Production of Perennial Vegetation in an Oasis-desert Transition Zone in NW China - Allometric Estimation,and Assessment of Flooding and Use Effects

River oases at the southern fringe of the Taklamakan desert in NW China are surrounded by belts of spontaneous vegetation that protect the oases from sand drift. As an important source of forage, fuel and construction wood, this foreland vegetation is also a component part of the agricultural system of the oases but has been, and still is, destroyed through overuse. Within a broader study that aimed to provide a basis for a sustainable management of this foreland vegetation, biomass and production were studied in four vegetation types dominated either by Alhagi sparsifolia, Calligonum caput-medusae, Populus euphratica, or Tamarix ramosissima that were thought to occur under different regimes of natural flooding in the foreland of Qira (Cele) oasis, Xinjiang, NW China. Shoot biomass components were closely correlated to basal area (Calligonum, Populus, Tamarix) or shrub volume and projection area (Alhagi), enabling non-destructive estimation of stand biomass from shoot diameters or shrub dimensions with sufficient precision using allometric regression equations. Relationships between shoot basal area and biomass of the woody species (Calligonum, Populus and Tamarix) agreed with predictions by a theoretical model of plant vascular systems, suggesting that they are determined by hydraulic and mechanical requirements for shoot architecture. Average aboveground biomass densities of typical stands in late summer were 2.97 Mg/ha in Alhagi, 3.6 Mg/ha in a row plantation and 10.9 Mg/ha in homogenous stands of Calligonum, 22–29 Mg/ha in 22 year-old Populus forests and 1.9–3.1 Mg/ha in Tamarix-dominated vegetation. Annual aboveground production including wood and assimilation organs ranged from 2.11 to 11.3 Mg/ha in plantations of Calligonum, 3.17 to 6.12 Mg/ha in Populus, and 1.55 to 1.74 Mg/ha (based on total ground area) or 3.10 to 7.15 Mg/ha (in homogenous stands) in Tamarix. Production of Alhagi is equal to peak biomass. A thinning treatment simulating use by the local population enhanced productivity of Calligonum, Populus and Tamarix. A complete harvest of Alhagi in late August decreased production in the following year. An artificial flood irrigation treatment did not sufficiently increase soil water content except in the uppermost layer and had no clear beneficial effect on growth of the four species and even a negative effect on Alhagi, which was due to increased competition from annual species. As biomass and production with or without artificial irrigation were much higher than values expected for rain-fed desert vegetation at a mean annual precipitation of 35 mm, it is concluded that the existence of all vegetation types studied is probably based on permanent access to groundwater and that natural floods or precipitation do not contribute to their water supply. The effects of agricultural groundwater use in the oasis on groundwater in the foreland of the oasis need further study. Sustainable use of this productive vegetation is possible but requires proper management.     

Life-cycle assessment and techno-economic analysis of biochar produced from forest residues using portable systems

The International Journal of Life Cycle Assessment - Producing biochar from forest residues can help resolve environmental issues by reducing forest fires and mitigating climate change. However,...     

Nitric oxide induces TIMP-1 expression by activating the transforming growth factor beta-Smad signaling pathway

