Influence of the margin vegetation on the conservation of aphid biological control in apple orchards

The influence of three margin strip treatments (wildflower strips, grass strips and spontaneous vegetation) adjacent to apple orchards on the biological control of Dysaphis plantaginea Passerini (Hemiptera: Aphididae) was compared during two consecutive years. The wildflower strips provided the highest amount of floral resources. Within the margin strips, hoverflies responded positively to higher resource provisioning whereas ladybird abundance did not differ between strip treatments. Within the orchards, the presence of parasitoids, hoverflies, and ladybirds in aphid colonies and the predation of sentinel aphids were not significantly affected by the adjacent strip treatments. The number of natural enemies observed in aphid colonies was mainly driven by aphid number. Aphid numbers were higher close to the margin strips suggesting that aphid colonization from orchard edges may counteract the positive effect of wildflower strips on natural enemy abundance and on a reduction of aphid infestation. The results confirm the positive influence of floral resource provisioning by wildflower strips on the conservation of aphid natural enemies, but also suggest that effects of wildflower strips on aphid regulation inside orchards are not very strong compared with spontaneous vegetation naturally occurring in the margins.     

The dioxygenase GIM2 functions in seed germination by altering gibberellin production in Arabidopsis

The phytohormones gibberellic acid (GA) and abscisic acid (ABA) antagonistically control seed germination. High levels of GA favor seed germination, whereas high levels of ABA hinder this process. The direct relationship between GA biosynthesis and seed germination ability need further investigation. Here, we identified the ABA‐insensitive gain‐of‐function mutant germination insensitive to ABA mutant 2 (gim2) by screening a population of XVE T‐DNA‐tagged mutant lines. Based on two loss‐of‐function gim2‐ko mutant lines, the disruption of GIM2 function caused a delay in seed germination. By contrast, upregulation of GIM2 accelerated seed germination, as observed in transgenic lines overexpressing GIM2 (OE). We detected a reduction in endogenous bioactive GA levels and an increase in endogenous ABA levels in the gim2‐ko mutants compared to wild type. Conversely, the OE lines had increased endogenous bioactive GA levels and decreased endogenous ABA levels. The expression levels of a set of GA‐ and/or ABA‐related genes were altered in both the gim2‐ko mutants and the OE lines. We confirmed that GIM2 has dioxygenase activity using an in vitro enzyme assay, observing that GIM2 can oxidize GA₁₂. Hence, our characterization of GIM2 demonstrates that it plays a role in seed germination by affecting the GA metabolic pathway in Arabidopsis.     

渔游蛇（Xenochrophis piscator）的脑及脑神经

了解渔游蛇的脑及脑神经,方法 解剖整体和观察蛇头标本。其形态特点与乌稍蛇相似但逼神经已与迷走神经分开并单独出颅,出颅后第一脊神经,然后进入脑颈干。     

Inhibition of the oxidative stress-induced miR-23a protects the human retinal pigment epithelium (RPE) cells from apoptosis through the upregulation of glutaminase and glutamine uptake

The degeneration of retinal pigment epithelium (RPE) cells in the sub retinal pigment epithelial space and choroid is an initial pathological characteristic for the age-related macular degeneration which is the leading cause of severe vision loss in old people. Moreover, oxidative stress is implicated as a major inducer of RPE cell death. Here, we assessed the correlation between the H₂O₂-induced RPE cell death and glutamine metabolism. We found under low glutamine supply (20 %), the ARPE-19 cells were more susceptive to H₂O₂-induced apoptosis. Moreover, the glutamine uptake and the glutaminase (GLS) were suppressed by H₂O₂ treatments. Moreover, we observed miR-23a was upregulated by H₂O₂ treatments and overexpression of miR-23a significantly sensitized ARPE-19 cells to H₂O₂. Importantly, Western blotting and luciferase assay demonstrated GLS1 is a direct target of miR-23a in RPE cells. Inhibition of the H₂O₂-induced miR-23a by antagomiR protected the RPE cells from the oxidative stress-induced cell death. In addition, recovery of GLS1 expression in miR-23a overexpressed RPE cells rescued the H₂O₂-induced cell death. This study illustrated a mechanism for the protection of the oxidative-induced RPE cell death through the recovery of glutamine metabolism by inhibition of miR-23a, contributing to the discovery of novel targets and the developments of therapeutic strategies for the prevention of RPE cells from oxidative stress.     

p62 links the autophagy pathway and the ubiqutin–proteasome system upon ubiquitinated protein degradation

The ubiquitin–proteasome system (UPS) and autophagy are two distinct and interacting proteolytic systems. They play critical roles in cell survival under normal conditions and during stress. An increasing body of evidence indicates that ubiquitinated cargoes are important markers of degradation. p62, a classical receptor of autophagy, is a multifunctional protein located throughout the cell and involved in many signal transduction pathways, including the Keap1–Nrf2 pathway. It is involved in the proteasomal degradation of ubiquitinated proteins. When the cellular p62 level is manipulated, the quantity and location pattern of ubiquitinated proteins change with a considerable impact on cell survival. Altered p62 levels can even lead to some diseases. The proteotoxic stress imposed by proteasome inhibition can activate autophagy through p62 phosphorylation. A deficiency in autophagy may compromise the ubiquitin–proteasome system, since overabundant p62 delays delivery of the proteasomal substrate to the proteasome despite proteasomal catalytic activity being unchanged. In addition, p62 and the proteasome can modulate the activity of HDAC6 deacetylase, thus influencing the autophagic degradation.     

Conformational rearrangements of tail-less complex polypeptide 1 (TCP-1) ring complex (TRiC)-bound actin

The mechanism of chaperonins is still under intense investigation. Earlier studies by others and us on the bacterial chaperonin GroEL points to an active role of chaperonins in unfolding the target protein during initial binding. Here, a natural eukaryotic chaperonin system [tail-less complex polypeptide 1 (TCP-1) ring complex (TRiC) and its target protein actin] was investigated to determine if the active participation of the chaperonin in the folding process is evolutionary-conserved. Using fluorescence resonance energy transfer (FRET) measurements on four distinct doubly fluorescein-labeled variants of actin, we have obtained a fairly detailed map of the structural rearrangements that occur during the TRiC-actin interaction. The results clearly show that TRiC has an active role in rearranging the bound actin molecule. The target is stretched as a consequence of binding to TRiC and further rearranged in a second step as a consequence of ATP binding; i.e., the mechanism of chaperonins is conserved during evolution.