The rapid yellowing of spruce at a mountain site in the Central Black Forest (Germany). Combined effects of Mg deficiency and ozone on biochemical, physiological and structural properties of the chloroplasts

Biochemical, physiological and ultrastructural changes of the chloroplasts were examined in the course of the rapid yellowing process of spruce (Picea abies (L.) Karst.) at a Mg-deficient and ozone polluted mountain site (Sch?llkopf mountain, Central Black Forest, Germany, 840 m a.s.l.). While at an early stage of yellowing the chlorophyll (Chl) content of the needles decreased slowly, significant changes occurred in the chloroplasts: The lability of the light-harvesting Chl a/b protein complex LHC II increased; the thylakoid cross-sectional area of chloroplasts in the outer mesophyll of the needles decreased, and their Chl fluorescence showed typical changes like the decrease of Fv/Fm and the increase of the photoinhibitory Fv quenching. Later on, the Chl content decreased rapidly, the changes in the chloroplasts continued and the needles turned yellow. Lutein and the pigments of the xanthophyll cycle were enhanced in relation to Chl a. Light and dark reactions of the xanthophyll cycle were highly active indicating efficient proton pumping and NADPH formation. The ratio of nonappressed to appressed thylakoid membranes increased with decreasing Fv/Fm suggesting that structural and fluorescence properties of the chloroplasts were related. The response of the needles to defined shading and improved Mg supply was also examined. The combined effects of strong sun light, low levels of non-Chl-bound Mg (Mg(free)) and ozone concentrations exceeding 80 microg m(-3) are shown to be necessary to induce the rapid yellowing process. For needles with Mg(free) < 0.12 mg g(-1) needle dry matter, the lability of the LHC II was correlated with the ozone concentration suggesting that the destabilization of the LHC II plays a central role in the rapid yellowing process.     

Identification of voltage-gated K+ channel beta 2 (Kvβ2) subunit as a novel interaction partner of the pain transducer Transient Receptor Potential Vanilloid 1 channel (TRPV1)

The Transient Receptor Potential Vanilloid 1 (TRPV1, vanilloid receptor 1) ion channel plays a key role in the perception of thermal and inflammatory pain, however, its molecular environment in dorsal root ganglia (DRG) is largely unexplored. Utilizing a panel of sequence-directed antibodies against TRPV1 protein and mouse DRG membranes, the channel complex from mouse DRG was detergent-solubilized, isolated by immunoprecipitation and subsequently analyzed by mass spectrometry. A number of potential TRPV1 interaction partners were identified, among them cytoskeletal proteins, signal transduction molecules, and established ion channel subunits. Based on stringent specificity criteria, the voltage-gated K⁺ channel beta 2 subunit (Kvβ2), an accessory subunit of voltage-gated K⁺ channels, was identified of being associated with native TRPV1 channels. Reverse co-immunoprecipitation and antibody co-staining experiments confirmed TRPV1/Kvβ2 association. Biotinylation assays in the presence of Kvβ2 demonstrated increased cell surface expression levels of TRPV1, while patch-clamp experiments resulted in a significant increase of TRPV1 sensitivity to capsaicin. Our work shows, for the first time, the association of a Kvβ subunit with TRPV1 channels, and suggests that such interaction may play a role in TRPV1 channel trafficking to the plasma membrane.     

Periodic lamellipodial contractions correlate with rearward actin waves

Cellular lamellipodia bind to the matrix and probe its rigidity through forces generated by rearward F-actin transport. Cells respond to matrix rigidity by moving toward more rigid matrices using an unknown mechanism. In spreading and migrating cells we find local periodic contractions of lamellipodia that depend on matrix rigidity, fibronectin binding and myosin light chain kinase (MLCK). These contractions leave periodic rows of matrix bound beta3-integrin and paxillin while generating waves of rearward moving actin bound alpha-actinin and MLCK. The period between contractions corresponds to the time for F-actin to move across the lamellipodia. Shortening lamellipodial width by activating cofilin decreased this period proportionally. Increasing lamellipodial width by Rac signaling activation increased this period. We propose that an actin bound, contraction-activated signaling complex is transported locally from the tip to the base of the lamellipodium, activating the next contraction/extension cycle.     

