The Combined Effects of Moss-Dominated Biocrusts and Vegetation on Erosion and Soil Moisture and Implications for Disturbance on the Loess Plateau,China

Biological soil crusts (BSCs, or biocrusts) have important positive ecological functions such as erosion control and soil fertility improvement, and they may also have negative effects on soil moisture in some cases. Simultaneous discussions of the two-sided impacts of BSCs are key to the rational use of this resource. This study focused on the contribution of BSCs while combining with specific types of vegetation to erosion reduction and their effects on soil moisture, and it addressed the feasibility of removal or raking disturbance. Twelve plots measuring 4 m × 2 m and six treatments (two plots for each) were established on a 15° slope in a small watershed in the Loess Plateau using BSCs, bare land (as a control, BL), Stipa bungeana Trin. (STBU), Caragana korshinskii Kom. (CAKO), STBU planted with BSCs (STBU+BSCs) and CAKO planted with BSCs (CAKO+BSCs). The runoff, soil loss and soil moisture to a depth of 3 m were measured throughout the rainy season (from June to September) of 2010. The results showed that BSCs significantly reduced runoff by 37.3% and soil loss by 81.0% and increased infiltration by 12.4% in comparison with BL. However, when combined with STBU or CAKO, BSCs only made negligible contributions to erosion control (a runoff reduction of 7.4% and 5.7% and a soil loss reduction of 0.7% and 0.3%). Generally, the soil moisture of the vegetation plots was lower in the upper layer than that of the BL plots, although when accompanied with a higher amount of infiltration, this soil moisture consumption phenomenon was much clearer when combining vegetation with BSCs. Because of the trivial contributions from BSCs to erosion control and the remaining exacerbated consumption of soil water, moderate disturbance by BSCs should be considered in plots with adequate vegetation cover to improve soil moisture levels without a significant erosion increase, which was implied to be necessary and feasible.     

Encapsulation of recombinant <Emphasis Type="Italic">E. coli</Emphasis> expressing cyclopentanone monooxygenase in polyelectrolyte complex capsules for Baeyer–Villiger biooxidation of 8-oxabicyclo[3.2.1]oct-6-en-3-one

Recombinant Escherichia coli cells, over-expressing cyclopentanone monooxygenase activity, were immobilized in polyelectrolyte complex capsules, made of sodium alginate, cellulose sulfate, poly(methylene-co-guanidine), CaCl₂ and NaCl. More than 90% of the cell viability was preserved during the encapsulation process. Moreover, the initial enzyme activity was fully maintained within encapsulated cells while it halved in free cells. Both encapsulated and free cells reached the end point of the Baeyer–Villiger biooxidation of 8-oxabicyclo[3.2.1]oct-6-en-3-one to 4,9-dioxabicyclo[4.2.1]non-7-en-3-one at the same time (48 h). Similarly, the enantiomeric excess above 94% was identical for encapsulated and free cells.     

Peroxisome Proliferator-activated Receptor-D (PPARD) Coordinates Mouse Spermatogenesis by Modulating Extracellular Signal-regulated Kinase (ERK)-dependent Signaling

Ppard^−/− mice exhibit smaller litter size compared with Ppard^+/+ mice. To determine whether peroxisome proliferator-activated receptor-D (PPARD) could possibly influence this phenotype, the role of PPARD in testicular biology was examined. Atrophic testes and testicular degeneration were observed in Ppard^−/− mice compared with Ppard^+/+ mice, indicating that PPARD modulates spermatogenesis. Higher expression of p27 and decreased expression of proliferating cellular nuclear antigen in Sertoli cells were observed in Ppard^+/+ mice as compared with Ppard^−/− mice, and these were associated with decreased Sertoli cell number in Ppard^+/+ mice. Cyclin D1 and cyclin D2 expression was lower in Ppard^+/+ as compared with Ppard^−/− mice. Ligand activation of PPARD inhibited proliferation of a mouse Sertoli cell line, TM4, and an inverse agonist of PPARD (DG172) rescued this effect. Temporal inhibition of extracellular signal-regulated kinase (ERK) activation by PPARD in the testis was observed in Ppard^+/+ mice and was associated with decreased serum follicle-stimulating hormone and higher claudin-11 expression along the blood-testis barrier. PPARD-dependent ERK activation also altered expression of claudin-11, p27, cyclin D1, and cyclin D2 in TM4 cells, causing inhibition of cell proliferation, maturation, and formation of tight junctions in Sertoli cells, thus confirming a requirement for PPARD in accurate Sertoli cell function. Combined, these results reveal for the first time that PPARD regulates spermatogenesis by modulating the function of Sertoli cells during early testis development.     

