Fragmentation effects on diversity of wasp community and its impact on fig/fig wasp interaction in Ficus racemosa L.

Habitat fragmentation usually results in alteration of species composition or biological communities. However, little is known about the effect of habitat fragmentation on the fig/fig wasp system. In this study, we compared the structure of a fig wasp community and the interaction between figs and fig wasps of Ficus racemosa L. in a primary forest, a locally fragmented forest and a highly fragmented forest. Our results show that, in the highly fragmented forest, the proportion of pollinator wasps is lower and the proportion of non-pollinator wasps is higher compared with the primary forest and locally fragmented forest. The proportion of fruits without pollinator wasps in mature fruits is also greatly increased in the highly fragmented forest. The proportion of galls in all female flowers increases in the highly fragmented forest, whereas the proportion of viable seeds does not change considerably. The disruption of groups of fig trees results in a decrease in pollinator wasps and even might result in the extinction of pollinator wasps in some extreme cases, which may transform the reciprocal interaction between figs and fig wasps into a parasite/host system. Such an effect may lead to the local extinction of this keystone plant resource of rain forests in the process of evolution, and thereby, may change the structure and function of the tropical rain forest.

GPIb is involved in platelet aggregation induced by mucetin, a snake C-type lectin protein from Chinese habu (Trimeresurus mucrosquamatus) venom

Mucetin (Trimeresurus mucrosquamatus venom activator, TMVA) is a potent platelet activator purified from Chinese habu (Trimeresurus mucrosquamatus) venom. It belongs to the snake venom heterodimeric C-type lectin family and exists in several multimeric forms. We now show that binding to platelet glycoprotein (GP) lb is involved in mucetin-induced platelet aggregation. Antibodies against GPIb as well as the GPIb-blocking C-type lectin echicetin inhibited mucetin-induced platelet aggregation. Binding of GPIb was confirmed by affinity chromatography and Western blotting. Antibodies against GPVI inhibited convulxin- but not mucetin-induced aggregation. Signalling by mucetin involved rapid tyrosine phosphorylation of a number of proteins including Syk, Src, LAT and PLCgamma2. Mucetininduced phosphorylation of the Fcgamma chain of platelet was greatly promoted by inhibition of alpha(llb)beta(3) by the peptidomimetic EMD 132338, suggesting that phosphatases downstream Of alpha(llb)beta(3) activation are involved in dephosphorylation of Fcgamma. Unlike other multimeric snake C-type lectins that act via GPIb and only agglutinate platelets, mucetin activates alpha(llb)beta(3). Inhibition Of alpha(llb)beta(3) strongly reduced the aggregation response to mucetin, indicating that activation Of alpha(llb)beta(3) and binding of fibrinogen are involved in mucetin-induced platelet aggregation. Apyrase and aspirin also inhibit platelet aggregation induced by mucetin, suggesting that ADP and thromboxaneA(2) are involved in autocrine feedback. Sequence and structural comparison with closely related members of this protein family point to features that may be responsible for the functional differences.

Prolonged cardiac allograft survival in presensitized rats after a high activity Yunnan-cobra venom factor therapy

Complement-dependent antibody-mediated acute humoral rejection is the major obstacle of clinical transplantation across ABO incompatibility and human leukocyte antigen presensitization. We previously demonstrated that Yunnan-cobra venom factor (Y-CVF) cou