Excessive accumulation of the extracellular matrix is a hallmark of many inflammatory and fibrotic diseases, including those of the kidney. This study addresses the question whether NO, in addition to inhibiting the expression of MMP-9, a prominent metalloprotease expressed by mesangial cells, additionally modulates expression of its endogenous inhibitor TIMP-1. We demonstrate that exogenous NO has no modulatory effect on the extracellular TIMP-1 content but strongly amplifies the early increase in cytokine-induced TIMP-1 mRNA and protein levels. We examined whether transforming growth factor beta (TGFbeta), a potent profibrotic cytokine, is involved in the regulation of NO-dependent TIMP-1 expression. Experiments utilizing a pan-specific neutralizing TGFbeta antibody demonstrate that the NO-induced amplification of TIMP-1 is mediated by extracellular TGFbeta. Mechanistically, NO causes a rapid increase in Smad-2 phosphorylation, which is abrogated by the addition of neutralizing TGFbeta antisera. Similarly, the NO-dependent increase in Smad-2 phosphorylation is prevented in the presence of an inhibitor of TGFbeta-RI kinase, indicating that the NO-dependent activation of Smad-2 occurs via the TGFbeta-type I receptor. Furthermore, activation of the Smad signaling cascade by NO is corroborated by the NO-dependent increase in nuclear Smad-4 level and is paralleled by increased DNA binding of Smad-2/3 containing complexes to a TIMP-1-specific Smad-binding element (SBE). Reporter gene assays revealed that NO activates a 0.6-kb TIMP-1 gene promoter fragment as well as a TGFbeta-inducible and SBE-driven control promoter. Chromatin immunoprecipitation analysis also demonstrated DNA binding activity of Smad-3 and Smad-4 proteins to the TIMP-1-specific SBE. Finally, by enzyme-linked immunosorbent assay, we demonstrated that NO causes a rapid increase in TGFbeta(1) levels in cell supernatants. Together, these experiments demonstrate that NO by induction of the Smad signaling pathway modulates TIMP-1 expression.     

Expression of the xylulose 5-phosphate phosphoketolase gene, xpkA, from Lactobacillus pentosus MD363 is induced by sugars that are fermented via the phosphoketolase pathway and is repressed by glucose mediated by CcpA and the mannose phosphoenolpyruvate phosphotransferase system

Purification of xylulose 5-phosphate phosphoketolase (XpkA), the central enzyme of the phosphoketolase pathway (PKP) in lactic acid bacteria, and cloning and sequence analysis of the encoding gene, xpkA, from Lactobacillus pentosus MD363 are described. xpkA encodes a 788-amino-acid protein with a calculated mass of 88,705 Da. Expression of xpkA in Escherichia coli led to an increase in XpkA activity, while an xpkA knockout mutant of L. pentosus lost XpkA activity and was not able to grow on energy sources that are fermented via the PKP, indicating that xpkA encodes an enzyme with phosphoketolase activity. A database search revealed that there are high levels of similarity between XpkA and a phosphoketolase from Bifidobacterium lactis and between XpkA and a (putative) protein present in a number of evolutionarily distantly related organisms (up to 54% identical residues). Expression of xpkA in L. pentosus was induced by sugars that are fermented via the PKP and was repressed by glucose mediated by carbon catabolite protein A (CcpA) and by the mannose phosphoenolpyruvate phosphotransferase system. Most of the residues involved in correct binding of the cofactor thiamine pyrophosphate (TPP) that are conserved in transketolase, pyruvate decarboxylase, and pyruvate oxidase were also conserved at a similar position in XpkA, implying that there is a similar TPP-binding fold in XpkA.     

Characterization of PROPPIN-Phosphoinositide Binding and Role of Loop 6CD in PROPPIN-Membrane Binding

PROPPINs (β-propellers that bind polyphosphoinositides) are a family of PtdIns3P- and PtdIns(3,5)P₂-binding proteins that play an important role in autophagy. We analyzed PROPPIN-membrane binding through isothermal titration calorimetry (ITC), stopped-flow measurements, mutagenesis studies, and molecular dynamics (MD) simulations. ITC measurements showed that the yeast PROPPIN family members Atg18, Atg21, and Hsv2 bind PtdIns3P and PtdIns(3,5)P₂ with high affinities in the nanomolar to low-micromolar range and have two phosphoinositide (PIP)-binding sites. Single PIP-binding site mutants have a 15- to 30-fold reduced affinity, which explains the requirement of two PIP-binding sites in PROPPINs. Hsv2 bound small unilamellar vesicles with a higher affinity than it bound large unilamellar vesicles in stopped-flow measurements. Thus, we conclude that PROPPIN membrane binding is curvature dependent. MD simulations revealed that loop 6CD is an anchor for membrane binding, as it is the region of the protein that inserts most deeply into the lipid bilayer. Mutagenesis studies showed that both hydrophobic and electrostatic interactions are required for membrane insertion of loop 6CD. We propose a model for PROPPIN-membrane binding in which PROPPINs are initially targeted to membranes through nonspecific electrostatic interactions and are then retained at the membrane through PIP binding.