Silencing NFBD1/MDC1 enhances the radiosensitivity of human nasopharyngeal cancer CNE1 cells and results in tumor growth inhibition

NFBD1 functions in cell cycle checkpoint activation and DNA repair following ionizing radiation (IR). In this study, we defined the NFBD1 as a tractable molecular target to radiosensitize nasopharyngeal carcinoma (NPC) cells. Silencing NFBD1 using lentivirus-mediated shRNA-sensitized NPC cells to radiation in a dose-dependent manner, increasing apoptotic cell death, decreasing clonogenic survival and delaying DNA damage repair. Furthermore, downregulation of NFBD1 inhibited the amplification of the IR-induced DNA damage signal, and failed to accumulate and retain DNA damage-response proteins at the DNA damage sites, which leaded to defective checkpoint activation following DNA damage. We also implicated the involvement of NFBD1 in IR-induced Rad51 and DNA-dependent protein kinase catalytic subunit foci formation. Xenografts models in nude mice showed that silencing NFBD1 significantly enhanced the antitumor activity of IR, leading to tumor growth inhibition of the combination therapy. Our studies suggested that a combination of gene therapy and radiation therapy may be an effective strategy for human NPC treatment.Nasopharyngeal carcinoma (NPC) is a non-lymphomatous, squamous cell carcinoma that occurs in the epithelial lining of the nasopharynx, which is a prevalent tumor in people of southern Chinese ancestry in southern China and Southeast Asia, and the incidence is still increasing.¹ Although radiotherapy is routinely used to treat patients with NPC, local recurrences and distant metastasis often occur in 30–40% of NPC patients at advanced staged.² Thus, new therapeutic strategies are required to improve the poor prognosis of NPC.Among the various types of DNA damage, DNA double-strand breaks (DSBs) are the most serious and require elaborated networks of proteins to signal and repair the damage.³ It has recently been shown that the histone H2A variant H2AX specifically controls the recruitment of DNA repair proteins to the sites of DNA damage.⁴ H2AX is phosphorylated extensively on a conserved serine residue at its carboxyl terminus in chromatin regions bearing DSBs, which is mediated by members of the phos-phoinositide-3-kinase-related protein kinase (PIKK) family.^{5, 6} Of these PIKKs, ataxia telangiectasia mutated (ATM) and DNA-dependent protein kinase catalytic subunit (DNA-PKcs) phosphorylate H2AX in response to DSBs in a partially redundant manner.^{7, 8} NFBD1 (Nuclear Factor with BRCT Domain Protein 1), also known as MDC1 (mediator of DNA damage checkpoint protein 1), is a recently identified nuclear protein that regulates many aspects of the DNA damage-response pathway, such as intra-S phase checkpoint, G2/M checkpoint, spindle assembly checkpoint and foci formation of NBS/MRE/Rad50 (MRN complex), 53BP1 and BRCA1.^{9, 10, 11, 12, 13} Human NFBD1 comprises 2089 amino acid residues and has a predicted molecular weight of ∼220 kDa. Motifs found in the protein include an FHA (Forkhead Associated) domain, two BRCT (BRCA1 carboxy terminal) domains and around 20 in terminal repeats of ∼41 amino acid residues each.¹⁴ Following DNA damage, NFBD1 serves as a bridging molecule and directly interacts with ATM and phospho-H2AX (γ-H2AX) through its FHA and BRCT domains, respectively, which leads to the expansion of γ-H2AX region surrounding DNA strand breaks and provides docking sites for many DNA damage and repair proteins including the MRN complex, 53BP1, BRCA1, RNF8, RNF4 and so on, ensuring genomics stability.^{11, 15, 16, 17, 18} In mammalian cells, DSBs are mainly repaired by two mechanisms, homologous recombination (HR) or non-homologous end-joining (NHEJ).^{19, 20, 21} For NHEJ repair, it is estimated that following exposure to ionizing radiation (IR), 80–90% of the DSBs in G1 are rejoined with fast kinetics in a manner dependent upon the NHEJ core components, Ku, DNA-PKcs, XRCC4 and DNA ligase IV. In contrast, HR predominates in late S- and G2-phase cells, when the sister chromatid is available to act as the template, representing those normally repaired with slow kinetics, require Rad51, Rad52, Rad54, XRCC2, XRCC3, the Rad51 paralogs and the breast cancer susceptibility genes BRCA1 and BRCA2.^{22, 23, 24, 25, 26}Since NFBD1 contains protein–protein interaction domains, and participate in the DNA damage-response (DDR) pathway. However, the mechanism by which NFBD1 regulates so many aspects of the DNA damage-response pathway in NPC cells is not fully understood. In addition, the physiological function of NFBD1 in NPC cells has been not investigated. With these goals in mind, we generated NFBD1-knockdown NPC cells and studied the physiological function of NFBD1 in DDR.     

