The specialization and structure of antagonistic and mutualistic networks of beetles on rainforest canopy trees

Different kinds of species interactions can lead to different structures within ecological networks. Antagonistic interactions (such as between herbivores and host plants) often promote increasing host specificity within a compartmentalized network structure, whereas mutualistic networks (such as pollination networks) are associated with higher levels of generalization and form nested network structures. However, we recently showed that the host specificity of flower‐visiting beetles from three different feeding guilds (herbivores, fungivores, and predators) in an Australian rainforest canopy was equal to that of herbivores on leaves, suggesting that antagonistic herbivores on leaves are no more specialized than flower‐visitors. We therefore set out to test whether similarities in the host specificity of these different assemblages reflect similarities in underlying network structures. As shown before at the species level, mutualistic communities on flowers showed levels of specialization at the network scale similar to those of the antagonistic herbivore community on leaves. However, the network structure differed, with flower‐visiting assemblages displaying a significantly more nested structure than folivores, and folivores displaying a significantly more compartmentalized structure than flower‐visitors. These results, which need further testing in other forest systems, demonstrate that both antagonistic and mutualistic interactions can result in equally high levels of host specialization among beetle assemblages in tropical rainforests. If this is a widespread phenomenon, it may alter our current perceptions of food web dynamics, species diversity patterns, and co‐evolution in tropical rainforests. © 2014 The Linnean Society of London, Biological Journal of the Linnean Society, 2015, 114 , 287–295.     

Enhanced Specificity of Minimally Modified Anti-c-myc Oligonucleotides

Abstract

The sequence-specificity of antisense oligonucleotides (ODN) against c-myc mRNA was tested by Northern blot analysis. Rat smooth muscle cells were treated with antisense or control ODN against c-myc modified by the “minimal protection strategy”. At 0.3 μM concentration the ODN show a very specific reduction in c-myc mRNA levels. Use of the “minimal protection strategy” minimizes nonspecific effects as observed for all-phosphorothioate ODN containing four consecutive guanine residues.     

The U11/U12 snRNP 65K protein acts as a molecular bridge, binding the U12 snRNA and U11-59K protein

U11 and U12 interact cooperatively with the 5' splice site and branch site of pre-mRNA as a stable preformed di-snRNP complex, thereby bridging the 5' and 3' ends of the intron within the U12-dependent prespliceosome. To identify proteins contributing to di-snRNP formation and intron bridging, we investigated protein-protein and protein-RNA interactions between components of the U11/U12 snRNP. We demonstrate that the U11/U12-65K protein possesses dual binding activity, interacting directly with U12 snRNA via its C-terminal RRM and the U11-associated 59K protein via its N-terminal half. We provide evidence that, in contrast to the previously published U12 snRNA secondary structure model, the 3' half of U12 forms an extended stem-loop with a highly conserved seven-nucleotide loop and that the latter serves as the 65K binding site. Addition of an oligonucleotide comprising the 65K binding site to an in vitro splicing reaction inhibited U12-dependent, but not U2-dependent, pre-mRNA splicing. Taken together, these data suggest that U11/U12-65K and U11-59K contribute to di-snRNP formation and intron bridging in the minor prespliceosome.     

Ecology of Microbial Saprophytes and Pathogens in Tissue Culture and Field-Grown Plants: Reasons for Contamination Problems In Vitro

This review compares published surveys of microbial populations in plant tissue and cell cultures with the microbial saprophytes and pathogens found on field grown plants and microbial populations in the laboratory environment. From this comparison and the measured reduction in contamination after improvements in working practices in the laboratory, conclusions can be drawn about the importance of the explant and the laboratory as sources of contamination.

Mechanisms of pathogenicity in vitro are described to explain why bacteria, fungi, and yeasts that are not pathogenic to plants in the field become pathogens in plant tissue cultures. Conversely, plant metabolism and its effect on the tissue culture environment are described to explain why prokaryotes, viruses, and viroids that cause disease in the field can stay latent in vitro.

Detection methods for latent contaminants in plant tissue cultures are summarized, and the strategies and methods for prevention or treatment of contamination are discussed.     

Epitope mapping with a recombinant human 68-kDa (U1) ribonucleoprotein antigen reveals heterogeneous autoantibody profiles in human autoimmune sera

Several cDNA fragments encoding parts of the (U1)RNP specific 68-kDa autoantigen were expressed in Escherichia coli and the fusion proteins were used as substrate for localization of the autoreactive epitopes. We have identified a region of approximately 30 amino acids reacting with more than 90% (16 of 17) of all human anti-p68 sera tested, regions which carry only a few and a region with no autoepitopes. Comparative analysis of epitopes recognized on partially degraded fusion proteins indicated that the anti-p68 autoimmune response is polyclonal. It involves generation of antibodies to several epitopes including one in a region with retroviral gag protein homology speculated to play a role in the initiation of the autoimmune response. Each of the 17 sera tested contained a different set of autoantibody specificities. These data are not consistent with random mutation as a sole mechanism of anti-p68 autoantibody induction and argue for an Ag-driven autoimmune response.     

Regurgitation and choke in rats

Male and female F344 rats choked on fecal pellets and regurgitant during the course of two long-term experiments. Each study involved feeding standard and high bulk diets containing 10% wood cellulose or 10% chrysotile asbestos fiber. Choke deaths occurred at all stages of the experiments. A total of 36 of 774 (4.6%) rats in the two studies died of choke. Females died of choke more frequently (26/382 or 6.8%) than did males (10/392 or 2.6%). Rats on high bulk diets were affected more frequently (33/571 or 5.8%), especially those on 10% asbestos diet (26/311 or 8.4%, than rats consuming standard diet (3/190 or 1.6%). The reason for the difference between females and males was not determined. Although choke may be related to some characteristics of high nonnutritive bulk feed fed in pellet form, the higher risk for females even on standard diet (3/95 or 3.2%) than for males (0/95) indicated that more than one factor operated in the etiology of these events.