Category: Nature

A group from Ecological Security and Protection Key Laboratory of Sichuan Province, Mianyang Normal University, Mianyang, China, etc. has reported Burkholderia gladioli strain KJ-34 exhibiting broad-spectrum antifungal activity. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10020716/ It was shown that Burkholderia gladioli strain KJ-34 is a potential biocontrol bacterium isolated from the rhizosphere soil of rice and can fight multiple fungal pathogens (i.e. Ustilaginoidea virens, Alternaria solani, Fusarium oxysporum, Phytophthora capsica, Corynespora cassiicola). Metabolites of this strain exhibiting antifungal activity appeared to be Ac-Yvad-cho, benzoylstaurosporine, TAXOL C, morellin, jubanine B, trichostatin A, thapsigargin, kabiramide B, scopolamine, enniatin B, latrunculin A, rifaximin, rigin, and garcinone C. We have to be careful that some Burkholderia bacteria are pathogenic. For instance, Burkholderia gladioli BSR3 infects rice, causing bacterial blight, and another rice seed−borne bacterium, B. glumae, causes rice grain rot.

A group from Department of Horticulture and Landscape Architecture, Center for Root and Rhizosphere Biology, Colorado State University, Fort Collins, CO USA, etc. has reported that root exudate compounds (galactinol, threonine, and 4-hydroxybutyric acid) induced under low P conditions can stimulate the ability of bacteria to solubilize P. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10006420/ The effect of the three root-exudate derived compounds on the enhancement of P solubilization by bacteria was assessed. In the calcium phosphate (inorganic) media, threonine, 4-hydroxybutyric acid, galactinol, and the combination of compounds significantly increased dissolved P in the medium for Enterobacter cloacae and Pseudomonas pseudoalcaligenes. For Bacillus thuringiensis, only threonine and 4-hydroxybutyric acid increased dissolved P. In phytin (organic phosphate) media, the effect of the compound additions on the enhancement of P solubilization was not significant for any of the bacterial strains.

A group from Catarina Hioe, Icahn School of Medicine at Mount Sinai, New York, USA, etc. has reported that HIV infection is enhanced by interaction with an O-glycan-specific bacterial lectin. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9949255/ I was shown that the O-glycan-specific lectin SLBR-N, which is expressed on oral commensal Streptococcus gordonii strains and recognizes α2–3 sialylated O-glycans on HIV-1, was found to enhance HIV-1 infection in the context of both cell-free virus infection and a CD4-dependent cell-to-cell viral transfer assay. Surprisingly, virus treatment with SLBR-N enhanced virus infection up to 4-fold in a dose-dependent manner, while strangely, the interaction with high-mannose N-glycan-binding bacterial lectins FimH and Msl did not affect infectivity. This strange mechanisms by which SLBR-N and other O-glycan-binding lectins increase HIV-1 infectivity are not fully understood. CMU06 and C.Z331M are full length infectious molecular clones oh HIV-1.

A group from Institute for Advanced Biosciences, Université Grenoble Alpes, Grenoble, France, etc. has reported changes in glycosylation of melanoma tumor cells and its impacts on functionality of dendritic cells. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9986448/ It was found that higher levels of GalNAc and NeuAc residues (revealed by the interaction of WFA and MAA respectively) were observed in melanoma tumor cell lines when compared to healthy melanocytes. The global view of tumor glyco-code profiles upon separation of patients based on better or worse overall survival (median OS) or progression-free survival (median PFS) revealed a pattern of higher expression of Thomsen-Friedenreich antigen (TF-antigen), GlcNAc, Fuc and NeuAc residues (detected by ACA, WGA, RPL-αMan, UEA-I, MAA and SNA) in tumor cell lines from patients with worse clinical outcome. Strikingly, tumor cells with higher levels of f TF-antigen and GlcNAc residuesi (detected by ACA and WGA respectively) were found in patients with worse OS, whereas tumor cells with higher levels of terminal αGalNAc (seen by HPA) were found in patients with a better PFS. It should be highlighted that higher levels of Man/Glc residues on tumor cell lines (detected by ConA) correlate with better PFS, whereas higher levels of NeuAc and Fuc residues (detected by SNA, MAA or UEA-I respectively) predict a worse clinical outcome in melanoma patients Interestingly, there was positive correlations between levels of Man/Glc and GlcNAc residues on tumor cells and proportions of tumor-infiltrating cDC1s. Man/Glc were linked with a good clinical outcome, and GlcNAc was a candidate to boost cDC1s’ functionality. Strikingly, levels of Fuc residues on tumors negatively correlated with infiltration by T cells, and were associated with a poor outcome. In addition, levels of TF-antigen residues on tumor cells from melanoma patients negatively correlated with tumors’ infiltration by CD8+ T cells, and were linked to a shorter survival.

