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Sensitive analysis of glycans by liquid chromatography/mass spectrometry is significantly hampered by the lack of chromogenic or fluorescent groups on the glycan structures, as well as, their poor ionization properties. In the present, a heterobifunctional chromogenic reagent 3-amino-1-phenyl-2-pyrazoline-5-ketone (PAP) bearing amino and active methylene groups, which readily reacts with reducing glycans, was used for detection of the pre-column-labeled glycans via high-performance liquid chromatography/electrospray ionization mass spectrometry (HPLC/ESI-MS). The PAP derivatives with active methylene and amino groups were obtained via reductive amination in acidic medium and condensation of an active PAP methylene group with the reducing end of glycans in alkaline medium, respectively, and the PAP derivatives could be further functionalized, e.g., via glycan microarray preparation. The conditions for the two reaction modes were optimized, the HPLC separation method of PAP derivatives was investigated, and the PAP derivatives of some glycans derived from biological samples were obtained and analyzed by ESI-MS and LC-MS. Using this new reagent, reducing glycans can be selectively derivatized by different reaction mechanisms, having great importance for functional glycomics studies.

The whitefly, Bemisia tabaci, has developed a high level of resistance to thiamethoxam, a second generation neonicotinoid insecticide that has been widely used to control this pest. In this study, we assessed the level of cross-resistance, the activities of detoxifying enzymes, and the expression profiles of 23 glutathione S-transferase (GST) genes in a thiamethoxam-resistant ant and -susceptible strain of Bemisia tabaci Q. The thiamethoxam-resistant strain showed a moderate level of cross-resistance to another nicotinoid insecticide imidacloprid, a low level of cross-resistance to acetamiprid and nitenpyram, and no significant cross-resistance to abamectin and bifenthrin. Among detoxifying enzymes, only GSTs had significantly higher activity in the resistant strain than in the susceptible strain. Seven of 23 GST genes were over-expressed in the resistant strain relative to the susceptible strain. Using the technology of RNA interference to knockdown a GST gene (GST14), the results showed that silencing GST14 increased the mortality of whiteflies to thiamethoxam in Bemisia tabaci.

Background Sweetpotato whitefly, Bemisia tabaci MED/Q and MEAM1/B, are two economically important invasive species that cause considerable damages to agriculture crops through direct feeding and indirect vectoring of plant pathogens. Recently, a draft genome of B. tabaci MED/Q has been assembled. In this study, we focus on the genomic comparison between MED/Q and MEAM1/B, with a special interest in MED/Q’s genomic signatures that may contribute to the highly invasive nature of this emerging insect pest. Results The genomes of both species share similarity in syntenic blocks, but have significant divergence in the gene coding sequence. Expansion of cytochrome P450 monooxygenases and UDP glycosyltransferases in MED/Q and MEAM1/B genome is functionally validated for mediating insecticide resistance in MED/Q using in vivo RNAi. The amino acid biosynthesis pathways in MED/Q genome are partitioned among the host and endosymbiont genomes in a manner distinct from other hemipterans. Evidence of horizontal gene transfer to the host genome may explain their obligate relationship. Putative loss-of-function in the immune deficiency-signaling pathway due to the gene loss is a shared ancestral trait among hemipteran insects. Conclusions The expansion of detoxification genes families, such as P450s, may contribute to the development of insecticide resistance traits and a broad host range in MED/Q and MEAM1/B, and facilitate species’ invasions into intensively managed cropping systems. Numerical and compositional changes in multiple gene families (gene loss and gene gain) in the MED/Q genome sets a foundation for future hypothesis testing that will advance our understanding of adaptation, viral transmission, symbiosis, and plant-insect-pathogen tritrophic interactions. Electronic supplementary material The online version of this article (10.1186/s12864-018-4448-9) contains supplementary material, which is available to authorized users.

The sweetpotato whitefly Bemisia tabaci is a highly destructive agricultural and ornamental crop pest. It damages host plants through both phloem feeding and vectoring plant pathogens. Introductions of B. tabaci are difficult to quarantine and eradicate because of its high reproductive rates, broad host plant range, and insecticide resistance. A total of 791 Gb of raw DNA sequence from whole genome shotgun sequencing, and 13 BAC pooling libraries were generated by Illumina sequencing using different combinations of mate-pair and pair-end libraries. Assembly gave a final genome with a scaffold N50 of 437 kb, and a total length of 658 Mb. Annotation of repetitive elements and coding regions resulted in 265.0 Mb TEs (40.3%) and 20 786 protein-coding genes with putative gene family expansions, respectively. Phylogenetic analysis based on orthologs across 14 arthropod taxa suggested that MED/Q is clustered into a hemipteran clade containing A. pisum and is a sister lineage to a clade containing both R. prolixus and N. lugens. Genome completeness, as estimated using the CEGMA and Benchmarking Universal Single-Copy Orthologs pipelines, reached 96% and 79%. These MED/Q genomic resources lay a foundation for future ‘pan-genomic’ comparisons of invasive vs. noninvasive, invasive vs. invasive, and native vs. exotic Bemisia, which, in return, will open up new avenues of investigation into whitefly biology, evolution, and management.

Dear Editor: Ulcerate colitis (UC), the main type of inflammatory bowel disease (IBD), is an unexplained immune-mediated intestinal mucosal inflammation with higher cancer risk. Because of an interaction between inflammation and coagulation in the disease progression, hypercoagulative state is often seen in patients of UC. Endothelial cell damage plays an important role in the activation of coagulation system in patients with UC, while protein C (PC) system, a well-characterized anticoagulant system located on the vascular endothelial cell surface, which consists of protein S (PS), endothelial cell protein C receptor (EPCR), PC, protein C inhibitor, and thrombomodulin (TM), is a mediator of endothelial function. Recent studies indicated that PC system plays an important role in regulating intestinal homeostasis both in human intestinal microvascular endothelial cells and animal models of colitis. Therefore, we speculate that the imbalance of PC system may be one of the pathogenesis of UC patients. Our in vivo study verified that the degree of inflammation was negatively correlated with the PC activity, and mouse colonic macrophages and mucosa microvascular endothelial cells are suggested as the major mediators involved. Until today, it is unclear why PC system changed, and how macrophages and mucosa microvascular endothelial cells interact with each other in UC pathology, so it is important to investigate the changes and mechanisms of PC system, and to find new drug target. Further research in vitro revealed that TNF-α and IL-6 levels were increased in the supernatant of macrophages from dextran sulfate sodium (DSS) mice colonic tissue, and these conditions were only seen in CD14+CD64+ subtype macrophages. In addition, after incubation of TNF-α or IL-6 with colonic mucosal microvascular endothelial cells, the activity of PC system was inhibited, manifested as decreased APC activity, and downregulated expression of EPCR. Furthermore, β-arrestin-pJNK MAPK expressions were upregulated by real-time PCR and Western blot. Taken together into account, due to complex UC mechanism, its pathogenesis is unclear, and there is little research about colonic mucosal microvascular, especially the study for PC system changes in the pathogenesis of UC is rare. In our study, we found that in DSS-induced mouse colitis, colonic CD14+CD64+ macrophages produced more inflammatory cytokines, which result in inhibited PC pathway via mucosal microvascular endothelial cells, and β-arrestin-pJNK MAPK signal pathway may involved. Therefore, enhancing the activity of PC system provides a major theoretical and clinical significance to find new drug target for the treatment of UC.