Mechanisms of long-distance seed dispersal

Growing recognition of the importance of long-distance dispersal (LDD) of plant seeds for various ecological and evolutionary processes has led to an upsurge of research into the mechanisms underlying LDD. We summarize these findings by formulating six generalizations stating that LDD is generally more common in open terrestrial landscapes, and is typically driven by large and migratory animals, extreme meteorological phenomena, ocean currents and human transportation, each transporting a variety of seed morphologies. LDD is often associated with unusual behavior of the standard vector inferred from plant dispersal morphology, or mediated by nonstandard vectors. To advance our understanding of LDD, we advocate a vector-based research approach that identifies the significant LDD vectors and quantifies how environmental conditions modify their actions.     

Serum Amyloid A Complexed with Extracellular Matrix Induces the Secretion of Tumor Necrosis Factor-α by human T-lymphocytes

Summary Serum amyloid A (SAA), an acute-phase reactant, exists naturally as a minor protein in the sera of healthy individuals. However, its levels in sera are increased markedly during various transient and chronic inflammatory diseases, often concomitantly with accumulation at inflicted sites. SAA is synthesized mainly in the liver following the synergistic action of cytokines, mainly tumor necrosis factor-α (TNF-α) and interleukin-1 and-6 (IL-1 and IL-6). It was already shown by us that upon interaction with SAA or amyloid A (AA), the extracellular matrix (ECM) and laminin induced the adhesion of resting human CD4⁺ T-cells in an apparently β₁-integrin-mediated manner. Herein we have shown that the SAA-ECM complex modulates the regulation of cytokine synthesis by human T-lymphocytes. The SAA-ECM complex dramatically enhanced the release of TNF-α by human T-cells in a dose-dependent manner, reaching its maximal effect in the presence of 100 μM recombinant SAA. The SAA domain, responsible for the enhanced release of TNF-α by human T-lymphocytes, is apparently the amyloid A protein (AA, i.e. SAA2-82). Specifically, TNF-α enhanced secretion is mediated through intimate interactions of SAA/AA, with laminin. Thus, the ECM serving as a temporary anchorage site for SAA and AA seems to be involved in regulating TNF-α secretion and the recruitment and accumulation of immunocytes in extravascular, inflammatory compartments.     

Molecular Basis for Zinc Transporter 1 Action as an Endogenous Inhibitor of L-type Calcium Channels

The L-type calcium channel (LTCC) has a variety of physiological roles that are critical for the proper function of many cell types and organs. Recently, a member of the zinc-regulating family of proteins, ZnT-1, was recognized as an endogenous inhibitor of the LTCC, but its mechanism of action has not been elucidated. In the present study, using two-electrode voltage clamp recordings in Xenopus oocytes, we demonstrate that ZnT-1-mediated inhibition of the LTCC critically depends on the presence of the LTCC regulatory β-subunit. Moreover, the ZnT-1-induced inhibition of the LTCC current is also abolished by excess levels of the β-subunit. An interaction between ZnT-1 and the β-subunit, as demonstrated by co-immunoprecipitation and by fluorescence resonance energy transfer, is consistent with this result. Using surface biotinylation and total internal reflection fluorescence microscopy in HEK293 cells, we show a ZnT-1-dependent decrease in the surface expression of the pore-forming α₁-subunit of the LTCC. Similarly, a decrease in the surface expression of the α₁-subunit is observed following up-regulation of the expression of endogenous ZnT-1 in rapidly paced cultured cardiomyocytes. We conclude that ZnT-1-mediated inhibition of the LTCC is mediated through a functional interaction of ZnT-1 with the LTCC β-subunit and that it involves a decrease in the trafficking of the LTCC α₁-subunit to the surface membrane.     

Comparison of the ovaries and oogenesis of some Australian and South African viviparid clinid fishes (Clinidae,Blennioidei, Perciformes)

The ovaries of the studied 16 viviparous blenny species of the fish family Clinidae (Teleostei, Perciformes) from Australia and South Africa, are of the cystovarian type and bilobed, ending in a common short oviduct at the gonopore; they are elongated in juvenile fish, becoming bottle-shaped or oval with maturation and onset of embryogenesis, when they comprise 18–20% of the total body weight. The ovarian lumen is covered by the germinal epithelium, resting on a basal membrane. The primordial germ cells are situated along the inner side of each lobe, juxtaposed internally to the lumenal epithelium. Single primary oocytes or nests of such, each in a follicular envelope and covered externally by the lumenal epithelium forming clusters protruding into the lumen, along which the inoculated sperm settle. Two different types of reproductive strategies are demonstrated by the Australian species of Heteroclinus and Cristiceps and the South African species of Clinus and related forms. The Australian species produce high numbers of small (350 ± 50 μm in diameter) eggs that develop synchronously, while the South African species produce much fewer and larger (1.0 ± 0.1 mm) eggs, asynchronous in development. An exception in the latter group is Blennophis striatus, with eggs of ca.1.4 mm that develop synchronously. The Australian species are thus mass releasers that bear and release up to 1000 small (11 ± 1.5 mm in length) embryos/spawn, while the South African Clinus species are discrete releasers that bear eggs of various sizes and small numbers of mature for release embryos that reach up to 22 mm in length, and are released throughout the year. The cytogenesis of the oocytes and surrounding envelopes is discussed.     

