The larva of Rhyacophila ferox Graf, 2006 (Trichoptera: Rhyacophilidae) from the Eastern Alps (Carinthia,Austria)

The hitherto unknown larva of Rhyacophila ferox Graf, 2006, is described and discussed in the context of contemporary Rhyacophilidae keys. In addition, zoogeographical and ecological notes are included.     

Description of the female and new data on the distribution of Annitella apfelbecki Klapálek, 1899 (Insecta: Trichoptera)

Annitella apfelbecki is one of three Annitella species with distribution ranges restricted to the Balkan Peninsula. In this paper, we describe the hitherto unknown female of A. apfelbecki and give the most important morphological features to enable its identification and separation from the other Annitella females. Additionally, we provide new data on distribution and discuss zoogeography, life cycle and ecology of this species.     

Can tree-ring δ<Superscript>15</Superscript>N be used as a proxy for foliar δ<Superscript>15</Superscript>N in European beech and Norway spruce?

Key message

For long-term environmental investigations, tree-ring δ ¹⁵ N values are inappropriate proxies for foliar δ ¹⁵ N for both Fagus sylvatica and Picea abies under moderate N loads.

Abstract

Currently it is unclear whether stable nitrogen isotope signals of tree-rings are related to those in foliage, and whether they can be used to infer tree responses to environmental changes. We studied foliar and tree-ring nitrogen (δ¹⁵N) and carbon (δ¹³C) isotope ratios in European beech (Fagus sylvatica L.) and Norway spruce (Picea abies L.) from six long-term forest monitoring sites in Switzerland together with data on N deposition and soil N availability, as well as a drought response index over the last two decades. For both species, tree-ring δ¹⁵N and δ¹³C values were less negative compared to foliar δ¹⁵N and δ¹³C values, most likely due to recycling and reallocation of N within the tree and fractionation processes associated with the transport of sucrose and the formation of tree-rings, respectively. Temporal trends recorded in foliar δ¹⁵N were not reflected in tree-ring δ¹⁵N, with much higher variations in tree-rings compared to foliage. Soil N availability and N deposition were partially able to explain changes in foliar δ¹³C, while there were no significant correlations between environmental variables and either tree-ring or foliar δ¹⁵N. Our results suggest an uncoupling between the N isotopic composition of tree-rings and foliage. Consequently, tree-ring δ¹⁵N values are inappropriate proxies of foliar δ¹⁵N values under low-to-moderate N deposition loads. Furthermore, at such low levels of deposition, tree-ring δ¹⁵N values are not recommended as archives of tree responses to soil C/N or bulk N deposition.

     

The redox-switch domain of Hsp33 functions as dual stress sensor

The redox-regulated chaperone Hsp33 is specifically activated upon exposure of cells to peroxide stress at elevated temperatures. Here we show that Hsp33 harbors two interdependent stress-sensing regions located in the C-terminal redox-switch domain of Hsp33: a zinc center sensing peroxide stress conditions and an adjacent linker region responding to unfolding conditions. Neither of these sensors works sufficiently in the absence of the other, making the simultaneous presence of both stress conditions a necessary requirement for Hsp33's full activation. Upon activation, Hsp33's redox-switch domain adopts a natively unfolded conformation, thereby exposing hydrophobic surfaces in its N-terminal substrate-binding domain. The specific activation of Hsp33 by the oxidative unfolding of its redox-switch domain makes this chaperone optimally suited to quickly respond to oxidative stress conditions that lead to protein unfolding.     

Inhibition of glucose transport by cyclic GMP in cardiomyocytes

Recent evidence points to a potential role of cyclic GMP (cGMP) in the control of cardiac glucose utilization. The present work examines whether the glucose transport system of cardiac myocyte is a site of this cGMP-dependent regulation. Treatment of isolated rat cardiomyocytes (for 10 min) with the membrane-permeant cGMP analogue 8-(4-chlorophenylthio)-cGMP (8-p-CPT-cGMP, 200 microM) caused a decrease in glucose transport in non-stimulated (basal) myocytes, as well as in cells stimulated with insulin or with the mitochondrial inhibitor oligomycin B by up to 40%. An inhibitory effect was also observed with another cGMP analogue (8-bromo-cGMP), and in cells stimulated by hydrogen peroxide or anoxia. In contrast, 8-p-CPT-cAMP (200 microM), or the beta-adrenergic agonist isoprenaline (which increases cAMP levels) did not depress glucose transport, and even potentiated the effect of insulin. Blockade of endogenous cGMP formation with the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 10 microM) significantly increased basal and insulin-dependent glucose transport (by 25%), whereas addition of the guanylate cyclase activator 3-(5'-hydroxymethyl-2'furyl)-1-benzylindazol (YC-1, 30 microM) produced a depression of glucose transport (by 20%). Confocal laser scanning microscopic studies revealed that cGMP partially prevents the insulin-induced redistribution of the glucose transporter GLUT4 from intracellular stores to the cell surface. These observations suggest that the glucose transport system of cardiomyocytes represents a metabolic target of inhibition by cGMP, and that this regulation occurs at the level of the trafficking of glucose transporters.     

