Insecticidal genes of Yersinia spp.: taxonomical distribution, contribution to toxicity towards Manduca sexta and Galleria mellonella, and evolution

<p>Abstract</p> <p>Background</p> <p>Toxin complex (Tc) proteins termed TcaABC, TcdAB, and TccABC with insecticidal activity are present in a variety of bacteria including the yersiniae.</p> <p>Results</p> <p>The <it>tc </it>gene sequences of thirteen <it>Yersinia </it>strains were compared, revealing a high degree of gene order conservation, but also remarkable differences with respect to pseudogenes, sequence variability and gene duplications. Outside the <it>tc </it>pathogenicity island (<it>tc</it>-PAI^<it>Ye</it>) of <it>Y. enterocolitica </it>strain W22703, a pseudogene (<it>tccC2'</it>/<it>3'</it>) encoding proteins with homology to TccC and similarity to tyrosine phosphatases at its C-terminus was identified. PCR analysis revealed the presence of the <it>tc</it>-PAI^{<it>Ye </it>}and of <it>tccC2'</it>/<it>3'</it>-homologues in all biotype 2–5 strains tested, and their absence in most representatives of biotypes 1A and 1B. Phylogenetic analysis of 39 TccC sequences indicates the presence of the <it>tc</it>-PAI^{<it>Ye </it>}in an ancestor of <it>Yersinia</it>. Oral uptake experiments with <it>Manduca sexta </it>revealed a higher larvae lethality of <it>Yersinia </it>strains harbouring the <it>tc</it>-PAI^{<it>Ye </it>}in comparison to strains lacking this island. Following subcutaneous infection of <it>Galleria mellonella </it>larvae with five non-human pathogenic <it>Yersinia </it>spp. and four <it>Y. enterocolitica </it>strains, we observed a remarkable variability of their insecticidal activity ranging from 20% (<it>Y. kristensenii</it>) to 90% (<it>Y. enterocolitica </it>strain 2594) dead larvae after five days. Strain W22703 and its <it>tcaA </it>deletion mutant did not exhibit a significantly different toxicity towards <it>G. mellonella</it>. These data confirm a role of TcaA upon oral uptake only, and suggest the presence of further insecticidal determinants in <it>Yersinia </it>strains formerly unknown to kill insects.</p> <p>Conclusion</p> <p>This study investigated the <it>tc </it>gene distribution among yersiniae and the phylogenetic relationship between TccC proteins, thus contributing novel aspects to the current discussion about the evolution of insecticidal toxins in the genus <it>Yersinia</it>. The toxic potential of several <it>Yersinia </it>spp. towards <it>M. sexta </it>and <it>G. mellonella </it>demonstrated here for the first time points to insects as a natural reservoir for yersiniae.</p

Polymer-derived Ni/SiOC materials structured by vat-based photopolymerization with catalytic activity in CO2 methanation

A new concept for the additive manufacturing of nickel-modified polymer-derived ceramics via vat-based photopolymerization is presented. A photoactive polysiloxane resin system modified by nickel nitrate via methacrylic acid complexation was developed and modified to facilitate vat-based photopolymerization. Through pyrolysis of the Ni-modified preceramic polymer at temperatures between 600 and 800 °C, amorphous SiOC components with well-dispersed Ni nanoparticles can be obtained. The modified polymer and the fabricated structures were characterized by photorheology, thermal analysis, scanning and transmission electron microscopy, optical coherence tomography, and powder X-ray diffraction. In addition, the effect of pyrolysis temperature on specific surface area, crystallinity, and shrinkage was investigated. The developed material systems enable additive manufacturing of porous SiOC structures containing crystalline, uniformly distributed, and bimodally sized Ni nanoparticles, exhibiting catalytic activity suitable for CO2 methanation. The developed printable SiOC/Ni materials represent a promising approach for combining metal-modified polymer-derived ceramic systems and additive manufacturing for prospective catalysis applications

Discoidin domain receptor 1 controls linear invadosome formation via a Cdc42-Tuba pathway.

International audienceAccumulation of type I collagen fibrils in tumors is associated with an increased risk of metastasis. Invadosomes are F-actin structures able to degrade the extracellular matrix. We previously found that collagen I fibrils induced the formation of peculiar linear invadosomes in an unexpected integrin-independent manner. Here, we show that Discoidin Domain Receptor 1 (DDR1), a collagen receptor overexpressed in cancer, colocalizes with linear invadosomes in tumor cells and is required for their formation and matrix degradation ability. Unexpectedly, DDR1 kinase activity is not required for invadosome formation or activity, nor is Src tyrosine kinase. We show that the RhoGTPase Cdc42 is activated on collagen in a DDR1-dependent manner. Cdc42 and its specific guanine nucleotide-exchange factor (GEF), Tuba, localize to linear invadosomes, and both are required for linear invadosome formation. Finally, DDR1 depletion blocked cell invasion in a collagen gel. Altogether, our data uncover an important role for DDR1, acting through Tuba and Cdc42, in proteolysis-based cell invasion in a collagen-rich environment