Lamellipodial actin mechanically links myosin activity with adhesion-site formation

Cell motility proceeds by cycles of edge protrusion, adhesion, and retraction. Whether these functions are coordinated by biochemical or biomechanical processes is unknown. We find that myosin II pulls the rear of the lamellipodial actin network, causing upward bending, edge retraction, and initiation of new adhesion sites. The network then separates from the edge and condenses over the myosin. Protrusion resumes as lamellipodial actin regenerates from the front and extends rearward until it reaches newly assembled myosin, initiating the next cycle. Upward bending, observed by evanescence and electron microscopy, results in ruffle formation when adhesion strength is low. Correlative fluorescence and electron microscopy shows that the regenerating lamellipodium forms a cohesive, separable layer of actin above the lamellum. Thus, actin polymerization periodically builds a mechanical link, the lamellipodium, connecting myosin motors with the initiation of adhesion sites, suggesting that the major functions driving motility are coordinated by a biomechanical process.     

The epilepsy-linked Lgi1 protein assembles into presynaptic Kv1 channels and inhibits inactivation by Kvbeta1

The voltage-gated potassium (Kv) channel subunit Kv1.1 is a major constituent of presynaptic A-type channels that modulate synaptic transmission in CNS neurons. Here, we show that Kv1.1-containing channels are complexed with Lgi1, the functionally unassigned product of the leucine-rich glioma inactivated gene 1 (LGI1), which is causative for an autosomal dominant form of lateral temporal lobe epilepsy (ADLTE). In the hippocampal formation, both Kv1.1 and Lgi1 are coassembled with Kv1.4 and Kvbeta1 in axonal terminals. In A-type channels composed of these subunits, Lgi1 selectively prevents N-type inactivation mediated by the Kvbeta1 subunit. In contrast, defective Lgi1 molecules identified in ADLTE patients fail to exert this effect resulting in channels with rapid inactivation kinetics. The results establish Lgi1 as a novel subunit of Kv1.1-associated protein complexes and suggest that changes in inactivation gating of presynaptic A-type channels may promote epileptic activity.     

Die Entwicklung der Brutvogelbest?nde am Bodensee: Vergleich halbquantitativer Rasterkartierungen 1980/81 und 1990/91

Zusammenfassung Die halb-quantitative Rasterkartierung Bodensee wurde 1990/91 auf 88.3 % der zehn Jahre zuvor kartierten Fläche wiederholt. Nur 25 % der Rasterfelder wurden von denselben Beobachtern kartiert wie vor zehn Jahren. Daher wurden Veränderungen nur dann als gesichert betrachtet, wenn sie mindestens auf dem 2 %-Niveau signifikant waren. Dies war bei 62 Arten der Fall, wovon 29 Arten zu- und 33 abnahmen. 145 Vogelarten wurden registriert (vorher 143), die Artenzahl pro Rasterfläche ist jedoch ebenso rückläufig wie der Gesamtbestand aller Vogelarten. Neben Zunahmen bei einigen Vogelarten der menschlichen Siedlungsflächen und des Waldes ragen solche von Feuchtgebiets- und Wasservögeln hervor, die am Bodensee effizient geschützt sind. Bemerkenswert sind der erhebliche Bestandsrückgang beim Haussperling und die insgesamt stark negative Entwicklung bei den Langstreckenziehern, unter denen keine Singvogelart mehr eine gesicherte Zunahme verzeichnen konnte. Drastische Bestandseinbrüche fast aller Bodenbrüter des offenen Kulturlandes wurden festgestellt.

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The development in the breeding birds of Lake Constance: comparison of grid mapping in 1980/81 and 1990/91

Summary The distribution and number of breeding birds at Lake Constance was mapped on 278 grids of 4 km² in 1990/91, covering 88.3 % of the area of 1980/81. As only 25 % of the grids were censused by the same observers as in 1980/81, changes were only considered real if significant on the 2 % level at least. This was the case in 62 species, 29 of which were increasing, 33 decreasing. A total of 145 breeding species was found (143 before), however, the number of species per grid and the total number of territories registered were lower than ten years ago. Apart from increases of species of urban settlements (e.g. Feral Pigeon, Collared dove, Black Redstart, Serin) and forests (e.g. Sparrowhawk, Goshawk, Great Spotted Woodpecker, Mistle thrush), the favourable development in species living in reedbeds and in waterbirds was notable. The latter is due to effective conservation measures at Lake Constance. Remarkable was the considerable loss in breeding numbers of the House Sparrow and the generally negative development of long-distance migrants, especially passerine species. A drastic population decline was found for almost the complete guild of ground-nesting birds in open habitats.