Fine-scale substrate heterogeneity does not affect arthropod communities on green roofs

Green roofs, which are roofs with growing substrate and vegetation, can provide habitat for arthropods in cities. Maintaining a diversity of arthropods in an urban environment can enhance the functions they fill, such as pest control and soil development. Theory suggests that the creation of a heterogeneous environment on green roofs would enhance arthropod diversity. Several studies have examined how arthropod diversity can be enhanced on green roofs, and particularly whether substrate properties affect the arthropod community, but a gap remains in identifying the effect of substrate heterogeneity within a green roof on the arthropod community. In this paper, it is hypothesized that creating heterogeneity in the substrate would directly affect the diversity and abundance of some arthropod taxa, and indirectly increase arthropod diversity through increased plant diversity. These hypotheses were tested using green roof plots in four treatments of substrate heterogeneity: (1) homogeneous dispersion; (2) mineral heterogeneity—with increased tuff concentration in subplots; (3) organic heterogeneity—with decreased compost concentrations in subplots; (4) both mineral and organic heterogeneity. Each of the four treatments was replicated twice on each of three roofs (six replicates per treatment) in a Mediterranean region. There was no effect of substrate heterogeneity on arthropod diversity, abundance, or community composition, but there were differences in arthropod communities among roofs. This suggests that the location of a green roof, which can differ in local climatic conditions, can have a strong effect on the composition of the arthropod community. Thus, arthropod diversity may be promoted by building green roofs in a variety of locations throughout a city, even if the roof construction is similar on all roofs

Sialyl Residues Modulate LPS-Mediated Signaling through the Toll-Like Receptor 4 Complex

We previously reported that neuraminidase (NA) pretreatment of human PBMCs markedly increased their cytokine response to lipopolysaccharide (LPS). To study the mechanisms by which this occurs, we transfected HEK293T cells with plasmids encoding TLR4, CD14, and MD2 (three components of the LPS receptor complex), as well as a NFκB luciferase reporting system. Both TLR4 and MD2 encoded by the plasmids are α-2,6 sialylated. HEK293T cells transfected with TLR4/MD2/CD14 responded robustly to the addition of LPS; however, omission of the MD2 plasmid abrogated this response. Addition of culture supernatants from MD2 (sMD2)-transfected HEK293T cells, but not recombinant, non-glycosylated MD2 reconstituted this response. NA treatment of sMD2 enhanced the LPS response as did NA treatment of the TLR4/CD14-transfected cell supplemented with untreated sMD2, but optimal LPS-initiated responses were observed with NA-treated TLR4/CD14-transfected cells supplemented with NA-treated sMD2. We hypothesized that removal of negatively charged sialyl residues from glycans on the TLR4 complex would hasten the dimerization of TLR4 monomers required for signaling. Co-transfection of HEK293T cells with separate plasmids encoding either YFP- or FLAG-tagged TLR4, followed by treatment with NA and stimulation with LPS, led to an earlier and more robust time-dependent dimerization of TLR4 monomers on co-immunoprecipitation, compared to untreated cells. These findings were confirmed by fluorescence resonance energy transfer (FRET) analysis. Overexpression of human Neu1 increased LPS-initiated TLR4-mediated NFκB activation and a NA inhibitor suppressed its activation. We conclude that (1) sialyl residues on TLR4 modulate LPS responsiveness, perhaps by facilitating clustering of the homodimers, and that (2) sialic acid, and perhaps other glycosyl species, regulate MD2 activity required for LPS-mediated signaling. We speculate that endogenous sialidase activity mobilized during cell activation may play a role in this regulation