Methyl jasmonate induces cell cycle block and cell death in the amitochondriate parasite Trichomonas vaginalis

Jasmonates are a group of small lipids produced in plants and function as stress hormones. They are selectively cytotoxic against cancer cells. Methyl jasmonate (MJ), one of the naturally occurring jasmonates, has direct mitochondriotoxic effects, strongly suggesting that mitochondria are target organelles of jasmonates. We have previously shown that jasmonates are cytotoxic to two human parasites -Schistosoma mansoni and Plasmodium falciparum. Both the cancer cells and the parasites mentioned above possess mitochondria. The present work aimed to examine whether jasmonates are able to damage cells lacking mitochondria, e.g., some unicellular human parasitic flagellates. We found that MJ induced death of the amitochondriate Trichomonas vaginalis parasites. MJ caused fragmentation and condensation of the DNA of T. vaginalis, resembling phenomena associated with apoptotic death. However, DNA laddering, a sub-G(1) cell cycle stage peak and caspase-3 activation were not observed. Thus, MJ-induced T. vaginalis cell death appears to be non-apoptotic. We found that MJ induced cell cycle block at the G(2)/M phase in T. vaginalis, similar to the effect of metronidazole. We examined the influence of MJ on the bioenergetic pathways of T. vaginalis, and found that depletion of ATP did not precede death of the parasites, but rather reflected it. Nevertheless, 2-deoxy-d-glucose, a glycolysis blocker, was synergistic with MJ in causing death of T. vaginalis cells, suggesting that MJ does perturb the bioenergetic homeostasis of the parasites. Finally, MJ was found to be cytotoxic towards a metronidazole-resistant strain of T. vaginalis (ATCC 50143), suggesting that it may be effective for the treatment of nitroimidazole-refractory trichomoniasis. In conclusion, MJ was found to exhibit mitochondria-independent cytotoxicity and presents a potentially novel agent against T. vaginalis.     

Prostaglandin E2 inhibits the proliferation of human gingival fibroblasts via the EP2 receptor and Epac

Elevated levels of prostaglandins such as PGE₂ in inflamed gingiva play a significant role in the tissue destruction caused by periodontitis, partly by targeting local fibroblasts. Only very few studies have shown that PGE₂ inhibits the proliferation of a gingival fibroblast (GF) cell line, and we expanded this research by using primary human GFs (hGFs) and looking into the mechanisms of the PGE₂ effect. GFs derived from healthy human gingiva were treated with PGE₂ and proliferation was assessed by measuring cell number and DNA synthesis and potential signaling pathways were investigated using selective activators or inhibitors. PGE₂ inhibited the proliferation of hGFs dose‐dependently. The effect was mimicked by forskolin (adenylate cyclase stimulator) and augmented by IBMX (a cAMP‐breakdown inhibitor), pointing to involvement of cAMP. Indeed, PGE₂ and forskolin induced cAMP generation in these cells. Using selective EP receptor agonists we found that the anti‐proliferative effect of PGE₂ is mediated via the EP₂ receptor (which is coupled to adenylate cyclase activation). We also found that the effect of PGE₂ involved activation of Epac (exchange protein directly activated by cAMP), an intracellular cAMP sensor, and not PKA. While serum increased the amount of phospho‐ERK in hGFs by ～300%, PGE₂ decreased it by ～50%. Finally, the PGE₂ effect does not require endogenous production of prostaglandins since it was not abrogated by two COX‐inhibitors. In conclusion, in human gingival fibroblasts PGE₂ activates the EP₂—cAMP—Epac pathway, reducing ERK phosphorylation and inhibiting proliferation. This effect could hamper periodontal healing and provide further insights into the pathogenesis of inflammatory periodontal disease. J. Cell. Biochem. 108: 207–215, 2009. © 2009 Wiley‐Liss, Inc.     

Phylogeny of the Baldratiina (Diptera: Cecidomyiidae) inferred from morphological, ecological and molecular data sources, and evolutionary patterns in plant-galler relationships

The phylogeny of the gall-midge subtribe Baldratiina (Diptera: Cecidomyiidae) was reconstructed from molecular (partial sequence of the mitochondrial 12S rDNA), morphological and ecological data sets, using 16 representative species of most of the genera. The morphological and ecological data were combined in a single character matrix and analyzed separately from the molecular data, resulting in an eco-morphological cladogram and a molecular cladogram. Attributes of galls and host associations were superimposed on the molecular cladogram in order to detect possible trends in the evolution of these traits. The cladograms resulting from the two independent analyses were statistically incongruent, although both provide evidence for the monophyly of the genera Baldratia and Careopalpis and the paraphyly of the genera Stefaniola and Izeniola. The results suggest a minor impact of the morphological characters traditionally used in the classification of the Baldratiina, whereas ecological data had a major impact on the phylogenetic inference. Mapping of gall and host attributes on the molecular cladogram suggests that multi-chambered stem galls constitute the ancestral state in the subtribe, with several subsequent shifts to leaf galls. It is concluded that in contrast to other studied groups of gall insects, related baldratiine species induce different types of galls, attesting to speciation driven by gall-type shifts at least as often as host shifts.