Epstein-Barr virus encodes a novel homolog of the bcl-2 oncogene that inhibits apoptosis and associates with Bax and Bak

The sequenced gammaherpesviruses each contain a single viral bcl-2 homolog (v-bcl-2) which may encode a protein that functions in preventing the apoptotic death of virus-infected cells. Epstein-Barr virus (EBV), a gammaherpesvirus associated with several lymphoid and epithelial malignancies, encodes the v-Bcl-2 homolog BHRF1. In this report the previously uncharacterized BALF1 open reading frame in EBV is identified as having significant sequence similarity to other v-bcl-2 homologs and cellular bcl-2. Transfection of cells with a BALF1 cDNA conferred apoptosis resistance. Furthermore, a recombinant green fluorescent protein-BALF1 fusion protein suppressed apoptosis and associated with Bax and Bak. These results indicate that EBV encodes a second functional v-bcl-2.     

Neurexins induce differentiation of GABA and glutamate postsynaptic specializations via neuroligins

Formation of synaptic connections requires alignment of neurotransmitter receptors on postsynaptic dendrites opposite matching transmitter release sites on presynaptic axons. beta-neurexins and neuroligins form a trans-synaptic link at glutamate synapses. We show here that neurexin alone is sufficient to induce glutamate postsynaptic differentiation in contacting dendrites. Surprisingly, neurexin also induces GABA postsynaptic differentiation. Conversely, neuroligins induce presynaptic differentiation in both glutamate and GABA axons. Whereas neuroligins-1, -3, and -4 localize to glutamate postsynaptic sites, neuroligin-2 localizes primarily to GABA synapses. Direct aggregation of neuroligins reveals a linkage of neuroligin-2 to GABA and glutamate postsynaptic proteins, but the other neuroligins only to glutamate postsynaptic proteins. Furthermore, mislocalized expression of neuroligin-2 disperses postsynaptic proteins and disrupts synaptic transmission. Our findings indicate that the neurexin-neuroligin link is a core component mediating both GABAergic and glutamatergic synaptogenesis, and differences in isoform localization and binding affinities may contribute to appropriate differentiation and specificity.     

Vascular endothelial cells express a functional fas-receptor due to lack of hemodynamic forces

The fas system is present in atherosclerotic lesions. However, its role in the initiation and progression is still unclear. Here we show that in endothelial cells (EC) the expression of the fas receptor is regulated by flow conditions. The EC of the vascular system are regularly exposed to a range of hemodynamic forces with great impact on cellular structures and functions. Recently it was reported that in endothelial cells the lack of hemodynamic forces as well as irregular flow conditions trigger apoptosis by induction of a mechanosensitive autocrine loop of thrombospondin-1 and the _V3 integrin/integrin-associated protein complex. Here we show that EC cultivated under regular laminar flow conditions are devoid of the fas-receptor whereas cultivation under static conditions as well as under turbulence leads to its expression. Stimulation of the fas-receptor by its ligand increases the amount of apoptotic cells by twofold; the increase can be prevented by blocking the fas-receptor. The availability of the expressed fas receptor for stimulation by its ligand hints at a role as a tool for progression of atherosclerosis.     

Mechanosensitive induction of apoptosis in fibroblasts is regulated by thrombospondin-1 and integrin associated protein (CD47)

Fibroblasts are cultured in three-dimensional collagen matrices to investigate the effect of mechanical tension on the regulation of apoptosis. Under the influence of mechanical loading, the cells show little apoptosis whereas releasing of tension leads to an increase up to tenfold during the first 24 h and remains constant for further 48 h. An autocrine loop of the integrin _V3/CD47 receptor complex and thrombospondin-1 is identified as the molecular coupling device between mechanical loading and apoptosis: The integrin _V3 is expressed under mechanical loading as well as unloading whereas the CD47 could only be identified after the release of tension. The secreted thrombospondin binds to the active receptor and induces apoptosis. The presented mechanosensitive regulation of apoptosis in fibroblast cultures could be an essential mechanism for the regression of the granulation tissue by apoptosis in the process of wound healing.