN值上升等;干旱胁迫(土壤含水量低于10%)严重抑制植株的生长,表现为qN值上升,而qP、ETR、Fv'/Fm'和净光合速率下降,处理19 d后干旱组植株死亡.轻度干旱(土壤含水量在15%～25%之间)适宜植物生长,表现为3次测定的qP、ETR、Fv'/Fm'、Fv/Fm和净光合速率都较高且稳定.土壤含水量日变化在15%～25%以内受轻度干旱胁迫是园林中刺槐的最佳灌溉方式,既不影响景观效果,同时也能节约灌溉用水.     

Mite allergen Der-p2 triggers human B lymphocyte activation and Toll-like receptor-4 induction

Background

Allergic disease can be characterized as manifestations of an exaggerated inflammatory response to environmental allergens triggers. Mite allergen Der-p2 is one of the major allergens of the house dust mite, which contributes to TLR4 expression and function in B cells in allergic patients. However, the precise mechanisms of Der-p2 on B cells remain obscure.

Methodology/Principal Findings

We investigated the effects of Der-p2 on proinflammatory cytokines responses and Toll-like receptor-4 (TLR4)-related signaling in human B cells activation. We demonstrated that Der-p2 activates pro-inflammatory cytokines, TLR4 and its co-receptor MD2. ERK inhibitor PD98059 significantly enhanced TLR4/MD2 expression in Der-p2-treated B cells. Der-p2 markedly activated mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1) and decreased p38 phosphorylation in B cells. MKP-1-siRNA downregulated TLR4/MD2 expression in Der-p2-treated B cells. In addition, Der-p2 significantly up-regulated expression of co-stimulatory molecules and increased B cell proliferation. Neutralizing Der-p2 antibody could effectively abrogate the Der-p2-induced B cell proliferation. Der-p2 could also markedly induce NF-κB activation in B cells, which could be counteracted by dexamethasone.

Conclusions/Significance

These results strongly suggest that Der-p2 is capable of triggering B cell activation and MKP-1-activated p38/MAPK dephosphorylation-regulated TLR4 induction, which subsequently enhances host immune, defense responses and development of effective allergic disease therapeutics in B cells.