A group from School of Food Science, Henan Institute of Science and Technology, Xinxiang, China, etc. has reported about Paenibacillus polymyxa 7F1 suppressing fusarium head blight of wheat. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9963053/ Fusarium head blight is a severe disease of wheat, corn, barley, and other grain and occurs in all regions worldwide. Several bacteria and fungi have been found to inhibit the growth of Fusarium graminearum. Among the antimicrobial agents identified, Bacillus is the most compelling antibiotic-producing strain, and it has more advantages than other biocontrol microorganisms due to its inherent endospore formation and resistance to extreme conditions. Paenibacillus polymyxa 7F1 was isolated from the rhizosphere of a wheat field, and it was shown that Paenibacillus polymyxa 7F1 showed high antifungal activity against all fungi strains tested in this study. Antifungal activity of Paenibacillus polymyxa 7F1 against seven pathogenic fungi. 1. Fusarium equiseti, 2. Fusarium verticillioide, 3. Fusarium semitectum, 4. Fusarium graminearum, 5. Colletotrichum gloeosporioides, 6. Fusarium proliferatum, 7. Fusarium oxysporum The antibiotics produced by Paenibacillus polymyxa 7F1 included lipopeptides such as iturin A and surfactin.

A group from Nantes Université, CHU Nantes, INSERM, Center for Research in Transplantation and Translational Immunology, France, etc. has reported about structural and functional analysis of BK polyomavirus mutants regarding the infectivity. https://pubmed.ncbi.nlm.nih.gov/36790933/ BK polyomavirus (BKPyV) is a small, non-enveloped, double-stranded DNA virus with an icosahedral capsid formed by 72 capsomers, where a capsomer is an association of a pentamer of the VP1 protein. BKPyV is known to interact with the urothelium and kidney epithelium through the gangliosides GT1b and GD1b, but also via other b-series gangliosides characterized by their α2-8-linked-disialyl moieties attached to the first galactose from the reducing end. BKPyV is an opportunistic virus with a prevalence of 80% in the worldwide population. Usually, infections occur asymptomatically during childhood and then lead to latency or persistence in the kidneys. In this study, four variant forms of the VP1 protein were discussed. These variants had accumulated multiple mutations in the BC loop region of the VP1 protein, which is involved in the direct interaction of the virus with sialic acids. Those variants contained double mutant K69N E82Q (N-Q), E73Q mutant, E73A mutant, and triple mutant A72V E73Q E82Q (VQQ). Cell lines 293TT and RS were used to test the infectivity of all variant pseudoviruses as well as wild-type (WT) subtype Ib2 pseudovirus. Both cell lines were shown to contain monosialylated GM2 and GM3 a-series gangliosides along with neutral globosides from the structural studies using MS. In addition, RS cells specifically expressed b-series disialylated gangliosides GD2 and GD3 carrying α2-8-linked-disialyl epitopes. The followings were found. The N-Q variant lost all ganglioside-binding activity but retained infectivity in 293TT cells through a sialic acid-independent pathway, whereas VQQ showed enhanced ganglioside binding but almost completely lost infectivity in 293TT cells. One plausible explanation of these observations is that the VQQ variant may have lost the ability to interact with the unknown entry receptor employed by the N-Q variant to infect 293TT cells, and that this interaction is required, in addition to sialic acid binding, for infectious entry.