Seed germinating characteristics of 54 gramineous species in the alpine meadow on the eastern Qinghai-Tibet plateau

The germination experiment was started on March 3, 2004, and seeds were collected from July to October in 2003. We analyzed the percentage of germination, days to first germination, germination period and days to 50% germination. Among the 54 examined species, 26 species exceeded 80% germination, 11 species exceeded 60%–80% germination, 8 exceeded 40%–0%, 5 exceeded 20%–40%, and 4 showed less than 20%. A principal-component analysis revealed that the species were distributed along two statistically independent axes, the first primarily represented the germination rate and the second represented the time of germination process. Based on scores of germination characteristics, cluster analysis of the 54 gramineous species could be divided into 4 distinct groups: rapid, slow, intermediate germinating (germination percentage > 50%), and low germinating (germination percentage < 50%). The meaning of different groups to the vegetation regeneration was discussed. __________ Translated from Journal of Plant Ecology, 2006, 30(4): 624–632 [译自: 植物生态学报]     

重组马g-干扰素抗病毒活性测定及单克隆抗体抑制活性鉴定

为了测定大肠杆菌和杆状病毒表达的重组马g-干扰素是否具有抗病毒活性, 利用这两种干扰素处理马胎肾细胞(EFK-78), 然后接种表达绿色荧光蛋白(GFP)的重组水泡性口炎病毒(VSV*GFP), 观察干扰素对病毒表达GFP的抑制, 测出其抗病毒活性单位分别为1×103 AU/mL、1×105 AU/mL。评价了制备的九株抗重组马g-干扰素单克隆抗体是否可抑制重组马g-干扰素抗病毒活性, 证实其中一株可中和重组马g-干扰素的抗病毒活性。结果表明: 杆状病毒表达的马g-干扰素具有较高的抗病毒活性, 其活性可被一株制备的抗重组马g-干扰素单克隆抗体抑制; 首次获得原核表达的具有抗病毒活性的马g-干扰素。     

Mitogen-activated protein kinase activity may not be necessary for the neuropathology of Niemann-Pick type C mice

Hyperphosphorylation of neurofilament and tau, and formation of cytoskeletal lesions, are notable features of several human neurodegenerative diseases, including Niemann-Pick Disease Type C (NPC). Previous studies suggested that the MAPKs, extracellular signal regulated kinase 1 and 2 (ERK1/2) may play a significant role in this aspect of NPC. To test this idea, we treated npc mice with PD98059, a specific and potent inhibitor of MAPK activation. Although activity of ERK1/2 was inhibited by 40%, a 2-week intracerebroventricular infusion of PD98059 just prior to onset of cytoskeletal pathology and symptoms in npc mice did not delay or inhibit prominent hallmarks of NPC. Unexpectedly, ERK1/2 inhibition led to aggravation of tau hyperphosphorylation, particularly in oligodendroctyes, in a manner similar to that of certain human tauopathies. Our results suggest that ERK1/2 does not play a major role in NPC neuropathology, and therefore, that MAPK inhibition is unlikely to be a useful strategy for managing the disease.     

红树林源白骨壤链霉菌中多环稠合大环内酰胺类化合物的结构多样性研究

【目的】通过基因组挖掘的方法,研究红树林来源白骨壤链霉菌Streptomyces avicenniae 9-9中多环稠合大环内酰胺(PTMs)类化合物的结构多样性。【方法】通过生物信息学分析白骨壤链霉菌基因组序列,寻找PTMs类化合物的生物合成相关基因;利用UPLC-MS/MS技术对该菌的次级代谢产物进行分析。【结果】在白骨壤链霉菌基因组中发现PTMs生物合成基因簇(aviA-D);从菌液提取物中鉴定出5个PTMs类化合物,其中包括ikarugamycin(化合物1)和capsimycin B(化合物2);基于PTMs类化合物5-6-5环类型的MS/MS碎裂规律,对化合物3–5的结构进行了推测。【结论】红树林来源白骨壤链霉菌S.avicenniae 9-9具有产生5-6-5环类型的PTMs类化合物的能力。     

Surprising low diversity of the plant pathogen Phytophthora in Amazonian forests

The genus Phytophthora represents a group of plant pathogens with broad global distribution. The majority of them cause the collar and root-rot of diverse plant species. Little is known about Phytophthora communities in forest ecosystems, especially in the Neotropical forests where natural enemies could maintain the huge plant diversity via negative density dependence. We characterized the diversity of soil-borne Phytophthora communities in the North French Guiana rainforest and investigated how they are structured by host identity and environmental factors. In this little-explored habitat, 250 soil cores were sampled from 10 plots hosting 10 different plant families across three forest environments (Terra Firme, Seasonally Flooded and White Sand). Phytophthora diversity was studied using a baiting approach and metabarcoding (High-Throughput Sequencing) on environmental DNA extracted from both soil samples and baiting-leaves. These three approaches revealed very similar communities, characterized by an unexpected low diversity of Phytophthora species, with the dominance of two cryptic species close to Phytophthora heveae. As expected, the Phytophthora community composition of the French Guiana rainforest was significantly impacted by the host plant family and environment. However, these plant pathogen communities are very small and are dominated by generalist species, questioning their potential roles as drivers of plant diversity in these Amazonian forests.